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4,100 | Torsades de pointes ventricular tachycardia induced by mosapride and flecainide in the presence of hypokalemia. | We report a 68-year-old man who developed torsades de pointes ventricular tachycardia induced by combined use of mosapride and flecainide. He had a permanent pacemaker (DDD mode) implanted because of sick sinus syndrome (bradytachy syndrome) 6 years earlier. The patient had started taking mosapride for upper abdominal discomfort 2 weeks earlier. On admission, ECG showed prolongation of the QTc interval from 0.48 to 0.56 seconds and self-terminating torsades de pointes occurred. We considered that this proarrhythmia was induced by mosapride in combination with antiarrhythmic agents. |
4,101 | [Determinants of survival after implantation of an automatic defibrillator. Report of 127 patients]. | The authors present a retrospective and longitudinal study of the predictive factors of mortality in patients having an implanted automatic defibrillator. The population comprised 127 patients implanted between September 1988 and September 1997. There were 107 men with a mean age of 57.7 +/- 13 years. The left ventricular ejection fraction was 39.3%. The proportion of coronary patients was 68%; 20% of patients had atrial fibrillation and 5% were in Class III of the NYHA classification. The indications were: resuscitated cardiac arrest (N = 56) and poorly tolerated ventricular tachycardia (N = 71). The follow-up period was 30 +/- 25 months. There were 23 early and 10 late complications. Seventy-two patients had received an electric shock; 57 had an appropriate shock. There were 23 arrhythmic storms (ventricular arrhythmia requiring at least 2 shocks in less than 24 hours) in 17 patients. The operative mortality was 1.1%; at 1 year, the global survival was 93.9 +/- 2.2%; cardiac survival was 94.7 +/- 2.1%; survival without sudden death was 98.3 +/- 1.2%. Multivariate analysis isolated predictive factors for mortality; atrial fibrillation was predictive for global mortality; an ejection fraction < 30% and the fact of having received an appropriate shock were predictive of cardiac mortality; and an arrhythmic storm was predictive of sudden death. |
4,102 | Is electrical storm in ICD patients the sign of a dying heart? Outcome of patients with clusters of ventricular tachyarrhythmias. | Electrical storm in patients with implanted cardioverter defibrillators (ICDs) is purported to carry an ominous prognosis.</AbstractText>We retrospectively compared 40 patients with electrical storm (defined as three or more episodes of ventricular arrhythmia requiring ICD therapy in a 24 h period) with those only having isolated appropriate ICD therapy (n=57) and with patients having no or only inappropriate ICD therapy (n=125). All patients received ICDs for documented sustained VT or VF. There was no significant difference in age, sex, ejection fraction, total follow-up time, or underlying heart disease between any of the three groups. Patients who had electrical storm received their first appropriate ICD therapy 275 +/- 369 days post-implant (35% had storm as their first event) with storm occurring an average of 599 +/- 710 days post-implant. Patients had 1.5 +/- 1.0 storms in total (median= 1), with 55 +/- 91 episodes per storm. There were no significant differences in actuarial survival at 5-year follow-up between the three groups. Eighty percent of storm patients were alive 5 years post-implant.</AbstractText>Storm is a common occurrence in ICD patients, can occur at any time during the follow-up period, and does not independently confer increased mortality.</AbstractText> |
4,103 | Effects of intravenous amiodarone on ventricular refractoriness, intraventricular conduction, and ventricular tachycardia induction. | Intravenous amiodarone has recently emerged as an important drug for the acute treatment of ventricular tachyarrhythmias. However, electrophysiological actions and the efficacy of the drug in the suppression of ventricular tachycardia inducibility have not yet been fully established. The present study was designed to address these issues.</AbstractText>The study group consisted of 18 patients (all males, mean age 75 +/- 14 years), who underwent electrophysiological study due to a history of sustained ventricular tachyarrhythmia or syncope with non-sustained ventricular tachycardia detected on ambulatory ECG monitoring. The effects of 5 mg.kg(-1) or 10 mg.kg(-1) of intravenous amiodarone on (1) ventricular refractoriness (QTc interval, right ventricular effective refractory period and monophasic action potential duration), (2) intraventricular conduction (paced-QRS and signal-averaged QRS duration), and (3) ventricular tachycardia inducibility, were examined. The drug had no significant effect on ventricular refractoriness. However, a relatively small but significant slowing of intraventricular conduction was seen (paced-QRS duration: 182 +/- 27 ms vs 191 +/- 28 ms, P<0.0007; 183 +/- 32 ms vs 195 +/- 33 ms, P<0.0007; and 177 +/- 21 ms vs 192 +/- 24 ms, P<0.003, at the cycle lengths of 600, 500 and 400 ms, respectively). This effect was more evident during extrasystolic beats than during stable pacing (for example, at the cycle length of 600 ms, the magnitude of amiodarone-induced lengthening of QRS duration was 23.9 +/- 17.6 ms vs 9.7 +/- 7.2 ms, P<0.009, respectively). Intravenous amiodarone did not prevent induction of sustained ventricular tachycardia in any of five patients inducible at baseline. Of six patients with non-sustained ventricular tachycardia, five had sustained ventricular tachycardia or fibrillation induced after amiodarone infusion.