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2,900 | Carrier-mediated norepinephrine release and reperfusion arrhythmias induced by protracted ischemia in isolated perfused guinea pig hearts: effect of presynaptic modulation by alpha(2)-adrenoceptor in mild hypothermic ischemia. | Yohimbine, an alpha(2)-adrenoceptor antagonist, has been reported to protect hypoxic myocardium and inhibit carrier-mediated norepinephrine (NE) release and reperfusion arrhythmias (ventricular fibrillation; VF) in normothermic ischemia. In heart surgery, mild hypothermic (tepid) cardioplegia has been reported to reduce metabolic demand and permit immediate recovery of cardiac function. Therefore, we determined the effect of yohimbine on NE release and reperfusion arrhythmias in isolated perfused guinea pig hearts of tepid temperature (32 degrees C) ischemia model. Stepwise increase of global ischemia period (20, 40, and 60 min) induced a progressive increase of NE release and duration of VF. Neuronal uptake 1 inhibitor desipramine (100 nM) and Na(+)-H(+) exchanger inhibitor 5-N-ethyl-N-isopropyl-amiloride (10 microM) decreased NE and VF in 60-min hypothermic ischemia. This indicated that NE release induced by protracted tepid ischemia was due to carrier-mediated release. Yohimbine (1 microM) markedly reduced NE release and VF (p < 0.01 versus control) and 5-bromo-N-(4,5-dihydro-1H-imidazol-2-yl)-6-quinoxalinamine [UK 14,304 (UK); 10 microM], an alpha(2)-adrenoceptor agonist, increased NE release and VF (p < 0.01 versus control). Yohimbine (1 microM) prevented the potentiated effect of UK (10 microM) in hypothermia (p < 0.01 versus UK). Our findings indicate that presynaptic reduction of carrier-mediated NE release seems to be one of the most important factors controlling reperfusion arrhythmias, and alpha(2)-adrenoceptor blockade by yohimbine (1 microM) in tepid ischemia may contribute to effective myocardial protection in terms of NE release and reperfusion arrhythmia. |
2,901 | On the mechanism of the probabilistic nature of ventricular defibrillation threshold. | The probabilistic nature of the ventricular defibrillation threshold (DFT) remains poorly understood. We hypothesized that shock outcome is a function of the amount of myocardium in its vulnerable period (VP). The endocardial surface of five isolated, perfused swine right ventricles was mapped with 477 bipolar electrodes during ventricular fibrillation (VF). Shock parameters and VF cycle length were not significantly different in the successful (S; n = 26) and failed (F; n = 26) trials. At the instant of the shock, the number of sites with 45- to 55-ms recovery was significantly smaller in the S trials than the F trials (P < 0.04). No significant difference in the number of sites with recovery intervals outside the 45- to 55-ms range was seen in S and F shocks. Endocardial action potential showed that a recovery time of 45-55 ms corresponded to the VP spanning -15 to -60 mV in 92% of the regenerative action potentials. We conclude that the probabilistic nature of the DFT is related to the amount of myocardium in its VP. |
2,902 | Slow rate during AF improves ventricular performance by reducing sensitivity to cycle length irregularity. | Atrial fibrillation (AF) is characterized by short and irregular ventricular cycle lengths (VCL). While the beneficial effects of heart rate slowing (i.e., the prolongation of VCL) in AF are well recognized, little is known about the impact of irregularity. In 10 anesthetized dogs, R-R intervals, left ventricular (LV) pressure, and aortic flow were collected for >500 beats during fast AF and when the average VCL was prolonged to 75%, 100%, and 125% of the intrinsic sinus cycle length by selective atrioventricular (AV) nodal vagal stimulation. We used the ratio of the preceding and prepreceding R-R intervals (RR(p)/RR(pp)) as an index of cycle length irregularity and assessed its effects on the maximum LV power, the minimum of the first derivative of LV pressure, and the time constant of relaxation by using nonlinear fitting with monoexponential functions. During prolongation of VCL, there was a pronounced decrease in curvature with the formation of a plateau, indicating a lesser dependence on RR(p)/RR(pp). We conclude that prolongation of the VCL during AF reduces the sensitivity of the LV performance parameters to irregularity. |
2,903 | Advanced life support drugs: do they really work? | Basic life support and rapid defibrillation for ventricular fibrillation or pulseless ventricular tachycardia are the only two interventions that have been shown unequivocally to improve survival after cardiac arrest. Several drugs are advocated to treat cardiac arrest, but despite very encouraging animal data, no drug has been reliably proven to increase survival to hospital discharge after cardiac arrest. This review focuses on recent experimental and clinical data concerning the use of vasopressin, amiodarone, magnesium, and fibrinolytics during advanced life support (ALS). Animal data indicate that, in comparison with epinephrine (adrenaline), vasopressin produces better vital organ blood flow during cardiopulmonary resuscitation (CPR). These apparent advantages have yet to be converted into improved survival in large-scale trials of cardiac arrest in humans. Data from two prospective, randomized trials suggest that amiodarone may improve short-term survival after out-of-hospital ventricular fibrillation cardiac arrest. On the basis of anecdotal data, magnesium is recommended therapy for torsades de pointes and for shock-resistant ventricular fibrillation associated with hypomagnesemia. In the past, CPR has been a contraindication to giving fibrinolytics, but several studies have demonstrated the relative safety of fibrinolysis during and after CPR. Fibrinolytics are likely to be beneficial when cardiac arrest is associated with plaque rupture and fresh coronary thrombus or massive pulmonary embolism. Fibrinolysis may also improve cerebral microcirculatory perfusion once a spontaneous circulation has been restored. A planned, prospective, randomized trial may help to define the role of fibrinolysis during out-of-hospital CPR. |
2,904 | Feasibility of public access to defibrillation. | Immediate defibrillation is the single most effective therapy to reverse ventricular fibrillation cardiac arrest today. The once physician-only skill of defibrillation has entered mainstream society and is saving the lives of many sudden cardiac arrest (SCA) victims in a variety of settings. The automated external defibrillator (AED) and the concept of public access defibrillation (PAD) are a result of collaborative efforts between the American Heart Association (AHA) and medical manufacturers. Today, airports, airlines, casinos, cruise ships, and other public venues have modernized their first aid kits to include an AED. The success of these programs has ignited a trend in public safety and subsequently marketed the worth of AEDs in the home. Although optimal placement of AEDs remains uncertain, PAD is showing great promise in reducing the death rate from SCA. The lay public, both trained and untrained, is emerging as the next level of emergency care responders able to use a defibrillator. |
2,905 | Regional differences in ventricular fibrillation in the open-chest porcine left ventricle. | It has been hypothesized that during ventricular fibrillation (VF), the fastest activating region, the dominant domain, contains a stable reentrant circuit called a mother rotor. This hypothesis postulates that the mother rotor spawns wavefronts that propagate to maintain VF elsewhere and implies that the ratio of wavefronts propagating off a region to those propagating onto it (propoff/propon) should be >1 for the dominant domain but <1 elsewhere. To test this prediction in the left ventricular (LV) epicardium of a large animal, most of the LV free wall was mapped with 1008 electrodes in 7 pigs. VF activation rate was faster in the posterior than in the anterior LV (10.0+/-1.3Hz versus 9.3+/-1.3Hz; P<0.001). The anterior LV had a higher fraction of wavefronts that blocked than did the posterior LV and had a propoff/propon ratio <1 (P<0.001). The mean conduction velocity vectors of the VF wavefronts pointed in the direction from the posterior to the anterior LV. Although these findings favor a dominant domain in the posterior LV, the facts that the anterior LV had a higher incidence of reentry than did the posterior LV and that the posterior LV did not have propoff/propon significantly different from 1 do not. Thus, quantitative regional differences are present over the porcine LV epicardium during VF. Although these differences are not totally consistent with the presence of a dominant domain within the LV free wall, the mean conduction velocity vector is consistent with one in the septum. |
2,906 | Progressive increases in complexity of T-wave oscillations herald ischemia-induced ventricular fibrillation. | T-wave alternans (TWA), an ABAB oscillation, has been postulated as the initial pattern in a stepwise progression to higher-order oscillations, culminating in sudden arrhythmic death. The present study is the first to provide experimental evidence to support this intriguing concept. Epicardial and endocardial ECGs from 12 dogs were monitored during 8-minute left anterior descending coronary artery occlusion with right atrial pacing at 150 bpm. TWA magnitude was measured by modified moving average beat analysis, and the complexity of T-wave oscillations was assessed by complex demodulation. In 6 animals with subsequent ventricular fibrillation (VF), TWA achieved a threshold of 5.00+/-1.30 mV in epicardial ischemic-zone electrograms, which then exhibited a stepwise increase in T-wave oscillation complexity to quadrupling (ABCDABCD, 3 cases) or tripling (ABCABC, 2 cases) and to more complex forms (5 cases) preceding VF (6 cases). In dogs without VF, peak TWA levels did not increase from baseline, measuring a maximum of 0.35+/-0.10 mV (P=NS), or only 7% the value of those with VF, and T-wave multupling was not observed (0 of 6 versus 5 of 6, P<0.005). Discordant TWA episodes, with T waves alternating out of phase, were associated with increased T-wave complexity and fibrillation in 4 of 6 dogs with VF but in none of the 6 dogs without VF (P<0.025). TWA appears to be the first step in an orderly progression of T-wave complexity, episodes of discordant TWA, and VF. This demonstrated increase in T-wave complexity points to a fundamental mechanistic link underlying the ability of TWA to predict lethal arrhythmias. |
2,907 | Time to first shock by emergency medical technicians with automated external defibrillators. | The interval from collapse to electrical rescue shock is a critical determinant of successful defibrillation in cardiac arrest. In order to achieve the earliest possible defibrillation, many emergency medical services (EMS) systems equip first-responding units with an automated external defibrillator (AED).</AbstractText>To measure the time from on-scene emergency medical technician (EMT) recognition of cardiac arrest to AED application and shock in ventricular fibrillation (VF) arrest. In addition, the authors sought to understand the reasons for delays.</AbstractText>Using the AED recordings and written EMS reports, the authors conducted a retrospective cohort study of all persons who experienced an EMS-attended VF cardiac arrest in which an AED was applied and a shock delivered by an EMT, from January 1999 through December 2000 (n = 177). Based on the bimodal distribution of times, two groups were assembled: no delay (time to shock < or = 90 seconds) and delayed (time to shock > 90 seconds). Patient and event characteristics associated with delay status were determined using Mantel-Haenszel methods.</AbstractText>The median (25th, 75th percentile) time from cardiac arrest recognition to shock was 51 (43, 64) seconds. Ninety-four percent (n = 166) of the cohort received a shock within 90 seconds. Delayed shock was associated with unwitnessed arrest status (odds ratio = 9.3, 95% confidence interval = 2.3, 36.8) and nursing home location (odds ratio = 10.0, 95% confidence interval = 2.1, 47.5).</AbstractText>The findings suggest that a 1-minute goal and a 90-second minimum standard for time to first shock are appropriate for EMT AED defibrillation in the field.</AbstractText> |
2,908 | Azathioprine in refractory sprue: results from a prospective, open-label study. | Refractory sprue is a rare and severe malabsorptive disorder that mimics celiac disease but is refractory to a gluten-free diet and is without initial evidence of overt lymphoma. Treatment is largely empiric and often ineffective, with steroids and immunosuppression being the mainstream therapeutic options. The aim of this study was to evaluate prospectively the effect of azathioprine on a group of patients diagnosed with refractory sprue.</AbstractText>We studied seven consecutive patients (five women and two men) with a well-defined diagnosis of refractory sprue and a lack of response to oral or parenteral steroids. At diagnosis, five patients had endoscopic evidence of ulcerative jejunitis, and five underwent exploratory laparotomy for exclusion of malignancies. The characteristic monoclonal TCRgamma gene rearrangement was shown in five of six patients studied. Patients were treated for a mean of 11 months (range 8-12 months), and clinical, biochemical, molecular, and histological parameters were reassessed at the end of the trial. The study was a prospective, open-label, non-placebo-controlled study using azathioprine (2 mg/kg/ day) plus oral prednisone (1 mg/kg/day). A gluten-free diet (n = 7) as well as enteral (n = 6) and parenteral nutrition (n = 5) were administered during the trial.</AbstractText>After treatment, five patients had a complete clinical remission, and biochemical and nutritional parameters were significantly improved. Steroids were tapered after the onset of azathioprine, and no patient was on steroids at the end of the trial. Intestinal histology improved significantly in all cases (normal histology in three cases and minor infiltration in the lamina propria in two). Two patients did not respond to treatment at any time and died in months 10 and 9, of an irreversible ventricular fibrillation and sepsis, respectively. No overt lymphoma was demonstrated during the follow-up.</AbstractText>The present study confirms earlier anecdotal reports on the efficacy of azathioprine in refractory sprue, with clear clinical and histological improvement shown in most patients. However, monoclonality persisted after treatment. We consider that a larger number of patients should be evaluated before a definitive recommendation is adopted for use of this drug in refractory sprue.</AbstractText> |
2,909 | Transmural reentry triggered by epicardial stimulation during acute ischemia in canine ventricular muscle. | Ischemia depresses tissue excitability more rapidly in the ventricular epicardium than in the endocardium. We hypothesized that this would provide the substrate for transmural reentry originating in the epicardium. We mapped transmural conduction in isolated and perfused wedges taken from canine left ventricles during global ischemia while pacing alternately between the epicardium and endocardium. Ischemia reduced conduction velocity more in the epicardium than in the endocardium. We observed that the epicardial-initiated activation penetrated the ventricular wall transmurally while failing to conduct laterally along the epicardium, then conducted laterally along the endocardium and midmyocardium, and reentered the epicardium in 9 of 16 wedges during epicardial stimulation after 600 +/- 182 s of ischemia. Endocardial stimulation applied immediately before or after the epicardial stimulation initiated activation that spread quickly along the endocardium and then transmurally to the epicardium without reentry in six of the nine wedges. The transmural asymmetric conduction was not observed in four separate wedges after the endocardium was removed. Therefore, ischemia-induced transmural gradient of excitability provided the substrate for reentry during epicardial stimulation. |
2,910 | [Myotonic dystrophy and bundle-branch re-entrant tachycardia]. | We report the case of a 37-year-old man diagnosed with myotonic dystrophy who presented atrial fibrillation with high ventricular rate. While being treated with amiodarone, he suffered cardiac arrest. The electrophysiological study disclosed bundle-branch reentrant ventricular tachycardia and ventricular fibrillation. Catheter ablation of the right bundle branch was performed and a bicameral defibrillator was implanted. The mechanisms and treatment of arrhythmias in these patients are discussed. |
2,911 | [Role of coronary artery revascularization and aneurysmectomy in ventricular arrhythmias in the chronic phase of myocardial infarction]. | The influence of coronary artery revascularization on the control of ventricular arrhythmias in patients with chronic myocardial infarction is uncertain. However, ablation of the arrhythmogenic circuit in these patients by aneurysm resection is useful for controlling ventricular arrhythmias. We made a prospective analysis of our clinical strategy in patients who were candidates for coronary artery revascularization and/or aneurysmectomy to determine its influence on the recurrence of ventricular arrhythmias.</AbstractText>Prospective study of 17 consecutive patients with chronic myocardial infarction and ventricular arrhythmias unrelated with an acute ischemic event, who had coronary artery disease and/or ventricular aneurysm susceptible to aggressive treatment. We evaluated our clinical strategy and the recurrence of ventricular arrhythmias during a mean follow-up period of 33.64 months.</AbstractText>Two groups of patients were studied: patients with ventricular aneurysm (group I: 12 patients) and patients without ventricular aneurysm (group II: 5 patients). Seven patients of group I underwent endoaneurysmorrhaphy and endocardial resection (4 of these patients had associated revascularization procedures). Three patients were not candidates for aneurysmectomy or revascularization procedures. Two patients underwent only revascularization procedures. All the patients in group II were revascularized. The patients who underwent aneurysmectomy did not have recurrence of arrhythmias. In 5 of the 6 patients who underwent programmed electrophysiological stimulation after aneurysmectomy, no sustained arrhythmia could be induced. Patients who were only revascularized had a high rate of recurrence of ventricular arrhythmias (57%), which were inducible after revascularization.</AbstractText>Aneurysmectomy and endocardial resection constituted, in our experience, an effective tool for controlling ventricular arrhythmias associated with left ventricular aneurysm. Coronary artery revascularization in patients with ventricular arrhythmias and chronic myocardial infarction probably does not prevent the recurrence of ventricular arrhythmias.</AbstractText> |
