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4,900 | Cardioprotective effects of the calcineurin inhibitor FK506 and the PAF receptor antagonist and free radical scavenger, EGb 761, in isolated ischemic/reperfused rat hearts. | Effects of the calcineurin inhibitor FK506, the platelet-activating factor (PAF) antagonist, and free radical scavenger Ginkgo biloba extract, EGb 761, and their combination on reperfusion-induced ventricular fibrillation (VF), ventricular tachycardia (VT), and recovery of cardiac function were studied after 30 min of global ischemia followed by 2 h of reperfusion in isolated rat hearts. In the first series of studies, rats received a daily (oral) dose of 0, 1, 5, 10, 20, or 40 mg/kg/day FK506 for 10 days. FK506 dose-dependently reduced the incidence of reperfusion-induced total (irreversible plus reversible) VF from a value of 92% for untreated animals to 92% (NS), 83% (NS), 67% (NS), 33% (p<0.05), and 25% (p<0.05), for doses of 1-40 mg/kg/day, respectively, with effects on incidence of VT showing the same pattern. FK506, between 20 and 40 mg/kg/day, also resulted in significant recovery of postischemic cardiac function. In the second series of studies, rats were treated with EGb 761 alone or in combination with FK506. Whereas no significant reduction in arrhythmias or improvement in cardiac function resulted from a single intervention of EGb 761 at 25 mg/kg/day, combined treatment of rats with 25 mg/kg/day of EGb 761 and 1 or 5 mg/kg/day of FK506 resulted in a reduction in total and irreversible VF of 92% and 92% to 42% (p<0.05) and 33% (p<0.05), 25% (p<0.05) and 8% (p<0.05), respectively, versus untreated control animals, paralleled by similar effects on the incidence of VT and accompanied by significant improvements in postischemic cardiac function. Our results demonstrate a novel cardioprotective characteristic of FK506 and suggest that combination therapy by using FK506 plus EGb 761 synergistically improves postischemic cardiac function, while reducing the incidence of reperfusion-induced VF and VT, which may expand the clinical utility of FK506 and allow therapy with FK506 at lower doses than are currently useful. |
4,901 | Modulation of ventricular fibrillation in the isolated heart: the role of slow calcium channel activity under continuous perfusion. | The individual activities of sodium versus calcium channels in the initiation and maintenance of ventricular fibrillation (VF) have not been fully elucidated. Therefore we studied in isolated heart under nonischemic conditions (a) VF characteristics in untreated hearts, (b) initiation and maintenance of VF during attenuation and blockade of slow calcium channel activity by verapamil, (c) the effect of these interventions on the characteristics of the induced arrhythmia, and (d) the impact of heart weight on the observed results. Measurements were carried out in both ventricles of isolated feline hearts during ventricular pacing and 8 min of electrically induced tachyarrhythmias. Measurements during ventricular pacing included epicardial conduction time (CON), refractoriness (VRP), and all tissue resistivity (ATR; an indirect measure of changes in intercellular electrical coupling). Measurements during arrhythmia included ATR, peak frequency [PKF; a measure of the prevailing frequency based on Fast Fourier Transform (FFT) analysis], and normalized entropy (ENTROP; a measure of the degree of arrhythmia organization). Measurements during sinus rhythm and arrhythmia were repeated after blocking of calcium channel activity by verapamil at a high concentration (1.8x10(-4) M; n = 8) and at two low concentrations (1.5 and 3.0x10(-7) M; n = 8). In untreated hearts, mainly VF episodes were induced, exhibiting a low degree of organization with no significant change in this parameter throughout the arrhythmia (8 min). In the left ventricle (LV; and to a much smaller extent in the right ventricle; RV), a gradual increase in PKF was observed throughout the arrhythmia, with no significant change in ATR. Verapamil at a high concentration increased CON, but did not affect VRP. These findings were similar in both ventricles. In lower verapamil concentrations, CON was not affected, and VRP was slightly shortened. After treatment with a high verapamil concentration, VF could not be induced in small hearts but was always inducible in large hearts. Transient arrhythmia episodes appeared in 9% of untreated hearts, in 25% with "high" verapamil, and in 25-37% with "low" verapamil. With all verapamil concentrations, the induced arrhythmia was modulated from a predominantly VF to PVT or MVT type, manifested by a decrease in ENTROP. This effect was less pronounced with increasing heart weight. No significant change in PKF and in ATR was obtained with verapamil throughout the arrhythmia. It is suggested that verapamil modulation of arrhythmia organization is associated mainly with a direct blockade of calcium channel activity (perhaps by causing reduction in the safety factor for conduction), rather than with indirect modulation of electrophysiological parameters. |
4,902 | Antidysrhythmics. Emergent. | The emergent treatment of dysrhythmias in the ED continues to evolve. Classic medications such as bretylium and lidocaine are given with newer drugs like amiodarone, ibutilide, and sotalol. Studies in progress will examine their efficacy in the ED. The emergency physician must keep abreast of the growing body of literature. |
4,903 | Role of structural barriers in the mechanism of alternans-induced reentry. | Previously, using an animal model of T-wave alternans in structurally normal myocardium, we demonstrated that repolarization can alternate with opposite phase between neighboring myocytes (ie, discordant alternans), causing spatial dispersions of repolarization that form the substrate for functional block and reentrant ventricular fibrillation (VF). However, the mechanisms responsible for cellular discordant alternans and its electrocardiographic manifestation (ie, T-wave alternans) in patients with structural heart disease are unknown. We hypothesize that electrotonic uncoupling between neighboring regions of cells by a structural barrier (SB) is a mechanism for discordant alternans. Using voltage-sensitive dyes, ventricular action potentials were recorded from 26 Langendorff-perfused guinea pig hearts in the absence (ie, control) and presence of an insulating SB produced by an epicardial laser lesion. Quantitative analysis of magnitude and phase of cellular alternans revealed that in controls, action potential duration alternated in phase at all ventricular sites above a critical heart rate (269+/-17 bpm), ie, concordant alternans. Also, above a faster critical heart rate threshold (335+/-24 bpm), action potential duration alternated with opposite phase between sites, ie, discordant alternans. In contrast, only discordant but not concordant alternans was observed in 80% of hearts with the SB, and discordant alternans always occurred at a significantly slower heart rate (by 68+/-28 bpm) compared with controls. Therefore, the SB had a major effect on the alternans-heart rate relation, which served to facilitate the development of discordant alternans. Whether a SB was present or not, discordant alternans produced considerable increases (by approximately 170%) in the maximum spatial gradient of repolarization, which in turn formed the substrate for unidirectional block and reentry. However, by providing a structural anchor for stable reentry, discordant alternans in the presence of a SB led most often to sustained monomorphic ventricular tachycardia rather than to VF, whereas in the absence of a SB discordant alternans caused VF. SBs facilitate development of discordant alternans between cells with different ionic properties by electrotonically uncoupling neighboring regions of myocardium. This may explain why arrhythmia-prone patients with structural heart disease exhibit T-wave alternans at lower heart rates. These data also suggest a singular mechanism by which T-wave alternans forms a substrate for initiation of both VF and sustained monomorphic ventricular tachycardia. |
4,904 | Ventricular fibrillation: how do we stop the waves from breaking? | Combined experimental and theoretical developments have demonstrated that in addition to preexisting electrophysiological heterogeneities, cardiac electrical restitution properties contribute to breakup of reentrant wavefronts during cardiac fibrillation. Developing therapies that favorably alter electrical restitution properties have promise as a new paradigm for preventing fibrillation. |
4,905 | Cardiac arrhythmias and stroke: increased risk in men with high frequency of atrial ectopic beats. | With the exception of atrial fibrillation (AF), little scientific attention has been given the associations between cardiac arrhythmias and incidence of stroke. We sought to study whether atrial and ventricular arrhythmias assessed during a 24-hour ambulatory ECG registration are associated with incidence of stroke.</AbstractText>The population-based cohort "Men Born in 1914" was examined with 24-hour ambulatory ECG registrations at 68 years of age. Four hundred two men without previous myocardial infarction or stroke were included, and 236 of them had hypertension (>/=160/95 mm Hg or treatment). Fourteen-year rates of stroke (fatal and nonfatal) and all-cause mortality were updated from national and regional registers. Frequent or complex ventricular arrhythmias was defined as Lown class 2 to 5. A high frequency of atrial ectopic beats (AEB) was defined as the fifth quintile (ie, >/=218 AEB per 24 hours).</AbstractText>Fifty-eight men suffered a first stroke during the follow-up. Stroke rates (per 1000 person-years) among men with AF (n=14), with frequent AEB (n=77), and without AF or frequent AEB (n=311) were 34.5, 19.5, and 11.6, respectively. The corresponding values among men with hypertension were 40.7, 32.3, and 14.7, respectively. Frequent AEB (compared with absence of AF and frequent AEB) was significantly associated with stroke among all men (relative risk=1.9; 95% CI, 1.02 to 3.4; P:=0.04) and among hypertensive men (relative risk=2.5; 95% CI, 1.3 to 4.8; P:=0.009) after adjustments for potential confounders. The increased stroke rates among men with Lown class 2 to 5 did not reach statistical significance.</AbstractText>A high frequency of AEB is associated with an increased incidence of stroke.</AbstractText> |
4,906 | Electrophysiological deterioration during long-duration ventricular fibrillation. | Probability of survival from sudden cardiac arrest caused by ventricular fibrillation (VF) decreases rapidly with fibrillation duration. We hypothesized that cellular ischemia/fibrillation-induced electrophysiological deterioration underlies decreased survival.</AbstractText>We determined fibrillation monophasic action potential (MAP) morphology including action potential frequency content, duration, cycle length, developing diastolic intervals, and amplitude as a function of ischemic fibrillation duration in 10 isolated rabbit hearts. We also correlated ECG frequency (used clinically) and MAP amplitude and frequency. Fibrillation cycle length and diastole duration increased, whereas APD(100) shortened significantly with time (P:<0.001). Between 1 and 3 minutes, diastole appeared primarily as the result of APD(100) shortening, with only small changes in cycle length. Between 2 and 5 minutes, diastole increased primarily as the result of increased cycle length. Diastole developed progressively from 5% of VF cycles at 5 seconds to approximately 100% of VF cycles by 120 seconds (P:<0.001). Diastole increased from 1% of cycle length at 5 seconds to 62% at 5 minutes. Its duration increased from 4.7 ms at 5 seconds to 90 ms at 5 minutes (P:<0.001). Both MAP and ECG 1/frequency closely correlated with fibrillation cycle length.</AbstractText>These results show a rapid and progressive electrophysiological deterioration during fibrillation, leading to electrical diastole between fibrillation action potentials. This rapid deterioration may explain the decreased probability of successful resuscitation after prolonged fibrillation. Therefore, a greater understanding of cellular deterioration during fibrillation may lead to improved resuscitation methods, including development of specific defibrillator waveforms for out-of-hospital cardiac arrest.</AbstractText> |
4,907 | Exogenous GSH protection during hypoxia-reoxygenation of the isolated rat heart: impact of hypoxia duration. | The objective of this study was to determine the interaction between duration of myocardial hypoxia and presence of exogenous glutathione (GSH) on functional recovery upon subsequent reoxygenation. Isolated perfused rat hearts were subjected to 20, 30, 40, or 50 min hypoxia (HYP), which resulted in a progressive decline in the amount of contractile recovery (% of normoxic rate-pressure product (RPP) and developed pressure) during 30 min reoxygenation. Supplementation with 5 mM GSH throughout normoxia, hypoxia, and reoxygenation significantly improved contractile recovery during reoxygenation after 20 and 30 min hypoxia (p < 0.05), but had no effect after longer durations of hypoxia when contractile recovery was typically below 40% of RPP and significant areas of no-reflow were observed. ECG analysis revealed that GSH shifted the bell-shaped curve for reperfusion ventricular fibrillation to the right resulting in attenuated fibrillation after 20 and 30 min hypoxia then increased incidences after 40 min when Control hearts were slow to resume electrical activity. ECG conduction velocity was well preserved in all hearts after 20 and 30 min hypoxia, but GSH administration significantly attenuated the decline that occurred with longer durations. GSH supplementation did not attenuate the 35% decline in intracellular thiols during 30 min of hypoxia. When 5 mM GSH was added only during 40 min of hypoxia, RPP recovery after reoxygenation was improved compared to unsupplemented Controls (73% vs. 55% of pre-hypoxia value, p < 0.05). Administration of GSH only during reoxygenation following 40 min of hypoxia did not alter RPP recovery compared to Control hearts. We conclude that cardioprotection by exogenous GSH is dependent on the duration of hypoxia and the functional parameter being evaluated. It is not due to an enhancement of intracellular GSH suggesting that exogenous GSH acts extracellularly to protect sarcolemmal proteins against thiol oxidation during the phase of hypoxia when oxidative stress is a major contributor to cardiac dysfunction. Furthermore, if enough damage accrues during oxygen deprivation, supplementing with GSH during reoxygenation will not impact recovery. |
4,908 | Definitive palliation with cavopulmonary or aortopulmonary shunts for adults with single ventricle physiology. | To compare the relative merits of cavopulmonary or aortopulmonary shunts, or both, as definitive non-Fontan palliations for patients with single ventricle physiology.</AbstractText>Clinical data, ECG, echocardiographic data, surgical records, and available postmortem material were reviewed in all patients with single ventricle physiology identified from the University of Toronto Congenital Cardiac Centre for Adults (UTCCCA) database who had not undergone a Fontan operation. Current status of patients was assessed from clinic reviews and patient contact. Two groups of patients were identified: those with cavopulmonary shunt (group 1, n = 35); and those with aortopulmonary shunt(s) only (group 2, n = 15).</AbstractText>50 adults (21 male/29 female) who underwent the last palliation at a median age of 11 years (range 1 day to 53 years) were identified. During a mean (SD) follow up of 13.0 (6.2) years at the UTCCCA, 19 patients died. Survival is 89.4% and 51.9% at 10 and 20 years, respectively, from the time patients were first seen at UTCCCA, with no differences between the groups. Most recent New York Heart Association (NYHA) classification was I-II in 21 patients, III in 25, and IV in four patients; mean haemoglobin was 190 (28) g/l, and oxygen saturation was 82 (4)%, with no group differences. Arrhythmia developed in 25 patients (atrial flutter/fibrillation in 20 and/or sustained ventricular tachycardia in 11). Atrial flutter/fibrillation was more common in patients in group 2, who also showed a greater decline in ventricular function with time. Age at last palliation, cardiothoracic ratio, and inclusion in group 2 were predictive of atrial flutter/fibrillation, poor ventricular function predictive of ventricular tachycardia, NYHA class > III, and prior ventricular tachycardia predictive of death.</AbstractText>Cavopulmonary or aortopulmonary shunts, or both, provide sustained palliation for selected patients with single ventricle physiology. Survival for both compares favourably with published Fontan series. Compared to aortopulmonary shunts, cavopulmonary shunts convey a beneficial long term effect on ventricular function. Arrhythmia is a major cause of late morbidity in these patients, relating to both ventricular dysfunction and death. Onset of sustained ventricular tachycardia is an ominous sign.</AbstractText> |
4,909 | Ventricular pre-excitation in the general population: a study on the mode of presentation and clinical course. | To describe the mode of presentation and the clinical course of patients with ventricular pre-excitation (Wolff-Parkinson-White (WPW) syndrome), with special emphasis on asymptomatic cases in the general population.</AbstractText>Over an eight year period (1990-97) a prospective population based survey of cases with WPW pattern was conducted in a defined population in north west Greece (340 000 inhabitants). ECGs with WPW pattern were obtained from a widespread pool of ECGs within the health system.</AbstractText>During the study period, 157 cases with WPW pattern were identified (49 female, 108 male). Ages ranged from infants to 84 years, mean (SD) 49.1 (21.0) years in female and 39.6 (20.6) years in male subjects (p < 0.01); 78 (49%) had no history of syndrome related symptoms. Asymptomatic subjects (n = 77; 24 female, 53 male) were older than symptomatic subjects (mean age 46.7 (21.0) v 38.5 (20.6) years, p < 0.03). Documented supraventricular tachycardia was recorded in 27 patients (17%) and atrial fibrillation in 12 (8%) (mean age at first episode 31.2 (18.3) and 51.6 (20.7) years, respectively, p < 0.01). During follow up (mean 55 months) no case of sudden death occurred. Three asymptomatic subjects reported episodes of brief palpitation.</AbstractText>WPW pattern is more common, and diagnosed at a younger age, in men than in women. About half the patients with WPW pattern on ECG are asymptomatic at diagnosis and tend to remain so thereafter. No sudden cardiac death occurred during the study period.</AbstractText> |
4,910 | Cardiac Na(+) channel dysfunction in Brugada syndrome is aggravated by beta(1)-subunit. | Mutations in the gene encoding the human cardiac Na(+) channel alpha-subunit (hH1) are responsible for chromosome 3-linked congenital long-QT syndrome (LQT3) and idiopathic ventricular fibrillation (IVF). An auxiliary beta(1)-subunit, widely expressed in excitable tissues, shifts the voltage dependence of steady-state inactivation toward more negative potentials and restores normal gating kinetics of brain and skeletal muscle Na(+) channels expressed in Xenopus oocytes but has little if any functional effect on the cardiac isoform. Here, we characterize the altered effects of a human beta(1)-subunit (hbeta(1)) on the heterologously expressed hH1 mutation (T1620M) previously associated with IVF.</AbstractText>When expressed alone in Xenopus oocytes, T1620M exhibited no persistent currents, in contrast to the LQT3 mutant channels, but the midpoint of steady-state inactivation (V(1/2)) was significantly shifted toward more positive potentials than for wild-type hH1. Coexpression of hbeta(1) did not significantly alter current decay or recovery from inactivation of wild-type hH1; however, it further shifted the V(1/2) and accelerated the recovery from inactivation of T1620M. Oocyte macropatch analysis revealed that the activation kinetics of T1620M were normal.</AbstractText>It is suggested that coexpression of hbeta(1) exposes a more severe functional defect that results in a greater overlap in the relationship between channel inactivation and activation (window current) in T1620M, which is proposed to be a potential pathophysiological mechanism of IVF in vivo. One possible explanation for our finding is an altered alpha-/beta(1)-subunit association in the mutant.</AbstractText> |
4,911 | Dietary intake of long-chain n-3 polyunsaturated fatty acids and the risk of primary cardiac arrest. | Whether the dietary intake of long-chain n-3 polyunsaturated fatty acids (PUFAs) from seafood reduces the risk of ischemic heart disease remains a source of controversy, in part because studies have yielded inconsistent findings. Results from experimental studies in animals suggest that recent dietary intake of long-chain n-3 PUFAs, compared with saturated and monounsaturated fats, reduces vulnerability to ventricular fibrillation, a life-threatening cardiac arrhythmia that is a major cause of ischemic heart disease mortality. Until recently, whether a similar effect of long-chain n-3 PUFAs from seafood occurred in humans was unknown. We summarize the findings from a population-based case-control study that showed that the dietary intake of long-chain n-3 PUFAs from seafood, measured both directly with a questionnaire and indirectly with a biomarker, is associated with a reduced risk of primary cardiac arrest in humans. The findings also suggest that 1) compared with no seafood intake, modest dietary intake of long-chain n-3 PUFAs from seafood (equivalent to 1 fatty fish meal/wk) is associated with a reduction in the risk of primary cardiac arrest; 2) compared with modest intake, higher intakes of these fatty acids are not associated with a further reduction in such risk; and 3) the reduced risk of primary cardiac arrest may be mediated, at least in part, by the effect of dietary n-3 PUFA intake on cell membrane fatty acid composition. These findings also may help to explain the apparent inconsistencies in earlier studies of long-chain n-3 PUFA intake and ischemic heart disease. |