</AbstractText>Intravenous amiodarone does not prolong ventricular refractoriness, slows intraventricular conduction and may facilitate inducibility of sustained ventricular arrhythmias.</AbstractText> |
4,104 | Detection of ventricular fibrillation in implantable defibrillators with automatic gain control amplifiers: effects of programming sensitivity. | In newer implantable cardioverter-defibrillators with automatic gain control amplifiers the maximum possible sensitivity is programmed with the aim of securing optimal detection of ventricular fibrillation. This study was designed to prove that a reduction in maximum sensitivity is safe with respect to appropriate sensing of ventricular fibrillation, while avoiding sensing of extracardiac signals.</AbstractText>Forty-two consecutive patients, undergoing defibrillator implantation/replacement with programmable maximum auto-gain sensing sensitivity (Ventak Mini III, Ventak AV , Guidant, St. Paul, MN, U.S.A.), were prospectively investigated. Thirty-four patients were implanted with a dual-coil lead system, providing integrated bipolar sensing (Endotak, Guidant, St. Paul, MN, U.S.A.), eight patients received a single-coil lead system with true bipolar sensing (Sprint, Medtronic, Minneapolis, MN, U.S.A.). During device implantation and pre-discharge testing, arrhythmia detection times of induced ventricular fibrillation were compared at programmed maximum (0.18 mV) and minimum (0.43 mV) sensitivity in a randomized manner. Seventy-six induced episodes of ventricular fibrillation were analysed. The mean arrhythmia detection times did not differ between the programmed sensing levels (maximum sensitivity: 1612 +/- 307 ms, vs minimal sensitivity: 1,602 +/- 330 ms; P = ns). The results were not affected by the type of implanted lead system (integrated bipolar versus true bipolar sensing).</AbstractText>In the implantable defibrillator devices, reduction in maximum sensitivity did not impair the detection of induced episodes of ventricular fibrillation.</AbstractText> |
4,105 | Fractally coated defibrillation electrodes: is an improvement in defibrillation threshold possible? | In patients with implantable cardioverter-defibrillators (ICD), the goals of lowering the defibrillation threshold (DFT) can be achieved by means of higher defibrillation safety margins, more rapid charging of capacitors, improved battery longevity, implying smaller devices. Whether an increase in the electrically active surface of ICD leads by fractal coating results in decreased DFTs is unknown.</AbstractText>In this prospective randomized cross-over study the defibrillation efficacy of a novel right ventricular endocardial defibrillation electrode fractally coated with iridium was compared with an uncoated but otherwise identical electrode in 30 patients undergoing ICD implantation. In each patient, DFT testing was performed twice according to a binary search protocol introducing the two different electrodes in a random order. The mean DFT was 8.4 +/- 4.1 J with the fractally coated lead and 9.6 +/- 3.6 J using the uncoated lead. The improvement of 1.2 J was statistically not significant (P = 0.11). No differences were observed between the patients with an improved DFT (n =12) and those with an unchanged or worsened DFT (n = 18) concerning age, underlying cardiac disease, NYHA class, or left ventricular ejection fraction, respectively.</AbstractText>Increasing the electrical surface of defibrillation leads by fractal coating does not lead to a substantial clinically relevant reduction in defibrillation thresholds. Defibrillation impedance is not influenced by the increased electrical surface of the defibrillation lead.</AbstractText> |
4,106 | Pregnancy with an ICD and a documented ICD discharge. | We report a successful pregnancy in a patient affected by idiopathic ventricular fibrillation 3 years after insertion of an ICD, with a documented defibrillator discharge. |