2,912 | New insights into onset mechanisms of atrial fibrillation and flutter after coronary artery bypass graft surgery. | To determine by means of a monitoring study the onset mechanisms of atrial fibrillation (AF) after coronary artery bypass graft surgery (CABG).</AbstractText>During elective CABG, 81 patients had one bipolar atrial and one ventricular epicardial electrode attached. These were connected to a Vitatron 900E external pacing device, which monitored the patients for four consecutive days. 12 lead ECGs were obtained if AF was clinically detected and Holter ECGs were obtained in 8 (33%) of these patients.</AbstractText>24 patients (30%) developed paroxysmal AF (50%), atrial flutter (17%), or both (33%). The number of AF episodes varied from 1-169 a day (median 5) and were usually of short duration (median 2.25 minutes). Pacemaker diagnostics showed much intrapatient and interpatient variability in onset mechanisms but the majority of AF onsets (71%) were preceded by either short runs of AF or multiple atrial extrasystoles. The final trigger was a conducted atrial extrasystole in 72% of cases. There were no bradycardic triggers. The Holter ECGs confirmed the device's data.</AbstractText>The onset mechanisms of post-CABG AF are dominated by atrial extrasystoles with multiple atrial extrasystoles and short runs of AF preceding the main AF onset in the majority of cases. These results have major implications for the development of new preventive pacing algorithms.</AbstractText> |
2,913 | Surgical closure of atrial septal defects in adults: effect of age at operation on outcome. | To determine whether age has an effect on the long term outcome after surgical closure of atrial septal defects in patients aged 35 years and over.</AbstractText>Retrospective analysis of 89 patients (64 women) operated on between 1989 and 1999. Patients were divided into two age groups: group I (aged 35-50 years, n = 51) and group II (> 50 years, n = 38). Follow up was between 1-11 years.</AbstractText>One operative death and two late deaths occurred in the study period (both in group II). Preoperatively, 29 (57%) patients were in New York Heart Association functional class III-IV in group I compared with 22 (58%) patients in group II (NS). After operation, 44 (86.2%) patients in group I were found to be in class I-II compared with 25 (71.5%, p < 0.05) in group II. Group I patients had a lower incidence of preoperative atrial fibrillation than those in group II (12 (23.5%) v 17 (43.6%), p < 0.05) and only four (7.8%) patients in group I were in atrial fibrillation requiring long term warfarin after surgery compared with 12 (34%, p < 0.05) in group II. Furthermore, echocardiography showed a greater reduction in right ventricular dimension in group I patients (mean (SD) 4.26 (0.82) v 2.71 (0.41) cm, p < 0.001) than in group II patients (4.36 (0.43) v 3.87 (0.29) cm, p = 0.21). No residual intracardiac shunts were identified during follow up.</AbstractText>Surgical closure of atrial septal defects in adult patients can improve clinical status and prevent right ventricular dilatation. The greatest benefit is seen in younger patients.</AbstractText> |
2,914 | Heart transplantation as last resort against Brugada syndrome. | We report the first case, to the best of our knowledge, of a patient with Brugada syndrome who required heart transplantation to control multiple "electrical storms." |
2,915 | Programmed electrical stimulation in Brugada syndrome: how reproducible are the results? | Inducibility of ventricular arrhythmias at programmed electrical stimulation (PES) ranges between 50% and 80% of patients with Brugada syndrome. However, the variety of PES protocols and the lack of data relative to a control group or to ventricular arrhythmia reproducibility contribute to a still undefined interpretation of PES outcome in Brugada syndrome.</AbstractText>Twenty-one patients with Brugada syndrome (18 men and 3 women; mean age 34 years; 9/21 symptomatic; 8/21 with SCN5A gene mutation) underwent a PES protocol from two right ventricular sites. The endpoint was PES protocol completion or induction of sustained or reproducible (>6 consecutive inductions) nonsustained (>6 beats) fast ventricular arrhythmia. In 17 of 21 patients with Brugada syndrome, PES was repeated 2 months later to test ventricular arrhythmia reproducibility. Twenty-five healthy patients (17 men; mean age 36 years) formed the control group. In patients with Brugada syndrome, ventricular arrhythmia inducibility rate at PES was high (18/21 patients [85%]) and increased with protocol aggressiveness, independent of clinical presentation. In control subjects, no ventricular arrhythmias were induced. Among patients with Brugada syndrome, 14 (82%) of 17 patients remained inducible at a second PES.</AbstractText>In our experience, ventricular arrhythmia inducibility in patients with Brugada syndrome, at variance with healthy controls, is high and does not correlate with clinical presentation. PES inducibility is deeply influenced by the protocol used. PES outcome is reproducible at a mid-term follow-up mainly if a categorical endpoint (inducible vs noninducible) is used. The need to assess the predictive value of specific PES protocols in targeted studies is widely emerging and is confirmed by our results.</AbstractText> |
2,916 | Anatomy of a murder: telemetric footprints. | A man with complete heart block received a Pacesetter Affinity pacemaker, programmed DDD. Two months later, the patient was beaten to death and the coroner requested telemetric information. Pacemaker stored Event Records for the previous 40 hours were retrieved and using the zoom scale, the events leading to death were examined. This included sinus tracking during the beating followed by atrial and ventricular pacing interpreted as an unconscious vagal response associated with profound blood loss. Then followed a chaotic rapid ventricular activity or terminal ventricular fibrillation. The telemetric footprints provided valuable time stamps on the events preceding the victim's death. |
2,917 | Implantable cardioverter defibrillator dysfunction during and after magnetic resonance imaging. | This report describes a patient in whom a MRI of the brain was performed without realizing that an ICD had been implanted 8 days previously. Electromagnetic noise induced during the MRI was detected as ventricular fibrillation and nearly caused inappropriate shocks. Charge time during MRI was prolonged. The battery indicator switched to "end of life," but this was reversed by capacitor reformation. These problems could have been avoided by inactivating the ICD prior to MRI. Three months later, the pacing threshold increased from 0.4 V per 0.5 ms at implantation to 2.8 V per 0.5. It is still uncertain whether radiofrequency current heating at the electrode tip caused the increased pacing threshold or if this would have occurred independently of the MRI. MRI of patients with an active ICD may cause life-threatening complications, and it is unknown if MRI may be safely performed if the ICD is inactivated. Therefore, MRI of patients with an ICD remains contraindicated. |
2,918 | Shock coordinated with high power of morphology electrogram improves defibrillation success in patients with implantable cardioverter defibrillators. | Animal studies have suggested that the success of defibrillation may depend on the properties of VF waveform obtained from the morphology electrogram (ME) at the time of the shock. The reliable identification of depolarization events in the fibrillatory signal can be achieved using adaptive estimation of the instantaneous signal power (P). The aim of this study was to investigate if a high P of the ME (P(ME)) was related to ventricular DFT and if the upslope in ME can be associated with the depolarization event. A total of 575 VF (mean duration 10 s) episodes recorded and stored during ICD implantation in 77 patients with ventricular arrhythmias were used for analysis. The DFT was defined using a double step-down test. The values of P(ME) immediately before pulse delivery (P(shock)) and shock outcomes were registered. The differences between P(shock) of successful and failed defibrillation were tested with the Mann-Whitney U test. The relationship between individual medians of P(shock) (P(med)) and DFT was analyzed using the Kruskall-Wallis H-test. The coincidence between identified depolarization and upslope in ME was tested using the chi-square test. A P value of 0.05 was set for an error probability. The P(shock) in case of failed defibrillation was significantly lower than P(shock) in successful cases by the pulses of any strength (P < 0.001). The test revealed a significant inverse correlation between P(med) and DFT with P < 0.001. The depolarization corresponded to the upslope of ME in 85% of cases. This study demonstrated that a high value of instantaneous power of ME indicates the optimal time for shock delivery. The implementation of this algorithm in ICDs may improve the defibrillation efficacy. |
2,919 | Prognosis of patients with ventricular fibrillation in out-of-hospital cardiac arrest in Hong Kong: prospective study. | To determine the prognosis of patients with ventricular fibrillation in out-of-hospital cardiac arrest in Hong Kong and examine its relationship with the other links in the chain of survival.</AbstractText>Prospective descriptive study.</AbstractText>Three accident and emergency departments, Hong Kong.</AbstractText>Patients older than 18 years with non-traumatic out-of-hospital cardiac arrest who were transported to the hospitals by ambulance between 15 March 1999 and 15 October 1999.</AbstractText>Demographic data, characteristics of the cardiac arrest and the response times of the emergency medical service according to the Utstein style, and survival to hospital discharge rate.</AbstractText>Three hundred and twenty patients were included. The incidence of ventricular fibrillation in this group of patients was 14.1%. The chance of survival to hospital discharge was significantly higher for patients with ventricular fibrillation than those with other rhythms of cardiac arrest (4.4% versus 0.7%). Approximately 40.0% of all cardiac arrests were witnessed. The bystander cardiopulmonary resuscitation rate was low at 15.6%. The median intervals for recognition to activation of the emergency medical service, time to cardiopulmonary resuscitation, time to defibrillation, and time to advanced life support were 1, 8, 9, and 27 minutes, respectively.</AbstractText>Patients with ventricular fibrillation in out-of-hospital cardiac arrest have a better chance of survival than those with other cardiac rhythms. Further improvement requires simultaneous strengthening of all four links in the chain of survival.</AbstractText> |
2,920 | Use of topological charge to determine filament location and dynamics in a numerical model of scroll wave activity. | The unique time course of an excitable element in cardiac tissue can be represented as the phase of its trajectory in state space. A phase singularity is defined as a spatial point where the surrounding phase values changes by a total of 2 pi, thereby forming the organizing center for a reentrant excitatory wave, a phenomenon which occurs in cardiac fibrillation. In this paper, we describe a methodology to detect the singular filament in numeric simulations of three-dimensional (3-D) scroll waves by using the concept of topological charge. Here, we use simple two-variable models of cardiac activity to construct the state space, generate the phase field, and calculate the topological charge as a summation of 3-D convolution operations. We illustrate the usage of the algorithm on the basic dynamics of vortex ring filament behavior as well as the more complex spatiotemporal behavior observed in fibrillation. We also compare the motion of filament wavetips as determined by the phase field produced by two-variable state space and single-variable, time-delay embedded state space. Finally, we examine the state spaces produced by a more complex three-variable model. We conclude that the use of state-space analysis, along with the unique properties of topological charge, allows for a novel means of filament localization. |
2,921 | Ionic and cellular basis for the predominance of the Brugada syndrome phenotype in males. | The Brugada syndrome displays an autosomal dominant mode of transmission with low penetrance. Despite equal genetic transmission of the disease, the clinical phenotype is 8 to 10 times more prevalent in males than in females. The basis for this intriguing sex-related distinction is unknown. The present study tests the hypothesis that the disparity in expression of the Brugada phenotype is a result of a more prominent I(to)-mediated action potential notch in the right ventricular (RV) epicardium of males versus females.</AbstractText>We studied epicardial tissue slices, arterially perfused wedge preparations, and dissociated epicardial myocytes isolated from male and female canine hearts. RV epicardium action potential phase 1 amplitude was 64.8+/-2.0% of that of phase 2 in males compared with 73.8+/-4.4% in females (P<0.05) at a cycle length of 2000 ms. I(to) density was 26% smaller and time constant for inactivation 17% smaller at +40 mV in female versus male RV epicardial cells (P<0.05). The other functional characteristics of I(to), including the voltage dependence of inactivation and time course of reactivation, were no different between the sexes. Pinacidil caused loss of action potential dome in male, but not female, RV epicardial tissue slices. Terfenadine (5 micromol/L) induced phase 2 reentry in 6 of 7 male but only 2 of 7 female arterially perfused wedge preparations. Two of 6 male and 1 of 2 female preparations developed polymorphic ventricular tachycardia/ventricular fibrillation.</AbstractText>Our results suggest that the predominance of the Brugada phenotype in males is a result of the presence of a more prominent I(to) in males versus females.</AbstractText> |
2,922 | Alternans of atrial action potentials during atrial flutter as a precursor to atrial fibrillation. | The mechanisms underlying the transition of typical atrial flutter (Afl) to fibrillation (AF) remain unclear. We set out to test the hypothesis that Afl disorganizes to AF via alternans of atrial action potentials.</AbstractText>In 38 patients with Afl, monophasic action potentials (MAPs) were recorded at the isthmus and either high or low right atrium (HRA, LRA) during overdrive pacing to 160 ms or to the initiation of AF, whichever came first. MAP duration measured at 90% repolarization was longer at the isthmus in all patients, and failed to shorten with rate, compared with the HRA (n=38) or LRA (n=5). In 20 patients who developed AF, progressive pacing first caused alternans of isthmus MAP duration and amplitude at mean cycle length of 219+/-45 ms, followed by AF at a mean onset cycle length of 184+/-38 ms. Subsets of this group showed spontaneous action potential duration alternans at the isthmus (11 of 20 patients) and 2:1 isthmus conduction block immediately preceding AF (4 of 20 patients). In the 18 patients who did not develop AF, MAP alternans was less common (9 of 18 patients; P<0.0003), and occurred only at faster pacing (cycle length=169+/-25 ms; P<0.05).</AbstractText>In patients with typical Afl, action potential duration rate maladaptation at the isthmus may lead to action potential duration alternans and conduction block preceding the transition to AF. These isthmus characteristics may enable the spontaneous initiation of AF through wavefront fractionation and may explain the benefits of isthmus ablation in preventing AF recurrence.</AbstractText> |
2,923 | [New approaches in first aid for cardiovascular patients]. | Sudden cardiac arrest is a major problem of our society. Ventricular fibrillation strikes without any warning. It leads to unconsciousness and death occurs within minutes. Every year at least 100,000 people die from sudden cardiac arrest in Germany alone. The following article is concerned with how todays rescue system can be improved in order to increase survival rates. The time which passes between occurrence of the ventricular fibrillation and the therapeutic defibrillation plays a major role. It is being observed that decentralizing the rescue system is of great advantage. The idea of the "first responder", involving laymen, family members, and company paramedics, reduces the rescue time extraordinarily. The introduction of a digital emergency health record which provides the doctor with all the important data on the patient briefly seems to be of equal importance. Hereby, delays based on false information can be reduced to a minimum. Optimizing the equipment by means of implementing automatic procedures which enable the application by laymen is just as important. But the key to medical success appears to be educating and repeatedly training as many people as possible. |
2,924 | [Acute cardiovascular failure and its treatment--value of defibrillation in preclinical management]. | Ventricular fibrillation is the most common cause of cardiac arrest. The only scientifically proved therapy that guarantees a long time survival is the early electrical defibrillation. As early as 200 years ago electricity was employed in trying to regain circulation in cases of unexpected death. In the field of emergency medicine almost all rescue services are equipped with defibrillators nowadays and the personnel is trained in using them. Since the application of electricity on the myocardium can lead to damage, there are devices with a varied defibrillation pulse available since recently. The advantage of the biphasic defibrillation is a less harmful impact on the myocardium at lower shock intensity. A further novelty which enables the application by groups other than the rescue services, is the automatic external defibrillator (AED). Extending the availability of defibrillators can contribute to an increase in the presently low success rates of resuscitation. |
2,925 | [New aspects of ICD therapy: from rhythm therapy to complex cardiac monitoring. Development of an implantable, ICD-assisted, intrathoracic 6-channel ECG for continuous monitoring of high infarct risk patients]. | Implantable defibrillator systems (ICD) are therapy of choice for the treatment of life-threatening ventricular arrhythmias and in prevention of sudden cardiac death. In more than 80% of patients who receive an ICD, the underlying cardiac disease is a coronary heart disease. Since arrhythmogenic sudden cardiac death can be reliably prevented in these patients by the use of ICD technology, the cardiac prognosis for these patients is determined by the occurrence of myocardial ischemia and myocardial infarction, as well as from the heart failure which develops in consequence. An intrathoracic 6-channel ECG comparable to the standard surface ECG can be reconstructed by further technical development of the electrode configurations currently present in ICD systems. The importance of this development in early diagnosis of myocardial ischemias and myocardial infarction can hardly be adequately estimated at the moment. The chronic consequences of myocardial infarction can be completely prevented or at least greatly reduced by means of such diagnostics and inclusion of immediate initiation of effective, appropriate early therapeutic measures before more serious symptoms even occur. In the development and pilot studies thus far, it has been found that the intrathoracic 6-channel ECG which can be generated in the ICD is capable of reliably recognizing acute myocardial ischemia, irrespective of localization or extent earlier and better than the standard surface ECG. Continuous preventive ischemia monitoring using the implanted ICD thus appears possible in patients at risk of infarction. |