4,912 | Prevention of fatal cardiac arrhythmias by polyunsaturated fatty acids. | In animal feeding studies, and probably in humans, n-3 polyunsaturated fatty acids (PUFAs) prevent fatal ischemia-induced cardiac arrhythmias. We showed that n-3 PUFAs also prevented such arrhythmias in surgically prepared, conscious, exercising dogs. The mechanism of the antiarrhythmic action of n-3 PUFAs has been studied in spontaneously contracting cultured cardiac myocytes of neonatal rats. Adding arrhythmogenic toxins (eg, ouabain, high Ca(2+), lysophosphatidylcholine, beta-adrenergic agonist, acylcarnitine, and the Ca(2+) ionophore) to the myocyte perfusate caused tachycardia, contracture, and fibrillation of the cultured myocytes. Adding eicosapentaenoic acid (EPA: 5-15 micromol/L) to the superfusate before adding the toxins prevented the expected tachyarrhythmias. If the arrhythmias were first induced, adding the EPA to the superfusate terminated the arrhythmias. This antiarrhythmic action occurred with dietary n-3 and n-6 PUFAs; saturated fatty acids and the monounsaturated oleic acid induced no such action. Arachidonic acid (AA; 20:4n-6) is anomalous because in one-third of the tests it provoked severe arrhythmias, which were found to result from cyclooxygenase metabolites of AA. When cyclooxygenase inhibitors were added with the AA, the antiarrhythmic effect was like those of EPA and DHA. The action of the n-3 and n-6 PUFAs is to stabilize electrically every myocyte in the heart by increasing the electrical stimulus required to elicit an action potential by approximately 50% and prolonging the relative refractory time by approximately 150%. These electrophysiologic effects result from an action of the free PUFAs to modulate sodium and calcium currents in the myocytes. The PUFAs also modulate sodium and calcium channels and have anticonvulsant activity in brain cells. |
4,913 | Response to repeated equal doses of epinephrine during cardiopulmonary resuscitation in dogs. | Advanced cardiac life support (ACLS) guidelines recommend a 3- to 5-minute interval between repeated doses of epinephrine. This recommendation does not take into account the dose of epinephrine used, and only very limited data exist regarding the hemodynamic responses to repeated "high" doses of epinephrine. The objective of this study was to analyze the hemodynamic responses to repeated, equal, high doses of epinephrine administered during cardiopulmonary resuscitation (CPR) in a canine model of ventricular fibrillation (VF).</AbstractText>This study used a secondary analysis of data collected in a prospective, randomized study, primarily designed to assess the effects of acid buffers in a canine model of cardiac arrest. VF was electrically induced. After 10 minutes, CPR was initiated, including ventilation with FIO(2)=1.0, external chest compressions, administration of epinephrine (0.1 mg/kg repeated every 5 minutes) and defibrillation. Animals were randomized to receive either NaHCO(3), Carbicarb, tromethamine (THAM), or NaCl. The hemodynamic variables were sampled from each experiment's paper chart at 1-minute intervals, and the responses to the first 4 doses of epinephrine were compared.</AbstractText>Thirty-six animals (9 in each buffer group) were included in this analysis. Systolic, diastolic, and coronary perfusion pressures increased steeply (by 100%, 130%, and 190%, respectively) only after the first epinephrine dose. These pressures peaked at 2 to 3 minutes and decreased only slightly and insignificantly during the rest of the 5-minute interval, until the next epinephrine dose. No further significant increases in arterial pressures were observed in response to the next 3 doses of epinephrine, administered 5 minutes apart.</AbstractText>The hemodynamic effects of high-dose epinephrine (0.1 mg/kg) during CPR appear to last longer than 5 minutes. Therefore, longer intervals between doses may be justified with high doses of epinephrine.</AbstractText> |
4,914 | Dispersion of ventricular repolarization and ventricular fibrillation in left ventricular hypertrophy: influence of selective potassium channel blockers. | This study tested the hypothesis that combination ion channel blockers of the transient outward current (I(to)) and the rapid component of the delayed rectifying current (I(Kr)) would produce greater prolongation of the ventricular action potential duration (APD) and increased dispersion of the APD in hypertrophied hearts compared with control hearts. Isolated rabbit hearts were studied 48 +/- 5 days postabdominal aortic banding. Left ventricular endocardial and epicardial APDs were significantly greater at baseline in the hypertrophied group than in controls (P <.05). The magnitude of APD prolongation induced by the I(to) blocker 4-aminopyridine (4-AP) and combination 4-AP and the I(Kr) blocker dofetilide was greater in the hypertrophied hearts than in the normal hearts (P <.01). Mean APD dispersion was significantly greater in the hypertrophied group than in the control hearts at baseline (P <.05). 4-AP increased APD dispersion by a similar magnitude in the hypertrophied hearts (10 +/- 10 ms) and the control hearts (8 +/- 8 ms, P = NS), whereas the combination 4-AP and dofetilide increased APD dispersion by a greater magnitude in the hypertrophied hearts (41 +/- 28 ms) than the control hearts (21 +/- 11 ms, P <.05). Ventricular fibrillation occurred spontaneously in four hypertrophied hearts (40%) during combination drug perfusion and in none of the control hearts (P <.05). Thus, combination I(to) and I(Kr) blockers cause greater prolongation APD and increased APD dispersion in left ventricular hypertrophy, and this is associated with the development of ventricular fibrillation. |
4,915 | Quality of life in atrial fibrillation. | In patients with atrial fibrillation (AF), the restoration and maintenance of sinus rhythm is the primary therapeutic goal. Once sinus rhythm is maintained, physiological rate control is restored, and left ventricular ejection fraction, cardiac output, and exercise capacity are increased. This improved cardiovascular performance thereby enhances the patient's ability to perform the functions of normal daily life. The primary intervention for maintaining sinus rhythm after restoration is the use of anti-arrhythmic agents. Although physicians mostly use class 1A anti-arrhythmic drugs, these oral agents only maintain sinus rhythm in a limited number of cases and are accompanied by considerable side effects. Therefore, more effective tools are needed. Effective treatment for AF is based on the above objective criteria, but subjective criteria such as the quality of life are growing in importance. To address these quality-of-life issues, we have initiated a prospective study in which patients are assigned to one of two groups: those with paroxysmal AF who are candidates for permanent implantable atrial defibrillators and those with chronic or paroxysmal AF who are not candidates for atrial defibrillators. Specifically designed questionnaires and various standardized and validated instruments are used to measure quality of life. The questionnaires cover social demographic data, including age, education, occupation level, driving behavior, return to work, and sexual activity. Quality of life is a multidimensional construct, and thus its definition must consider the many factors mentioned above. In the final analysis, therefore, both objective and subjective criteria are necessary to define appropriate treatment of AF. |
4,916 | Design and preliminary data of the Metrix Atrioverter expanded indication trial. | The Metrixtrade mark Atrioverter Expanded Indication Trial evaluates the safety and efficacy of an implantable atrial defibrillator in patients with symptomatic, recurrent and drug refractory atrial fibrillation who also have structural heart disease. In this ongoing multicenter study, all patients are anticoagulated and concomitant antiarrhythmic drug treatment is left to the preference of the physician. Holter monitoring is performed prior to enrollment in the study. Spontaneous episodes of atrial fibrillation (AF) are treated under physician observation and when patients are ambulatory, the device is programmed in a monitoring mode. The atrial defibrillation threshold is measured at implantation and at 3, 6 and 12 months thereafter. The performance of the AF detection and R-wave synchronization algorithm is assessed at implantation, at regular follow-up intervals, and each time the patient visits the hospital for treatment of a spontaneous episode of AF. An echocardiogram is performed prior to implantation, at 3 and 6 month follow-up and for patients with an implanted heart valve, after 20 and 50 atrial defibrillation shocks have been delivered. The study started on October 1997 and will end after the last patient enrolled completes his/her six-month post-implantation follow-up, unless a safety issue arises. As of September 1998, 6 patients (2 patients with tachycardia induced cardiomyopathy, 1 patient with a mitral valve prosthesis, 2 patients with hypertrophic cardiomyopathy and 1 patient with congenital heart disease) have been enrolled in the study. Over 350 shocks have been delivered for atrial defibrillation testing or termination of spontaneous AF episodes. There have been no reported cases of ventricular proarrhythmia or inaccurately synchronized shocks and no complications of device therapy in this population. |
4,917 | Clinical experience with implantable atrial and combined atrioventricular defibrillators. | The high prevalence of atrial fibrillation (AF) and its clinical complications, the poor efficacy of medical therapy for preventing recurrences, and dissatisfaction with alternative modes of therapy stimulated interest in implantable atrial and combined atrioventricular defibrillators. In a multicenter study, the safety and efficacy of a stand alone implantable atrial defibrillator, the Metrix system, were evaluated. The device was implanted in 51 patients with highly symptomatic episodes of AF refractory to pharmacological treatment. During a follow-up of 9 months, 96% of 227 spontaneous AF episodes were successfully converted to sinus rhythm in 41 patients. In 62 episodes (27%), several shocks and/or additional drug treatment were required to maintain stable sinus rhythm because of early recurrences of AF. A total of 3719 shocks were delivered and no induction of ventricular proarrhythmia or inaccurately synchronized shocks occurred. The AF detection algorithm exhibited a 100% specificity for the recognition of sinus rhythm and a 92.3% sensitivity for the detection of AF. The combined atrioventricular defibrillator, Jewel AF 7250, was evaluated in a multicenter, randomized, cross-over trial. The primary study objectives included: overall safety as determined by complications-free survival at 6 months, efficacy of tiered atrial pacing and defibrillation therapies for termination of spontaneous atrial tachycardias (AT) and AF, and relative sensitivity of a new dual-chamber detection algorithm. The device was implanted in 211 patients with either a history of ventricular tachyarrhythmias (VT/VF) alone or with a history of both AT/AF and VT/VF. During a mean follow-up of 4.5 months, it has been shown that the Jewel AF is safe and effective in treating atrial and ventricular tachyarrhythmias. Pace termination of 85% of AT episodes were achieved with painless delivery of antitachycardia pacing; additional 35% of AT episodes were terminated by high frequency burst pacing.</AbstractText>The stand alone implantable atrial defibrillator may be safe and clinically useful in selected patients for the treatment of highly symptomatic, drug resistant recurrences of AF. The combined atrioventricular defibrillator may be particularly indicated in patients presenting with both a history of atrial and ventricular tachyarrhythmias.</AbstractText> |
4,918 | Combining antiarrhythmic drugs and implantable devices therapy: benefits and outcome. | At least 50% of patients who received an ICD have been treated with antiarrhythmic drugs (AAD). The potential indications for combining antiarrhythmic drugs and ICD are generally the following: reduction of the number of episodes of ventricular tachycardia or ventricular fibrillation and therefore of the number of shocks, improving patient's quality of life and extending the battery life of the ICD, prevention of supraventricular arrhythmias and/or control of their rate, lengthening of the tachycardia cycle length to allow ventricular tachycardia conversion by antitachycardia pacing and reduction of the number of episodes of syncope. Although previous papers reported conflicting results about pharmacologic therapy in reducing the frequency of iCD shocks, some recent randomized prospective studies showed the efficacy of pharmacologic therapy in reducing the frequency of ICD shocks. The use of antiarrhythmic drugs can have also adverse effect: an increase in the defibrillation threshold, an increase in the pacing threshold and an increase in the VT cycle length leading to detection failure. We have also to consider that some advantages derived from antiarrhythmic drugs can be reached by the new devices with atrial sensing and pacing and/or the possibility of atrial defibrillation or by using catheter ablation as adjunctive therapy to ICD. For these reasons, the concomitant use of antiarrhythmic drugs and ICD should be evaluated in each patient in relation to specific clinical and electrophysiologic features including: the frequency, the rate and the clinical presentation of the ventricular arrhythmia, the effect of the selected drug on the defibrillation threshold, the defibrillation threshold at the implant, the effect of the selected drug on the ventricular function and the likelihood of proarrhythmic events. |
4,919 | The role of EP-guided therapy in ventricular arrhythmias: beta-blockers, sotalol, and ICD's. | Arrhythmic death can be reduced by antiarrhythmic drugs to a range of 24%. Electrophysiologic study by testing noninducibility of ventricular arrhythmia represents the classic method for evaluating the effectiveness of drug therapy. Several clinical studies have shown thaat sotalol suppresses VT induction and prevents arrhythmias recurrences at long term follow-up in 23% to 67% of patients. The efficacy of sotalol EP guided therapy in preventing VT/VF is not necessarily related to prevention of sudden death. In the ESVEM study the superiority of d,l-sotalol to other antiarrhythmic drugs was confirmed. The response to programmed ventricular stimulation was found to be strongly predictive for arrhythmia free state while the failure of sotalol therapy to suppress VT at the EP study was associated with an high recurrence rate (40%). However, EP study failes to predict freedom from sudden death. The beta-blocking activity of racemic sotalol may account for some of the observed survival benefit.Beta-blockers therapy reduces mortality in patients after myocardial infarction primarily by a reduction of sudden death. A reduction of death, worsening heart failure and life threatening ventricular arrhythmias was shown in a recent study on carvedilol. In the prospective study of Steinbeck the EP guided-therapy did not improve the overall outcome when compared to metoprolol. Suppression of inducible arrhythmias by antiarrhythmic drugs was associated with a better outcome. The effectiveness of defibrillator therapy in reducing overall mortality, has been uncertain since great clinical trials have been concluded. MADIT, AVID and CASH trials confirmed the superiority of ICD therapy over antiarrhythmic drugs therapy: ICD should be considered the first choice therapy in post-cardiac arrest patients. The ongoing BEST Trial will give us further responses about the interaction between EP study and metoprolol effect compared to ICD in patients post myocardial infarction also focusing on tolerability and compliance of the beta-blocking therapy in patients with low ejection fraction. In this study will be useful to optimize therapy in patients at high risk of sudden death. |
4,920 | Amiodarone: maximising survival benefit with empiric or guided therapy. | Review of available data suggests that serial drug testing in patients with a history of sustained ventricular tachyarrhythmias using various antiarrhythmic drugs including amiodarone is able to identify subgroups with favorable and unfavorable outcome (patient groups with suppression vs. no suppression of inducibility of VT/VF). These results more likely reflect patient selection rather than drug effects, thus limiting the role of electrophysiologically guided antiarrhythmic therapy to actively modify outcome. All major and actual antiarrhythmic drug trials including an amiodarone arm, have chosen to deliver this drug empirically in both patients with asymptomatic as well as severely symptomatic life-threatening sustained ventricular tachyarrhythmias instead of a guided approach. The empiric approach is therefore adequate until new valid data comparing the empiric with the guidedor the invasive with the non invasiveapproach tell us otherwise. |
4,921 | Acute coronary syndrome and cardiac arrest: using simulation to assess resident performance and program outcomes. | Simulation training has emerged as an effective method of educating residents in cardiac emergencies. Few studies have used emergency simulation scenarios as an outcome measure to identify training deficiencies within residency programs.</AbstractText>The purpose of this study was to evaluate postgraduate year-1 (PGY-1) residents on their ability to manage an acute coronary syndrome and cardiac arrest scenario before and after internship in order to provide outcome data to improve program performance.</AbstractText>A total of 58 PGY-1 residents from 10 medical specialties were evaluated using a human patient simulator before and after internship. They were given 12 minutes to manage a patient with acute coronary syndrome and ventricular fibrillation due to hyperkalemia. An objective checklist following basic and advanced cardiac life support guidelines was used to assess performance.</AbstractText>A total of 58 interns (age, 25 to 44 years [mean, 29.1]; 38 [65.6%] men; 41 [70.7%] allopathic medical school graduates) participated in both the incoming and outgoing examination. Overall chest pain scores increased from a mean of 60.0% to 76.1% (P < .01). Medical knowledge performance improved from 51.1% to 76.1% (P < .01). Systems-based practice performance improved from 40.9% to 71.0% (P < .01). However, patient care performance declined from 93.4% to 80.2% (P < .01).</AbstractText>A simulated acute coronary syndrome and cardiac arrest scenario can evaluate incoming PGY-1 competency performance and test for interval improvement. This assessment tool can measure resident competency performance and evaluate program effectiveness.</AbstractText> |
4,922 | Heart failure in acute ischemic stroke. | Heart failure (HF) is a complex clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood. Due to the aging of the population it has become a growing public health problem in recent decades. Diagnosis of HF is clinical and there is no diagnostic test, although some basic complementary testing should be performed in all patients. Depending on the ejection fraction (EF), the syndrome is classified as HF with low EF or HF with normal EF (HFNEF). Although prognosis in HF is poor, HFNEF seems to be more benign. HF and ischemic stroke (IS) share vascular risk factors such as age, hypertension, diabetes mellitus, coronary artery disease and atrial fibrillation. Persons with HF have higher incidence of IS, varying from 1.7% to 10.4% per year across various cohort studies. The stroke rate increases with length of follow-up. Reduced EF, independent of severity, is associated with higher risk of stroke. Left ventricular mass and geometry are also related with stroke incidence, with concentric hypertrophy carrying the greatest risk. In HF with low EF, the stroke mechanism may be embolism, cerebral hypoperfusion or both, whereas in HFNEF the mechanism is more typically associated with chronic endothelial damage of the small vessels. Stroke in patients with HF is more severe and is associated with a higher rate of recurrence, dependency, and short term and long term mortality. Cardiac morbidity and mortality is also high in these patients. Acute stroke treatment in HF includes all the current therapeutic options to more carefully control blood pressure. For secondary prevention, optimal control of all vascular risk factors is essential. Antithrombotic therapy is mandatory, although the choice of a platelet inhibitor or anticoagulant drug depends on the cardiac disease. Trials are ongoing to evaluate anticoagulant therapy for prevention of embolism in patients with low EF who are at sinus rhythm. |