4,107 | Comparison of QT dispersion during atrial fibrillation and sinus rhythm in the same patients, at normal and prolonged ventricular repolarization. | Drug-induced increase in QT dispersion has been associated with increased risk of ventricular proarrhythmia. The aim of the present study was to compare QT dispersion during atrial fibrillation and sinus rhythm in the same patients at normal and prolonged ventricular repolarization.</AbstractText>Sixty-one patients who had had chronic atrial fibrillation for 8 +/- 14 months received a 6 h infusion of the Ikr-blocker almokalant, the first 90 min of which are used for this analysis. The following day, after conversion to sinus rhythm, by almokalant (n = 19) or direct current cardioversion (n=42), an identical 90 min infusion was administered. Prior to infusion, there was no difference in precordial QT dispersion between atrial fibrillation and sinus rhythm (29 +/- 12 vs 36 +/- 17 ms, P=ns). During infusion, at prolonged repolarization, the increase in QT dispersion was greater during sinus rhythm than during atrial fibrillation (58 +/- 49 vs 30 +/- 15 ms, P=0.0011, after 30 min infusion). No correlation was found between QT dispersion and the QT or RR interval.</AbstractText>QT dispersion during atrial fibrillation does not differ from QT dispersion during sinus rhythm during normal repolarization. while measurement of QT dispersion during prolonged repolarization, induced by an Ikr-blocker, yielded larger values during sinus rhythm than during atrial fibrillation.</AbstractText> |
4,108 | Maintenance of sinus rhythm as a therapy goal. | Despite recent advances in our understanding of the mechanisms and consequences of atrial fibrillation, appropriate management of this common condition presents something of a dilemma. Control of ventricular rate alone is a common strategy, considered by many physicians to be the safest treatment option and a relatively simple approach to preserving left ventricular function. Rhythm control using antiarrhythmic agents, however, offers a number of important advantages, with the potential to correct abnormal physiology, increase exercise tolerance, reduce thromboembolic risk, prevent atrial remodelling and eliminate the risk of tachycardia-induced cardiomyopathy. Selection of an appropriate antiarrhythmic agent for such long-term prophylaxis is however problematic. Class I agents are associated with an unacceptable proarrhythmic risk especially in patients with structural heart disease and long-term therapy with the class III agent amiodarone can result in serious non-cardiac adverse effects. It is apparent, therefore, that there is little consensus on appropriate management strategies for atrial fibrillation and less still on the antiarrhythmic agent to be used. A number of studies are, however, ongoing which attempt to determine the benefits of rhythm versus rate control. These include the PIAF (Pharmacological Intervention in Atrial Fibrillation), AFFIRM (Atrial Fibrillation Follow-up Investigation of Rhythm Management) and RACE (Rate Control versus Electrical Cardioversion) studies, which should provide valuable answers which will help to guide physicians in their therapy choices. |
4,109 | [Interatrial electromechanic resynchronization by dual atrial pacing in the prevention of paroxysmal atrial fibrillation --report of a case]. | We presented the case of a 78 year old woman who five years ago underwent myectomic surgery, and aortic valvular replacement, for obstructive cardiomyopathy and valvular aortic stenosis. After surgery, the aortic transvalvular gradient was insignificant (20 mm/Hg). In spite of this she suffers from frequent AF crises, (3 times a month), with a cardiac frequency of 140-150/min. She was in sinus bradycardia (40-45/min), which was a clear counter-indication for the use of antiarrhythmic drugs. Her ECG showed sinusal bradycardia with 45/min, a two-phase P-wave (positive-negative) in DII, DIII aVF, and bimodal P-wave in DI. Furthermore, she showed a 1st degree auriculo-ventricular block with complete left-branch block. In her echocardiogram there was concentric left ventricular hypertrophy, with diastolic disfunction and left atrial dilatation. In the auricular IEGM we observed a slowed-down interauricular conduction (right atrium-left atrium = 120 msecs); The A-wave was fragmented. The auriculo-ventricular Wenckbach point was at 90/min. In view of these findings we proceeded with the implantation of a DDD-pacemaker with biauricular stimulation, as follows: 1. We used two auricular electrodes, one with an active fixation to the crista terminalis of the right atrium and the other (having in mind the stimulation of the left atrium) applied to the proximal coronary sinus. These two electrodes were connected to the auricular pin of the pacemaker by means of an "Y"--type Biotronick adaptor. 2. The right ventricular stimulation was done with a normal, bipolar ventricular electrode, on the apex of the ventricle. After biauricular, simultaneous, stimulation, we proceeded with interauricular re-synchronization. After this procedure, the A-wave no longer appeared fragmented, and the right auricular--left auricular waves were then simultaneous and with two-phase morphology. Three months later the interauricular resynchronization procedure was induced and without any antiarrhythmic drugs, the Holter showed no cardiac arrhythmias, there is no auricular fibrillation. The morphology of the P-wave has changed. The patient has an improved exercise capacity and a better quality of life. |