2,926 | [The future of electrical defibrillators for the heart]. | The aim of electric defibrillation of the heart is to salvage a greater percentage of victims of cardiac arrest in the future. An initial decisive pathway towards this goal is to get a defibrillator to the victim as quickly as possible and apply an electric shock. This has now been implemented on a large scale--by means of the widespread propagation of (semi-)automatic external defibrillators (AED) and their PAD (Public Access Defibrillator) variant for use by laypersons. This is an initial necessary prerequisite which, however, is not sufficient to have a real impact on saving lives. For experience has shown that, despite the early use of AEDs, an appreciable proportion of the victims cannot be saved. The intention is to improve this situation by increasing the efficacy and reducing the harmful downside of the defibrillation waveforms applied. The solution is optimally dimensioned biphasic waveforms with high efficacy at low energy levels. In this connection, it is shown that the efficacy of high-energy defibrillation shocks is exceeded by their injurious effects, thus thwarting life-saving defibrillation. Examples of new waveforms of particularly high efficacy are presented. It is shown how such impulses should be physiologically dimensioned, and clinical results of cardioversion (atrial defibrillation) and initial out-of-hospital results of emergency defibrillation are discussed. In addition, new approaches for future waveforms enabling pulsed pulse-pause-modulated biphasic shocks are described. In this way, waveforms with a physiologically optimal effect on the heart can be produced which were previously impossible with portable defibrillators. Waveforms that have already been tested or are still in the research stage, justify hopes that improved survival of cardiac arrest victims may be expected. These new waveforms may also be of benefit in other types of defibrillators (e.g. cardioversion or implanted defibrillators). |
2,927 | [The shock for life: early defibrillation in first aid and by the professional paramedic]. | The Automated External Defibrillation is the key link of the chain of survival for patients in cardiac arrest. A lot of case series and trials have shown the effectiveness of early defibrillation by first rescuers and trained lay persons. The earlier the defibrillation is performed, the better is the rate of survival to hospital discharge. To increase the survival rate healthcare providers, first rescuer citizens at worksites and trained lay rescuers should be authorized, equipped and encouraged to perform early defibrillation combined with effective cardiopulmonary resuscitation (CPR). The new generation of Automated External Defibrillators (AED) are sophisticated, computerized devices that are reliable and simple to operate, enabling also lay rescuers to administer this lifesaving intervention to victims of cardiac arrest. For the concept of recurrent adequate and qualified training in the use of the AED integrated in effective DPR is recommended. |
2,928 | Treatment of medically uncontrolled coronary artery spasm in the normal coronary artery with coronary stenting. | We present a 53-year-old male with recurrent episodes of vasospastic angina and serious complications of coronary artery spasm including ventricular fibrillation and myocardial infarction, who was treated with coronary stenting at the site of ergonovine-induced coronary vasospasm where the coronary artery appeared angiographically normal, i.e., without evidence of atherosclerotic lesion. |
2,929 | Cardiac arrest related to coronary spasm in patients with variant angina: a three-case study. | We present three patients with variant angina pectoris and episodes of cardiac arrest. All of them had typical clinical symptoms, ST-segment changes in electrocardiogram, and coronary artery spasm confirmed by arteriography. They were treated with high doses of calcium antagonists and nitrates. An automatic cardioverter-defibrillator was implanted in the patient who developed ventricular fibrillation despite therapy with calcium antagonists. In another patient a DDD pacemaker was implanted because of high-degree atrioventricular block. |
2,930 | Teaching hospital physicians' skills and knowledge of resuscitation algorithms are deficient. | The resuscitation skills of 78 on-call physicians in a tertiary referral center were evaluated in a simulated sudden cardiac arrest (SCA).</AbstractText>The study subjects consisted of physicians whose on-call duty included handling emergency situations. First they were drawn without warning to a simulated witnessed cardiac arrest (ventricular fibrillation (VF)). They were provided with two nurses and all the equipment and medicine needed to treat SCA. Second, they were asked to write the current treatment protocols for basic life support (BLS) and VF.</AbstractText>The median time to defibrillation was 2.38 min, and only 31% of the physicians were able to use the defibrillator correctly. Thirty per cent treated asystole according to the guidelines of the time. Twenty-four per cent were able to return the spontaneous circulation and the median time to ROSC (return of spontaneous circulation) was 5.75 min Only 25% of the physicians wrote the guideline for treatment of VF and basic life support correctly or nearly correctly.</AbstractText>Regular resuscitation education should be compulsory to all physicians responsible for on-call duties in hospitals. Hospitals should have at least one employee part-time responsible for this duty.</AbstractText> |
2,931 | Cardiotoxic interaction of metabolites from a prodrug segment cilexetil (cyclohexyloxy-carbonyloxy-ethyl) with digoxin in the canine failing heart. | Potential risks of cyclohexanol (CH) and cyclohexanediol (CHD) isomers, which are the metabolites derived from cilexetil ester side-chain of several prodrugs such as antibiotics (e.g. cefotiam hexetil) and an antihypertensive agent (candesartan cilexetil), were examined in beagles that were made congestive heart failure (CHF) by rapid ventricular pacing. The following three experiments tested the cardiac effects of i.v. doses of: (1) the metabolites alone, (2) the metabolites under the digoxin-induced bradycardia, and (3) the metabolites given concomitantly with digoxin (0.02 mg kg(-1)). Experiment 1: t-1,2- or 1,4-CHD alone (0.1-12 mg kg(-1)) exerted transient yet reproducible supraventricular or ventricular arrhythmia dose-dependently, whereas CH and 1,3-CHD at 12 mg kg(-1) showed no cardiac effect at all. Experiment 2: t-1,2-CHD (0.1-4 mg kg(-1)), but not CH or 1,3-CHD, induced the additive arrhythmia dose-dependently; t-1,2-CHD (12 mg kg(-1)) caused frequent premature supraventricular contractions and/or irreversible paroxysmal supraventricular tachycardia. Experiment 3: t-1,2-CHD, not CH or 1,3-CHD, caused fatal arrhythmia: one dog showed torsade de pointes followed by ventricular fibrillation, while another showed 3rd degree atrioventricular block and eventually cardiac arrest. In both Experiments 2 and 3, saline vehicle added onto digoxin never caused the irreversible, fatal arrhythmia. In a separate study using healthy dogs without CHF, none of these metabolites did produce cardiac effect. Given the potential risk of generating cardiotoxic metabolites from cilexetil-bearing prodrugs, the use of such prodrugs should be avoided from the patients with CHF, particularly from those who are receiving cardiac glycosides. |
2,932 | Dietary fats and coronary heart disease pathogenesis. | The intake of saturated fat seems to be the main environmental factor for coronary heart disease (CHD). However, decreasing the intake of saturated fat and replacing it in part with linoleic acid in primary or secondary intervention trials did not satisfactorily reduce CHD clinical manifestations. It is only when omega-3 fatty acids, alpha-linolenic acid (ALA), or eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) were added to the diet that sudden cardiac death (ALA, EPA plus DHA) and nonfatal myocardial infarction (only ALA) were significantly lowered. The protective effect of omega-3 fatty acids occurs rapidly, within weeks. The mechanism for preventing ventricular fibrillation seems to be through a direct effect on myocytes. The additional effect of ALA on nonfatal myocardial infarction may be through thrombosis, at least partly caused by an effect on platelets. |
2,933 | [Medication reducing therapy of atrial fibrillation: a new approach to an old problem]. | To study influence of different rate-reducing medicine groups on atrial electrical activity and ventricular thyrhms structure in chronic atrial fibrillation (CAF) and thus to optimize treatment.</AbstractText>57 patients with CAF treated with digitalis, beta-blockers, their combinations, verapamil, amiodaron and sotalol were studied. Repeatedly highly-resolution ECG analysis was made.</AbstractText>Atrial fibrillation is characterized by ff-waves basic period from 0.12 s to 0.20 s. Ventricular characteristics were determined both by AV conduction and basic ff-waves periods. The reducing of basic ff-period is the leading mechanism of digitalis rate-reducing actions in typical cases. The direct AV block appears on the late stage of therapy and is moderate.</AbstractText>Combined therapy by medicines with different mechanisms of rate-reducing actions is the most efficient. The choice of the drug and its doses is determined by basic ff-waves periods value and the ventricular rhythm structure.</AbstractText> |
2,934 | Rationale and design of a study assessing treatment strategies of atrial fibrillation in patients with heart failure: the Atrial Fibrillation and Congestive Heart Failure (AF-CHF) trial. | Nonrandomized studies suggest that atrial fibrillation is independently associated with increased mortality in patients with heart failure. Whether restoring and maintaining sinus rhythm will have a beneficial impact on cardiovascular mortality in patients with heart failure has never been tested in an adequately powered randomized trial.</AbstractText>The primary objective of the Atrial Fibrillation and Congestive Heart Failure (AF-CHF) trial is to determine whether restoring and maintaining sinus rhythm significantly reduces cardiovascular mortality compared with a rate-control strategy in patients with atrial fibrillation and CHF.</AbstractText>AF-CHF is a prospective multicenter trial (109 centers in Canada, United States, South America, Europe, and Israel), that will randomize 1450 patients with CHF with left ventricular ejection fraction < or =35% and atrial fibrillation to 1 of 2 treatment strategies: (1) rhythm control with the use of electrical cardioversion combined with antiarrhythmic drugs (amiodarone or other class III agents), (2) rate control with the use of beta-blockers, digoxin, or pacemaker and AV nodal ablation. Cardiovascular mortality is the primary end point and the intention-to-treat approach the primary method of analysis. We anticipate an 18.75% 2-year cardiovascular mortality in the rate control arm with a 25% mortality reduction in the rhythm control group.</AbstractText>As of August 13, 2002, 334 patients have been enrolled from 68 participating centers. Enrollment is expected to be concluded in May 2003 with a minimum follow-up of 2 years.</AbstractText>The results of this trial should provide definitive information concerning 2 widely applicable treatment strategies of atrial fibrillation in a large cohort of patients with CHF.</AbstractText> |
2,935 | Atrial fibrillation: the nonpharmacologic strategy. | Pharmacologic treatment has been used for decades for conversion and prevention of recurrent atrial fibrillation (AF). But the use of antiarrhythmic drugs is associated with substantial side effects and mortality in some patients. Accordingly, it is not surprising that nonpharmacologic techniques have been developed for the management of AF, including the use of atrial defibrillators, atrial pacing methods, and several surgical and radiofrequency catheter ablation procedures. The atrial defibrillator has been found to detect and treat atrial and ventricular arrhythmias appropriately, with successful termination of spontaneous AF through low energy shocks. Although these devices are promising, the factor which limits their widespread use is not safety or efficacy, but patient comfort. Several studies suggest that atrial-based cardiac pacing may have a beneficial effect in decreasing and preventing AF episodes in patients with sick sinus syndrome. Palliative ablative procedures also available for the treatment of atrial fibrillation include AV junctional modification and AV nodal ablation with permanent pacing, the latter technique being associated with improvements in ejection fraction. Two potentially curative procedures are the surgical MAZE and endocardial catheter ablation. These techniques are based on placing strategically located lesions in the atrium to disrupt the conduction pathway(s). Recent studies have focused on ablative therapies aimed at the area of the pulmonic veins. The main therapy for maintaining sinus rhythm after conversion is predominantly pharmacologic. Similarly, in the absence of heart block, if conversion to sinus rhythm is not successful, pharmacologic modalities may be required to control ventricular rate. In any case, planning a treatment regimen for the management of AF should include evaluation of the risks inherent in the use of various drugs as well as more invasive strategies. |
2,936 | Two types of ventricular fibrillation in isolated rabbit hearts: importance of excitability and action potential duration restitution. | The combined effects of excitability and action potential duration (APD) restitution on wavefront dynamics remain unclear.</AbstractText>We used optical mapping techniques to study Langendorff-perfused rabbit hearts. In protocol IA (n=10), D600 at increasing concentrations was infused during ventricular fibrillation (VF). With concentration increased to 0.5 mg/L, fast VF (dominant frequency, 19.1+/-1.8 Hz) was consistently converted to ventricular tachycardia (VT). However, increasing D600 further to 2.5 or 5.0 mg/L converted VT to slow VF (11.9+/-2.3 Hz, P=0.0011). In an additional 4 hearts (protocol IB), tetrodotoxin converted a preexisting VT to slow VF (11.0+/-1.4 Hz). Optical maps show wandering wavelets in fast VF, organized reentry in VT, and spatiotemporal periodicity in slow VF. In protocol II, we determined APD and conduction time(-1) (CT(-1)) restitutions during D600 infusion. CT(-1) was used as an estimate of excitability. At 0.1 mg/L, APD and CT(-1) restitutions were steep and flat, respectively. APD restitution became flattened when D600 increased to 0.5 mg/L, converting fast VF to VT. Further increasing D600 to 2.5 or 5.0 mg/L steepened CT(-1) restitution and widened the range of S(1) pacing cycle lengths over which CT(-1) decreased, converting VT to slow VF.</AbstractText>Two types of VF exist in isolated rabbit hearts. Fast (type I) VF is associated with a steep APD restitution, a flat CT(-1) restitution, and wandering wavelets. Slow (type II) VF is associated with a flat APD restitution, a steep CT(-1) restitution, and spatiotemporal periodicity. Both excitability and APD restitution are important in VF maintenance.</AbstractText> |
2,937 | Ventricular rate control by selective vagal stimulation is superior to rhythm regularization by atrioventricular nodal ablation and pacing during atrial fibrillation. | Selective atrioventricular nodal (AVN) vagal stimulation (AVN-VS) has emerged as a novel strategy for ventricular rate (VR) control in atrial fibrillation (AF). Although AVN-VS preserves the physiological ventricular activation sequence, the resulting rate is slow but irregular. In contrast, AVN ablation with pacemaker implantation produces retrograde activation (starting at the apex), with regular ventricular rhythm. We tested the hypothesis that, at comparable levels of VR slowing, AVN-VS provides hemodynamic benefits similar to those of ablation with pacemaker implantation.</AbstractText>AVN-VS was delivered to the epicardial fat pad that projects parasympathetic nerve fibers to the AVN in 12 dogs during AF. A computer-controlled algorithm adjusted AVN-VS beat by beat to achieve a mean ventricular RR interval of 75%, 100%, 125%, or 150% of spontaneous sinus cycle length. The AVN was then ablated, and the right ventricular (RV) apex was paced either irregularly (i-RVP) using the RR intervals collected during AVN-VS or regularly (r-RVP) at the corresponding mean RR. The results indicated that all 3 strategies improved hemodynamics compared with AF. However, AVN-VS resulted in significantly better responses than either r-RVP or i-RVP. i-RVP resulted in worse hemodynamic responses than r-RVP. The differences among these modes became less significant when mean VR was slowed to 150% of sinus cycle length.</AbstractText>AVN-VS can produce graded slowing of the VR during AF without destroying the AVN. It was hemodynamically superior to AVN ablation with either r-RVP or i-RVP, indicating that the benefits of preserving the physiological antegrade ventricular activation sequence outweigh the detrimental effect of irregularity.</AbstractText> |
2,938 | Emotional and physical precipitants of ventricular arrhythmia. | Observational studies have suggested that psychological stress increases the incidence of sudden cardiac death. Whether emotional or physical stressors can trigger spontaneous ventricular arrhythmias in patients at risk has not been systematically evaluated.</AbstractText>Patients with implantable cardioverter-defibrillators (ICDs) were given diaries to record levels of defined mood states and physical activity, using a 5-point intensity scale, during 2 periods preceding spontaneously occurring ICD shocks (0 to 15 minutes and 15 minutes to 2 hours) and during control periods 1 week later. ICD-stored electrograms confirmed the rhythm at the time of shock. A total of 107 confirmed ventricular arrhythmias requiring shock were reported by 42 patients (33 men; mean age, 65 years; 78% had coronary artery disease) between August 1996 and September 1999. In the 15 minutes preceding shock, an anger level > or =3 preceded 15% of events compared with 3% of control periods (P<0.04; odds ratio, 1.83; 95% confidence intervals, 1.04 to 3.16) Other mood states (anxiety, worry, sadness, happiness, challenge, feeling in control, or interest) did not differ. Patients were more physically active preceding shock than in control periods. Anger and physical activity were independently associated with the preshock period.</AbstractText>Anger and physical activity can trigger ventricular arrhythmias in patients with ICDs. Future investigations of therapies aimed at blocking a response to these stressors may decrease ventricular arrhythmias and shocks in these patients.</AbstractText> |