4,923 | Effect of catheter ablation on the left ventricular mass index and other echocardiograph parameters in atrial fibrillation patients: comparison with antiarrhythmic drug treatment. | Catheter ablation (CA) is reported to improve left ventricular (LV) function in patients with atrial fibrillation (AF). This study compared the effects of CA and antiarrhythmic drug treatment (AT) on LV remodeling and other echocardiography parameters in AF.</AbstractText>We performed a non-randomized prospective study involving 72 drug-resistant AF patients who were treated with either CA (n = 42) or who declined CA and continued on AT (n = 30). Baseline and follow-up (mean 20.7 ± 7.5 months) echocardiography was performed in all patients. The maintenance of sinus rhythm was determined based on clinical interview, electrocardiography, and 24-h Holter and event recording.</AbstractText>There were no significant differences between the two groups in regard to demographic features, blood pressure, and medication. CA was superior to AT with respect to sinus rhythm maintenance, LV ejection fraction, left atrium (LA) diameter, and LA volume index. In addition, CA resulted in decreases in the LV mass [from 190.5 ± 36.1 to 179.3 ± 32.4 g (p = 0.02)] and the LV mass index [from 104.2 ± 20.5 to 98.2 ± 18.3 g/m(2) (p = 0.03)]. No parameter improved in AT patients. These improved echocardiographic parameters were observed in both groups with maintained sinus rhythm.</AbstractText>Reverse LV remodeling after CA may include a reduction in the LV mass index, which appears to be associated with sinus rhythm maintenance.</AbstractText> |
4,924 | [Ventricular arrhythmias, sudden death and heart failure]. | Despite therapeutic advances, the mortality rate associated with congestive heart failure remains as high as 20% per year. Among patients with severe left ventricular dysfunction, more than 60% of deaths result from ventricular tachycardia or fibrillation, 20% from bradyarrhythmias (including advanced atrio-ventricular block or asystole), and 20% from terminal ventricular pump failure. Ventricular arrhythmias and sudden death result from an interaction between a trigger and a substrate with neurohumoral factors (enhanced activity of the adrenergic and renin-angiotensin systems, electrolyte disturbances, etc.). Left ventricular structural lesions result in complex electrophysiological changes, but those mainly responsible for arrhythmias are conduction slowing, changes in the refractory period, inhomogeneous activation and repolarization, and abnormal automaticity. It is important but difficult to identify those patients most at risk. According to current guidelines, most patients with left ventricular dysfunction (left ventricular ejection fraction below 35%) and symptomatic heart failure may qualify for prophylactic implantation of cardioverter defibrillators (ICD), which have been shown to reduce the risk of sudden cardiac death by 26% in randomized trials. The challenge is now to better identify and select patients who will benefit from implanted devices and resynchronization therapy. We review the literature and report our personal experience of the prognostic value of various Holter--ECG parameters providing information on the autonomic nervous system (sinus variability, baroreflex sensitivity), repolarization dynamics (QT dispersion, T alternance, ventricular late potentials) and the results of programmed ventricular stimulation. Combining electrocardiographic stratification with etiologic and clinical information may help to select the best candidates for defibrillator implantation and resynchronization. These devices, combined with optimal pharmacologic treatment, have been shown to reduce overall mortality and sudden death in recent multicenter randomized controlled trials. |
4,925 | [Sudden cardiac death, a major scientific challenge]. | Sudden death is responsible for 350,000 deaths each year in Europe, or 1000 deaths each day, equivalent to the combined mortality from the most lethal cancers (breast, lung and colorectal). Unfortunately, sudden death is widely considered to be "natural", being due to unknown but critical cardiac disorders leading to sudden arrest of cardiac activity. Awareness of its potential preventability is inadequate. Indeed, 80% of cases of sudden death are associated with extremely rapid heartbeats, an "electric tornado" called ventricular fibrillation, caused by ultrarapid firing of ectopic foci or chaotic wave propagation. This arrhythmia strikes like lightning Although it can be associated with myocardial infarction, most victims have structurally normal or slightly altered hearts. The cells which cause this ultrarapid firing originate from the Purkinje system, which constitutes just a fraction (2%) of total cardiac mass. This is borne out by the fact that the risk of fatal arrhythmic events can be reduced by focal thermoablation. What is most important is to identify subjects at risk of such events. It has been suggested that there exists an unidentified subclinical electrical disharmony, which converts into a tornado of ultimately fatal clinical events at a certain threshold level. High-resolution bioelectrical cardiac mapping, functional imaging, and treatment of electrical field disorders are major scientific challenges given their complexity, intraindividual dynamics and interindividual variability. |
4,926 | A case report of atrial fibrillation potentially induced by hydroxycut: a multicomponent dietary weight loss supplement devoid of sympathomimetic amines. | Multicomponent dietary weight loss supplements comprise the single largest segment of herbal preparations available to the public. As a result of limited de novo regulatory oversight, supplement-related adverse events are underreported secondary to the lack of adequate pharmacodynamic, pharmacokinetic, and clinical data. Here we report the case of an obese 63-year-old caucasian female with a 2-day history of symptomatic paroxysmal atrial fibrillation (AF) with rapid ventricular response following a 2-week course of therapy with hydroxycut, a multicomponent dietary weight loss supplement devoid of sympathomimetic amines. Upon presentation, the patient received 2 doses of intravenous diltiazem, was loaded with intravenous digoxin, and spontaneously converted to normal sinus rhythm 36 hours following her last dose of the product. Epigallocatechin (EGCG), a principal ingredient in the hydroxycut preparation is the suspected causative component. EGCG blocks the atrial-specific KCNA5 potassium channel. Loss of KCNA5 function has been reported in patients with familial lone AF. Thus, causal relationship between hydroxycut and AF in this patient is probable. Given the serious risks associated with AF, patients at risk of developing AF should avoid dietary supplements containing EGCG until more information on the adverse effects of EGCG is known. |
4,927 | Survival of a refractory ventricular fibrillation by cooperative treatments. | In the case of acute myocardial infarction (AMI), prompt and appropriate initial treatment is essential for increasing the rate of survival and early reperfusion is a main determinant factor for long-term prognosis. The survival of a patient with refractory ventricular fibrillation was made possible by cooperative emergency medical care including air medical transport, despite long distance to the hospital. The patient was a 60-year-old man. Under a diagnosis of AMI, a helicopter emergency medical service (HEMS) with medical staff on board was requested. Although ventricular fibrillation (VF) occurred at the scene, quick and appropriate advanced cardiovascular life support (ACLS) was provided by the attending doctor, leading to the return of heartbeat. Since the patient still exhibited serious bradycardia and cardiac failure, he was airlifted while undergoing transcutaneous pacing. Upon arrival at the hospital, the patient underwent emergency percutaneous coronary intervention (PCI). During the PCI, VF recurred and chest compressions and a total of 17 defibrillations were performed. The PCI was continued with percutaneous cardiopulmonary support (PCPS). The patient survived without sequelae. Smoother cooperation between pre-hospital medical procedures and post-hospital emergency care is considered to be essential for the survival of patients such as this case. |
4,928 | Embolized Amplatzer septal occluder device presenting with ventricular fibrillation. | The Amplatzer septal occluder device is used with high success and low-complication rate. Device embolization occurs in around 0.3-0.55% of cases. We report the case of a 44-year-old man with ventricular fibrillation (VF) due to embolization of Amplatzer septal occluder into the right ventricle, 1 h after the successful closure of secundum ASD with a 26-mm Amplatzer septal occluder device. The patient was immediately defibrillated. Bedside echocardiography revealed a free floating device in transit in the right chambers. Percutaneous retrieval attempt was unsuccessful. He was referred to surgery immediately. To our knowledge, VF has not been reported yet. |
4,929 | Lesson of the month (1). Myotonic dystrophy and out-of-hospital arrest. | Myotonic dystrophy (MD) is an autosomal dominant disorder which affects both smooth and skeletal muscles. The incidence is approximately 1 in 8,000 births. It is the most common muscular dystrophy to manifest in adulthood, and the second most common skeletal muscle disorder after Duchenne MD. Cardiac rhythm disturbances are a common cause of death in these patients. This lesson describes a case in which a previously undiagnosed case of MD presented with an episode of ventricular fibrillation. |
4,930 | [The use of hypothermia in intensive therapy]. | The authors discuss the usefulness of therapeutic hypothermia for neuroprotection in patients with hypoxic cerebral damage. Although first reports on this method were published more than 50 years ago, it gained wider popularity at the end of 20th century. This popularity was related to the fact that deep hypothermia (below 30 degrees C) was displaced by mild hypothermia using higher temperatures (32-35 degrees C). The therapeutic benefit of mild hypothermia is based on the decrease of cerebral metabolism (5-7% per one degree Celsius). The ATP consumption by neurons is decreased despite the lack of glucose and oxygen associated with cardiac arrest, and membrane function is longer preserved. Hypothermia also prevents cerebral oedema, both of vascular and cytotoxic origin, and other reactions associated with reperfusion injury. Recently, the American Heart Association and European Resuscitation Council recommended the use of mild hypothermia (32-34 degrees C) in adult patients after ventricular fibrillation. Some clinical data also indicates that induced hypothermia reduces cerebral hypoxic ischemic injury. Randomized clinical trials in newborns with hypoxic ischemic encephalopathy confirm improved neurological outcomes and survival at 18 months of age with therapeutic hypothermia. The use of hypothermia after craniocerebral and spinal trauma, or ischemic brain damage is controversial, and not widely recommended. The authors describe various methods of inducing hypothermia in clinical settings; perhaps the most effective is intravenous infusion of cold fluids together with superficial cooling. Side effects and complications are discussed. They conclude that mild hypothermia can be regarded as a useful therapy in adult patients after VF cardiac arrest, and in neonates with hypoxic cerebral brain damage. |
4,931 | [Hurst index based analysis of ventricular tachycardia and ventricular fibrillation]. | In our laboratory, the normal ECG signal, the ECG signals of ventricular tachycardia (VT) and of ventricular fibrillation (VF) are studied with the use of Hurst index value. The Hurst index values of the normal ECG signal, VT, VF are calculated separately. There exist obvious differences among the Hurst values of the three kinds of signals,but they are all higher than 0.5 which is a value indicating the long-term relevant character. The long-term relevant character of the normal ECG signal is the best, and the character of VT is better than that of VF. Therefore, the Hurst Index can be used as an identification criterion for distinguishing normal ECG, VT and VF. |
4,932 | [Doubts of the cardiologist regarding an electrocardiogram presenting QRS V1-V2 complexes with positive terminal wave and ST segment elevation. Consensus Conference promoted by the Italian Cardiology Society]. | When an ECG shows (or is suspicious for) a Brugada pattern, i.e., the association of a positive terminal deflection and ST segment elevation in the right precordial leads, the cardiologist often faces several problems. Three important questions are raised by this ECG pattern: (1) is this really a Brugada ECG pattern? (2) How can be determined whether this patient is at risk for sudden death? and (3) Should this patient receive an implantable cardioverter-defibrillator (ICD)? The term "Brugada syndrome" should be restricted to patients who have diagnostic ECG changes, as well as a history of symptoms. Asymptomatic subjects, in contrast, should be categorized as having a "Brugada ECG pattern" rather than the syndrome. Diagnostic ECG (type 1) is characterized by a J wave (a terminal positive wave) whose amplitude is > or =2 mm, and a "coved" type ST segment elevation located in the right precordial leads. These signs are usually present in leads V1 and/or V2 (lead V3 is more rarely involved, and is never the only affected one), but occasionally also can be observed in some of the limb leads. Types 2 and 3 ECGs, which are not truly diagnostic of Brugada pattern, are characterized by a "saddle back" ST segment elevation, that is > or =1 mm in type 2 and <1 mm in type 3. In Brugada ECG pattern, the QRS complex characteristically shows a positive terminal deflection that mimics an r' prime wave (the wave occurring in right bundle branch block), in the right precordial leads. Actually, it is a J wave that is very similar to the "Osborn" one observed during hypothermia. The J wave of Brugada ECG pattern is generated by a voltage gradient across the myocardial wall of the right ventricular outflow tract. This abnormal potential can be recorded only by electrodes located very close to the site where that phenomenon is originating. Displacement of the right precordial leads electrodes one or two intercostal spaces above their normal positions may, at times, disclose the diagnostic pattern when conventional leads, recorded at the fourth intercostal space, are non-diagnostic or even normal. High right precordial leads should be recorded whenever standard V1-V3 leads raise the suspicion of Brugada pattern. For example, when a relatively large positive terminal wave, even of low amplitude, is recorded, placing high right precordial leads is an option that should be considered. The ECG may show a marked variation over time, ranging from the typical pattern to a completely normal ECG and back again. In subjects with a non-diagnostic ECG, a pharmacological test with sodium channel blockers may disclose the typical Brugada pattern. In order to establish the diagnosis, several conditions that can mimic Brugada pattern must be excluded. These include right bundle branch block, early repolarization, acute myocardial ischemia, pericarditis, hypercalcemia, hyperkalemia, hypothermia and primary right ventricular diseases, particularly arrhythmogenic right ventricular dysplasia. Some drugs (e.g., some antiarrhythmic drugs, psychotropic agents or antihistamines), hyperthermia and enhanced vagal tone, as it occurs after a full meal, may render Brugada pattern more evident on the ECG. Typical ventricular arrhythmia in Brugada syndrome is a polymorphic ventricular tachycardia, that can evolve into ventricular fibrillation; its mechanism is assumed to be phase 2 reentry. Monomorphic ventricular tachycardia is rarely seen. Atrial fibrillation occurs more frequently in patients with the Brugada ECG pattern than in the general population. A mutation in the SCN5A gene, which encodes the alpha subunit of the cardiac sodium channel, is found in about 20% of the subjects with Brugada pattern; mutations in other genes have less frequently been described. Genetic testing is not very helpful in formulating the diagnosis, but when a mutation is found it could be useful to extend testing to first degree relatives, enabling early detection of abnormal gene carriers. Patients who have experienced an aborted sudden death have a high risk of recurrence and should receive an ICD. A history of syncope, spontaneous type 1 ECG and male sex, not family history of sudden death, are independent risk factors. The role of programmed ventricular stimulation in risk stratification remains the subject of debate. Asymptomatic patients with a Brugada ECG pattern should: (1) receive adequate information on current knowledge concerning this topic, (2) be given the list of forbidden drugs, (3) be informed to promptly treat hyperthermia, (4) be informed that clinical evaluation should be extended to their first degree relatives, 5) undergo regular cardiology follow-up. Also in this group the role of programmed ventricular stimulation in risk stratification is debated. Subjects showing a Brugada pattern after a pharmacological challenge should be followed-up with ECG and 12-lead Holter monitoring, if available, to identify the appearance of spontaneous type 1 ECG. Symptoms should be promptly reported. |
4,933 | Statins Do Not Reduce Atrial Fibrillation After Cardiac Valvular Surgery: A Single Centre Observational Study. | INTRODUCTION: Statins may theoretically reduce postoperative atrial fibrillation (AF) in patients after cardiac valvular surgery due to preservation of endothelial function and anti-ischaemic, anti-inflammatory and anti-remodelling effects. METHODS: Two hundred seventy-two patients who underwent cardiac workup and subsequently cardiac valvular surgery without AF and concomitant coronary artery bypass grafting (CABG) at our hospital were selected. Preoperative drug use and postoperative AF were recorded. AF was defined as any episode of AF longer than 10 s. In addition, results from echocardiography and blood samples were retrieved. RESULTS: BASELINE CHARACTERISTICS WERE AS FOLLOWS: mean age was 65 ± 11 years, 142 (52%) patients were male, 189 (70%) had undergone aortic valve surgery and the mean left ventricular ejection fraction was 57 ± 12%. Statins were used by 79 patients (29%). Statin users, more often, had a prior percutaneous coronary intervention (25% vs 9%, p < 0.001) or CABG (24% vs 4%, p < 0.001), diabetes mellitus (22% vs 5%, p < 0.001) and more often used β-blockers (51% vs 24%, p < 0.001). Patients in the non-statin group more often had surgery on more than one valve (10% vs 3%, p = 0.043) and had a higher cholesterol level (222 ± 48 vs 190 ± 43 mg/dl, p < 0.001). Postoperative AF occurred in 54% (43/79) of the patients with and in 55% (106/193) of the patients without statins (p = 0.941). There was also no difference in the timing of onset of AF or duration of hospital stay. CONCLUSION: In this observational study, statin use was not associated with a reduced incidence of AF in patients after cardiac valvular surgery. |
4,934 | Influence of preoperative serum N-terminal pro-brain type natriuretic peptide on the postoperative outcome and survival rates of coronary artery bypass patients. | The N-terminal fragment of pro-brain type natriuretic peptide (NT-proBNP) is an established biomarker for cardiac failure.</AbstractText>To determine the influence of preoperative serum NT-proBNP on postoperative outcome and mid-term survival in patients undergoing coronary artery bypass grafting (CABG).</AbstractText>In 819 patients undergoing isolated CABG surgery preoperative serum NT-proBNP levels were measured. NT-proBNP was correlated with various postoperative outcome parameters and survival rate after a median follow-up time of 18 (0.5-44) months. Risk factors of mortality were identified using χ², Mann-Whitney test, and Cox regression.</AbstractText>NT-proBNP levels > 430 ng/ml and > 502 ng/ml predicted hospital and overall mortality (p < 0.05), with an incidence of 1.6% and 4%, respectively. Kaplan-Meier analysis revealed decreased survival rates in patients with NT-proBNP > 502 ng/ml (p = 0.001). Age, preoperative serum creatinine, diabetes, chronic obstructive pulmonary disease, low left ventricular ejection fraction and BNP levels >502 ng/ml were isolated as risk factors for overall mortality. Multivariate Cox regression analysis, including the known factors influencing NT-proBNP levels, identified NT-proBNP as an independent risk factor for mortality (OR = 3.079 (CI = 1.149-8.247), p = 0.025). Preoperative NT-proBNP levels >502 ng/ml were associated with increased ventilation time (p = 0.005), longer intensive care unit stay (p=0.001), higher incidence of postoperative hemofiltration (p = 0.001), use of intra-aortic balloon pump (p < 0.001), and postoperative atrial fibrillation (p = 0.031)</AbstractText>Preoperative NT-proBNP levels > 502 ng/ml predict mid-term mortality after isolated CABG and are associated with significantly higher hospital mortality and perioperative complications.</AbstractText> |