4,110 | Mitral annulus calcification--a window to diffuse atherosclerosis of the vascular system. | Mitral annulus calcification (MAC) is a chronic, non-inflammatory, degenerative process of the fibrous support structure of the mitral valve. It occurs more often in women and the elderly. MAC is associated with known atherosclerotic risk factors such as diabetes mellitus, hypertension and hypercholesterolemia. It is also known that patient with MAC have higher prevalence of left atrial and left ventricular enlargement, hypertrophic cardiomyopathy, atrial fibrillation, aortic valve calcification and stenosis, various cardiac conduction defects, bacterial endocarditis, cardiovascular events and stroke, though the etiological basis is unknown. Pathological studies from the 80s present a theory that MAC is a form of atherosclerosis. In order to test this theory we conducted during the last years a few clinical studies to examine the association of MAC and known atherosclerotic phenomena. We found higher prevalence of aortic atheroma in patients with MAC and atheroma thickness. We also found in MAC patients higher prevalence of carotid artery stenosis, coronary artery stenosis, peripheral artery stenosis and higher levels of beta2-Glycoprotein I antibodies in patients with MAC thickness equal or greater than 5 mm. These studies support the theory that MAC is a form of atherosclerosis and define a group of patients with higher prevalence of atherosclerotic disease in multiple blood vessels. The purpose of this review is to summarize the data concerning MAC and atherosclerotic processes, emphasizing that MAC in itself may be an atherosclerotic process. |
4,111 | [Dilated cardiomyopathy and panuveitis as presenting symptoms of Lyme disease. General review of one case]. | The clinical expression of Lyme disease is highly variable. If a patient presents clinical findings consistent with a systemic Lyme borreliosis, this disease must be considered in an endemic area because of its favorable outcome with adequate treatment.</AbstractText>The authors report and discuss the case of a patient with an unusual history of dilated cardiomyopathy and supraventricular fibrillation followed by bilateral panuveitis. Enzyme-linked immunosorbent assay and Western blot were positive for Borrelia burgdorferi antigens. The diagnosis of Lyme disease was made after other infectious, inflammatory and autoimmune disorders were excluded by clinical, instrumental and biological investigations. The treatment by ceftriaxone and amoxicillin resolved the ophthalmologic manifestations and improved the cardiac condition.</AbstractText>This report underlines the possibility of an unusual presentation of Lyme disease. Ophthalmologic and cardiac involvement should be known by clinicians.</AbstractText> |
4,112 | Impact directly over the cardiac silhouette is necessary to produce ventricular fibrillation in an experimental model of commotio cordis. | In an experimental model of sudden death from chest wall impact (commotio cordis), we sought to define the chest wall areas important in the initiation of ventricular fibrillation (VF).</AbstractText>Sudden death can result from an innocent chest blow by a baseball or other projectile. Observations in humans suggest that these lethal blows occur over the precordium. However, the precise location of impact relative to the risk of sudden death is unknown.</AbstractText>Fifteen swine received 178 chest impacts with a regulation baseball delivered at 30 mph at three sites over the cardiac silhouette (i.e., directly over the center, base or apex of the left ventricle [LV]) and four noncardiac sites on the left and right chest wall. Chest blows were gated to the vulnerable portion of the cardiac cycle for the induction of VF.</AbstractText>Only chest impacts directly over the heart triggered VF (12 of 78: 15% vs. 0 of 100 for noncardiac sites: p < 0.0001). Blows over the center of the heart (7 of 23; 30%) were more likely to initiate VF than impacts at other precordial sites (5 of 55; 9%, p = 0.02). Peak LV pressures generated instantaneously by the chest impact were directly related to the risk of VF (p < 0.0006).</AbstractText>For nonpenetrating, low-energy chest blows to cause sudden death, impact must occur directly over the heart. Initiation of VF may be mediated by an abrupt and substantial increase in intracardiac pressure. Prevention of sudden death from chest blows during sports requires that protective equipment be designed to cover all portions of the chest wall that overlie the heart, even during body movements and positional changes that may occur with athletic activities.</AbstractText> |