2,939 | [Frecuency of adverse events during the hygiene of the critical care patient]. | The hygiene of the patient in critical condition is a common nursing technique in the intensive care unit, which does not mean that doing it is exempt of risk for the patient's state. We carry out a study to measure the frequency of the appearance of certain adverse events during the hygiene care and their clinical repercussion.Hygiene of the critical patients was monitored, measuring the appearance of certain events at the time of hygiene and until one hour after to assess if the complications were at the moment or had a greater repercussion on the state of the patient.During the study period, some adverse event appeared in 48% (CI 95%: 43-52) of the hygiene performed while none appeared in 52% (CI 95%: 48-56) of it. The events that appeared most frequently were: desaturation in 18% (CI 95%: 15-21) of the hygiene performed, the deadaptation of the mechanical ventilation in 11% (CI 95%: 9-14), arterial hypertension in 21% (CI 95%: 18-25) and arterial hypotension in 11% (CI 95%: 9-14). The intracranial hypertension appeared in 42% (CI 95%: 26-61) of the hygiene performed to patients who were carriers of intraventricular catheter, 9% (CI 95%: 2-25) continued with elevated values 1 hour after concluding the hygiene. The rest of the events monitored presented a lower frequency, although the appearance of one episode of cardiorespiratory arrest and two of auricular fibrillation with rapid ventricular response, one of which required cardioversion, stand out. We conclude that it is an essential job of the nursing staff to correctly assess the risks that the performance of hygiene means for the critical patient, so that the technique should be applied rationally and under strict monitoring and control. |
2,940 | [Asystole after combination anesthesia]. | A 55-year-old man with liver cancer underwent partial hepatectomy under combined lumbar epidural and general anesthesia. Asystole during postoperative recovery was followed by ventricular fibrillation. After unsuccessful cardiopulmonary resuscitation efforts, brain death was diagnosed. In the absence of anemia, acidosis, electrolytic alterations or hypothermia, and after ruling out hemoperitoneum, acute myocardial infarction and stroke, we conclude that the clinical picture described was the result of autonomic imbalance due to spreading of the sympathetic block. |
2,941 | Pulmonary gas exchange after cardiopulmonary resuscitation with either vasopressin or epinephrine. | It is well established that epinephrine administered during cardiopulmonary resuscitation results in pulmonary gas exchange disturbances. It is uncertain how vasopressin affects gas exchange after cardiopulmonary resuscitation.</AbstractText>Prospective, randomized experimental study.</AbstractText>Animal research laboratory.</AbstractText>Twenty domestic pigs.</AbstractText>Animals were subjected to ventricular fibrillation and cardiopulmonary resuscitation by using either vasopressin or epinephrine. Hemodynamic and pulmonary gas exchange (multiple inert gas elimination technique) variables were recorded before cardiopulmonary resuscitation and 10, 30, 60, and 120 mins after return of spontaneous circulation when either epinephrine (control) or vasopressin was used.</AbstractText>At 10 mins after return of spontaneous circulation, blood flow to low V /Q lung units was increased in animals treated with epinephrine (17.8 +/- 6 vs. 2.6 +/- 3%, mean +/- sd, p<.01). Resulting carbon dioxide elimination was impaired in animals treated with epinephrine but not in animals treated with vasopressin (PaCO2, 55 +/- 2 vs. 46 +/- 4 torr, p<.05). Thirty minutes after return of spontaneous circulation, blood flow to lung units with a normal VA /Q ratio was reduced in animals treated with epinephrine (79 +/- 1 vs. 84 +/- 12%, p<.05), resulting in a depressed PaO2 (147 +/- 4 vs. 127 +/- 10 torr, p<.05).</AbstractText>Vasopressin compared with epinephrine for cardiopulmonary resuscitation resulted in better gas exchange variables in the early postresuscitation phase.</AbstractText> |
2,942 | Hypertonic-hyperoncotic solutions reduce the release of cardiac troponin I and s-100 after successful cardiopulmonary resuscitation in pigs. | In some patients, cardiopulmonary resuscitation (CPR) can revive spontaneous circulation (ROSC). However, neurological outcome often remains poor. Hypertonic-hyperoncotic solutions (HHS) have been shown to improve microvascular conductivity after regional and global ischemia. We investigated the effect of infusion of HHS in a porcine CPR model. Cardiac arrest was induced by ventricular fibrillation. Advanced cardiac life support was begun after 4 min of nonintervention and 1 min of basic life support. Upon ROSC, the animals randomly received 125 mL of either normal saline (placebo, n = 8) or 7.2% NaCl and 10% hydroxyethyl starch 200,000/0.5 (HHS, n = 7). Myocardial and cerebral damage were assessed by serum concentrations of cardiac troponin I and astroglial protein S-100, respectively, up to 240 min after ROSC. In all animals, the levels of cardiac troponin I and S-100 increased after ROSC (P < 0.01). This increase was significantly blunted in animals that received HHS instead of placebo. The use of HHS in the setting of CPR may provide a new option in reducing cell damage in postischemic myocardial and cerebral tissues.</AbstractText>Infusion of hypertonic-hyperoncotic solutions (HHS) after successful cardiopulmonary resuscitation in pigs significantly reduced the release of cardiac troponin I and cerebral protein S-100, which are sensitive and specific markers of cell damage. Treatment with HHS may provide a new option to improve the outcome of cardiopulmonary resuscitation.</AbstractText> |
2,943 | [Malignant lymphoma with various cardiac manifestations: a case report]. | A 49-year-old woman presented with malignant lymphoma manifesting as dyspnea, palpitation and leg edema. Chest radiography demonstrated cardiomegaly, electrocardiography(ECG) showed first degree atrioventricular block, and echocardiography showed concentric left ventricular hypertrophy with granular sparkling texture and mild pericardial effusion. The diagnosis was malignant lymphoma(B-cell) based on lymph node biopsy. Chemotherapy(CHOP) was performed under a suspected diagnosis of cardiac invasion of malignant lymphoma. Immediately after chemotherapy, ECG showed complete atrioventricular block with sinus arrest, ventricular fibrillation and atrial fibrillation. ECG was normalized after 2 weeks on chemotherapy. Left ventricular hypertrophy was improved and pericardial effusion disappeared. However, she died of recurrence of malignant lymphoma on day 116. |
2,944 | [Brugada syndrome occurring in an identical twin: a case report]. | A 51-year-old man was admitted for evaluation of palpitation and syncope. Electrocardiography showed right bundle branch block with ST segment elevation. Intravenous administration of pilsicainide(50 mg) converted the saddle-back type into coved type ST elevation. Ventricular fibrillation was induced with double extrastimuli applied to the right ventricular outflow tract. His identical younger twin had neither symptoms nor abnormality by electrocardiography. Intravenous administration of pilsicainide(50 mg) induced no significant changes in the younger twin. Although SCN5A mutation is considered to be associated with Brugada syndrome, the present results suggest that the genetic factor is not the only factor responsible for the pathogenesis of Brugada syndrome. |
2,945 | Twenty-five years' experience with the arterial switch operation. | The arterial switch operation was introduced in 1976 to correct transposition of the great arteries and has since replaced atrial palliation. This study examines the long-term outcomes of the arterial switch operation.</AbstractText>Included in the study were 195 patients who underwent the arterial switch operation from 1977 through June 2000. Patients were evaluated for functional class, pulmonary stenosis, left ventricular function, arrhythmias, aortic sequelae, and coronary disease.</AbstractText>Overall perioperative mortality was 15%, but rates dropped in the last 5 years to 4% for complex transposition and 0% for simple transposition. Of 151 survivors, 2 died late; 1 died of persisting pulmonary hypertension and 1 died of ventricular fibrillation after coronary pathologic changes. At last follow-up, a total of 145 patients were in New York Heart Association functional class I and 4 patients were in class II. The most frequent complication was pulmonary stenosis, necessitating 45 reinterventions in 26 patients. Left ventricular dysfunction was noted in 5 patients. Arrhythmias were seen in 5 patients: 2 patients had ventricular fibrillation (1 died and 1 required a defibrillator implantation), 1 had sick sinus syndrome, 1 had atrial flutter, and 1 had a single attack of supraventricular tachycardia. Aortic valve incompetence was absent or trivial in 146 patients, 3 had mild incompetence, 1 had moderate incompetence, and 1 had severe incompetence. Coronary sequelae were found in 5 of the 61 patients who underwent angiography.</AbstractText>Long-term clinical outcome of the arterial switch operation is good, and perioperative mortality is now low. Morbidity is dominated by pulmonary stenosis and coronary artery disease, with the potential for lethal arrhythmias.</AbstractText> |
2,946 | Refibrillation, resuscitation and survival in out-of-hospital sudden cardiac arrest victims treated with biphasic automated external defibrillators. | Defibrillation is essential for victims of sudden cardiac arrest (SCA) with ventricular fibrillation (VF), yet it does not terminate the underlying causes of VF. Prior to more definitive interventions, these same causes may result in recurrence of VF following defibrillation (refibrillation). The incidence and course of refibrillation, and its relation to patient outcomes, has not been previously described in the context of treatment of out-of-hospital SCA with biphasic waveform automated external defibrillators (AEDs).</AbstractText>ECGs were recovered from all shocks delivered with biphasic AEDs by Basic Life Support (BLS) first responders, primarily police, in witnessed cardiac arrests occurring from December 1996 to December 2001 in the Rochester, MN public service area. Only events prior to administration of cardio-active medications were considered. Frequency and time to occurrence of refibrillation were compared in patients in relation to the progress of their resuscitation and survival.</AbstractText>One hundred and sixteen of 128 shocks delivered under BLS care to 49 patients with witnessed cardiac arrests presenting with VF terminated VF. Most patients (61%) refibrillated while under BLS care, many (35%) more than once. Occurrence of and time to refibrillation were unrelated to achievement of return of spontaneous circulation (ROSC) under BLS care (BLS ROSC), to survival to hospital discharge and to neurologically intact survival.</AbstractText> |
2,947 | Mock loop testing of On-x prosthetic mitral valve with Doppler echocardiography. | Previous in vitro testing (mainly in aortic position) and clinical experience (often based on Doppler echocardiographic observations) demonstrated an excellent hemodynamic behavior of the On-X valve. However, integrative studies including simultaneous hemodynamic pressure and flow measurements and Doppler echocardiography are lacking. Using our computer-controlled mock loop system, two samples of the Mitral 27/29 and one sample of the Conform-X Mitral 25/33 are tested in mitral position. Data include transvalvular pressure gradient and flow as well as transthoracic Doppler echocardiography. The valves are tested under three pressure conditions (ventricular systolic pressure of 100, 130, and 160 mm Hg) at three different heart rates (60, 100, and 140 beats/min). In addition, ventricular pressure conditions simulating fibrillation are imposed. Both valve types show similar hydrodynamic characteristics and have an effective orifice area of 2.1 cm2 and a performance index of 0.56 for a cardiac output of 3.5 L/min. Regurgitant volumes remain below 6 ml. |
2,948 | Cardioversion of atrial fibrillation with ibutilide: when is it most effective? | Atrial fibrillation (AF) is found in 1% of persons above the age of 60 years. More than 5% of the population older than 69 years and about 14% of octogenarians are at risk for this arrhythmia. It is estimated that 1.5 to 3 million persons in the United States alone suffer from AF. The public health implications and attendant morbidity are a significant drain on our health care system.</AbstractText>The purpose of this study was to determine the clinical and echocardiographic predictors of success in converting AF of > or = 24 h duration.</AbstractText>Demographic and clinical and echocardiographic parameters of 101 patients with recent onset AF (> 24 h) who received ibutilide were studied.</AbstractText>Of 101 patients, 56 (55%) converted to sinus rhythm. Age, gender, hypertension, diabetes mellitus, left ventricular ejection fraction (< or = 35%), congestive heart failure, and previous medication for rate control had no significant effect on the conversion rate. Conversion rate was only 30% (9/30 patients) in the presence of an enlarged left atrium (LA > or = 5 cm) and 37.7% (23/61 patients) in the presence of mitral valve disease (MVD), whereas the conversion rate was 82.5% (33/40 patients) in the absence of MVD and 85% (29/34 patients) in the absence of both enlarged LA and MVD (p = <0.001). Patients with coronary artery disease (CAD) also exhibited a significantly greater response to ibutilide than patients without CAD (77 vs. 46%, p-value 0.005).</AbstractText>As a therapy for cardioversion of AF, ibutilide is most effective in a selected subgroup patients, such as in patients with CAD and in patients without MVD and/or markedly enlarged left atrium.</AbstractText> |
2,949 | [Simultaneous hypertrophic obstructive cardiomyopathy and long QT syndrome: a potentially malignant association]. | Hypertrophic obstructive cardiomyopathy (HOCM) and long-QT syndrome (LQTS) are cardiac diseases with known genetic disorders. They are inherited in an autosomal-dominant way. From a clinical point of view, both diseases share a disturbed repolarization and the risk of sudden cardiac death. In 1998, during the annual meeting of the German Cardiac Society, we presented the case report of two patients (mother and daughter) with the combination of both diseases, being the first scientific communication on this subject. Both patients experienced sudden cardiac death due to ventricular fibrillation more than 10 years after the first diagnosis of the diseases. Resuscitation resulted in an apallic syndrome in both. The mother died from complications during the course of the apallic syndrome. In contrast to actual therapeutic strategies and data on prophylactic ICD-implantation available today, the daughter received no defibrillator. Sudden death in the presented cases may be due to either disease or their possible malignant association. Thus, the combination of both diseases forms the argument for early prophylactic ICD-implantation in these rare cases. Moleculargenetic studies are needed in large families to elucidate the potential of a common etiology. |
2,950 | Success of serial external electrical cardioversion of persistent atrial fibrillation in maintaining sinus rhythm; a randomized study. | The aim of this prospective, randomized study was to determine the efficacy of a serial external electrical cardioversion strategy in maintaining sinus rhythm after 12 months in patients with recurrent persistent atrial fibrillation.</AbstractText>Ninety patients with persistent atrial fibrillation lasting more than 72 h but less than 1 year were randomized in a one to one fashion to repetition of up to two electrical cardioversions in the event of relapse of atrial fibrillation detected within 1 month of the previous electrical cardioversion (Group AGG), or to non-treatment of atrial fibrillation relapse (Group CTL). ECGs were scheduled at 6 h, 7 days, and 1 month. Clinical examination and ECGs were repeated during the 6-month and 12-month follow-up examinations. Echocardiography was repeated during the 6-month follow-up examination. Clinical and echocardiographic characteristics were similar in the two groups. All patients were treated with antiarrhythmic drugs before electrical cardioversion and throughout follow-up. After 12 months, sinus rhythm was maintained in 53% of Group AGG patients and in 29% of Group CTL patients (P<0.03). After 6 months, left ventricular ejection fraction had recovered significantly only in Group AGG (56.8 +/- 9.0% at enrollment vs 60.4 +/- 9.4% at 6 months,P <0.001).</AbstractText>These results demonstrate that an aggressive policy towards persistent atrial fibrillation by means of repetition of electrical cardioversion after early atrial fibrillation recurrence is useful in maintaining sinus rhythm after 12 months.</AbstractText>Copyright 2002 The European Society of Cardiology</CopyrightInformation> |
2,951 | Vasopressin: new uses in critical care. | The science of medicine has evolved dramatically over recent years, with better understanding of the mechanisms of disease leading to innovative new treatments. However, the critical care patient still suffers from a high mortality rate with few advances from the traditional modalities of therapy. Arginine vasopressin has been explored as a vasoconstrictor in the treatment of the hypotension associated with septic shock. This drug has also recently been added to the advanced cardiac life support protocol for the resuscitation of pulseless ventricular tachycardia and ventricular fibrillation. Studies of arginine vasopressin in these situations have been promising but still have yet to prove a survival benefit over traditional therapies. Newer and larger trials are necessary to determine whether any mortality benefit can be sustained from the use of arginine vasopressin in critical care patients with septic shock and cardiac arrest secondary to pulseless ventricular tachycardia and ventricular fibrillation. |