4,935 | Use of digoxin for heart failure and atrial fibrillation in elderly patients. | Digoxin has been reported to improve symptoms and reduce hospitalization in patients with heart failure as well as to control rapid ventricular rate in patients with atrial fibrillation. Both of these are high-prevalence diseases in the elderly, and yet studies have indicated that digoxin may not be used appropriately in this population. Clinical trials evaluating digoxin use specifically in the elderly are scarce.</AbstractText>This article discusses the evidence on the therapeutic use of digoxin in the elderly and the changes in the pharmacokinetics of digoxin with aging to provide recommendations about the appropriate use of this drug in this population.</AbstractText>Peer-reviewed clinical trials, review articles, and relevant treatment guidelines limited to those evaluating patients aged >65 years were identified from MEDLINE and the Current Contents database (both from 1966 to May 1, 2010) using the search terms digoxin, pharmacokinetics, heart failure, and atrial fibrillation. Citations from available articles were also reviewed for additional references.</AbstractText>One pharmacokinetic study, 8 clinical trials, and 2 guidelines were identified as relevant to digoxin use specifically in the elderly. In an elderly population (aged ≥65 years; n = 7) compared with a younger population (aged <65 years; n = 6), the elderly had a significant increase in digoxin t(1/2) (mean [SD]: oral dosing, 69.6 [13.1] vs 36.8 [4.5] hours; N dosing, 68.8 [12.3] vs 38.2 [3.5] hours; both, P < 0.05) and a decrease in total-body clearance (0.8 [0.2] vs 1.7 [0.2] mL/min/kg; P < 0.05). The use of digoxin in heart failure has been found to reduce the risk of hospitalization (risk ratio = 0.72; 95% CI, 0.66-0.79; P < 0.001). This beneficial effect of digoxin was found to be not significantly different across age groups in those aged >18 years. In terms of atrial fibrillation, the ability of digoxin to control the ventricular rate is believed to be caused by its vagotonic effect on the atrioventricular node. Therefore, digoxin is recommended for ventricular rate control only in patients with heart failure or sedentary lifestyle (ie, low sympathetic tone), or in those who cannot tolerate other rate-control agents. Because the prevalence of heart failure is high among the elderly (15.2 per 1000 population at age 65-74 years, 31.7 per 1000 population at age 75-84 years, and 65.2 per 1000 population at age ≥85 years), many of whom have a relatively sedentary lifestyle, digoxin may be an appropriate agent for ventricular rate control in the elderly.</AbstractText>The elderly population appears to gain comparable benefits as does a younger population from the use of digoxin for heart failure management in terms of symptom improvement and reduction of hospitalization. In atrial fibrillation, digoxin does not control the ventricular rate as efficaciously during exercise and in high adrenergic states as do R-blockers and calcium channel blockers. The elderly have reduced elimination of digoxin, so if digoxin is to be used, the dosing strategy must be conservative and therapeutic monitoring is needed. Further clinical studies are needed to confirm the pharmacokinetic parameters of digoxin in elderly patients with heart failure and/or atrial fibrillation.</AbstractText>Copyright © 2010 Elsevier HS Journals, Inc. Published by EM Inc USA.. All rights reserved.</CopyrightInformation> |
4,936 | [Accidental hypothermia]. | Accidental hypothermia is an infrequent and under-diagnosed pathology, which causes fatalities every year. Its management requires thermometers to measure core temperature. An esophageal probe may be used in a hospital situation, although in moderate hypothermia victims epitympanic measurement is sufficient. Initial management involves advance life support and body rewarming. Vigorous movements can trigger arrhythmia which does not use to respond to medication or defibrillation until the body reaches 30°C. External, passive rewarming is the method of choice for mild hypothermia and a supplementary method for moderate or severe hypothermia. Active external rewarming is indicated for moderate or severe hypothermia or mild hypothermia that has not responded to passive rewarming. Active internal rewarming is indicated for hemodynamically stable patients suffering moderate or severe hypothermia. Patients with severe hypothermia, cardiac arrest or with a potassium level below 12 mmol/l may require cardiopulmonary bypass treatment. |
4,937 | Metabolic syndrome does not impose greater atrial fibrillation risk in elderly hypertensive patients. | Metabolic syndrome (MS) increases the risk of atrial fibrillation (AF). It is not clear if MS imposes a greater risk of AF in elderly hypertensive patients.</AbstractText>The data were gathered from surveys of 3,775 patients participating in the LIFE survey from November 2005 to July 2006. From this database there were 2,055 patients with MS, and 125 patients were diagnosed with AF.</AbstractText>The prevalence of AF was not different between the MS and non-MS group. With an increasing number of MS components, the prevalence of AF did not change. Univariate analysis revealed that AF patients were older, male-predominant, and had more left ventricular hypertrophy (LVH), heart failure, and coronary artery disease. There were higher levels of uric acid and creatinine in AF patients. AF patients were prescribed antihypertensive drugs, especially diuretics, but less frequently statins. Upon multivariate analysis, age, LVH, heart failure, use of diuretics, and use of statins were the independent predictors of AF. None of the MS components could predict AF attack.</AbstractText>MS does not impose more AF risk in elderly hypertensive patients. Aging, heart failure, LVH, and drugs used may play more important roles.</AbstractText> |
4,938 | Cardiac gene expression profiling - the quest for an atrium-specific biomarker. | Biomarkers are gaining increasing interest to predict risk but also to aid in diagnostics. Tissue-specific biomarkers are of utmost importance to detect diseases of respective organs. As of yet there are no atrium-specific biomarkers for risk stratification of atrial disease, such as atrial fibrillation. Bioinformatics such as mRNA microarrays can help to detect tissue-enriched and possibly tissue-specific expressed genes that can be targets for biomarkers. We describe an approach to identify genes preferably expressed in atrial cardiomyocytes compared with ventricular cardiomyocytes by RNA microarray and confirmed by quantitative real-time polymerase chain reaction. By this approach we identified several atrium-enriched genes but also ventricle-enriched genes. As expected atrial natriuretic peptide (ANP) mRNA showed higher expression in atrial cardiomyocytes while with adrenergic stimulation expression was almost as high in ventricular as in atrial cells. Brain-type natriuretic peptide (BNP), however, was not different between atrial and ventricular cells giving a possible explanation for increased levels of NT-proBNP in atrial fibrillation patients. Interesting identified candidates are serpine1 and ltbp2 as atrium-enriched genes whereas alpha-adrenergic receptor subtype 1b and S100A1 expression was significantly higher in ventricular cells. The identified genes need to be confirmed in human tissue and might ultimately be tested as potential biomarkers for atrial stress. (Neth Heart J 2010;18:610-4.). |
4,939 | Long QT syndrome provoked by induction of general anesthesia -A case report-. | Long QT syndrome (LQTS) is an arrhythmogenic cardiovascular disorder resulting from mutations in cardiac ion channels. LQTS is characterized by prolonged ventricular repolarization and frequently manifests itself as QT interval prolongation on the electrocardiogram (ECG). A variety of commonly prescribed anesthetic drugs possess the adverse property of prolonging cardiac repolarization and may provoke serious ventricular tachyarrhythmia called 'torsades de pointes', ventricular fibrillation, and sudden death. We experienced a case of ventricular tachycardia and ventricular fibrillation after anesthetic induction and it came out into the open that anesthetic induction provoked long QT syndrome. |
4,940 | Right ventricular outflow tract pacing: an alternative, safe, and effective pacing site. | The right ventricular apex (RVA) has traditionally been preferred for the insertion of permanent cardiac pacemaker leads because of vast experience with their use, their ease of implantation, and the stability of passive fixation leads in the RVA trabeculae. However, prolonged RVA pacing is associated with progressive left ventricular dysfunction due to dysynchronous ventricular activation, and often results in substantial functional, hemodynamic, electrical, and structural changes, as previously demonstrated in many studies. Only in recent years has interest in the use of alternate pacing sites developed. The right ventricular outflow tract (RVOT) is now the preferred site of pacing because of potential advantages such as ease of application, better hemodynamics, synchronous activation, fewer myocardial perfusion defects, and a narrower QRS complex compared with RVA pacing. This review article comprehensively discusses this novel technique in terms of its beneficial effects, long-term safety, and performance measures compared with RVA pacing, and as an alternative method for biventricular pacing. |
4,941 | Prevalence of early postoperative arrhythmias in children with delayed open-heart surgery for severe congenital heart disease.<Pagination><StartPage>386</StartPage><EndPage>391</EndPage><MedlinePgn>386-91</MedlinePgn></Pagination><Abstract><AbstractText Label="UNLABELLED">BACKGROUND; Our aim was to determine the incidence, risk factors and outcome of early postoperative arrhythmias in children with delayed treatment of severe congenital heart disease.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">A prospective study was conducted in 141 consecutive children with delayed referral from emerging countries, who underwent open-heart surgery.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">Sinus node dysfunction was noted in 5 cases. Preoperative moderate extrasystoly was common and its incidence significantly increased in the postoperative phase. Overall, 9 patients required specific antiarrhythmic therapy: 6 for sustained atrioventricular reciprocating tachycardia, and 3 respectively for atrial flutter, atrial fibrillation and junctional ectopic tachycardia. Non-sustained atrioventricular and ventricular tachycardia required no therapy in respectively 6 and 1 case. Postoperative complete atrioventricular block was observed in 6 patients and remained permanent in 3. No major complications resulted from those arrhythmias. Preoperative low oxygen saturation, preoperative arrhythmias, as well as long cardiopulmonary bypass time and aortic cross-clamp time, were risk factors for early postoperative arrhythmias.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">Children with delayed surgery for congenital heart disease are at risk of developing early postoperative arrhythmias depending on the complexity of their disease and of its treatment. However, their prevalence (14%) is not higher than in the general population of cardiac children.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Massin</LastName><ForeName>M</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Division of Paediatric Cardiology at Queen Fabiola Children's University Hospital (HUDERF), Brussels, Belgium. [email protected]</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Malekzadeh-Milani</LastName><ForeName>S G</ForeName><Initials>SG</Initials></Author><Author ValidYN="Y"><LastName>Demanetz</LastName><ForeName>H</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Wauthy</LastName><ForeName>P</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Deuvaert</LastName><ForeName>F E</ForeName><Initials>FE</Initials></Author><Author ValidYN="Y"><LastName>Dessy</LastName><ForeName>H</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Verbeet</LastName><ForeName>T</ForeName><Initials>T</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Acta Clin Belg</MedlineTA><NlmUniqueID>0370306</NlmUniqueID><ISSNLinking>1784-3286</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000293" MajorTopicYN="N">Adolescent</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001145" MajorTopicYN="N">Arrhythmias, Cardiac</DescriptorName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName><QualifierName UI="Q000453" MajorTopicYN="Y">epidemiology</QualifierName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002648" MajorTopicYN="N">Child</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002675" MajorTopicYN="N">Child, Preschool</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003906" MajorTopicYN="Y">Developing Countries</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006330" MajorTopicYN="N">Heart Defects, Congenital</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000601" MajorTopicYN="Y">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007223" MajorTopicYN="N">Infant</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015995" MajorTopicYN="N">Prevalence</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011446" MajorTopicYN="N">Prospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012307" MajorTopicYN="N">Risk Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013997" MajorTopicYN="N">Time Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016896" MajorTopicYN="N">Treatment Outcome</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2011</Year><Month>1</Month><Day>29</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2011</Year><Month>1</Month><Day>29</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2011</Year><Month>3</Month><Day>25</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">21268951</ArticleId><ArticleId IdType="doi">10.1179/acb.2010.65.6.003</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">21268293</PMID><DateCompleted><Year>2011</Year><Month>04</Month><Day>04</Day></DateCompleted><DateRevised><Year>2016</Year><Month>10</Month><Day>18</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">1019-5297</ISSN><JournalIssue CitedMedium="Print"><Issue>3-4</Issue><PubDate><Year>2010</Year><Season>Apr-Jun</Season></PubDate></JournalIssue><Title>Likars'ka sprava</Title><ISOAbbreviation>Lik Sprava</ISOAbbreviation></Journal>[Some clinical-pathogenetical characteristics of arrhythmias in patients with myocardial infarction and diabetes mellitus type 2]. | In spite of considerable success in the study of basic pathogenetic mechanisms of arrhythmias development in patients without diabetes mellitus 2 type (DM), the problem of impact of DM on disorders of the cardiac rhythm of patients with acute myocardial infarction is still not resolved. Disorders of the cardiac rhythm have been analyzed in all groups of patients. So, the first group of patients, for certain, had more patients with fibrillation and palpitation of auricles, i.e. hypoglycemia more frequent induced the development of supra ventricular disorders of cardiac rhythm. Fibrillation of auricles, for certain, was more frequently observed in the group of patients with Hba1c less than 7 mkmol/l (P < 0,001). Single VE (ventricular extra systoles) and SVE (supra ventricular extra systoles) prevailed in the 2nd group. Patients with Hba1c more than 9 mkmol/l and hyperglycemia episodes prevailed with ventricular disorders, namely ventricular extra systoles of high degree. Thus, hypoglycemia provokes the development of supra ventricular disorders of the cardiac rhythm in a greater degree, while hyperglycemia results in the development of ventricular disorders of the cardiac rhythm. |
4,942 | The effect of early and intensive statin therapy on ventricular premature beat or nonsustained ventricular tachycardia in patients with acute coronary syndrome. | To evaluate the prognostic value of early and intensive lipid-lowering treatment on ventricular premature beat or nonsustained ventricular tachycardia (NSVT) after acute coronary syndrome (ACS) (ST-elevation myocardial infarction [STEMI], non-STEMI, and unstable angina pectoris).</AbstractText>Provided that early and intensive lipid-lowering treatment can reduce ventricular premature beat or non-sustained ventricular tachycardia after ACS.</AbstractText>A total of 586 patients with ACS were randomly divided into 2 groups: group A (with conventional statin therapy, to receive 10 mg/day atorvastatin, n = 289) and group B (early and intensive statin therapy, 60 mg immediately and 40 mg/day atorvastatin, n = 297). The frequency of ventricular premature beat and NSVT was recorded with Holter monitoring after hospitalization (24 hours and 72 hours).</AbstractText>Seventy-seven (11.8%) patients had NSVT. When compared to patients with no documented NSVT, patients with NSVT were older and more often had myocardial infarction, diabetes mellitus, atrial fibrillation, and an ejection fraction < 40% in their history. Ventricular premature beats decreased significantly in the early and aggressive treatment group (24 hours, P < 0.01; 72 hours, P < 0.001). A significant reduction in NSVT was seen in the early and aggressive (24 hours, P < 0.01; 72 hours, P < 0.001) group. No side effects were observed in either group.</AbstractText>Early and intensive lipid-lowering treatment can obviously decrease ventricular premature beats and NSVT.</AbstractText>Copyright © 2010 Wiley Periodicals, Inc.</CopyrightInformation> |
4,943 | AVE4454B--a novel sodium-hydrogen exchanger isoform-1 inhibitor--compared less effective than cariporide for resuscitation from cardiac arrest. | We compared the efficacy of the novel sodium-hydrogen exchanger (NHE-1) inhibitor AVE4454B with cariporide for resuscitation from ventricular fibrillation (VF) assessing the effects on left ventricular myocardial distensibility during chest compression, myocardial function after the return of spontaneous circulation, and survival. Three groups of 10 rats each were subjected to 10 min of untreated VF and resuscitation attempted by providing chest compression for up to 8 min with the depth of compression adjusted to attain an aortic diastolic pressure between 26 and 28 mmHg (to secure a coronary perfusion pressure above 20 mmHg) followed by electrical shocks. Rats received AVE4454B (1 mg/kg), cariporide (1 mg/kg), or vehicle control immediately before chest compression. We observed that NHE-1 inhibition (NHEI) preserved left ventricular myocardial distensibility during chest compression evidenced by less depth of compression required to attain the target aortic diastolic pressure corresponding to (mean ± standard deviation) 14.1 ± 1.1 mm in the AVE4454B group (P < 0.001 versus control), 15.0 ± 1.4 mm in the cariporide group (P < 0.01 versus control), and 17.0 ± 1.2 mm in controls. When the depth of compression was related to the coronary perfusion pressure generated-an index of left ventricular distensibility-only the cariporide group attained statistical significance. Postresuscitation, both compounds ameliorated myocardial dysfunction evidenced by lesser reductions in mean aortic pressure and the maximal rate of left ventricular pressure increase as well as earlier normalization of left ventricular end-diastolic pressure increases. This effect was associated with improved survival corresponding to 55% in the AVE4454B group (not significant) and 70% in the cariporide group (P < 0.01 versus control by Gehan-Breslow analysis) at 240 min postresuscitation. An inverse correlation was found between plasma cytochrome c and indices of left ventricular function at 240 min postresuscitation suggesting that NHEI exerts beneficial effects in part by attenuating mitochondrial injury. We conclude that cariporide is more effective than AVE4454B for resuscitation from cardiac arrest given its more prominent effect on preserving left ventricular myocardial distensibility and promoting survival. |
4,944 | On the mechanism of antifibrillatory effect of afobazole. | Effect of afobazole on the threshold of electrical fibrillation of the heart was studied on anesthetized rats with intact myocardium. It was shown that the drug considerably increased the threshold of electrical fibrillation of the heart, being not inferior to reference class I antiarrhythmic drugs (lidocaine and procainamide) according to V. Williamse classification. Against the background of preliminary injection of σ-receptor antagonist haloperidol, afobazole exhibited no antifibrillatory activity. These findings and analysis of published reports suggest that antifibrillatory activity of afobazole is determined by its antagonistic influence on σ1-receptors localized in cardiomyocyte cytosol. |
4,945 | The effects of iron deficiency anemia on p wave duration and dispersion. | The association between P wave dispersion and iron deficiency anemia has not been documented in the literature. In this study, we evaluated P wave dispersion in patients with iron deficiency anemia and the possible relationships between P wave dispersion and other echocardiographic parameters.</AbstractText>The iron status of an individual may play an important role in cardiovascular health. Anemia is an independent risk factor for adverse cardiovascular outcomes. P wave dispersion is a simple electrocardiographic marker that has a predictive value for the development of atrial fibrillation. Apart from cardiovascular diseases, several conditions, such as seasonal variation, alcohol intake and caffeine ingestion, have been demonstrated to affect P wave dispersion.</AbstractText>The study included 97 patients who had iron deficiency anemia and 50 healthy subjects. The cases were evaluated with a clinical examination and diagnostic tests that included 12-lead electrocardiography and transthoracic echocardiography.</AbstractText>Compared to the control group, patients with iron deficiency anemia showed significantly longer maximum P wave duration (Pmax) (91.1 ± 18.0 vs. 85.8 ± 6.7 msec, p = 0.054), P wave dispersion (PWD) (48.1 ± 7.7 vs. 40.9 ± 5.6 msec, p < 0.001), mitral inflow deceleration time (DT) (197.5 ± 27.9 vs. 178.8 ± 8.9 msec, p < 0.001) and isovolumetric relaxation time (IVRT) (93.3 ± 9.2 vs. 77.4 ± 8.2 msec, p < 0.001); they also showed increased heart rate (85.7 ± 16.1 vs. 69.0 ± 4.4, p < 0.001) and frequency of diastolic dysfunction (7 (7.2%) vs. 0). Correlation analysis revealed that PWD was significantly correlated with IVRT, DT, heart rate, the presence of anemia and hemoglobin level.</AbstractText>Iron deficiency anemia may be associated with prolonged P wave duration and dispersion and impaired diastolic left ventricular filling.</AbstractText> |