2,952 | [Interactions of peripheral mu-opioid receptors and K(ATP)-channels in regulation of cardiac electrical stability in ischemia, reperfusion, and postinfarction cardiosclerosis]. | It has been shown that mu-opioid receptor stimulation by intravenous administration of the selective mu receptor agonist DALDA in a dose of 0.1 mg/kg prevented ischemic and reperfusion arrhythmias in rats subjected to coronary artery occlusion (10 min) and reperfusion (10 min), and also increased the ventricular fibrillation threshold in rats with postinfarction cardiac fibrosis. These effects were abolished by pre-treatment with the selective mu receptor antagonist CTAP in a dose of 0.5 mg/kg or by prior injection of the opioid receptor antagonist naloxone methiodide (2 mg/kg) which does not penetrate the blood-braib barrier. Both antagonists by themselves had no effect on the incidence of occlusion or reperfusion-induced arrhythmias or on the ventricular fibrillation threshold. Pre-treatment with ATP-sensitive K+ channel (KATP channel) blocker glibenclamide in a dose of 0.3 mg/kg completely abolished the antiarrhythmic effect of DALDA. We believe that DALDA prevents occurrence of electrical instability during ischemia and reperfusion and increases the ventricular fibrillation threshold in rats with postinfarction cardiac fibrosis via stimulation of peripheral mu-opioid receptor which appear to be coupled to the KATP channel. |
2,953 | [Evaluation of emergency medicine knowledge and procedures after finishing the course "resuscitation specialty"]. | Emergency medical services are an indispensable part of out-patient medical care. For this purpose, special qualifications are necessary and these are taught within the framework of a course entitled "Certificate for Emergency Medical Services". These courses are organized either as a block course, that is a one-week course, or as weekend courses in progression. These two types of courses are compared here. Three block courses with 546 participants and five weekend courses with 599 participants were examined. The practical examination took the form of four practice stages, with 95 people from the courses taking the examination. The examination focussed on certain areas such as ECG diagnostics in the case of cardiac arrest, early defibrillation, removing helmets, immobilizing a fractured tibia, respiration with emergency equipment, vein punctures and volume substitution. Of the doctors attending the courses, 59.7% were residents, 35.7% were senior house officers and 4.6% were specialists or general practitioners. Thirty-nine (or 41.1%) of those examined attended a block course and 56 (58.9%) weekend courses. In diagnosing cardiac arrest, those attending a block course were more reliable (92.3% diagnosed correctly, compared with 67.9% in the other group). Fifteen per cent from both groups were not able to correctly diagnose ventricular fibrillation from the ECG. Of the block course participants, 39.1% chose defibrillation with the correct energy, compared with 24.2% of those attending weekend courses. One out of two participants recognized a deliberate fault in the ECG equipment. Thirty-seven per cent of participants of the block course and 35.9% from the weekend courses failed to choose the right size splint for neck immobilization. Regarding respiration, 67.2% of participants of the block course group and 71.4% of the weekend course group carried out manual artificial respiration. When using respirator equipment, 90% from the block course and 72.2% of the other group noticed an increase in respiratory tract pressure. When giving artificial respiration to an infant, 51.9% of the weekend course group and 35.9% of the block course group used an unsuitable emergency respirator. When choosing a central puncture point most participants picked the external jugular vein and gave their own previous experience as the reason (block course 48.2%, others 52.1%). Accuracy regarding the volume requirements in the case of large-scale burns, as well as choosing the quantity (16.7% compared with 7.4%) and the correct solution (47.9% compared with 40.7%) was unsatisfactory. For these reasons, we strongly recommend intensifying training in block courses for the future qualification of doctors in emergency services. It would also be useful to conduct an oral exam at the end of the entire course, which could also entitle candidates to use this professional designation as one of their qualifications. |
2,954 | [Surgical closure of atrial septal defect before or after the age of 25 years. Comparison with the natural history of unoperated patients]. | Surgical closure of an atrial septal defect (ASD) before the age of 25 years has been demonstrated to reduce complications during adulthood. However, the outcome for patients operated after the age of 25 is still debated.</AbstractText>In a retrospective study we examined the outcome of early and late surgical repair of ASD in adults, as compared with the natural evolution of unoperated patients. The study population was 280 patients (mean age 40 18 years) with non-restrictive ASD: 102 patients (group 1) underwent surgery before the age of 25 years, 90 patients (group 2) underwent surgery after the age of 25 years, and 88 unoperated patients were older than 25 years at the time of study (group 3). The variables analyzed were left ventricular systolic function, left atrial dimensions, systolic pulmonary pressure, right ventricular dimensions, the degree of mitral and tricuspid regurgitation, and the prevalence of late atrial fibrillation.</AbstractText>Left ventricular systolic function and the degree of mitral regurgitation were not statistically different between groups. Compared with the patients in group 2, the patients in group 1 had a significantly lower systolic pulmonary arterial pressure (p < 0.001) and less dilated right ventricle (p < 0.001) and left atrium (p < 0.001). The degree of tricuspid regurgitation (p < 0.001) and prevalence of atrial fibrillation (p < 0.001) were significantly higher in the patients of group 2. Compared with group 3, the patients in group 2 had a significantly lower systolic pulmonary arterial pressure (p < 0.001) and less dilated right ventricle (p < 0.001). However, the left atrial dimensions, degree of tricuspid regurgitation, and prevalence of atrial fibrillation did not differ in a statistically significant way between the two groups.</AbstractText>Surgical repair of an atrial septal defect in patients over 25 years of age does not fully prevent hemodynamic deterioration and the development of atrial arrhythmias. Therefore it seems that the surgical closure of ASD before adulthood should be strongly recommended.</AbstractText> |
2,955 | [Successful hybrid therapy combined with oral bepridil and ICD in a patient with amiodarone refractory life-threatening ventricular tachyarrhythmia associated with ischemic cardiomyopathy]. | A 68-year-old man was admitted to our hospital for the treatment of angina and ventricular tachyarrhythmia. A coronary and left ventricular angiography showed coronary artery disease and ischemic cardiomyopathy with severe left ventricular dysfunction. A percutaneous transluminal coronary angioplasty was performed successfully in the right coronary artery and his angina symptoms disappeared. However, ventricular tachycardia (VT)/ventricular fibrillation (VF) occurred spontaneously and converted to sinus rhythm with direct current shock (300 J). Oral amiodarone (200 mg/day) and continuous intravenous infusion of nifekalant and lidocaine were started. In addition, a dual chamber implantable cardioverter defibrillator (ICD) for his VT/VF was implanted. However, VT/VF occurred repeatedly after discontinuation of nifekalant. After the administration of bepridil (200 mg/day), VT/VF was completely prevented without nifekalant administration. The hybrid therapy with ICD and oral bepridil is very useful for the treatment of amiodarone resistant ventricular tachyarrhythmia. |
2,956 | ["Top-of-the-basilar" syndrome and Chagas' disease]. | As a chronic chagasic myocardiopathy, Chagas disease (CD) may give rise to cardiac insufficiency, arrhythmias, thromboembolism and stroke. Occlusive vascular disease of the rostral portion of the basilar artery or of its emergent branches may cause ischemia and necrosis in different areas of the midbrain, thalamic nuclei, cerebellum and occipital lobe.</AbstractText>We describe four patients (three males and a female, the average age being 54 years) with positive chagasic serology (indirect immunofluorescence and hemagglutination) and suffering from CD and top of the basilar syndrome. All of them underwent tests to determine proteins C and S, antithrombin III, factor V Leiden, and lupic anticoagulant, as well as being submitted to explorations using electrocardiogram (ECG), echocardiogram, carotid and transcranial echo Doppler, computerised tomography (CAT) and magnetic resonance imaging (MRI).</AbstractText>The coagulopathy studies were normal or negative in the four patients. We also describe the findings from the electrocardiograms (blockage in right branch, two cases; auricular fibrillation, one case; repolarization disorder, one case) and the echocardiograms (left ventricular dysfunction, two patients; apical aneurysm, one patient; mural thrombus, one patient). Neuroimaging revealed one case of each of the following infarctions: bilateral thalamic, bilateral cerebellar and occipital, cerebellar, thalamic mesencephalic and occipital, and thalamic mesencephalic and occipitotemporal.</AbstractText>In a patient with positive chagasic serology, with or without findings in the ECG and in the electrocardiogram that can be put down to a cardioembolic source, a vascular syndrome produced by occlusion of the distal basilar artery suggest a cardioembolism. We recommend secondary anticoagulation because of the high risk of recurrence.</AbstractText> |
2,957 | Cardiopulmonary resuscitation in the mouse. | We sought to develop a model of cardiac arrest and resuscitation on mice that would be comparable to that of large mammals and would allow for more fundamental investigations on cardiopulmonary arrest and cardiac resuscitation. A model of cardiopulmonary resuscitation previously developed by our group on rats was adapted to anesthetized, mechanically ventilated adult male Institute of Cancer Research mice that weighed 46 +/- 3 g. The trachea was intubated through the mouth, and end-tidal PCO(2) (PET(CO(2))) was measured with a microcapnometer. Catheters were advanced into the aorta and into the right atrium, and coronary perfusion pressure (CPP) was computed. A 1.5-mA alternating current was delivered to the right ventricular endocardium, which produced ventricular fibrillation or a pulseless rhythm. Precordial compression was begun 4 min later. Ten sequential studies were performed, during which five animals were successfully resuscitated and five failed resuscitation efforts. Successful resuscitation was contingent on the restoration of threshold levels of CPP and PET(CO(2)) during chest compression. As in rats, swine, and human patients, threshold levels of mean aortic pressure, CPP, and PET(CO(2)) were critical determinates of resuscitability in this murine model of threshold level of cardiac arrest and resuscitation. |
2,958 | New evidence for stroke prevention: clinical applications. | Stroke is a leading cause of morbidity and mortality in most developed nations. There is a significant body of evidence supporting strategies that target primary and secondary stroke prevention. This evidence cannot be broadly applied to all patients, and each patient's situation and values must be considered with regard to shared evidence-based decision making. Several models can be used to apply evidence to individual patients, including formal clinical decision analysis, decision aids, or simpler tools such as the likelihood of being helped vs harmed. Various programmatic models of providing patient care in stroke prevention may also be useful; these include specialized clinics or disease-management programs, anticoagulation management services, and self-testing and management of anticoagulation by patients. |
2,959 | Cariporide for pharmacologic defibrillation after prolonged cardiac arrest. | We hypothesized that cariporide, a sodium-hydrogen exchange inhibitor, would be as cardioprotective during the global myocardial ischemia of prolonged cardiac arrest as it is in settings of coronary occlusion.</AbstractText>Fifteen Sprague-Dawley rats were randomized to receive bolus injections of cariporide or placebo in a dose of 3 mgxkg(-1) into the right atrium either 5 minutes before, or at 8 minutes after, onset of ventricular fibrillation. Ventricular fibrillation was electrically induced and untreated for 8 minutes. Precordial compression, together with mechanical ventilation, was then started and continued for an interval of 8 minutes prior to attempted resuscitation. All but one placebo-treated animal were successfully resuscitated. Spontaneous defibrillation with restoration of circulation was observed in both cariporide-pretreatment and post-treatment groups but in none of the placebo-treated animals. Postresuscitation cardiac index, end-tidal CO(2), mean aortic pressure, left ventricular systolic pressure, left ventricular end-diastolic pressure, and left ventricular contractile and lusitropic functions (dP/dt(40), and -dP/dt) were significantly less impaired after cariporide, especially in the pretreated group, compared to electrically defibrillated controls. Postresuscitation ventricular premature beats were significantly reduced after cariporide. The duration of post-resuscitation survival was significantly increased in animals pretreated with cariporide.</AbstractText>Cariporide, when administered prior to and during cardiac arrest, improved both the success of resuscitation and postresuscitation myocardial function.</AbstractText> |
2,960 | [Spontaneous coronary spasm as a rare cause of survived sudden cardiac death]. | A 39-year-old man was admitted to our intensive care unit after successful resuscitation because of ventricular fibrillation with clinical and electrographic signs of acute myocardial infarction. Coronary angiography showed normal coronary arteries. MINC syndrome (myocardial infarction with angiographically normal coronary arteries) was due to a severe proximal spontaneous spasm of the left anterior descending artery (LAD). Intracoronary ultrasound imaging demonstrated an eccentric fibrous plaque in the proximal segment of LAD and a fibrofatty plaque distal to the spastic segment. At the time of electrophysiologic study, the patient was noninducible. After starting therapy with calcium antagonist, nitrate and molsidomine, the patient was stable and symptom-free.</AbstractText>Coronary spasm without significant organic stenosis is an important cause of sudden cardiac arrest and MINC syndrome. Because of the good prognosis under adequate treatment, exact diagnosis is important in the prevention of sudden death.</AbstractText> |
2,961 | Association of the human minK gene 38G allele with atrial fibrillation: evidence of possible genetic control on the pathogenesis of atrial fibrillation. | Human minK protein is the beta-subunit of I(Ks) potassium channel and plays an important role in cardiac cellular electrophysiology. We investigated the association between human atrial fibrillation and the polymorphism of minK gene (38G or 38S) with a case-control study.</AbstractText>We included 108 patients with atrial fibrillation and 108 control subjects. The case patients and control subjects were matched regarding age, sex, presence of valvular heart disease, and presence of left ventricular dysfunction. The genotype of minK was determined with polymerase chain reaction and restriction fragment analysis.</AbstractText>The results showed an association between the minK 38G allele and atrial fibrillation. The odds ratios for atrial fibrillation in patients with 1 and 2 minK 38G alleles were 2.16 (95% CI 0.81-5.74) and 3.58 (95% CI 1.38-9.27), respectively, when compared with patients without minK 38G allele. In a logistic regression model, the odds ratio for atrial fibrillation was 1.80 (95% CI 1.20-2.71, P <.0046) for patients with 1 more minK 38G allele.</AbstractText>We report the association between the minK 38G allele and clinical atrial fibrillation. Our findings suggest possible genetic control on the pathogenesis of atrial fibrillation.</AbstractText> |
2,962 | Prognostic value of baseline electrophysiology studies in patients with sustained ventricular tachyarrhythmia: the Antiarrhythmics Versus Implantable Defibrillators (AVID) trial. | We sought to determine the value of electrophysiology (EP) testing in patients with ventricular fibrillation (VF), ventricular tachycardia (VT) with syncope, or sustained VT in the setting of left ventricular dysfunction.</AbstractText>Traditionally, EP testing is part of the workup of patients with sustained VT or VF. Recently, some have suggested that EP testing is unnecessary in these patients, many of whom are likely to receive an implantable cardioverter-defibrillator (ICD).</AbstractText>Within a multicenter trial (Antiarrhythmics Versus Implantable Defibrillators) designed to evaluate whether drugs or ICD resulted in a better outcome, data were analyzed regarding EP testing. Although this testing was not required, it was performed in >50% of patients. Information regarding the results of EP testing was correlated to baseline clinical characteristics and outcome.</AbstractText>Of 572 patients subjected to an EP test, 384 (67%) had inducible sustained VT or VF. Inducible patients were more likely to have coronary artery disease, previous infarction, and VT as their index arrhythmic event. Inducibility of VT or VF did not predict death or recurrent VT or VF.</AbstractText>Information derived from EP testing in this patient population, particularly those with VF, is of limited value and may not be worth the risks and costs of the procedure, particularly in those patients likely to receive an ICD.</AbstractText> |
2,963 | Effect of risk stratification on cost-effectiveness of the implantable cardioverter defibrillator. | Implantable cardioverter defibrillators (ICDs) effectively prevent sudden cardiac death, but selection of appropriate patients for implantation is complex. We evaluated whether risk stratification based on risk of sudden cardiac death alone was sufficient to predict the effectiveness and cost-effectiveness of the ICD.</AbstractText>We developed a Markov model to evaluate the cost-effectiveness of ICD implantation compared with empiric amiodarone treatment. The model incorporated mortality rates from sudden and nonsudden cardiac death, noncardiac death and costs for each treatment strategy. We based our model inputs on data from randomized clinical trials, registries, and meta-analyses. We assumed that the ICD reduced total mortality rates by 25%, relative to use of amiodarone.</AbstractText>The relationship between cost-effectiveness of the ICD and the total annual cardiac mortality rate is U-shaped; cost-effectiveness becomes unfavorable at both low and high total cardiac mortality rates. If the annual total cardiac mortality rate is 12%, the cost-effectiveness of the ICD varies from $36,000 per quality-adjusted life-year (QALY) gained when the ratio of sudden cardiac death to nonsudden cardiac death is 4 to $116,000 per QALY gained when the ratio is 0.25.</AbstractText>The cost-effectiveness of ICD use relative to amiodarone depends on total cardiac mortality rates as well as the ratio of sudden to nonsudden cardiac death. Studies of candidate diagnostic tests for risk stratification should distinguish patients who die suddenly from those who die nonsuddenly, not just patients who die suddenly from those who live.</AbstractText> |