4,946 | Mortality rates and modes of death in heart failure patients with reduced versus preserved systolic function. | There are conflicting reports regarding the characteristics and mortality rates of heart failure patients with preserved (HFPSF) vs. reduced systolic left ventricular function (SHF).</AbstractText>We evaluated the clinical profiles, mortality rates and modes of death in 481 consecutive symptomatic heart failure patients. In 317(66%) patients LVEF was <40% (SHF), and in 164(34%) LVEF≥40% (HFPSF).</AbstractText>Compared to the HFPSF group, SHF patients were predominantly younger males with ischemic etiology and less cardiovascular comorbidities such as obesity, hypertension, diabetes mellitus and atrial fibrillation. Over a mean follow-up period of 2 years, 148(31%) patients died. Overall mortality was similar between the two groups: 53(32%) HFPSF patients and 95(30%) SHF patients died (p=0.6), even after adjusting for baseline variables, including age, gender and comorbidities (hazard ratio 1.09; 95% confidence interval 0.74-1.61; p=0.67). In contrast to the similar mortality rates, the modes of death were different. SHF patients had higher death rates due to pump failure compared to the HFPSF group {32/95(34%) vs. 9/53(17%) patients, p=0.03}. A trend towards higher rate of non-cardiac death was observed in HFPSF group {33/53(62%) patients vs. 45/95(47%) patients, respectively, p=0.08}. The prevalence of arrhythmic death was similar in both groups {17/95(18%) vs. 10/53(19%) patients, p=0.9}.</AbstractText>Although the characteristics of HFPSF and SHF patients are distinctively different, the mortality rates are similar. The mode of death is different among the two groups of patients, as pump failure death is significantly higher in SHF patients, while non-cardiac mortality is more prevalent in HFPSF patients.</AbstractText>Copyright © 2010 European Federation of Internal Medicine. Published by Elsevier B.V. All rights reserved.</CopyrightInformation> |
4,947 | Heart failure patients selection for cardiac resynchronization therapy. | Cardiac resynchronization therapy (CRT) is an established treatment for refractory chronic heart failure (CHF) patients with ventricular dyssynchrony. The patient selection for this therapy remains the basis for response improvement. Various parameters, methods and technology for identification of appropriate patient are under research. The influences of age and gender, disease progress stage such as mild and late stage CHF including right ventricular dysfunction, dyssynchrony and scar identified by imaging techniques like echocardiography, magnetic resonance and nuclear imaging, and atrial fibrillation on CRT benefits were respectively discussed. This review summarizes the current advancement in these areas. |
4,948 | Development of an ovine model of pediatric complete heart block. | Complete heart block is a significant clinical problem that can limit the quality of life in affected children. To understand the pathophysiology of this condition and provide for development of novel therapies, we sought to establish a large animal model of permanent, pacemaker-dependent atrioventricular block (AVB) that mimics the size and growth characteristics of pediatric patients.</AbstractText>We utilized nine immature lambs weighing 10.5 ± 1.4 kg. After implantation of dual-chamber pacemaker devices with fixed leads, AVB was produced by interrupting His-bundle conduction using radio-frequency ablation at the base of the non-coronary cusp of the aortic valve. Ablations (30 to 60 s in duration) were performed under fluoroscopic guidance with electrophysiological monitoring. Interrogation of pacemakers and electrocardiography (ECG) determined the persistence of heart block. Ovine hearts were also examined immunohistochemically for localization of conduction tissue.</AbstractText>AVB was produced in eight animals using an atypical approach from the left side of the heart. One animal died due to ventricular fibrillation during ablation proximal to the tricuspid annulus and one lamb was sacrificed postoperatively due to stroke. Four sheep were kept for long-term follow-up (109.8 ± 32.9 d) and required continuous ventricular pacing attributable to lasting AVB, despite significant increases in body weight and size.</AbstractText>We have created a large animal model of pediatric complete heart block that is stable and technically practicable. We anticipate that this lamb model will allow for advancement of cell-based and other innovative treatments to repair complete heart block in children.</AbstractText>Copyright © 2011 Elsevier Inc. All rights reserved.</CopyrightInformation> |
4,949 | General anaesthesia for insertion of an automated implantable cardioverter defibrillator in a child with Brugada and autism. | A 14-year-old autistic boy presented with acute gastroenteritis and hypotension. The electrocardiogram showed a ventricular fibrillation rhythm - he went into cardiorespiratory arrest and was immediately resuscitated. On investigation, the electrocardiogram showed a partial right bundle branch block with a "coved" pattern of ST elevation in leads v(1)-v(3). A provisional diagnosis of Brugada syndrome was made, for which an automated implantable cardioverter defibrillator (AICD) implantation was advised. Although the automated implantable cardioverter defibrillator implantation is usually performed under sedation, because this was an autistic child, he needed general anaesthesia. We performed the procedure uneventfully under general anaesthesia and he was discharged after a short hospital stay. |
4,950 | The S140G KCNQ1 atrial fibrillation mutation affects 'I(KS)' profile during both atrial and ventricular action potentials. | KCNQ1 is responsible for the pore-forming subunit of channels that mediate the cardiac 'IKs' potassium channel current. The S140G KCNQ1 gain-of-function mutation is responsible for a form of heritable atrial fibrillation. Here the action potential (AP) voltage clamp technique was used to elucidate the effect of S140G KCNQ1 on the profile of recombinant I(Ks) during atrial and ventricular APs applied to KCNQ1+KCNE1 expressing CHO cells, at 37°C. Under conventional voltage clamp the S140G KCNQ1 mutation shifted voltage-dependent activation by ≈-62 mV, with a marked instantaneous current component evident on membrane depolarisation. Under atrial AP clamp, cells expressing wild-type (WT) KCNQ1 exhibited modest outward currents during atrial repolarisation, whilst those expressing S140G KCNQ1 exhibited a marked instantaneous outward current and peak repolarising current >4-fold that for WT KCNQ1. Under ventricular AP clamp, both WT and mutant KCNQ1 conditions showed greater peak repolarising current than when an atrial AP command was used and the S140G mutation resulted in peak repolarising current that was >3-fold that for WT KCNQ1. We conclude that the S140G KCNQ1 mutation would be predicted to augment substantially repolarising current both early and throughout atrial APs and, in principle, also to influence markedly ventricular AP repolarisation. |
4,951 | Omega-3 fatty acids and atorvastatin suppress ventricular fibrillation inducibility in hypertriglyceridemic rat hearts: implication of intracellular coupling protein, connexin-43. | Omega-3 fatty acids (omega-3 FA) and statins exhibit besides lipid-lowering effects the antiarrhythmic ability in clinic, while definite mechanisms are not yet elucidated. Our goal was to examine whether these compounds can modulate inducibility of hypertriglyceridemic (HTG) rat heart to ventricular fibrillation (VF) and myocardial cell-to-cell coupling protein connexin-43 (Cx43). HTG and healthy Wistar rats were orally treated with omega-3 FA(30 mg/100 g/day/2 mth) and atorvastatin (Ato, 0.5 mg/100 g/day/2 mth) and compared to untreated rats. Susceptibility of the heart to electrically-inducible VF and functional parameters were monitored using Langendorff-perfused isolated heart. Ventricular tissues from treated and untreated HTG and Wistar rat hearts were processed for ultrastructure examination as well as for analysis of myocardial Cx43 distribution and expression using antiCx43 MAB, immunofluorescence and immunoblotting. Both, omega-3 FA and atorvastatin reduced elevated blood pressure, triglycerides and heart rate in HTG rats. Compared to Wistar the threshold to induce VF was lower in HTG rat hearts, which exhibited abnormal Cx43 distribution, decreased immunostaining and elevated phosphorylated form of Cx43. In contrast, an enhancement of immunostaining of Cx43, suppression of hyperphosphorylation of Cx43 and improvement of cardiomyocyte and intercellular junction integrity by omega-3 FA and atorvastatin was associated with a significant increase of threshold for VF. Moreover, treatment resulted in up-regulation of myocardial Cx43 and increase of VF threshold in healthy rats that was associated with up-regulation of Cx43. Results indicate that antiarrhythmic effects of omega-3 FA and atorvastatin are linked with modulation of expression and/or phosphorylation of Cx43 and protection of cardiomyocyte and cell-to-cell junction integrity. As both compounds are ligands for PPAR, a possible regulation of Cx43 gene expression and pathways involved in Cx43 phosphorylation should be investigated. |
4,952 | [Multiple organ damage in patients dying from acute decompensated heart failure]. | To detect the occurring and developing patterns of multiple organ damage in patients dying from acute decompensated heart failure (ADHF).</AbstractText>The clinical data of 30 hospitalized patients of ADHF were analyzed. The dying causes included renal, hepatic, respiratory dysfunctions, infection and anemia. All patients received continuous cardiac rhythm monitoring. Their renal, hepatic and respiratory function, infection and anemia were evaluated at admission and during the last 24 hours pre-death respectively. And the results were compared.</AbstractText>There were 19 males and 11 females. The average age was (55±22) years old. Among them, 7 cases were of NYHA class III and 23 cases NYHA class IV at admission. The causes of heart failure included valvular heart disease (n=17), dilated cardiomyopathy (n=6), ischemic cardiomyopathy (n=4), valvular heart disease and previous cardiac infarction (n=2) and restrictive cardiomyopathy (n=1). From admission to death, the average hospitalization duration was (8.8±7.4) days. Eleven cases suffered from sudden cardiac death due to lethal arrhythmias including ventricular tachycardia, ventricular fibrillation and sinus arrest. Another 19 cases had no lethal arrhythmias, but they suffered cardiac shock eventually. Among all 30 cases, there were 15 cases with pulmonary infection, 13 cases with hepatic dysfunction, 6 cases with renal dysfunction, 7 cases with respiratory failure, 7 cases with anemia and 15 cases with multiple organ damage at admission. However, the pre-death values increased to 26 (87%, P<0.01), 19 (63%, P<0.05), 24 (80%, P<0.01), 20 (67%, P<0.01), 9 (30%, P>0.05) and 29 (97%, P<0.01) respectively.</AbstractText>Multiple organ damage evolves and worsens to result in death in ADHF patients.</AbstractText> |
4,953 | Genetic testing of patients with long QT syndrome. | Congenital long QT syndrome is mainly caused by mutations in the KCNQ1, KCNH2 and SCN5A genes. The aim of this study was to investigate the prevalence of mutations in these three genes in patients with long QT syndrome or idiopathic ventricular fibrillation seen at our center. The study included nine patients with long QT syndrome and four with idiopathic ventricular fibrillation. The first-degree relatives of genotype-positive probands were also investigated. Missense mutations were found in seven patients with long QT syndrome and two with idiopathic ventricular fibrillation. Overall, 71.4% of mutations were in KCNH2 and 28.6% were in SCN5A. No mutations in KCNQ1 were found. Only two mutations had been previously observed. Mutations were also found in six of the 19 relatives studied. In conclusion, our initial experience shows that genetic testing had a high sensitivity for diagnosing long QT syndrome. Mutations were found most frequently in the KCNH2 gene. |
4,954 | [A comparative study on the efficacy and safety of intravenous esmolol, amiodarone and diltiazem for controlling rapid ventricular rate of patients with atrial fibrillation during anesthesia period]. | To evaluate the efficacy and safety of intravenous esmolol, amiodarone and diltiazem for controlling rapid ventricular rate in patients with atrial fibrillation (AF) during anesthesia period.</AbstractText>Ninety AF patients with rapid atrial ventricular rate (≥ 120 beats/min) in anesthesia period were randomly divided into 3 groups (n = 30 each: group I patients were treated with intravenous esmolol (0.5 mg/kg loading dose within 1 minute followed with infusion of 0.05 mg×kg(-1)×min(-1)); group II patients were treated with intravenous amiodarone (loading dose: 3 mg/kg for 10 minutes, followed with intravenous infusion of 1 mg/min); group III patients were treated with intravenous diltiazem (0.25 mg/kg for 5 minutes). The heart rate, blood pressure, rhythm were recorded before treatment, at 5, 10, 15, 30, 60 and 90 min after treatment. The reacting time, side effects including hypotension, bradycardia, nausea, vomiting, dizziness, etc, were analyzed.</AbstractText>The mean reacting time was significantly shorter in group I (4.3 ± 2.1) min than in group II (19.2 ± 8.5) min and in group III (8.5 ± 3.4) min (P < 0.05). The mean reacting time in group III was significantly shorter than in group II (P < 0.05). The total effective rate were similar among the groups (86.7%, 90.0% and 83.3% with a mean decrease in heart ventricular rate by 42.4%, 42% and 41.9% of the baseline level in group I, group II and group III, respectively). The incidence of total side effect was significantly lower in group II (10%) than in group I (16.7%) and group III (20%, P < 0.05).</AbstractText>Intravenous esmolol, amiodarone and diltiazem are all equally effective and safe on controlling rapid ventricular rate in patients with atrial fibrillation during the anesthesia period. Esmolol use is associated with the shortest mean reacting time and amiodarone use is associated with the lowest total side effect rate in this patient cohort.</AbstractText> |
4,955 | [Association between diastolic dysfunction evaluated by left ventricular flow propagation velocity and outcome in patients with hypertrophic cardiomyopathy]. | Left ventricular diastolic dysfunction is common in cardiovascular diseases. Hypertrophic cardiomyopathy(HCM) is a typical disease with diastolic dysfunction. We analyzed the association between the left ventricular flow propagation velocity (FPV), quantified by color M-mode Doppler and as an indicator for diastolic dysfunction, and clinical outcome in patients with HCM.</AbstractText>Standard echocardiography including FPV was performed in 43 cases with HCM and 22 control cases without a clear history of heart disease. All eligible cases were followed up to more than 1 year.</AbstractText>Hospitalization rate due to emerging atrial fibrillation/flutter was 21%, due to emerging ventricular tachycardia was 16%, due to heart failure was 26%, and due to other events was 14% in HCM patients. FPV [(31.6 ± 11.5) cm/s vs. (68.3 ± 18.3) cm/s, P < 0.01] and FPV/E (0.49 ± 0.20 vs. 1.18 ± 0.41, P < 0.01) were significantly lower in HCM group than in control group. PV/E was an independent predictor for atrial fibrillation/flutter and heart failure, IVST was independent predictor for VT (χ(2) = 5.181, P = 0.0228), LAD (χ(2) = 6.172, P = 0.0130) and FPV/E (χ(2) = 3.932, P = 0.0474) were independent risk factors for total cardiac events.</AbstractText>The incidence of atrial fibrillation and heart failure were closely related with left ventricular diastolic dysfunction in HCM patients and FPV/E was independent predictor for clinical cardiovascular events.</AbstractText> |
4,956 | [Safety and efficacy of intraoperative defibrillation threshold measured by defibrillation safety margin in 52 patients with implantable cardioverter defibrillator]. | To observe the safety and efficacy of implantable cardioverter defibrillator (ICD) intraoperative defibrillation threshold (DFT) measured by defibrillation safety margin (DSM).</AbstractText>Fifty-two patients underwent ICD implantation were enrolled in this study (25 single chamber ICD, 23 double chamber ICD, 4 three chamber ICD). DFT was measured by DSM method. All patients were followup regularly.</AbstractText>DFT was (13.27 ± 2.95) J and DSM was (17.40 ± 2.89) J in this patient cohort. There were no serious intraoperative complications. Malignant ventricular arrhythmia occurred in 38 patients post ICD, 469 episodes of nonsustained ventricular tachycardia (VT) were spontaneously terminated, 265 episodes were sustained VT and 245 (92.5%) episodes were successfully terminated by 1 antitachycardia pace treatment (ATP), 13 (4.89%) episodes successfully terminated by 2 ATP, and ATP failed to terminate VT in 7 (2.64%) episodes and VTs were terminated by low energy cardioversion. All 141 episodes of ventricular fibrillation (VF) were successfully identified, and 14 episodes spontaneously terminated before discharging, 127 VF episodes (91.34%) were terminated by 1 energy shock, defibrillation energy was (12.84 ± 3.18) J, 11 (12.2%) VF episodes were terminated by 2 energy shocks, defibrillation energy was (16.36 ± 2.34) J.</AbstractText>It is safe and feasible to use defibrillation threshold measured by DSM for patients receiving ICD implantation.</AbstractText> |
4,957 | [Association between electrocardiogram characteristics and long-term outcome in patients with idiopathic ventricular fibrillation]. | To explore the association between clinical and ECG characteristics and prognoses in patients with idiopathic ventricular fibrillation (VF).</AbstractText>We reviewed the data from 21 VF patients [male 47.6%, mean age (38.5 ± 19.0) years] with first event of VF, all patients were resuscitated after cardiac arrest and diagnosed as idiopathic VF. The prevalence of J wave was assessed and patients were divided into J wave positive (J+ group) and negative group (J- group). The end point was death or syncope from arrhythmia, and recorded VF recurrence during the follow-up.</AbstractText>J wave was frequent in subjects with idiopathic VF (71.4%). Among patients in the J+ group (15 cases), notch on the QRS wave was found in 7 subjects (46.7%), these patients were more likely to suffer from the sudden cardiac arrest during sleep at early morning than those with J wave but without notch on the QRS wave. Two patients dead suddenly in the J+ group and 1 dead from embolism in the J- group during follow-up [mean (42.4 ± 39.9) months]. The mean year-onset of VF or syncope was significantly higher in the J+ group than in the J-group [(1.3 ± 0.5) episodes/year vs. (0.4 ± 0.3) episodes/year, P < 0.01]. J wave positive was also associated with an increased risk of VF recurrence (RR 1.9, 95%CI 1.1 to 2.9, P = 0.03).</AbstractText>J wave prevalence is high in patients with history of idiopathic VF, and positive J wave is associated with high risk of recurrence of sudden cardiac death.</AbstractText> |
4,958 | [Clinical analyses of cardiovascular operations in patients with severe dilated left ventricle]. | To explore the perioperative features of surgical treatment in valvular patients with severe dilated left ventricle and investigate the structural changes of left ventricle and its correlation with cardiac functions.</AbstractText>A total of 126 patients with severe dilated left ventricle underwent mitral valve and/or aortic valve operation from January 2003 to December 2008, including mitral valve replacement (MVR) (n = 27), mitral valvuloplasty (MVP) (n = 13), aortic valve replacement (AVR) (n = 51), AVR+MVR (n = 25) and AVR + MVP (n = 10). There were 79 males and 47 females with a mean age of (52 ± 13) years old. The mean pathological course was (18 ± 12) years. The pathological changes were mainly of aortic and/or mitral incompetence. The concomitant procedures included Bentall procedure (n = 6), coronary artery bypass grafting (n = 3), tricuspid valvuloplasty (n = 58) and left atrial folding (n = 62).</AbstractText>The perioperative mortality was 3.17% (4/126). Two died of multiple organ failure (MOF) secondarily to severe low-output syndrome while another 2 died of sudden ventricular fibrillation. Forty-six (36.5%) patients suffered from ventricular arrhythmia during the earlier postoperative period and they required a venous injection of lidocaine and/or amiodarone. Fourteen (11.1%) patients suffered from severe low-output syndrome. Among them, 4 patients were resuscitated with an intra-aortic balloon pump for another 4 - 6 days. And 26 (20.6%) cases were complicated with multiple organ failure. The echocardiographic examinations showed that left ventricular dimensions decreased significantly at Days 7 - 14 postoperatively and progressively at Months 6 - 12 postoperatively. Left ventricular end-diastolic diameter (LVEDD) was (77 ± 6) mm preoperatively and (63 ± 12) mm (Days 7 - 14), (58 ± 10) mm (Months 6 - 12) postoperatively (P < 0.01). The contractile function of left ventricle temporarily decreased during the early postoperative stage and improved gradually afterwards. But it was not restored to normal range even until 6 - 12 m post-operation. Ejection fraction was 49% ± 12% preoperatively and 42% ± 9% (Days 7 - 14), 51% ± 7% (Months 6 - 12) postoperatively (P < 0.01). Left ventricular fraction shortness was 28% ± 7% preoperatively and 25% ± 4% (Days 7 - 14), 29% ± 5% (Months 6 - 12) postoperatively (P < 0.05).</AbstractText>For the patients with severe dilated left ventricle, cardiovascular operation can achieve an excellent outcome through a rigorous perioperative regiment. The prevention and treatment of postoperative ventricular arrhythmia should be emphasized. The dimension of left ventricle decreases progressively during the early postoperative period. There is a postoperative decline of cardiac functions.</AbstractText> |