2,964 | Management of ventricular arrhythmias in diverse populations in California. | The use of coronary angiography and revascularization is lower than expected among black patients. It is uncertain whether use of other cardiac procedures also varies according to race and ethnicity and whether outcomes are affected.</AbstractText>We analyzed discharge abstracts from all nonfederal hospitals in California of patients hospitalized for a primary diagnosis of ventricular tachycardia or ventricular fibrillation between 1992 and 1994. We compared mortality rates and use of electrophysiologic study (EPS) and implantable cardioverter-defibrillator (ICD) procedures according to the race and ethnicity of the patient.</AbstractText>Among 8713 patients admitted with ventricular tachycardia or ventricular fibrillation, 29% (n = 2508) had a subsequent EPS procedure, and 9% (n = 818) had an ICD implanted. After controlling for potential confounding factors, we found that black patients were significantly less likely than white patients to undergo EPS (odds ratio 0.72, CI 0.56-0.92) or ICD implantation (odds ratio 0.39, CI 0.25-0.60). Blacks discharged alive from the initial hospital admission had higher mortality rates over the next year than white patients, even after controlling for multiple confounding risk factors (risk ratio 1.18, CI 1.03-1.36). The use of EPS and ICD procedures was also significantly affected by several other factors, most notably by on-site procedure availability but also by age, sex, and insurance status.</AbstractText>In a large population of patients hospitalized for ventricular arrhythmia, blacks had significantly lower rates of utilization for EPS and ICD procedures and higher subsequent mortality rates.</AbstractText> |
2,965 | Trends in hospital treatment of ventricular arrhythmias among Medicare beneficiaries, 1985 to 1995. | Treatment options for patients with ventricular arrhythmias have undergone major changes in the last 2 decades. Trends in use of invasive procedures, clinical outcomes, and expenditures have not been well documented.</AbstractText>We used administrative databases of Medicare beneficiaries from 1985 to 1995 to identify patients hospitalized with ventricular arrhythmias. We created a longitudinal patient profile by linking the index admission with all earlier and subsequent admissions and with death records.</AbstractText>Approximately 85,000 patients aged > or =65 years went to hospitals in the United States with ventricular arrhythmias each year, and about 20,000 lived to admission. From 1987 to 1995, the use of electrophysiology studies and implantable cardioverter defibrillators in patients who were hospitalized grew substantially, from 3% to 22% and from 1% to 13%, respectively. Hospital expenditures rose 8% per year, primarily because of the increased use of invasive procedures. Survival improved, particularly in the medium term, with 1-year survival rates increasing between 1987 and 1994 from 52.9% to 58.3%, or half a percentage point each year.</AbstractText>Survival of patients who sustain a ventricular arrhythmia is poor, but improving. For patients who are admitted, more intensive treatment has been accompanied by increased hospital expenditures.</AbstractText> |
2,966 | Life after a ventricular arrhythmia. | There are few data from community-based evaluations of outcomes after a life-threatening ventricular arrhythmia (LTVA). We evaluated patients' quality of life (QOL) and medical costs after hospitalization and treatment for their first episode of an LTVA.</AbstractText>We prospectively evaluated QOL by use of the Duke Activity Status Index (DASI), Medical Outcomes Study SF-36 mental health and vitality scales, the Cardiac Arrhythmia Suppression Trial (CAST) symptom scale, and resource use in patients discharged after a first episode of an LTVA in a managed care population of 2.4 million members.</AbstractText>We enrolled 264 subjects with new cases of LTVA. Although functional status initially decreased compared with self-reports of pre-event functional status, both functional status and symptom levels improved significantly during the study period. These improvements were greater in patients receiving an implantable cardioverter defibrillator (ICD) than in patients receiving amiodarone. Ratings of mental health and vitality were not significantly different between the treatment groups and did not change significantly during follow-up. The total 2-year medical costs were higher for patients receiving an ICD than for patients receiving amiodarone, despite lower costs during the follow-up period for the patients receiving an ICD.</AbstractText>New onset of an LTVA has a substantial negative initial impact on QOL. With therapy, most patients have improvements in their QOL and symptom level, possibly more so after treatment with an ICD. The costs of treating these patients are very high.</AbstractText> |
2,967 | Role of signal-averaged electrocardiograms for predicting the inducibility of ventricular fibrillation in the syndrome consisting of right bundle branch block and ST segment elevation in leads V1-V3. | Right bundle branch block and ST segment elevation (RBBB-STE) in the right precordial leads have been reported as a distinct clinical and electrocardiographic syndrome in patients prone to ventricular fibrillation (VF) in the absence of structural heart disease (Brugada syndrome). The purpose of the study was to investigate the role of signal averaged electrocardiogram (SAECG) in identifying patients at high risk among asymptomatic RBBB-STE patients. Thirteen patients with the RBBB-STE ECG were identified. Symptoms were: syncope (n=3, cases 1, 3, and 11), atypical chest pain (n=3, cases 4, 10, and 12) and palpitations (n=2, cases 6, and 7). The other 5 patients were asymptomatic. SAECG and programmed electrical stimulation (PES) were conducted in all patients. Body surface late potentials (LPs) were present in 7 of 13 patients before PES. Vf was induced in 6 of 7 LP positive patients. Vf was induced in 3 of 6 LP negative patients, but LP became positive in 2 of 3 patients in whom Vf was induced. One patient with syncope due to VF (case 1), 1 patient without symptoms who died suddenly during follow up (case 2), and 1 asymptomatic patient (case 9) showed reproducibly positive LP. In a patient (case 9) with positive LP at baseline, LP transiently became negative during follow up. In RBBB-STE patients, reproducibly positive LP is at risk for malignant ventricular arrhythmias and sudden death. Repeated SAECG recording may be useful for screening high-risk patients who should receive electrophysiological study among asymptomatic RBBB-STE patients. |
2,968 | Effects of anti-vasospastic agents in Japanese patients with dilated cardiomyopathy and coronary vasospasm. | The pathogenesis of dilated cardiomyopathy (DCM) is unknown, but clinical evidence suggests that coronary vasospasm is associated with the development of DCM in some cases. In the present study, we aimed to clarify the prevalence of coronary vasospasm in patients with DCM, the characteristics of patients with DCM and coronary vasospasm, and the effects of anti-vasospastic agents on patients with DCM and coronary vasospasm. This study included 18 consecutive patients with DCM who underwent cardiac catheterization with ergonovine provocation testing. The patient was diagnosed as having coronary vasospasm if ergonovine induced coronary vasoconstriction > or = 75% diameter narrowing was observed compared to the diameter after nitroglycerin administration. Six (33%) patients were found to have coronary vasospasm and anti-vasospastic agents were added after the cardiac catheterization. The prevalence of atrial fibrillation in the patients with DCM and coronary vasospasm was greater than that in DCM without coronary vasospasm [67% vs 8% (P<0.05)]. The left ventricular end-diastolic dimension decreased from 61 mm (56/64) to 55 mm (53/56) (median, 25th/75th percentile, P<0.05) and the left ventricular ejection fraction increased from 36% (32/40) to 47% (46/48) (median, 25th/ 75th percentile, P<0.05) after the administration of anti-vasospastic agents and 4 of the 6 patients improved symptomatically. Therefore, ergonovine provocation testing is useful in identifying patients with DCM and coronary vasospasm, in whom cardiac performance is expected to be improved with anti-vasospastic agent therapy. DCM patients with atrial fibrillation may be a clue for identifying patients with coronary vasospasm. |
2,969 | Idiopathic ventricular fibrillation in a patient with Wolff-Parkinson-White syndrome. | Ventricular fibrillation in a patient with ventricular preexcitation is usually due to atrial fibrillation with an extremely rapid ventricular rate from which it degenerates. We present a case with Wolff-Parkinson-White syndrome and coexistent idiopathic ventricular fibrillation. The patient, a 23-year-old male, had had a cardiac arrest four years earlier. In electrophysiological study, the accessory pathway was located in the left posteroseptal region and successfully eliminated with radiofrequency catheter ablation. After the ablation procedure, ventricular fibrillation was induced with programmed ventricular stimulation. A dual chamber implantable cardioverter defibrillator was implanted in the patient. |
2,970 | Evolution of the stone heart after prolonged cardiac arrest. | We hypothesized that progressive impairment in diastolic function during cardiopulmonary resuscitation (CPR) precedes evolution of the "stone heart" after failure of CPR. We therefore measured sequential changes in left ventricular (LV) volumes and free-wall thickness of the heart during CPR in an experimental model.</AbstractText>Prospective, observational animal study.</AbstractText>Medical research laboratory in an university-affiliated research and educational institute.</AbstractText>Domestic pigs.</AbstractText>Ventricular fibrillation (VF) was induced in 40 anesthetized male domestic pigs weighing between 38 kg and 43 kg. After 4 min, 7 min, or 10 min of untreated VF, electrical defibrillation was attempted. Failing to reverse VF in each instance, precordial compression at a rate of 80/min was begun coincident with mechanical ventilation. Coronary perfusion pressures (CPPs) were computed from the differences in time-coincident diastolic aortic and right atrial pressures. Left ventricular (LV) systolic and diastolic ventricular volumes and thickness of the LV free wall were estimated with transesophageal echocardiography. The stroke volumes (SVs) were computed from the differences in decompression diastolic and compression systolic volumes. Free-wall thickness was measured on the hearts at autopsy.</AbstractText>Significantly greater CPPs were generated with the 4 min of untreated cardiac arrest. Progressive reductions in LV diastolic and SV and increases in LV free-wall thickness were documented with increasing duration of untreated VF. A stone heart was confirmed at autopsy in each animal that failed resuscitative efforts. Correlations with indicator dilution method and physical measurements at autopsy corresponded closely with the echocardiographic measurements.</AbstractText>Progressive impairment in diastolic function terminates in a stone heart after prolonged intervals of cardiac arrest.</AbstractText> |
2,971 | Amelioration of ischemia- and reperfusion-induced myocardial injury by the selective estrogen receptor modulator, raloxifene, in the canine heart. | We sought to investigate whether raloxifene reduces ischemia-reperfusion injury and what mechanisms are involved in the cardioprotective effects.</AbstractText>Estradiol-17-beta reduces myocardial infarct size in ischemia-reperfusion injury. Raloxifene, a selective estrogen receptor modulator, demonstrates immediate coronary artery vasorelaxing effects.</AbstractText>The myocardial ischemia-reperfusion model included anesthetized open-chest dogs after 90-min occlusion of the left anterior descending coronary artery (LAD) and subsequent 6-h reperfusion. Raloxifene and/or other drugs were infused into the LAD from 10 min before coronary occlusion to 1 h after reperfusion without an occlusion period.</AbstractText>Infarct size was reduced in the raloxifene (5 microg/kg per min) group compared with the control group (7.2 +/- 2.5% vs. 40.9 +/- 3.9% of the area at risk, p < 0.01). Either N(G)-nitro-L-arginine methyl ester (L-NAME), the inhibitor of nitric oxide (NO) synthase, or charybdotoxin, the blocker of Ca(2+)-activated K+ (K(Ca)) channels, partially attenuated the infarct size-limiting effect, and both of them completely abolished the effect. The incidence of ventricular fibrillation was also less in the raloxifene group than in the control group (11% vs. 44%, p < 0.05). Activity of p38 mitogen-activated protein (MAP) kinase increased with 15-min ischemia, and raloxifene pretreatment inhibited the activity. Myeloperoxidase activity of the 6-h reperfused myocardium was also attenuated by raloxifene.</AbstractText>These data demonstrate that raloxifene reduces myocardial ischemia-reperfusion injury by mechanisms dependent on NO and the opening of K(Ca) channels in canine hearts. Deactivation of p38 MAP kinase and myeloperoxidase by raloxifene may be involved in the cellular mechanisms of cardioprotection.</AbstractText> |
2,972 | Cardiac arrests treated by ambulance paramedics and fire fighters. | The Emergency Medical Response (EMR) program is a Victorian Government initiative in which fire fighters trained in cardiopulmonary resuscitation and equipped with automatic external defibrillators are dispatched to suspected cardiac arrests simultaneously with ambulance paramedics across metropolitan Melbourne. During the first 12 months (February 2000 to February 2001) of the expanded EMR program, 2942 events involved simultaneous dispatch of ambulance paramedics and fire fighters. In 430 events, patients had suffered a cardiac arrest of presumed cardiac cause, and resuscitation was attempted by the emergency medical services. Fire fighters provided the initial defibrillation to 41 (26.5%) patients presenting in ventricular fibrillation. Survival to hospital discharge for bystander-witnessed ventricular fibrillation cardiac arrests was 21.8%. The mean emergency services (fire and ambulance) response time to cardiac arrest patients was 6.03 (SD, 1.65) minutes. The mean time to defibrillation for ventricular fibrillation patients was 8.75 (SD, 2.07) minutes. |
2,973 | Two cases of a free-floating ball thrombus in the left atrium. | A free-floating ball thrombus in the left atrium is an unusual occurrence that may cause fatal systemic emboli or left ventricular inflow obstruction, often resulting in sudden death. The first of 2 cases was a 59-year-old female with mitral stenosis and chronic atrial fibrillation who presented with severe dyspnea. Transthoracic echocardiography revealed a free-floating ball thrombus and emergency thrombectomy and mitral valve replacement were performed successfully. A second thrombus, which was not found at preoperative examination, was attached to the anterior mitral leaflet and may have been the source of the free-floating ball thrombus. The second case was a 79-year-old female with chronic renal failure who underwent mitral valve replacement 11 years prior to admission. She had been dependent on hemodialysis for 10 years, and had suffered several recent transient cerebral ischemic attacks. Computed tomography showed a ring-shaped, high-density area in the left atrium and transthoracic echocardiography revealed a floating ball thrombus in the left atrium. Thrombectomy was performed, but the patient died as a result of postoperative pneumonia 2 months later. Case 2 appears to be the first reported case of a ball thrombus in a hemodialysis patient who had previously undergone mitral valve replacement. |
2,974 | [The relationship between QT dispersion and risk factors of sudden death in hypertrophic cardiomyopathy]. | Several risk factors are established for prediction of sudden cardiac death caused by ventricular arrhythmias in patients with hypertrophic cardiomyopathy (HCM). QT dispersion (QTd) is thought to reflect the heterogeneity of ventricular repolarization. The relation of QTd with ventricular arrhythmias and sudden cardiac death has been shown by several studies. The aim of this study is to examine whether there is a relationship between QTd and established risk factors of sudden cardiac death in patients with HCM.</AbstractText>In the present study 48 patients with HCM and 30 normal subjects were studied. The patients with electrocardiographic changes that could affect QT interval measurements and those in whom QTd was calculated in less than 9 leads were excluded from the study. A family history of sudden death due to HCM, a history of ventricular fibrillation, nonsustained ventricular tachycardia on Holter monitoring and a history of recurrent syncope were accepted as risk factors for sudden cardiac death.</AbstractText>QTd was significantly greater in patients with HCM than in normal controls (55+/-22 ms vs 34+/-13 ms, p<0.001). There was no significant difference in QTd between patients with and without risk factors (57+/-22 ms vs 53+/-20 ms, p>0.05). There was also no significant difference in QTd between patients with and without left ventricular outflow gradient p>30 mmHg (57+/-23 ms vs 53+/-19 ms, p>0.05).</AbstractText>Although QTd was significantly greater in patients with HCM than in normal controls, its relation to risk factors of sudden death could not be established.</AbstractText> |