4,959 | Sudden cause of cardiac death-be aware of me: a case report and short review on brugada syndrome. | Introduction. Brugada syndrome accounts for about 4% of sudden cardiac deaths (SCD). It is characterized by an ST-segment elevation in the right precordial electrocardiogram (EKG) leads. Case Presentation. We describe a 39-year-old healthy Caucasian man who was admitted to the intensive care unit after being cardioverted from ventricular fibrillation (VF) arrest. His past history was significant for an episode of syncope one month prior to this presentation for which he was admitted to an outlying hospital. EKG during that admission showed ST elevations in V1 and V2 leads, a pattern similar to Type 1 Brugada. A diagnosis of Brugada syndrome was missed and the patient had a cardiac arrest a month later. We discuss a short review of Brugada syndrome and emphasize the need to look for it in patients presenting with SCD and malignant arrhythmias. Conclusion. Physicians should always consider Brugada syndrome in the differential diagnosis of ST-segment elevation in anterior precordial leads of EKG and associated VT/VF. Although more than 17 years have passed since the first case was reported, increased awareness of this syndrome is needed to identify patients with EKG changes and treat them accordingly to prevent incidence of (SCD) and its deleterious complications. |
4,960 | Sudden death in a patient with Noonan syndrome. | We report here the case of a 27-year-old woman with Noonan syndrome presenting with ventricular fibrillation. After successful defibrillation, echocardiography revealed hypertrophic cardiomyopathy associated with left ventricular outflow tract obstruction. Normal echocardiographic cardiac structure and function were reported 11 years ago. This case emphasises the importance of regular follow-up in patients with congenital disorders in which cardiac manifestations might develop in early adulthood or later. |
4,961 | [The microvolt T-wave alternans test]. | Several clinical parameters and noninvasive tests have been developed to identify patients under the risk for sudden cardiac death (SCD). The microvolt T-wave alternans (MTWA) test is a noninvasive diagnostic method based on the measurement of subtle (microvolt) beat-to-beat alternation of the T-wave on the surface electrocardiogram and used for risk stratification of patients under the risk for SCD. Studies in the last decade have shown that the MTWA test is an effective method to distinguish patients with a high risk for arrhythmogenic mortality among patients suffering ischemic or nonischemic cardiomyopathies or with a history of myocardial infarction, with a high negative predictive value. This review revisits the MTWA test in the light of the most recent clinical studies. |
4,962 | Ruptured sinus of Valsalva aneurysm associated with aortic regurgitation and severe myocardial ischemia. | Sinus of Valsalva aneurysm (SVA) is a rare cardiac anomaly either presenting as a congenital heart disease or occurring secondary to cardiac surgical interventions. A 19-year-old male patient presented with chest pain and shortness of breath. On auscultation, a grade 4/6 early diastolic murmur was heard over the left lower sternal border and Erb's area with a thrill. Crepitating rales were heard over bilateral basal lung fields. The electrocardiogram showed right bundle branch block and ST depression. Troponin and CK-MB levels were increased. Shortly after admission, he developed ventricular fibrillation and was defibrillated three times. After restoration of hemodynamic stabilization, transthoracic echocardiography was performed, which showed grade 4 aortic regurgitation, patent foramen ovale, and an aneurysm of the sinus of Valsalva arising from the right coronary sinus, with rupture into the right ventricle. The patient underwent surgery under cardiopulmonary bypass, for repair of the ruptured SVA and patent foramen ovale and aortic valve replacement. He was discharged on the fifth postoperative day following an uneventful operation and postoperative course. |
4,963 | [Levosimendan and dobutamine have a similar profile for potential risk for cardiac arrhythmias during 24-hour infusion in patients with acute decompensated heart failure]. | Unlike traditional inotropic agents, levosimendan is thought to have a lower potential to induce arrhythmias because it does not increase intracellular calcium levels and myocardial oxygen consumption. We compared the potential effect of levosimendan and dobutamine to induce cardiac arrhythmias in patients with decompensated heart failure.</AbstractText>Fifty patients with acute decompensated heart failure (NYHA class III-IV, ejection fraction <35%) who were in need of inotropic support were randomized to dobutamine (n=25; mean age 69±10 years) or levosimendan (n=25; mean age 67.5±11.5 years) and underwent 24-hour Holter monitoring before and during inotropic infusion. Holter recordings were analyzed with respect to heart rate (HR), ventricular premature contraction (VPC), couplets of VPC, supraventricular premature contraction (SVPC), paroxysmal atrial fibrillation (PAF), and nonsustained ventricular tachycardia (NSVT).</AbstractText>Before infusions, the two groups were similar with respect to HR, VPC, couplets of VPC, SVPC, and PAF episodes, but the number of NSVT episodes was significantly higher in the levosimendan group. Heart rate and the number of VPCs increased significantly during infusions of levosimendan (p=0.036 and p<0.001, respectively) and dobutamine (for both p<0.001). Increase in couplets of VPC was significant only with dobutamine (p=0.012). The episodes of NSVT and PAF increased with levosimendan, without reaching significance. Levosimendan and dobutamine groups were similar in terms of percentage changes in arrhythmias (55±224% vs. 11±16% for VPC; 2±2.7% vs. 12±9% for couplets of VPC; 3.4±5.8% vs. 16±39% for SVPC, 0.4±2.8% vs. -2±0% for NSVT) and percentage change in total arrhythmias (41±190% vs. 18±35.4%), and the mean HR, VPC, couplets of VPC, SVPC, and episodes of NSVT and PAF (p>0.05).</AbstractText>Our findings suggest that levosimendan and dobutamine have a similar profile for potential risk for cardiac arrhythmias.</AbstractText> |
4,964 | Alternative stable scroll waves and conversion of autowave turbulence. | Rotating spiral and scroll waves (vortices) are investigated in the FitzHugh-Nagumo model of excitable media. The focus is on a parameter region in which there exists bistability between alternative stable vortices with distinct periods. Response functions are used to predict the filament tension of the alternative scrolls and it is shown that the slow-period scroll has negative filament tension, while the filament tension of the fast-period scroll changes sign within a hysteresis loop. The predictions are confirmed by direct simulations. Further investigations show that the slow-period scrolls display features similar to delayed after-depolarization and tend to develop into turbulence similar to ventricular fibrillation (VF). Scrolls with positive filament tension collapse or stabilize, similar to monomorphic ventricular tachycardia (VT). Perturbations, such as boundary interaction or shock stimulus, can convert the vortex with negative filament tension into the vortex with positive filament tension. This may correspond to transition from VF to VT unrelated to pinning. |
4,965 | First direct comparison of the late sodium current blocker ranolazine to established antiarrhythmic agents in an ischemia/reperfusion model. | There are few safe antiarrhythmics for ischemic heart disease. Whereas ranolazine is a promising late INa blocker with antiarrhythmic effects, and devoid of pro-arrhythmic properties, there are no direct comparisons between ranolazine and other antiarrhythmic agents in an ischemia/reperfusion setting. HYPOTHESIS AND METHODS: To determine whether ranolazine was as effective as sotalol and lidocaine to reduce ischemia/reperfusion-induced arrhythmias, anesthetized rats were subjected to 5 minutes of proximal left coronary artery occlusion plus 5 minutes of reperfusion, which causes severe ventricular arrhythmias. At 21 minutes prior to coronary occlusion, rats (n = 20 per group) were randomized to receive either sotalol (intravenous [IV] bolus 5 mg/kg, 10 mg/kg per hour infusion), lidocaine (IV bolus 2.5 mg/kg, 2.5 mg/kg/hr infusion), ranolazine (IV bolus 3.3 mg/kg, 3.2 mg/kg per hour infusion), or saline (control).</AbstractText>The incidence of ventricular arrhythmias in the sotalol (S), lidocaine (L), ranolazine (R), and control (C) groups was 7/20, 10/20, 9/20, and 16/20, respectively (P = .01 S vs C, P = .10 L vs C, and P = .048 R vs C). Duration of ventricular tachycardia (VT) episodes was reduced from 15.5 seconds (mean) in C to 1.3 seconds in S, 1.4 sec in L and 0.09 sec in R (P < .05 for S vs C and R vs C by Wilcoxon test). The number of rats with any (≥ 10 seconds) sustained VT was 3 in C versus 1, 0, and 0 in the S, L, and R groups, respectively. Two rats in C had reversible ventricular fibrillation versus 0 in the S, L, and R groups. The number of ventricular premature beats (VPBs) per rat was 10.9 in C, 2.3 in S, 4.9 in L, and 5.7 in R (P < .05 for S, L, or R vs C). P = NS for R versus L or S for all analyses.</AbstractText>In this first head-to-head comparison of R vs other antiarrhythmic agents at therapeutic doses in an ischemia/reperfusion model, ranolazine (which lacks pro-arrhythmic effects) was as effective as either sotalol or lidocaine to reduce reperfusion-induced ventricular arrhythmias.</AbstractText> |
4,966 | A new triterpene and an antiarrhythmic liriodendrin from Pittosporum brevicalyx. | A new triterpene, 21-O-senecioyl-R(1)-barrigenol (1) and 13 known compounds were isolated from the ethanol extracts of the leaves and bark of Pittosporum brevicalyx (Oliv.) Gagnep. Their structures were elucidated based on spectral data. The antiarrhythmic action of one furofuran lignan, liriodendrin (2), was tested on a model of CaCl(2)-induced arrhythmia and compared with the effect of verapamil. The prophylactic administration of liriodendrin (2) was effective in prolonging latency of arrhythmia and reducing the occurrence of ventricular fibrillation from 75% to 25%. The overall mortality rate was significantly reduced by the prophylactic administration of liriodendrin from 87.5% to 25%. The antiarrhythmic effect of liriodendrin (5.0 mg/kg) was similar to that of verapamil (1.05 mg/kg). Thus, liriodendrin may be a potent suppressor of CaCl(2)-induced arrhythmias. |
4,967 | Quinidine depresses the transmural electrical heterogeneity of transient outward potassium current of the right ventricular outflow tract free wall. | BACKGROUND#ENTITYSTARTX02014;: Electrical heterogeneity of the right ventricular outflow tract (RVOT) is regarded as one of the main electrophysiological substrates for Brugada syndrome. Recently quinidine has shown efficacy in patients with Brugada syndrome due to its ability to inhibit potassium current especially 4-aminopyridine-sensitive, non-Ca(2+) -dependent transient outward potassium current (Ito). However, much less is known on how extent quinidine in clinical therapeutic concentration range can inhibit this kind of electrical heterogeneity of RVOT Ito. METHODS AND RESULTS#ENTITYSTARTX02014;: Single RVOT free wall epicardial (Epi) cell, midmyocardial (M) cell and endocarcial (Endo) cells were used for whole-cell voltage clamping and Ito was recorded at 37°C, 0.2 Hz depolarization pulse. Evident Ito tranmural heterogeneity existed in RVOT free wall. Under the condition of baseline, of 10 μM quinidine perfusion 5 minutes (mins), and of 10 μM quinidine perfusion 7-10 mins, from 0 mV to 70 mV the whole transmural average Ito values of RVOT free wall were 10.2 pA/pF, 5.5 pA/pF and 3.5 pA/pF, respectively (between groups, P< 0.01). The inhibitory percentage of 10 μM quinidine at 5 mins and 7-10 mins steady-state level on the the whole Ito transmural heterogeneity of RVOT free wall were 46.3%±6% and 66.5%±11%, respectively. CONCLUSIONS#ENTITYSTARTX02014;: There exists a robust Ito transmural electrical heterogeneity in RVOT free wall and quinidine in clinical therapeutic concentration can depress this kind of heterogeneity effectively. |
4,968 | Anesthetic management of a patient with deteriorated cardiac function following cardiopulmonary resuscitation. | A 73-year-old woman suffering from an abdominal aortic aneurysm (AAA), unstable angina, and low cardiac function (32% of ejection fraction) was scheduled for abdominal aortic replacement and coronary artery bypass grafting. However, before the scheduled operation the patient fell into cardiopulmonary arrest with ventricular fibrillation due to rupture of the AAA. Immediate cardiopulmonary resuscitation (CPR) using epinephrine and electrical defibrillation restored the spontaneous circulation. Following CPR, a continuous high-dose dopamine infusion (15 µg/kg/min) was initiated and emergent abdominal aortic replacement was performed. On arrival at the operating room, the patient showed serious hypotension, atrial fibrillation with multifocal ventricular premature contractions, and metabolic acidosis. Transesophageal echocardiography (TEE) suggested that the circulatory collapse might have resulted from diastolic dysfunction and deteriorated compliance of the left ventricular (LV) wall, possibly due to myocardial stunning induced by myocardial ischemia, and tachycardia induced by hypovolemia, both of which are influenced by high doses of catecholamine. We accordingly transfused adequate amounts of blood products and gradually decreased the infusion rate of dopamine to 4 µg/kg/min, while carefully monitoring blood pressure, central venous pressure, and TEE. By the end of surgery hemodynamic parameters had recovered to near normal levels. In post-resuscitated and hypovolemic patients, caution should be taken when administering high levels of exogenous catecholamines, which can induce myocardial stunning and circulatory collapse. |
4,969 | Na+ channel distribution and electrophysiological heterogeneities in guinea pig ventricular wall. | We sought to explore the distribution pattern of Na(+) channels across ventricular wall, and to determine its functional correlates, in the guinea pig heart. Voltage-dependent Na(+) channel (Na(v)) protein expression levels were measured in transmural samples of ventricular tissue by Western blotting. Isolated, perfused heart preparations were used to record monophasic action potentials and volume-conducted ECG, and to measure effective refractory periods (ERPs) and pacing thresholds, in order to assess excitability, electrical restitution kinetics, and susceptibility to stimulation-evoked tachyarrhythmias at epicardial and endocardial stimulation sites. In both ventricular chambers, Na(v) protein expression was higher at endocardium than epicardium, with midmyocardial layers showing intermediate expression levels. Endocardial stimulation sites showed higher excitability, as evidenced by lower pacing thresholds during regular stimulation and downward displacement of the strength-interval curve reconstructed after extrasystolic stimulation compared with epicardium. ERP restitution assessed over a wide range of pacing rates showed greater maximal slope and faster kinetics at endocardial than epicardial stimulation sites. Flecainide, a Na(+) channel blocker, reduced the maximal ERP restitution slope, slowed restitution kinetics, and eliminated epicardial-to-endocardial difference in dynamics of electrical restitution. Greater excitability and steeper electrical restitution have been associated with greater arrhythmic susceptibility of endocardium than epicardium, as assessed by measuring ventricular fibrillation threshold, inducibility of tachyarrhythmias by rapid cardiac pacing, and the magnitude of stimulation-evoked repolarization alternans. In conclusion, higher Na(+) channel expression levels may contribute to greater excitability, steeper electrical restitution slopes and faster restitution kinetics, and greater susceptibility to stimulation-evoked tachyarrhythmias at endocardium than epicardium in the guinea pig heart. |
4,970 | Real-time electrogram analysis for monitoring coronary blood flow during human ventricular fibrillation: implications for CPR. | Effective chest compressions during prolonged ventricular fibrillation (VF) have been shown to increase the chances of successful defibrillation to a rhythm associated with a sustainable cardiac output. There is currently no effective method of recording the degree of antegrade coronary artery flow during chest compression in VF.</AbstractText>This study sought to quantify the relationship between the antegrade coronary flow and the characteristics of human VF using near real-time wavelet-based electrocardiographic markers.</AbstractText>VF experiments were conducted in 8 isolated human hearts. The Langendorff perfusion enabled different flow rates (perfusion) during VF, which allowed for the simulation of chest compression with different efficacies. After the initiation of VF, the hearts were maintained in ischemia (no flow) for 3 minutes, followed by a 2-minute reperfusion and defibrillation. The experiments were repeated at flows of 0%, 30%, and 100% of baseline perfusion, and volume-conducted surface electrograms were recorded and analyzed using continuous wavelet transform in 5-second frames.</AbstractText>Near real-time wavelet features were derived that demonstrated significant differences in the multicomponent nature of VF signals and predicted perfusion rate characteristics for different flow rates (i.e., 0%, 30%, and 100%; P < .0006). A pattern classifier was trained using the feature values from 5 hearts, and the flow rates for 3 additional hearts were predicted with an accuracy of 90%.</AbstractText>VF electrogram characteristics as measured by wavelet analysis relate to antegrade coronary flow rate during VF. These findings suggest that chest compression efficacy of physiological importance could be monitored using near real-time wavelet analysis.</AbstractText>Copyright © 2011 Heart Rhythm Society. Published by Elsevier Inc. All rights reserved.</CopyrightInformation> |
4,971 | Circadian pattern of life-threatening ventricular arrhythmia in patients with sleep-disordered breathing and implantable cardioverter-defibrillators. | Sleep-disordered breathing (SDB) has been associated with various benign cardiac arrhythmias occurring during sleep.</AbstractText>The purpose of this study was to demonstrate that SDB contributes to the development of life-threatening ventricular arrhythmias in patients with an established arrhythmic substrate.</AbstractText>We prospectively studied the association between SDB and timing of life-threatening ventricular arrhythmic events in 45 patients with an implantable cardioverter-defibrillator (ICD). SDB was defined as an apnea-hypopnea index (AHI) >10 events/hour based on an overnight sleep study. The primary outcome measure was appropriate ICD therapy, defined as antitachycardia pacing or shock for ventricular tachycardia or ventricular fibrillation during 1-year follow-up.</AbstractText>SDB was present in 26 (57.8%) patients. Appropriate ICD therapies were higher among patients with SDB (73% vs 47%, P = .02). Logistic regression identified SDB as a predictor of any appropriate ICD therapy (odds ratio 4.4, 95% confidence interval 1.4-15.3, P = .01). The risk for ventricular arrhythmias was higher in patients with SDB solely due to an increase in events occurring between midnight and 6 AM (odds ratio 5.6, 95% confidence interval 2.0-15.6, P = .001) with no discernible effect on appropriate ICD therapy during nonsleeping hours (odds ratio 0.7, 95% confidence interval 0.2-2.3, P = .61).</AbstractText>Patients with an ICD and SDB have a striking increase in the onset of life-threatening ventricular arrhythmic events during sleeping hours. These findings provide a rationale for SDB screening in patients with appropriate ICD therapy if device interrogation reveals a predominance of nocturnal onset of arrhythmias.</AbstractText>Copyright © 2011 Heart Rhythm Society. Published by Elsevier Inc. All rights reserved.</CopyrightInformation> |
4,972 | The impact of cardiac resynchronization therapy on the incidence of ventricular arrhythmias in mild heart failure. | Cardiac resynchronization therapy (CRT) decreases mortality, improves functional status, and induces reverse left ventricular (LV) remodeling in selected populations. However, the effect of CRT on ventricular arrhythmias is controversial. This is particularly important among patients with mild heart failure (HF), in whom sudden death is a leading cause of mortality.</AbstractText>This study sought to assess the impact of CRT on ventricular arrhythmias in mild HF.</AbstractText>The REsynchronization reVErses Remodeling in Systolic left vEntricular dysfunction (REVERSE) study is a multicenter randomized, double-blind trial of CRT among patients with mild systolic HF. The time to first appropriate, treated ventricular tachycardia/ventricular fibrillation (VT/VF) episode or spontaneous sustained VT in cardiac resynchronization therapy plus defibrillation device (CRT-D) patients was compared between groups, as were predictors of VT/VF.</AbstractText>The study randomized 508 patients who received CRT-D devices. There were no significant demographic differences between groups. There were no differences in VT/VF episodes or VT storm between groups. Specifically, in the CRT ON group, the estimated event rate was 18.7% at 2 years, compared with 21.9% in the CRT OFF group (hazard ratio 1.05, P = .84). However, among CRT ON patients, those with reverse remodeling had a reduced incidence of VT/VF compared with those without remodeling (5.6% vs. 16.3%, hazard ratio 0.31, P = .001).</AbstractText>CRT for up to 2 years does not impact VT/VF in mild HF despite marked clinical and remodeling effects of pacing. This neutral effect may be attributable to competing antiarrhythmic effects of reverse remodeling and proarrhythmic effect of pacing.</AbstractText>http://www.clinicaltrials.gov/ct2/show/NCT00271154.</AbstractText>Copyright © 2011 Heart Rhythm Society. Published by Elsevier Inc. All rights reserved.</CopyrightInformation> |
4,973 | Effects of mineralocorticoid receptor antagonist spironolactone on atrial conduction and remodeling in patients with heart failure. | Spironolactone was shown to reduce mortality in patients with heart failure (HF). However, the effect of spironolactone on the incidence of atrial fibrillation remains unknown. Therefore, we examined the effects of spironolactone on atrial conduction and remodeling in patients with HF.</AbstractText>A total of 21 patients with HF were divided into either spironolactone group (n=11) or control group (n=10). The patients were followed up for 12 months. Blood examination, echocardiogram, and signal-averaged electrocardiogram were performed at study enrollment and after 3 and 12 months of treatment. In the spironolactone group, atrial natriuretic peptide tended to reduce, left atrium dimension was significantly smaller, the ratio of E wave to A wave tended to improve, and P-duration was significantly shortened.</AbstractText>Spironolactone improves atrial conduction and remodeling in patients with HF.</AbstractText>Copyright © 2011 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.</CopyrightInformation> |
4,974 | Nurse-initiated defibrillation: are nurses confident enough? | To determine the capability of nurses to identify ventricular fibrillation (VF) and ventricular tachycardia (VT) rhythms on an ECG and carry out subsequent defibrillation on their own as soon as they identify and confirm cardiac arrest.</AbstractText>This was a prospective cohort study to determine the capability of emergency department (ED) nurses to recognise VF or pulseless VT correctly and their willingness to perform defibrillation immediately in an ED of a teaching hospital in Hong Kong. A questionnaire was completed before and after a teaching session focusing on the identification of rhythms in cardiac arrest and defibrillation skills. Correct answers for both ECG interpretation and defibrillation decisions scored one point for each question. The differences in mean scores between the pre-teaching and post-teaching questionnaires of all nurses were calculated.</AbstractText>51 pre-teaching and 43 post-teaching questionnaires were collected. There were no statistically significant changes in ECG scores after teaching. For defibrillation scores, there was an overall improvement in the defibrillation decision (absolute mean difference 0.42, p=0.014). Performance was also improved by the teaching (absolute mean difference 0.465, p=0.046), reflected by the combination of both scores. Two-thirds (67%) of nurses became more confident in managing patients with shockable rhythms.</AbstractText>Nurses improve in defibrillation decision-making skills and confidence after appropriate brief, focused in-house training.</AbstractText> |
4,975 | Therapeutic hypothermia for out-of-hospital cardiac arrest: implementation in a district general hospital emergency department. | The use of therapeutic hypothermia is recommended for unconscious adult patients with return of spontaneous circulation (ROSC) after out-of-hospital ventricular fibrillation cardiac arrest. There is evidence that the time taken to achieve target temperature impacts survival.</AbstractText>To audit the performance of an emergency department (ED) in implementing therapeutic hypothermia and achieving target temperature in survivors of out-of-hospital cardiac arrest admitted to the intensive care unit (ICU).</AbstractText>Data were extracted from the medical records of patients admitted to the ICU from the ED in the Royal United Hospital following out-of-hospital cardiac arrest (OHCA) between June 2002 and October 2008. The intervals between ROSC and initiation of cooling and between initiation of cooling and achieving the core temperature of 34°C were recorded.</AbstractText>During this period, 83 patients were admitted to the ICU following OHCA. Of these, 67 (81%) were actively cooled. All 16 patients who were not cooled had recognised exclusion criteria. The median time (IQR) from ROSC to initiation of cooling was 60 (40-165) minutes and the median time (IQR) to reach 34°C was 175 (40-420) minutes. Of the 67 who were cooled, 44 (66%) achieved the temperature of 34°C within 4 h, the audit standard published by the Royal College of Anaesthetists. In 29 (43%) patients, the temperature increased after leaving the ED.</AbstractText>Among OHCA patients who met recognised inclusion criteria, therapeutic hypothermia was implemented successfully by the ED staff. The temperature should be measured continuously from the same site in both the ED and the ICU. This will provide consistent and continuous temperature monitoring between the ED and the ICU and will enable prompt intervention to prevent temperature increases.</AbstractText> |
4,976 | Effect of previous statin use on the incidence of sustained ventricular tachycardia and ventricular fibrillation in patients presenting with acute coronary syndrome. | Recent studies suggest that statins have anti-arrhythmic effects. The aim of this study was to evaluate the effects of statins on sustained ventricular tachycardia or ventricular fibrillation (S-VT or VF) in patients presenting with acute coronary syndrome (ACS).</AbstractText>The population of this study consisted of consecutive patients admitted to coronary care unit. It was an observational case-controlled retrospective analysis performed on prospective cohort. From a total of 1000 patients presenting with ACS, 241 were on and 759 were not on statin. Patient demographics, clinical characteristics and previous medical treatment including statins were recorded. A S-VT or VF episode during hospitalization was accepted as endpoint. Multiple logistic regression model was performed which considered the occurrence of S-VT or VF as the response variable.</AbstractText>Sustained VT or VF occurred in 3.3% of patients in statin group and in 9% of patients in non-statin group. Univariate positive predictors of S-VT or VF were ST elevation myocardial infarction as clinical presentation, smoking and thrombolysis; univariate negative predictors of S-VT or VF were ejection fraction, use of acetylsalicylic acid before hospitalization, use of statin before hospitalization, initiation of clopidogrel at the hospital and normal coronary arteries. In the multiple logistic regression analysis, the only independent predictor of S-VT or VF was ejection fraction (OR 0.96; 95% CI 0.93 to 0.99; p=0.005).</AbstractText>Our results indicate that, although the incidence of S-VT/VF was significantly lower in patients with ACS and previous statin use; statin use is not an independent predictor of the occurrence of S-VT or VF in patients presenting with ACS.</AbstractText> |
4,977 | Out-of-hospital cardiac arrest-review of demographics in South Australia to inform decisions about the provision of automatic external defibrillators within the community. | Sudden, out-of-hospital cardiac arrest (OHCA) has an annual incidence of approximately 50 per 100,000 population. Public access defibrillation is seen as one of the key strategies in the chain-of-survival for OHCA. Positioning of these devices is important for the maximization of public health outcomes. The literature strongly advocates widespread public access to automated external defibrillatiors (AEDs). The most efficient placement of AEDs within individual communities remains unclear.</AbstractText>A retrospective case review of OHCAs attended by the South Australia Ambulance Service in metropolitan and rural South Australia over a 30-month period was performed. Data were analyzed using Utstein-type indicators. Detailed demographics, summative data, and clinical data were recorded.</AbstractText>A total of 1,305 cases of cardiac arrest were reviewed. The annual rate of OHCA was 35 per 100,000 population. Of the cases, the mean value for the ages was 66.3 years, 517 (39.6%) were transported to hospital, 761 (58.3%) were judged by the paramedic to be cardiac, and 838 (64.2%) were witnessed. Bystander cardiopulmonary resuscitation (CPR) was performed in 495 (37.9%) of cases. The rhythm on arrival was ventricular fibrillation (VF) or ventricular tachycardia (VT) in 419 (32.1%) cases, and 315 (24.1%) of all arrests had return of spontaneous circulation (ROSC) before or on arrival at the hospital. For cardiac arrest cases that were witnessed by the ambulance service (n=121), the incidence of ROSC was 47.1%. During the 30-month period, there only was one location that recorded more than one cardiac arrest. No other location recorded recurrent episodes.</AbstractText>This study did not identify any specific location that would justify defibrillator placement over any other location without an existing defibrillator. The impact of bystander CPR and the relatively low rate of bystander CPR in this study points to an area of need. The relative potential impact of increasing bystander CPR rates versus investing in defibrillators in the community is worthy of further consideration.</AbstractText> |
4,978 | Cardiac arrest in the out-of-hospital setting: when to halt resuscitation. | In out-of-hospital settings, when is it reasonable to halt attempts to resuscitate a victim of sudden cardiac arrest? To answer these questions, we reviewed the relevant literature using the standard Prescrire methodology. Retrospective studies of several thousand cases suggest that the chances of survival depend on how rapidly survival measures are implemented, how quickly medical help arrives, the type of cardiac arrhythmia, early defibrillation, and return of spontaneous circulation. The chances of survival without neurological sequelae are virtually nil when medical assistance does not arrive within 8 minutes and when the patient is already in asystole. Unless spontaneous circulation resumes after 30 minutes of medical resuscitation, the survival chances are also considered to be nil, except in case of hypothermia or persistent ventricular fibrillation (or tachycardia): it is then reasonable to cease resuscitation attempts. However, it may be appropriate to continue resuscitation procedures beyond 30 minutes in order to help relatives come to terms with the patient's death. In practice, when sudden cardiac arrest occurs in the community, those present must implement a chain of survival in order to optimise the patient's chances of survival. Physicians called to the scene must assess the victim's chances of survival in order to decide when to halt resuscitation attempts. |
4,979 | Thrombosuction with export aspiration catheter during PCI in acute MI. | The angiographic demonstration of thrombus laden LAD in a ventilated young man with IABP (to combat cardiogenic shock) demanded thrombosuction. Following thrombosuction no significant lesion was visible that could have mandated PTCA-Stenting. Follow-up coronary angiography in this hyperhomocysteinaemic young subject after one and a half month revealed normal coronaries. Thrombosuction alone unaccompanied by any other additional intervention is infrequently reported. |
4,980 | Beta blockers in arrhythmias: when and where to use? | Beta blockers are often the first line of medications used in treatment of arrhythmias. Their role has been established in treatment of Supraventricular tachycardia (SVT) and Ventricular tachyarrhythmias (VT). Beta Blockers are also used as prophylactic medications in SVT, VT and Sudden Cardiac Arrest survivors. They are important components of treatment in the management of VT storms, Atrial Fibrillation, arrhythmias during pregnancy, arrhythmias associated with congenital heart disease, Long QT syndrome, arrhythmias in cardiomyopathies and post-cardiac surgery arrhythmias.The choice of drug, dose and route of administration depends on the type of arrhythmia and clinical presentation and demographics of the patient. |
4,981 | [Pre-excitation pattern associated with accessory pathway related tachycardia: case report]. | Pre-excitation is based on an accessory conduction pathway between the atrium and ventricle. The term Wolff-Parkinson-White (WPW) syndrome is used for patients with the pre-excitation/WPW pattern associated with AP-related tachycardia.</AbstractText>We present a 52-year-old man with severe palpitation, fatigue, lightheadedness and difficulty breathing. The initial ECG showed tachyarrhythmia with heart rate between 240 and 300/min. He was treated with antiarrhythmics (Digitalis, Verapamil, Lidocaine) with no response. Then, the patient was treated with electrical cardioversion and was referred to our Clinic for further evaluation with the diagnosis: "Ventricular tachycardia". During in-hospital stay, the previously undiagnosed WPW pattern had been seen. Additional diagnostic tests confirmed permanent pre-excitation pattern (ECG Holter recording, exercises test). The patient was referred to an electrophysiologist for further evaluation. Mapping techniques provided an accurate assessment of the position of the accessory pathway which was left lateral. The elimination of the accessory pathway by radiofrequent catheter ablation is highly effective in termination and elimination of tacchyarrhythmias.</AbstractText>Symptomatic, life-threatening arrhythmia, first considered as ventricular tachycardia, reflected atrial fibrillation with ventricular pre-excitation over an accessory pathway in a patient with previously undiagnosed WPW syndrome.</AbstractText> |
4,982 | Cardioprotective effects of luteolin during ischemia-reperfusion injury in rats. | Antioxidants effectively reduce ischemia-reperfusion (IR) injury. The cardioprotective effects of luteolin, a flavonoid that exhibits antioxidant properties and is widely available in many fruits and vegetables, were examined in rats subjected to myocardial IR injury.</AbstractText>Rats were subjected to myocardial ischemia or reperfusion injury to evaluate the antiarrhythmic effects of luteolin. Myocardial infarct size was determined histochemically with triphenyltetrazolium chloride staining of the left ventricle. Luteolin was administered intravenously 15min before occlusion of the coronary artery. The incidence and duration of ventricular tachycardia and ventricular fibrillation and mortality during myocardial ischemia were significantly reduced by luteolin (10µg/kg). Similarly, luteolin (1µg/kg) reduced ventricular arrhythmias and mortality during the reperfusion phase. Pretreatment with luteolin decreased plasma lactate dehydrogenase and nitric oxide (NO) levels. Luteolin (10µg/kg) significantly reduced the myocardial infarct size, as well as malondialdehyde production in tissue samples of myocardial IR injury. Luteolin also downregulated inducible NO synthase protein and mRNA expression, but did not significantly alter neuronal NO synthase or endothelial NO synthase expression.</AbstractText>Luteolin is capable of protecting the myocardium against IR injury. The actions of luteolin are at least partly mediated through downregulation of NO production and its own antioxidant properties.</AbstractText> |
4,983 | Biological variation of brain natriuretic peptide and cardiac events in stable outpatients with nonischemic chronic heart failure. | To evaluate the biological variation and prognostic value of brain natriuretic peptide (BNP) for stable outpatients with nonischemic chronic heart failure (NICHF).</AbstractText>Biological variation in BNP was evaluated using an automated assay system in 140 outpatients with NICHF. The stable clinical condition during the 2-month study period was defined as unchanged NYHA and unchanged left ventricular ejection fraction; therefore, 7 patients were excluded during the 2 months. Thereafter, 133 patients were prospectively followed and the relationship between cardiac events and the plasma BNP concentrations (at baseline and after 2 months) were evaluated as well as the changes in BNP. The biological variation in BNP (2-month interval) was calculated as 22.3%. During a mean follow-up period of 42 months, 26 patients had cardiac events. According to stepwise multivariate analyses, plasma BNP after 2 months (P=0.0002) and % change in BNP (P=0.0067) were significant independent predictors of cardiac events.</AbstractText>These findings indicated that a combination of the absolute value of BNP after 2 months and % increase in BNP (2-month interval) is useful for predicting cardiac events in stable outpatients with NICHF.</AbstractText> |
4,984 | Effect of therapeutic hypothermia vs δ-opioid receptor agonist on post resuscitation myocardial function in a rat model of CPR. | This study is to compare the effect of the δ-opioid receptor agonist, D-Ala(2)-D-Leu(5) enkephalin (DADLE) with normothermic control and therapeutic hypothermia on post resuscitation myocardial function and 72-h survival in a rat model of cardiac arrest and resuscitation.</AbstractText>Ventricular fibrillation (VF) was induced in 15 male Sprague-Dawley rats. After 8 min of untreated VF, cardiopulmonary resuscitation was performed for 8 min before defibrillation. Animals were randomized to three groups of five: (a) normothermia; (b) hypothermia (32 °C); and (c) normothermia with DADLE intravenous infusion (1 mg/kg h(-1)). Hypothermia and drug infusion were started after successful defibrillation. Myocardial functions, including cardiac output (CO), left ventricular ejection fraction (LVEF), and myocardial performance index (MPI) were measured echocardiographically together with duration of survival.</AbstractText>The 72-h survival was significantly greater in the hypothermic group than in both DADLE and normothermic group (p = 0.02). However, the survival time of the DADLE treated animals was significantly longer than that of the normothermia group (51.8 ± 18.9 vs 18.8 ± 10.1h, p < 0.01). DADLE group showed significantly better CO (PR 60 min, p = 0.049), better LVEF (PR 60 min, p = 0.044; PR 240 min, p < 0.001) and lower MPI (PR 60 min, p = 0.043; PR 240 min, p = 0.045) than normothermic group. Hypothermia group also showed significantly better CO (PR 60m in, p = 0.044; PR 240 min, p = 0.007), better LVEF (PR 60 min, p = 0.001; PR 240 min, p < 0.001) and lower MPI (PR 60 min, p = 0.003; PR 240 min, p = 0.012) than the normothermic group.</AbstractText>DADLE attenuated post resuscitation myocardial dysfunction and increased short term survival time. However, the 72-h survival in the DADLE group was less than that in the hypothermia group.</AbstractText>Copyright © 2010. Published by Elsevier Ireland Ltd.</CopyrightInformation> |
4,985 | [Chinese risk stratification scoring system for coronary artery bypass grafting]. | To construct a scoring system for the prediction of in-hospital mortality in Chinese patients undergoing coronary artery bypass grafting (CABG).</AbstractText>From 2007 to 2008, complete clinical information of 9564 consecutive CABG patients was collected from Chinese coronary artery bypass grafting registry which recruited patients from 43 Chinese centers. This database was randomly divided into developmental and validation subsets (9:1). A risk model was developed using logistic regression. Calibration and discrimination characteristics were assessed in the validation dataset. Thresholds were defined for each model to distinguish different risk groups. The risk model was compared with EuroSCORE system in the validation dataset.</AbstractText>In the developmental dataset, calibration by Hosmer-Lemeshow (HL) test was P = 0.44 and discrimination by area under ROC (AUC) was 0.80. In the validation dataset, HL test was P = 0.34, AUC was 0.78. The performance turned out good for all three risk groups. Superiority were found over EuroSCORE (HL P = 0.60; AUC 0.73). The scoring system identified 11 risk factors (with weights in brackets): age over 65 (65 - 69, 3; 70 - 74, 5; over 75, 6), preoperative NYHA stage (NHYA III, 3; NHYA IV, 7), chronic renal failure (6), extracardiac arteriopathy (5), chronic obstructive pulmonary disease (4), Preoperative atrial fibrillation or flutter (within two weeks) (2), left ventricular ejection fraction < 50% (4), other than elective surgery (5), combined valve procedure (4), preoperative critical state (4), BMI (> 24 kg/m(2), -2; < 18 kg/m(2), 5).</AbstractText>This study constructs a simple, objective and accurate risk stratification system for Chinese patients undergoing CABG using the most up-to-date data.</AbstractText> |
4,986 | [An infant with unexplained epilepsy]. | A 6-month-old male infant with an unremarkable past medical history was admitted to the emergency department in an epileptic state. The seizures were resistant to treatment with conventional drugs. The child was sedated, intubated and admitted to the intensive care department. Despite extensive investigations no underlying disease was found. The seizures persisted and the child was repeatedly admitted to the hospital. Four months after the first presentation, ventricular fibrillation occurred from which the child was successfully resuscitated. His stomach appeared to contain a disinfectant and a severe ethanol-intoxication was found, leading to the diagnosis "Munchausen syndrome by proxy". The incidence of this syndrome is underestimated. Recognition of this potentially fatal phenomenon is often difficult, resulting in a delay in diagnosis. Paediatricians and general practitioners should be aware of this syndrome in children presenting with an unusual disease or an unusual medical history reported by the parents or care providers. |