2,975 | [Evaluation of "admission index of insulin resistance (AIRI)" as an early stage risk predictor in nondiabetic acute coronary syndromes]. | Insulin resistance is a risk predictor for many cardiovascular diseases, but its effect on etiology and prognosis of diseases has not been clearly identified. In this study, we aimed to investigate whether admission index of insulin resistance (AIRI), recently and practically presented for determination of insulin resistance, could be a new risk predictor of early prognosis in nondiabetic acute coronary syndromes.</AbstractText>One hundred and sixty nondiabetic patients admitted to the intensive coronary care unit and underwent coronary angiography with the diagnosis of acute myocardial infarction (AMI) (Group I; 72 patients; mean age - 58+/-12 years) or unstable angina pectoris (UAP) (Group II; 88 patients; mean age 58+/-10 years) were included in the study. In all patients blood glucose and insulin levels were measured on admission and AIRI was calculated by the formula of "admission glucose level X insulin level / normal blood glucose level (5 mmol/L) X normal insulin level (5 mU/L)" for each patient. After determining the left ventricular ejection fraction (LVEF) and wall motion score index (LVWMSI) echocardiographically and calculating the Gensini score index from coronary angiography, the patients were followed up for major cardiac events (heart failure, atrial fibrillation, reinfarction, life-threatening ventricular arrhythmias, atrio-ventricular block, need for revascularisation and mortality) for 30 days.</AbstractText>AIRI was found higher in Group I (7.2+/-5.3 versus 5.2+/-4.4, p< 0.01) than in Group II. AIRI was positively correlated with Gensini score and LVWMSI (r=0.41, p<0.01 and r=0.48, p<0.001, respectively) and negatively correlated with LVEF (r=-0.37, p=0.001) in Group I. In addition, it was seen that positive correlation of AIRI with Gensini score (r=0.23, p=0.01) and LVWMSI (r=0.43, p=0.0001) in Group I persisted on multivariate regression analysis. Again, AIRI was significantly correlated with heart failure (r=0.42, p<0.0001), atrial fibrillation (r=0.35, p=0.002) and reinfarction (r=0.23, p=0.04) in Group I. Along with this, in multivariate regression analysis, it was correlated with heart failure (r=0.21, p<0.007), atrial fibrillation (r=0.18, p=0.01) and reinfarction (r=0.18, p=0.01). On the other hand, there was no significant correlation between AIRI and these parameters in Group II.</AbstractText>AIRI can be used in early stage as a risk predictor to determine high-risk subgroups of nondiabetic patients presenting with AMI. Also AIRI, a parameter, which is practically calculated and easily used, is an independent risk factor detecting the extent of coronary artery disease and left ventricular dysfunction in patients with AMI.</AbstractText> |
2,976 | [Surgical treatment of aortic coarctation in adults: mid-term results and effects on the systolic blood pressure]. | To evaluate the outcome and the systolic blood pressure changes after surgical treatment of aortic coarctation in adults.</AbstractText>Between February 1995 and January 2001, 12 adult patients with a mean age of 29+/-10 years, underwent repair of aortic coarctation in our clinic. The diagnostic and operative data of these patients were retrospectively analyzed. Follow-up was complete in all hospital survivors.</AbstractText>The mean systolic blood pressure of 8 hypertensive patients decreased from 155+/-7 mmHg to 115+/-9 mmHg after surgical intervention. One patient with a dilated cardiomyopathy died one day after the operation due to an intractable ventricular fibrillation (mortality 8.3%). Four patients had been operated for coexisting cardiovascular pathologies during a mean follow-up period of 32+/-26 months.</AbstractText>Surgical treatment of aortic coarctation in adults can be safely performed with an acceptable mortality and morbidity, both resulting from coexisting cardiovascular disorders in our patient group. The systolic blood pressure may decrease significantly after the operation.</AbstractText> |
2,977 | Electrocardiographic findings predict short-term cardiac morbidity after transient ischemic attack. | Current guidelines recommend the use of electrocardiography (ECG) in the evaluation of transient ischemic attack (TIA), but the data supporting its value in acute management are sparse.</AbstractText>To determine whether ECG findings are useful as independent predictors of short-term cardiac or neurologic complications after TIA.</AbstractText>We included patients who presented to 1 of 16 emergency departments of a health maintenance organization in northern California and received a diagnosis of TIA from March 1, 1997, through February 28, 1998, for a 90-day follow-up. A cardiac event was defined as a hospitalization or a death due to myocardial infarction, ventricular arrhythmia, heart failure, or unstable angina.</AbstractText>Among the 1327 patients with TIA for whom ECG findings were available for diagnostic coding, cardiac events occurred in 2.9%, strokes in 10.9%, recurrent TIAs in 13.7%, and deaths in 2.6% during 90-day follow-up. The ECG findings disclosed a new diagnosis of atrial fibrillation in 28 (2.3%) of the 1200 patients with no history of this condition. The 90-day risk for a cardiac event was greater in those who had any abnormal ECG findings (4.2% vs 0.6%; P<.001). This association remained significant after adjustment for medical history and examination findings (odds ratio, 6.9; 95% confidence interval, 1.6-29.5; P =.009). Left ventricular hypertrophy, atrial fibrillation, and atrioventricular conduction abnormalities were each independently associated with more than doubling of the risk. The ECG abnormalities were not associated with risk for stroke or death.</AbstractText>Short-term cardiac morbidity is substantial after TIA. Electrocardiographic findings disclose new atrial fibrillation in a significant portion of patients with TIA and can identify a group of patients at a substantially higher risk for short-term cardiac events.</AbstractText> |
2,978 | [Noncompaction of the left ventricular myocardium. Case report and review of the literature]. | Left ventricular non-compaction is an unclassified cardiomyopathy characterized by an excessively prominent trabecular meshwork due to an arrest in myocardial morphogenesis. We report on a 51-year-old female patient with abnormal myocardial trabeculations associated with a congenital mitral valve stenosis post commissurotomy at the age of 14. In the present case report, clinical manifestation of the disorder included impaired left ventricular systolic function and atrial fibrillation. Noncompaction was diagnosed by echocardiography and levocardiography. In addition, a review of the literature on this rare disorder is presented. |
2,979 | Autologous right atrial patch for closure of atrial septal defect. | Prosthetic or pericardial patches used for the closure of atrial septal defects are associated with infrequent but definite problems. As an alternative, we used a right atrial free-wall patch in 12 patients, 7-54 years of age.</AbstractText>The presence of a large secundum atrial septal defect (n=2). associated mitral valve regurgitation (n=7), primum atrial septal defect (n=2) and sinus venosus defect (n=1) necessitated the use of a patch. The mitral valve was repaired in 9 patients (including 2 with a primum defect). One patient with a primum defect who was in congestive heart failure preoperatively died after 3 weeks due to refractory ventricular fibrillation. The remaining patients were discharged 5 to 7 days post procedure. No flow was detected across the septal patch on predischarge echocardiography. One patient underwent reoperation for failed mitral valve repair one month postprocedure. At reoperation, the patch was found to be intact with normal texture and without any suture dehiscence. Histopathological examination of the explanted patch revealed viable endothellum and subendothelial muscle on both surfaces of the patch. Follow-up ranged from 6 to 36 months. Echocardiography performed after 6 to 32 months post procedure showed an intact patch with no residual defect. All the patients are in sinus rhythm. Holter monitoring performed in 6 patients was normal in all of them. Electrophysiological study was performed in 2 patients using a mapping catheter 4 and 6 months post-procedure, respectively, and recorded normal atrial potentials from the site of the patch.</AbstractText>The use of an autologous free right atrial wall as a patch for atrial septal defect closure is a viable option.</AbstractText> |
2,980 | [Failure in the functioning of an implanted automatic defibrillator due to pneumothorax occurring during its implantation ]. | A 67-year-old man with chronic bronchitis and coronary artery disease was scheduled to receive an implantable cardioverter defibrillator (ICD) after an episode of sustained monomorphic ventricular tachycardia. During implantation through the left subclavian vein, oxygen saturation decreased to slightly below baseline. Nevertheless, the procedure continued, given that the patient experienced neither breathing difficulties nor pain. When the ICD failed to reverse ventricular fibrillation induced to test the device, an external defibrillator was used. At that point, left-sided pneumothorax was observed by x-ray. Air in the pleural cavity caused an increase in the defibrillation threshold. After insertion of a thoracic drain, the ICD implantation procedure was completed successfully. |
2,981 | Effect of intra-aortic occlusion balloon in external thoracic compressions during CPR in pigs. | This study was performed to compare the effectiveness of external thoracic compressions with and without intra-aortic occlusion balloon with capnography and coronary and cerebral perfusion pressure (CPP) in the normothermic and traumatic-less cardiopulmonary arrest provoked by a ventricular fibrillation in pigs. This was an experimental study (cross-over study) in 14 pigs with similar characteristics (23 +/- 2 kg, 10-12 weeks of age). After an 8-minute nonintervention period, the cardiopulmonary resuscitation (CPR) consists of 4 periods of 5 minutes alternating CPR with and without intra-aortic occlusion balloon. Main outcomes measured are end-tidal CO(2) (ETCO(2)); intra-aortic, coronary, and cerebral perfusion pressures; blood gas analysis; and blood lactate concentration. At the end of each period, levels are obtained. Postmortem study was made. Inflation of the occlusion balloon provokes an expansion in the ETCO(2) of about 38%. The coronary perfusion pressure initially goes from 10.21 to 29.0 mm Hg after the occlusion of the aorta, which means an increase of 150%. The CPP goes from 12.54 to 39.71 mm Hg after the balloon was inflated, which means an increase of 200%. In all cases the differences are statistically significant (P <.0001). These increases are less important in the final periods. Intra-aortic balloon occlusion increased ETCO(2), coronary, and cerebral perfusion pressures. An early application of this technique was important. |
2,982 | [Future potential indications for an oral thrombin inhibitor]. | By the use of conventional anticoagulants, significant improvements were achieved in all fields of medicine. Although efficacious and widely used, their use is limited in several respects. In particular, the use of vitamin K antagonists is restricted in the clinical routine setting. The main reasons are the delayed on- and off-set of action, the narrow therapeutic window, the necessity of individual laboratory-controlled dosing, and interactions with food ingredients and drugs. The search for new antithrombotics with an improved safety/efficacy profile led to the development of the direct oral thrombin-inhibitor ximelagatran. It can be administered without routine monitoring of coagulation parameters and does not possess any of the previously mentioned limitations. The results from clinical phase II studies obtained so far are very encouraging. After completion of the clinical development program focussing on prevention and treatment of venous thromboembolism, on stroke prevention in atrial fibrillation and on acute coronary syndromes, it is desirable to continue with investigations with regard to long-term prophylaxis in high risk surgery, in chronic peripheral artery disease, in patients with left ventricular thrombi, artificial heart valves, or thrombophilia, as an alternative anticoagulant in heparin induced thrombocytopenia and for prevention of thromboembolic complications in oncology. Because of the mitogenic effects of thrombin on the proliferation of tumour cells, additional experimental studies aiming at a potential inhibition of thrombin-triggered oncogenesis is of uttermost interest. |
2,983 | Significance and control of cardiac arrhythmias in patients with congestive cardiac failure. | A wide spectrum of ventricular and supraventricular tachyarrhythmias occurs in the setting of congestive cardiac failure. However, the two most clinically significant are atrial fibrillation and ventricular tachycardia and fibrillation. In the past there has been much emphasis on premature ventricular contractions and more recently, on nonsustained ventricular tachycardia. For the most part, these arrhythmias are asymptomatic in heart failure. They are markers of sudden arrhythmic death but their suppression by antiarrhythmic drugs have not resulted in a reduction of total mortality. Two approaches have been used to this end. The first is the use of beta-adrenergic blocking drugs and antiarrhythmic agents such as amiodarone. Beta-blockers have been shown to significantly reduce sudden death as well as total mortality, while the effects of amiodarone have been less decisive. The prospective role of the implantable cardioverter defibrillator (ICD) is undergoing critical evaluation in patients with cardiac failure at high risk for sudden death. The elective role of the ICD is well established as first-line therapy in patients with heart failure resuscitated from sudden death and in those with sustained ventricular tachycardia in conjunction with conventional therapies for cardiac decompensation. The prevalence of atrial fibrillation rises as a function of severity of cardiac failure, but it is also in known that persistent atrial fibrillation with an uncontrolled ventricular response may induce heart failure. Controlled ventricular response may prevent congestive heart failure and improve left ventricular function. The two most common causes of atrial fibrillation in cardiac failure in Europe and America are ischemic heart disease and hypertension, while mitral valve disease remains the prevalent cause elsewhere. The choice of antiarrhythmic drugs for maintaining sinus rhythm is critical in the prevention of heart failure aggravation and proarrhythmic reactions of antiarrhythmic drugs. Amiodarone and dofetilide are most widely used in this context. |
2,984 | Prevention of and medical therapy for atrial arrhythmias in heart failure. | A large proportion of heart failure patients suffer from atrial arrhythmias, prime amongst them being atrial fibrillation (AF). Ventricular dysfunction and the syndrome of heart failure can also be a concomitant pathology in up to 50% of patients with AF. However this association is more than just due to shared risk factors, research from animal and human studies suggest a causal relationship between AF and heart failure. There are numerous reports of tachycardia-induced heart failure where uncontrolled ventricular rate in AF results in heart failure, which is reversible with cardioversion to sinus rhythm or ventricular rate control. However the relationship extends beyond tachycardia-induced cardiomyopathy. Optimal treatment of AF may delay progressive ventricular dysfunction and the onset of heart failure whilst improved management of heart failure can prevent AF or improve ventricular rate control. Prevention and treatment of atrial arrhythmias, and in particular atrial fibrillation, is therefore an important aspect of the management of patients with heart failure. This review describes the incidence and possible predictors of AF and other atrial arrhythmias in patients with heart failure and discusses the feasibility of primary prevention. The evidence for the management of atrial fibrillation in heart failure is systematically reviewed and the strategies of rate versus rhythm control discussed in light of the prevailing evidence. |
2,985 | Anti-thrombotic strategies for patients with atrial fibrillation and heart failure. | Atrial fibrillation occurs commonly in the setting of congestive heart failure and, in fact can cause left ventricular dysfunction due to a rapid ventricular response over time, termed tachycardia-mediated cardiomyopathy. The combination of atrial fibrillation and congestive heart failure leads to a high risk of stroke for the patient and appropriate antithrombotic therapy can minimize this incidence of stroke. Stroke risk can be markedly reduced by treatment with warfarin and complications of anticoagulation minimized by close attention to maintaining the INR between 2.0 and 3.0. |
2,986 | Prevalence and incidence of arrhythmias and sudden death in heart failure. | Patients with heart failure are prone to a variety of arrhythmias, symptomatic and asymptomatic, that are prognostically significant and have an important bearing on the management of these patients. However there are some inherent problems in assessing the frequency of these arrhythmias within a large patient population, due to a lack of uniformity in defining heart failure and the transient nature of these rhythms. Patients with heart failure commonly die suddenly. The causes of these deaths are difficult to ascertain accurately and are often presumed arrhythmic. With the advent of effective interventions to prevent sudden death, accurately defining the causal relationship between the arrhythmias and sudden death has assumed great importance to appropriately target therapy. Several attempts have been made to predict such deaths on the basis of non-invasive and invasive diagnostic investigations with variable success. In this article we review the incidence and prevalence of atrial and ventricular arrhythmias and sudden deaths in epidemiological studies, surveys and randomised control trials of patients with heart failure. We discuss the prognostic significance of these arrhythmias, the inherent problems in their diagnosis and whether their presence predicts the risk of sudden deaths and the mode of such deaths in the heart failure population. The role of various investigations in risk stratification of sudden death has also been discussed. |
2,987 | Cocaethylene's effects on coronary artery blood flow and cardiac function in a canine model. | Cocaethylene is a toxic metabolite of cocaine formed in the presence of ethanol. Though cocaine causes coronary vasoconstriction, cocaethylene's effects on coronaryflow are unknown. The aim of our study was to describe cocaethylene 's effects on coronary flow and cardiac function.</AbstractText>Sixteen alpha-chloralose anesthetized dogs were monitored with Swan-Ganz, arterial and venous catheters, and an electrocardiogram. Dopplerflow probes were placed on the circumflex and left anterior descending coronary arteries. Dogs were allotted 15 mg/kg (n = 10) or 30mg/kg (n = 6) of cocaethylene given as a continuous intravenous infusion. Measurements were made at fixed time intervals during the 60-minute cocaethylene infusion and 2-hour observation period.</AbstractText>The cocaethylene concentrations were maximal at the end of the infusion and cocaethylene was rapidly metabolized to benzoylecognine. One low-dose animal died of ventricular fibrillation. Five high-dose dogs experienced ventricular arrhythmias or pulseless electrical activity (PEA), and three died. In the low-dose group, cocaethylene caused a 38% increase in mean arterial pressure relative to baseline, and increased systemic vascular resistance. In the high-dose group, at maximal cocaethylene concentrations, stroke volume decreased by 42% (p < 0.0002), and circumflex blood flow decreased by 30% (p = 0.03) relative to baseline, when arrhythmias occurred. The PR, QRS, and QTc intervals increased by 48, 209, and 29%, respectively (p < 0.001). As cocaethylene levels declined, circumflex blood flow increased by 77% (p = 0.05) and mean arterial pressure increased 49% (p < 0.01), also relative to baseline.</AbstractText>Cocaethylene caused hypertension and increased systemic vascular resistance. At high concentrations, it decreased myocardial function, slowed cardiac conduction, and was arrhythmogenic. The cocaethylene's toxicity does not appear to be mediated by effects on coronary blood flow.</AbstractText> |