4,987 | Impaired transport function of the left atrium in patients with lone paroxysmal atrial fibrillation. | Although lone paroxysmal atrial fibrillation (LPAF) is clinically defined as an arrhythmia that occurs in the absence of structural heart disease, it has been suggested that the presence of anatomical substrate is related to LPAF. The aim of the present study is to determine whether structural and functional remodeling of the left atrium (LA) occurs in patients with LPAF, and to identify whether frequent episodes of atrial fibrillation (AF) contribute to LA remodeling.</AbstractText>Forty-five patients who diagnosed as LPAF and age-, gender-, and body mass index-matched healthy control subjects (n = 45) were enrolled. Patients were grouped based on the frequency of AF episodes. An echocardiography was performed >2 weeks after last episode of AF without antiarrhythmic drugs. There were no statistical differences in left ventricular (LV) diastolic and systolic functions as well as baseline characteristics between patients and controls, whereas, patients had significantly larger LA volume (LAV), lower active LA emptying fraction (LAEF(active) , P = 0.009) and total LAEF (LAEF(total) , P = 0.005) compared with controls. Passive LAEF (LAEF(passive) ) was not different between patients and controls (P = 0.664). LAEF(active) was significantly depressed in patients with frequent episodes of AF than the others (P = 0.034).</AbstractText>Compared with healthy controls, patients with LPAF had increased LAV and depressed LAEF(active) and LAEF(total) without accompanying compensatory increase in LAEF(passive) . LAEF(active) was influenced by frequent episodes of AF. These findings may support the hypothesis that LPAF is "not-so-lone AF" and related to the concealed cardiac dysfunctions.</AbstractText>© 2010, Wiley Periodicals, Inc.</CopyrightInformation> |
4,988 | Vernakalant hydrochloride: A novel atrial-selective agent for the cardioversion of recent-onset atrial fibrillation in the emergency department. | Vernakalant is a relatively atrial-selective antiarrhythmic agent that has been shown to successfully convert atrial fibrillation (AF) to normal sinus rhythm for some patients whose onset of dysrhythmia occurred less than 7 days previously. This study sought to evaluate the efficacy and safety of vernakalant for patients with recent-onset AF.</AbstractText>This was a post hoc analysis of patients with recent-onset AF (> 3 to ≤ 48 hours) enrolled in the double-blind, placebo-controlled Atrial arrhythmia Conversion Trial (ACT) I and the open-label ACT IV trials. The studies enrolled adults presenting with AF to 78 emergency departments (ED) and cardiac clinics in six countries. Patients received a 10-minute intravenous infusion of vernakalant or placebo, followed by an additional infusion if necessary. Efficacy assessments included conversion to sinus rhythm within 90 minutes and median time to conversion. Safety evaluations included telemetry, Holter monitoring, and adverse events (AEs).</AbstractText>Of the 290 patients, 229 received vernakalant, 61 received placebo, and the overall mean age was 59 years. The vernakalant and placebo groups were similar. Of all patients given vernakalant, 136 (59.4%) converted to sinus rhythm within 90 minutes, compared with three (4.9%) placebo patients. The median time to conversion with vernakalant was 12 minutes (interquartile range = 7-24.5 minutes). Clinically significant bradycardia and hypotension were uncommon, and no cases of torsade de pointes or ventricular fibrillation occurred.</AbstractText>Vernakalant rapidly converted recent-onset AF to sinus rhythm in over half of patients, was well tolerated, and has the potential to offer an important therapeutic option for rhythm control of recent-onset AF in the ED.</AbstractText>© 2010 by the Society for Academic Emergency Medicine.</CopyrightInformation> |
4,989 | Effect of defibrillation energy dose during in-hospital pediatric cardiac arrest. | To examine the effectiveness of initial defibrillation attempts. We hypothesized that (1) an initial shock dose of 2 ± 10 J/kg would be less effective for terminating fibrillation than suggested in published historical data and (2) a 4 J/kg shock dose would be more effective.</AbstractText>This was a National Registry of Cardiopulmonary Resuscitation prospective, multisite, observational study of in-hospital pediatric (aged ≤18 years) ventricular fibrillation or pulseless ventricular tachycardia cardiac arrests from 2000-2008. Termination of ventricular fibrillation or pulseless ventricular tachycardia and event survival after initial shocks of 2 J/kg were compared with historic controls and a 4 J/kg shock dose.</AbstractText>Of 266 children with 285 events, 173 of 285 (61%) survived the event and 61 of 266 (23%) survived to discharge. Termination of fibrillation after initial shock was achieved for 152 of 285 (53%) events. Termination of fibrillation with 2 ± 10 J/kg was much less frequent than that seen among historic control subjects (56% vs 91%; P < .001), but not different than 4 J/kg. Compared with 2 J/kg, an initial shock dose of 4 J/kg was associated with lower rates of return of spontaneous circulation (odds ratio: 0.41 [95% confidence interval: 0.21-0.81]) and event survival (odds ratio: 0.42 [95% confidence interval: 0.18-0.98]).</AbstractText>The currently recommended 2 J/kg initial shock dose for in-hospital cardiac arrest was substantially less effective than previously published. A higher initial shock dose (4 J/kg) was not associated with superior termination of ventricular fibrillation or pulseless ventricular tachycardia or improved survival rates. The optimal pediatric defibrillation dose remains unknown.</AbstractText> |
4,990 | Postpartum spontaneous coronary dissection presenting with ventricular fibrillation. | Spontaneous coronary artery dissection is a rare cause of acute coronary syndromes; and one quarter of these patients present during the post-partum period. Furthermore, ventricular fibrillation is a rare presentation of this disease entity.</AbstractText>A 32-year-old woman presented 3 days post Cesarean-section delivery with chest pain, ischemic electrocardiogram changes, and ventricular fibrillation arrest. The patient was taken for cardiac catheterization and found to have a left anterior coronary artery dissection necessitating 6 stents to restore flow to the vessel.</AbstractText>We report the first case of survival after ventricular fibrillation arrest of a woman presenting with spontaneous coronary dissection in the post-partum period. Our case underscores the importance of recognizing ventricular fibrillation as a first presenting sign of spontaneous coronary artery dissection in the post-partum period.</AbstractText> |
4,991 | The impact of surgical ablation in patients with low ejection fraction, heart failure, and atrial fibrillation. | Surgical ablation procedures that use the Cox-Maze procedure lesion set were shown to be very effective. However, many surgeons are reluctant to perform the procedure, especially in high-risk patients such as those with reduced left ventricular (LV) function. This study explored the potential impact of the Cox-Maze III/IV procedure on patients with low ejection fraction (EF<40%) and symptoms of heart failure experiencing atrial fibrillation (AF) who present for cardiac surgery.</AbstractText>A prospective study whereby patients with persistent or long-standing persistent AF who had surgical ablation were followed. Echocardiograms (echo) were obtained; patients with preoperative EF <40% were included. Health-related quality of life (HRQL-SF-12) and AF symptom severity were obtained at baseline and follow-up. Rhythm was captured by electrocardiogram (EKG) and 24-h Holter.</AbstractText>In the past 5 years, 482 patients had surgical ablation (424 full Cox-Maze) of whom 44 patients met the inclusion criteria; however, two patients did not have an available follow-up echo, leaving 42 patients for analysis. Mean age was 61.1 ± 12.9 years, and additive European System for Cardiac Operative Risk Evaluation (EuroSCORE) of 7.5 ± 3.1. There was one operative death, there were no strokes or transient ischemic attacks (TIAs) at follow-up, and EF improved from 30 ± 5.0% to 45 ± 13.0% at a mean of 1.5 ± 11.3 months, postoperatively. The return to NSR at time of follow-up echo was 86% (35/40). The physical functioning HRQL scores improved (37.0 ± 12.3 to 46.8 ± 9.1, p = 0.02) at 12 months (population norm = 38.1 ± 9.9) with a significant improvement in symptom severity. Kaplan-Meier event-free survival at 24 months was 87% (confidence interval (CI): 80.4-91.6) (events considered were redo valve replacement, ventricular assist device or death).</AbstractText>This is a unique study assessing a high-risk group of patients. Surgical ablation in patients with low EF can be performed in a safe and effective way without added operative risk. Given the potential long-term clinical advantages of a successful surgical ablation in patients with low EF and heart failure, we believe that surgical ablation should be considered in such patients when they present to surgery.</AbstractText>Copyright © 2010. Published by Elsevier B.V.</CopyrightInformation> |
4,992 | Cardiovascular safety of QVA149, a combination of Indacaterol and NVA237, in COPD patients. | This study assessed the cardiovascular safety of QVA149, an inhaled, once daily, bronchodilator combination containing two 24-hour bronchodilators, the long-acting β(2)-agonist indacaterol and the long-acting muscarinic antagonist glycopyrronium (NVA237). In this randomised, double-blind, placebo-controlled, parallel-group study, 257 patients with moderate-to-severe chronic obstructive pulmonary disease (COPD) were randomised to receive QVA149 (indacaterol/NVA237) 600/100 microg, 300/100 microg or 150/100 microg, indacaterol 300 μg or placebo, once daily for 14 days. The primary endpoint was change from baseline in 24-h mean heart rate versus placebo on Day 14. 255 patients were included in the safety analysis (mean age 63.8 years, 76.5% male, post-bronchodilator forced expiratory volume in one second [FEV(1)] 53.2% predicted, FEV(1)/FVC [forced vital capacity] 50.0%, mean 24-h heart rate 79.6 bpm). There were no clinically significant differences in the 24-h mean heart rate on Day 14 between the three doses of QVA149 and placebo or indacaterol. The confidence intervals of these treatment differences (contrasts) were within the pre-specified equivalence limit (-5 to 5 bpm). No clinically relevant differences in QTc interval (Fridericia's) were observed between groups on Days 1, 7 and 14. Once-daily QVA149 was well tolerated in COPD patients with a cardiovascular safety profile and overall adverse event rates similar to placebo. |
4,993 | [Electrophysiological effect of atorvastatin on isolated rat hearts injured by ischemia/reperfusion]. | To investigate the myocardial electrophysiological effect and its underlying mechanisms of atorvastatin (Ator) on isolated rat hearts injured by ischemia/reperfusion (I/R).</AbstractText>Isolated SD rat hearts were mounted on Langendorff system, and a local I/R was induced by ligation (30 min) and release (15 min) of the left anterior descending artery. During the reperfusion period, the effect of Ator on diastolic excitation threshold (DET), effective refractory period (ERP) and ventricular fibrillation threshold (VFT) on rat heart were measured.</AbstractText>Compared with the control group, medium concentration of Ator prolonged the ERP in normal rat hearts; low, medium and high concentration of Ator significantly inhibited the decrease of DET, ERP and VFT induced by I/R. However, pretreatment with L-NAME cancelled these cardiac electrophysiological effects of Ator.</AbstractText>Ator reduced electrophysiological alteration induced by I/R in isolated rat hearts, which may be mediated by activating nitric oxide pathway to enhance the myocardial electrophysiological stability.</AbstractText> |
4,994 | Chronobiology of cardiac ventricular fibrillation development in experimental acute coronary failure. | Numerous experiments on simulation of acute coronary failure in initially intact rabbits showed that under the same experimental conditions irreversible ventricular fibrillation developed in some animals and did not develop in other. We hypothesize that the probability of fibrillation development was determined by the time of the day, during which acute coronary failure developed. The study was carried out on 2 groups of rabbits in winter in Moscow. In group 1, the failure was induced by ligation of the left descending coronary artery at the interface between its middle and lower thirds at 11.00-18.00 with 30-min intervals. In group 2, the microcirculatory status of the left-ventricular myocardium was studied by light microscopy and morphometry at 12.00 and 18.00. Induction of coronary failure during the period from 15.30 to 18.00 led to irreversible ventricular fibrillation and death in 100% cases. Modeling of the condition from 11.00 to 15.00 caused no ventricular fibrillation in 89% cases, and the animals survived. The area of left-ventricular myocardial capillaries at 12.00 virtually 2-fold surpassed that at 18.00. Presumably, the electrolyte balance and metabolic characteristics of the myocardium switch over to the nocturnal mode of functioning at 15.30 due to changes in blood filling of the myocardium. The appearance of an ischemic focus in the myocardium during this period inevitably leads to the development of irreversible ventricular fibrillation. |
4,995 | Enhanced dispersion of repolarization explains increased arrhythmogenesis in severe versus therapeutic hypothermia. | Hypothermia is proarrhythmic, and, as the use of therapeutic hypothermia (TH) increases, it is critically important to understand the electrophysiological effects of hypothermia on cardiac myocytes and arrhythmia substrates. We tested the hypothesis that hypothermia-enhanced transmural dispersion of repolarization (DOR) is a mechanism of arrhythmogenesis in hypothermia. In addition, we investigated whether the degree of hypothermia, the rate of temperature change, and cooling versus rewarming would alter hypothermia-induced arrhythmia substrates.</AbstractText>Optical action potentials were recorded from cells spanning the transmural wall of canine left ventricular wedge preparations at baseline (36°C), during cooling and during rewarming. Electrophysiological parameters were examined while varying the depth of hypothermia. On cooling to 26°C, DOR increased from 26±4 ms to 93±18 ms (P=0.021); conduction velocity decreased from 35±5 cm/s to 22±5 cm/s (P=0.010). On rewarming to 36°C, DOR remained prolonged, whereas conduction velocity returned to baseline. Conduction block and reentry was observed in all severe hypothermia preparations. Ventricular fibrillation/ventricular tachycardia was seen more during rewarming (4/5) versus cooling (2/6). In TH (n=7), cooling to 32°C mildly increased DOR (31±6 to 50±9, P=0.012), with return to baseline on rewarming and was associated with decreased arrhythmia susceptibility. Increased rate of cooling did not further enhance DOR or arrhythmogenesis.</AbstractText>Hypothermia amplifies DOR and is a mechanism for arrhythmogenesis. DOR is directly dependent on the depth of cooling and rewarming. This provides insight into the clinical observation of a low incidence of arrhythmias in TH and has implications for protocols for the clinical application of TH.</AbstractText> |
4,996 | Early diagnosis of left ventricular diastolic dysfunction in diabetic patients: a possible role for natriuretic peptides. | The aim of the present study was to verify whether BNP might detect pre-clinical diastolic dysfunction (LVDD) in type-2 diabetic patients.</AbstractText>One-hundred and twenty-seven consecutive outpatients with type-2 diabetes mellitus were enrolled into the study. Subjects with overt heart failure or NYHA class > 1, history of coronary artery disease, severe valvulopathy or chronic atrial fibrillation were excluded from the study. All patients underwent clinical evaluation, laboratory assessment of brain natriuretic peptide (BNP) and echocardiographic examination.</AbstractText>No patients showed systolic impairment of left ventricular function, whereas diastolic dysfunction was detected in 53 (42%) cases (all impaired relaxation). Median BNP was 27 pg/ml without any significant difference between 76 patients with normal left ventricular function and 53 with diastolic dysfunction; in 54 (43%) patients showing HBA1C≥8 (uncontrolled diabetes) normal function was found in 32 and diastolic dysfunction in 22, with a significant difference of BNP at multivariate analysis (OR = 1.02, 95%CI = 1.05-1.09, p = 0.003). In uncontrolled diabetic cohort, BNP was a strong predictor for LVDD (OR = 2.7, 95%CI = 1.3-5.6, p = 0.006) along with the duration of diabetes (OR = 1.6, 95%CI = 1.1-2.9, p = 0.046). BNP > 25 pg/ml was a cut-off value with high accuracy to detect a LVDD.</AbstractText>Early screening of high-risk patients for diabetic cardiomyopathy development might be useful to better control glycemic profile in order to reduce heart disease progression or even to reverse it</AbstractText>BNP could be a cheap, easy and useful tool to screen those ones with preclinical ventricular diastolic dysfunction in a subset of patients particularly prone to develop cardiovascular complications, like uncontrolled diabetic patients.</AbstractText> |
4,997 | Present concepts in management of atrial fibrillation: From drug therapy to ablation. | Atrial fibrillation (AF) management requires knowledge of its pattern of presentation, underlying conditions, and decisions about restoration and maintenance of sinus rhythm, control of the ventricular rate, and anti-thrombotic therapy. Maintenance of sinus rhythm is a desirable goal in AF patients because the prevention of recurrence may improve cardiac function, relieve symptoms and reduce the likelihood of adverse events. Anti-arrhythmic drug therapy is the first-line treatment for patients with paroxysmal and persistent AF based on current guidelines. However, currently used drugs have limited efficacy and cause cardiac and extracardiac toxicity. Thus, there is a continued need to develop new drugs, device and ablative approaches to rhythm management. Additionally, simpler and safer stroke prevention regimens are needed for AF patients on life-long anticoagulation, including occlusion of the left atrial appendage. The results of the Randomized Evaluation of Long-Term Anticoagulant Therapy study are encouraging in these settings. Knowledge on the pathophysiology of AF is rapidly expanding and identification of focally localized triggers has led to the development of new treatment options for this arrhythmia. Conversely, the clinical decision whether to restore and maintain sinus rhythm or simply control the ventricular rate has remained a matter of intense debate. In the minority of patients in whom AF cannot be adequately managed by pharmacological therapy, the most appropriate type of non-pharmacological therapy must be selected on an individualized basis. Curative treatment of AF with catheter ablation is now a legitimate option for a large number of patients. The evolution of hybrid therapy, in which two or more different strategies are employed in the same patient, may be an effective approach to management of AF. In any case, planning a treatment regimen for AF should include evaluation of the risks inherent in the use of various drugs as well as more invasive strategies. |
4,998 | Ultra-rapid delayed rectifier channels: molecular basis and therapeutic implications. | The ultrarapid delayed rectifier channels have attracted considerable interest as targets for 'atrial-selective' antiarrhythmic drugs because they contribute to atrial but not to ventricular repolarization. Thus, I(Kur) channel blockers are expected to prolong selectively the atrial effective refractory period without inducing proarrhythmic effects due to excessive ventricular action potential prolongation. Here we provide an overview of the properties of I(Kur) channels in expression systems and native cardiomyocytes. The ion conducting pore of the channel is formed by four Kv1.5 α-subunits, whereas the ancillary β-subunits Kvβ1.2, Kvβ1.3, and Kvβ2.1 control channel trafficking and plasma membrane integration as well as activation and inactivation kinetics. Investigation of I(Kur) channel blockers in cardiomyocytes is complicated (i) by substantial overlap of I(Kur) with other currents, notably the transient outward current I(to), (ii) by lack of drug selectivity, and (iii) by disease-induced regulation of I(Kur). Some new compounds developed as I(Kur) blockers are described and their efficacy in treatment of atrial fibrillation (AF) is discussed. Current evidence suggests that pure I(Kur) channel block may not be sufficient to suppress AF. |
4,999 | The development of familial hypertrophic cardiomyopathy: from mutation to bedside. | Hypertrophic cardiomyopathy (HCM) is a familial disorder characterized by left ventricular hypertrophy in the absence of other cardiac or systemic disease likely to cause this hypertrophy. HCM is considered a disease of the sarcomere as most causal mutations are identified in genes encoding sarcomeric proteins, although several other disorders have also been linked to the HCM phenotype. The clinical course of HCM is characterized by a large inter- and intrafamilial variability, ranging from severe symptomatic HCM to asymptomatic individuals. The general picture emerges that the underlying pathophysiology of HCM is complex and still scarcely clarified. Recent findings indicated that both functional and morphological (macroscopic and microscopic) changes of the HCM muscle are present before the occurrence of HCM phenotype. This review aims to provide an overview of the myocardial alterations that occur during the gradual process of wall thickening in HCM on a myofilament level, as well as the structural and functional abnormalities that can be observed in genetically affected individuals prior to the development of HCM with state of the art imaging techniques, such as tissue Doppler echocardiography and cardiovascular magnetic resonance imaging. Additionally, present and future therapeutic options will be briefly discussed. |
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