2,988 | Spontaneous T wave alternans and premature ventricular contractions during febrile illness in a patient with Brugada syndrome. | A 69-year-old man who had experienced syncope and ventricular fibrillation was referred to our hospital. ECG showed a right bundle branch block pattern with ST segment elevation in the right precordial leads. When the patient presented to the hospital with febrile illness, spontaneous T wave alternans and premature ventricular contractions were observed. When the patient became afebrile, ST segment elevation improved, and T wave alternans and premature ventricular contractions disappeared. |
2,989 | Body surface area of ST elevation and the presence of late potentials correlate to the inducibility of ventricular tachyarrhythmias in Brugada syndrome. | The value of noninvasive markers reflecting repolarization and/or conduction abnormalities in identifying patients with abnormal ECG showing a pattern of atypical right bundle branch block and ST elevation syndrome (Brugada syndrome) at risk for life-threatening arrhythmias is controversial. Because right precordial ST elevation reflects inhomogeneous repolarization, we hypothesized that a correlation between the area of ST elevation, that is, the area of inhomogeneous repolarization, and the inducibility of ventricular tachyarrhythmias (VT) exists. Therefore, the body surface area of ST elevation and the presence of late potentials were compared to the inducibility of VT in patients with the characteristic ECG of Brugada syndrome.</AbstractText>A 120-channel body surface potential map was recorded at rest and after administration of a Class I agent (ajmaline, 1 mg/kg) to measure the body surface area of ST elevation (> or = 0.2 mV) in 23 individuals (16 patients had been resuscitated from near sudden cardiac death or had suffered syncope) with an ECG compatible with the diagnosis of Brugada syndrome as well as in 15 healthy controls and in 15 patients with arrhythmogenic right ventricular cardiomyopathy. Late potentials were assessed in 20 of the Brugada patients using signal-averaged ECG. Programmed ventricular stimulation was performed at two ventricular sites with up to three extrastimuli. Mean body surface area of ST elevation (> or = 0.2 mV) of all Brugada syndrome patients was 154 +/- 139 cm2 (control 9 +/- 9 cm2; P < 0.001). In the group of patients with arrhythmogenic right ventricular cardiomyopathy, only one patient was found to have an area of ST elevation (165 cm2). In the presence of ajmaline, area size increased to 330 +/- 223 cm2 in Brugada syndrome patients (P < 0.05). In patients with inducible sustained (n = 15) and nonsustained VT (n = 3), a mean area of 183 +/- 139 cm2 was found, whereas the area was only 52 +/- 58 cm2 in those with no VT induction (P < 0.05). For an area > or = 50 cm2, there were positive and negative predictive values of 92% and 60%, respectively. Positive late potentials were found in 60% of patients and correlated to the inducibility during programmed ventricular stimulation (positive predictive value 100%, negative predictive value 75%; P < 0.001).</AbstractText>In patients with Brugada syndrome, the body surface area of ST elevation and the presence of late potentials correlate to the inducibility of VT during programmed ventricular stimulation and may be of value as a new noninvasive marker for risk stratification in these patients.</AbstractText> |
2,990 | The role of heme oxygenase-related carbon monoxide and ventricular fibrillation in ischemic/reperfused hearts. | Reperfusion-induced ventricular fibrillation (VF) and heme oxygenase (HO)-related carbon monoxide (CO) production in isolated ischemic/reperfused rat hearts were studied by gas chromatography. Hearts were subjected to 30 min ischemia followed by 2 h reperfusion, and the expression of HO-1 mRNA (about 4-fold) was observed in ischemic/reperfused-nonfibrillated hearts. In fibrillated hearts, the reduction (about 75%) in HO-1 mRNA expression was detected. These changes in HO-1 mRNA expression were reflected in tissue CO production. Thus, in the absence of VF, CO production was increased about 3.5-fold, while in the presence of VF, CO production was under the detectable level in comparison with the control group. Our results suggest that the stimulation of HO-1 mRNA expression may lead to the prevention of reperfusion VF via an increase in endogenous CO production. To prove this, hearts were treated with 1 microM of N-tert-butyl-alpha-phenylnitrone (PBN) as an inducer of HO-1. PBN treatment resulted in about 20 times increase in HO-1 mRNA expression, and even a higher production rate in endogenous CO. HO protein level and enzyme activity followed the same pattern, as it was observed in HO-1 mRNA expression, in fibrillated and nonfibrillated myocardium. Five mM/l of zinc-protoporphyrin IX (ZnPPIX) significantly blocked HO enzyme activity and increased the incidence of VF, therefore the application of ZnPPIX led to a significant reduction in HO-1 mRNA and protein expression. Our data provide direct evidence of an inverse relationship between the development of reperfusion-induced VF and endogenous CO production. Thus, interventions that are able to increase tissue CO content may prevent the development of reperfusion-induced VF. |
2,991 | Efficacy of a dual chamber defibrillator with atrial antitachycardia functions in treating spontaneous atrial tachyarrhythmias in patients with life-threatening ventricular tachyarrhythmias. | Atrial fibrillation has a high incidence in patients wearing an implantable cardioverter defibrillator for ventricular tachyarrhythmias and may lead to palpitations, heart failure, angina, stroke and inappropriate defibrillator discharge. The aim of the study was to evaluate the efficacy of a dual chamber defibrillator with atrial antitachycardia functions in treating spontaneous atrial tachyarrhythmias.</AbstractText>One hundred and twelve patients, 88 male, mean age 64+/-11 years, were enrolled. Seventy-six had ischaemic heart disease, 21 idiopathic dilated cardiomyopathy, nine other heart diseases, six no structural heart disease. The mean left ventricular ejection fraction was 40+/-11%. Sixty-two had prior atrial tachyarrhythmias.</AbstractText>Follow-up lasted 11+/-9 months (range 1-42). Among 933 ventricular tachyarrhythmia episodes, 100% of ventricular fibrillation and 92% of ventricular tachycardia were successfully cardioverted. Among 414 detected sustained atrial tachyarrhythmias, 195 were classified as atrial tachycardia (47.1%), 192 as atrial fibrillation (46.4%) and 27 (6.5%) as sinus rhythm. The detection-positive predictive value was 93.5%. Therapy success rates: antitachy pacing on atrial tachycardia = 71.3% (crude estimate); 66.1% (adjusted estimate); 50 Hertz on atrial fibrillation=36.2% (crude estimate); 13.5% (adjusted estimate); atrial shock on atrial fibrillation = 62.5% (mean energy 7.8+/-14.1J). Shock efficacy was 32% when delivered energy was < or = 2 atrial defibrillation threshold at implant and 92% when >2. Duration of successfully treated atrial episodes was significantly lower than that of unsuccessfully treated (6+/-26 min vs 42+/-60).</AbstractText>Atrial antitachy pacing and shock therapies demonstrated very high efficacy in treating atrial tachyarrhythmias in defibrillator patients.</AbstractText>Copyright 2002 The European Society of Cardiology. Published by Elsevier Science Ltd. All rights reserved.</CopyrightInformation> |
2,992 | Sodium channel blocking and antiarrhythmic actions of the novel arylpiperazine rsd992. | Bolus doses (4-128 micromolkg(-1)) and infusions (2-32 micromolkg(-1)min(-1)) of the novel arylpiperazine drug RSD992 produced bradycardia in rats and guinea pigs but had minimal effect on ECG variables. RSD992 (2-32 micromolkg(-1)min(-1)) increased threshold current (I(T)) for induction of extra-systoles and induction of sustained ventricular fibrillation (VF(T)) and also increased the effective refractory period (ERP) and decreased the maximum following frequency (MFF) in rat and guinea pig hearts. RSD992 (32-512 microM) significantly increased PR and QRS intervals in isolated rat hearts subjected to conditions that mimic ischaemia (pH 6.4, K(+) 11mM) but not in isolated hearts under normal perfusion conditions (pH 7.4, K(+) 3mM). RSD992 (0.1-3.0mM) reduced peak sodium current in rat cardiac (rNa(v)1.5) sodium channels more potently than neuronal (rNa(v)1.2a) sodium channels expressed in Xenopus oocytes. The voltage-dependence of sodium channel activation was unaffected whereas inactivation was shifted in a hyperpolarized direction thus suggesting RSD992 may preferentially interact with the inactive state of the sodium channel, a state usually associated with myocardial cell depolarization in ischaemic myocardium. RSD992 (2-24 micromolkg(-1)min(-1)) decreased the incidence of ventricular arrhythmias and mortality in rats subject to coronary artery ligation. RSD992 exhibits frequency- and ischaemia-selective actions on myocardial sodium currents and antiarrhythmic actions in ischaemic rat myocardium. |
2,993 | Torsade de pointes. | A case is described of torsade de pointes in a 41 year old woman with pre-existing QTc prolongation, potentially exacerbated by treatment with sotalol. Previous cardiac investigations had been normal and after a second episode of ventricular fibrillation the patient was referred for electrophysiological studies. The authors review the physiology, causes, and treatment of QTc prolongation and torsade de pointes. |
2,994 | Repeated physiologic stresses provide persistent cardioprotection against ischemia-reperfusion injury in rats. | We investigated the time course of myocardial tolerance to ischemia-reperfusion injury after repeated physiologic or pharmacologic stresses.</AbstractText>Sublethal stress provides cardiac tolerance to ischemia-reperfusion injury and increases the activity of manganese superoxide dismutase (Mn-SOD) in the myocardium in a biphasic manner. However, few studies have investigated the time course of the cardioprotective effects after repeated stresses.</AbstractText>One or two episodes of the same physiologic or pharmacologic stress (exercise, whole-body hyperthermia, or tumor necrosis factor-alpha treatment), or a combination of two different types of stress, were induced after a 48-h interval. The rats were then subjected to 20 min of left coronary artery occlusion, followed by 48 h of reperfusion. The interval between the last stimulus and the induced ischemia was between 0.5 h and 168 h. The incidence of ventricular fibrillation during ischemia and the size of the myocardial infarct after reperfusion were then examined.</AbstractText>When two episodes of physiologic or pharmacologic stress were induced, the beneficial effects against ischemia-reperfusion injury were observed in a monophasic manner. These effects persisted for a period of 0.5 to 60 h. One episode of sublethal stress provoked the same beneficial effects, but in a biphasic manner. The increase in Mn-SOD activity in the cardiac tissue resembled the time course for cardioprotection against ischemia-reperfusion injury.</AbstractText>Two episodes of physiologic or pharmacologic stress can provide persistent cardioprotective effects against ischemia-reperfusion injury.</AbstractText> |
2,995 | Myocardial dysfunction after electrical defibrillation. | We hypothesized that electrical shocks that defibrillate hearts successfully also produce myocardial injury, but only in settings in which the myocardium is underperfused. Myocardial function was measured in isolated, conventionally perfused or underperfused rat hearts during sinus rhythm and conventionally perfused or underperfused hearts during ventricular fibrillation (VF) after delivery of a sham, a 0.4 J, or a 0.7 J shock. In underperfused hearts, the dP/dt, negative dP/dt, left ventricular diastolic pressure and left ventricular pressure-volume relationships demonstrated significant impairment in myocardial function. Impairment increased with the higher energy shocks. This contrasted with normally perfused hearts, whether in sinus rhythm or during VF, in which shocks resulted in no significant impairment. Electrical shocks therefore produce myocardial injury but only when myocardial perfusion is reduced. |
2,996 | Body weight is a predictor of biphasic shock success for low energy transthoracic defibrillation. | Transthoracic impedance and current flow are determinants of defibrillation success with monophasic shocks. Whether transthoracic impedance, either independently or via its association with body weight, is a determinant of biphasic waveform shock success has not been determined.</AbstractText>We studied 22 swine, weighing 18-41 kg. After 15 s of ventricular fibrillation, each pig received transthoracic truncated exponential biphasic shocks (5/5 ms), 70-360 J. Shock success was strongly associated individually with body weight, leading-edge transthoracic impedance and current at low energy levels (70 and 100 J, all P<0.001). Multiple logistic regression analysis showed a significant association of body weight with shock success after adjusting for the effect of leading-edge impedance (odds ratio of success for 1 kg decrease in weight at 70 J was 1.29, 95% CI: 1.05-1.59, P=0.02; and at 100 J was 1.30, 95% CI: 1.14-1.49, P<0.0001). The same result was observed after adjusting for the effect of leading-edge current. At 150 J or higher energy levels, no significant association was observed.</AbstractText>Body weight is a determinant of shock success with biphasic waveforms at low energy levels in this swine model.</AbstractText> |
2,997 | Effects of hypertonic saline on myocardial blood flow in a porcine model of prolonged cardiac arrest. | To evaluate the effects of hypertonic saline (HS) on myocardial reperfusion pressure (MPP) and blood flow (MBF), and cardiac index (CI) during and after cardiopulmonary resuscitation (CPR).</AbstractText>In 21 domestic swine (16-23 kg) open chest cardiac massage was initiated after 10 min of ventricular fibrillation. With the onset of CPR animals randomly received HS (7.2%; 2 ml/kg per 10 min or 4 ml/kg per 20 min) or normal saline ((NS); 2 ml/kg per 10 min). Haemodynamic variables were monitored continuously, and coloured microspheres were used to measure MBF and CI before cardiac arrest (CA), during CPR and 5, 30 and 120 min after the return of spontaneous circulation.</AbstractText>During CPR HS significantly increased MPP, MBF, and CI in comparison to NS (P<0.05, resp., MANOVA). Doubling the volume of HS did not improve the haemodynamic effects seen after application of 2 ml/kg per 10 min. HS-infusion significantly increased the survival rate at 120 min, 6/7 and 5/7 animals receiving 2 ml/kg per 10 min or 4 ml/kg per 20 min versus 2/7 after NS-infusion (P<0.05, chi(2)-test).</AbstractText>HS applied during open chest cardiac massage enhanced MBF and CI, and significantly increased resuscitation success and survival rate. The positive effects of this promising new approach need to be confirmed in clinical studies.</AbstractText> |
2,998 | Automated external defibrillation as part BLS: implications for education and practice. | The latest Adult Basic Life Support (BLS) guidelines support the inclusion of the use of the automated external defibrillator (AED), as part of basic life support (BLS). Emphasis on the provision of early defibrillation as part of BLS acknowledges the importance of this manoeuvre in the successful termination of ventricular fibrillation. The ramifications of such changes for both first responders and organisations implementing the guidelines should not be underestimated. Issues relating to resourcing, content and duration of training and retraining, auditing and evaluation require further exploration. To consider these issues now seems particularly pertinent, given the recent launch of the UK Government's paper on public health, 'Saving Lives-Our Healthier Nation' which seeks to deploy AEDs in busy public places for use by trained members of the lay public. Additionally, defibrillation has been identified as one of the key competencies that all trained nurses and other health care providers should be able to undertake. This paper will consider the background to the current guideline changes, analyse the wider implications of translating the recommendations into practice, and offer possible solutions to address the issues raised. Whilst the analysis is particularly pertinent to the United Kingdom, many of the issues raised have international importance. |
2,999 | Ischaemia-induced cellular electrical uncoupling and ventricular fibrillation. | Sudden death resulting from ventricular fibrillation (VF) during acute myocardial ischaemia forms an important contribution to mortality associated with infarction. Its temporal distribution is not known, but 30% of mortality occurs within the first 60 minutes. Two distinct phases of arrhythmias have been demonstrated in laboratory animals subjected to coronary occlusion. The mechanism of the second, 1B phase (which is associated with more lethal events than the first, 1A phase) is largely unknown but appears to be related to cellular uncoupling, i.e. the closure of gap junctions. Gap junctions are intercellular communication channels that are permeable for ions and metabolites and are necessary for normal propagation of electrical activation. It has been suggested that closure of gap junctions results in a largely inhomogeneous substrate in which microreentry forms the electrophysiological mechanism for VF. However, there is growing support for the hypothesis that arrhythmias relate to the persistence of residual coupling rather than to the occurrence of uncoupling. With this, the ischaemic midmyocardium can depress the intrinsically viable tissue of the ischaemic subepicardium and subendocardium and cause conduction slowing and block leading to arrhythmias. Progression of uncoupling terminates this interaction and allows the subepicardium and subendocardium to recover. Indeed, electrophysiological properties recover subepicardially whereas the midmyocardial tissue becomes inexcitable. In addition, activation patterns during VF become restricted to the two-dimensional plane of the subepicardium. These observations support the hypothesis of residual coupling as an arrhythmogenic mechanism during the delayed phase of acute ischaemia. Whether this mechanism is equally important in patients with remodelled and failing hearts can at this time only be speculated upon. However, modifying intercellular coupling might turn out a new antiarrhythmic therapy. |
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