4,113 | Coronary artery revascularization in patients with sustained ventricular arrhythmias in the chronic phase of a myocardial infarction: effects on the electrophysiologic substrate and outcome. | The objective of this study was to analyze the influence of coronary artery revascularization in patients with ventricular arrhythmias.</AbstractText>Coronary artery revascularization is an effective treatment for myocardial ischemia; however, its effect on ventricular arrhythmias not related to an acute ischemic event has not been carefully studied.</AbstractText>Sixty-four patients (58 men, mean age 65 +/- 8 years old) with prior myocardial infarction, spontaneous ventricular arrhythmias not related to an acute ischemic event (55 ventricular tachycardia, 9 ventricular fibrillation) and coronary lesions requiring revascularization were studied prospectively. Electrophysiological study was performed before and after revascularization, and events during follow-up were analyzed.</AbstractText>At initial study 61 patients were inducible into sustained ventricular arrhythmias. After revascularization, in 62 survivors, 52 out of 59 patients previously inducible were still inducible (group A), and 10 patients were noninducible (group B). No differences were found in clinical, hemodynamic, therapeutic and electrophysiological characteristics between both groups. During 32 +/- 26 months follow-up, 28/52 patients in group A (54%) and 4/10 patients in group B (40%) had arrhythmic events (p = 0.46). An ejection fraction <30% predicted recurrent arrhythmic events (p = 0.02), but not the presence of demonstrable ischemia before revascularization (p = 0.42), amiodarone (p = 0.69) or beta-adrenergic blocking agent therapy (p = 0.53). Total mortality was 10% in both groups.</AbstractText>In patients with ventricular arrhythmias in the chronic phase of myocardial infarction, probability of recurrence is high despite coronary artery revascularization, but mortality is low if combined with appropriate antiarrhythmic therapy. Recurrences are related to the presence of a low ejection fraction but not to demonstrable ischemia before revascularization, amiodarone or beta-blocker therapy nor are they the results of electrophysiological testing after revascularization.</AbstractText> |
4,114 | Epidemiology and natural history of atrial fibrillation: clinical implications. | With a substantial impact on morbidity and mortality, the growing "epidemic" of atrial fibrillation (AF) intersects with a number of conditions, including aging, thromboembolism, hemorrhage, hypertension and left ventricular dysfunction. Currently, the epidemiology and natural history of AF govern all aspects of its clinical management. The ongoing global investigative efforts toward understanding AF are also driven by epidemiologic findings. New developments, by affecting the natural history of the disease, could eventually alter the nature of decision making in patients with AF. The crucial issue of rate versus rhythm control awaits completion of the AF Follow-up Investigation of Rhythm Management trial. The processes of electrical and structural remodeling that perpetuate AF appear to be reversible. In the era of functional genomics, the molecular basis of this ubiquitous arrhythmia is in the process of being defined. Unraveling the molecular genetics of AF might provide new insights into the structural and electrical phenotypes resulting from genetic mutations and, as such, new approaches to treatment of this arrhythmia at the ion channel and cellular levels. Thus, current adverse trends are superimposed on a background of a rapidly developing knowledge base and potentially exciting new therapeutic options. Consequently, an understanding of the epidemiology and natural history of AF is crucial to the future allocation of resources and the utilization of an expanding range of therapies aimed at reducing the impact of this disease on a changing patient population. |
4,115 | Effects of sustained low-flow ischemia and reperfusion on Ca2+ transients and contractility in perfused rat hearts. | We investigated changes in cytoplasmic Ca2+ concentration ([Ca2+]i) and in left ventricular contractility during sustained ischemia and reperfusion in isolated beating rat hearts. Hearts from male Sprague-Dawley rats were perfused retrogradely and were loaded with 4 microM fura-2. Low-flow global ischemia was induced by reducing perfusion flow to 10% and by electric pacing. The hearts were exposed to ischemia for 10 min or 30 min and then reperfused. [Ca2+]i was measured by monitoring the ratio of 500 nm fluorescence excited at 340 and 380 nm while simultaneously measuring left ventricular pressure (LVP). To determine diastolic [Ca2+]i, background autofluorescence was subtracted. LVP rapidly decreased from 82.3+/-8.2 to 17.1+/-2.9 mmHg , whereas the amplitude of the Ca2+ transient did not change significantly during the first 1 min of ischemia. After 10 min of ischemia, the amplitude decreased to 60.8+/-10.6% (p < 0.05) and diastolic [Ca2+]i increased by 26.3+/-2.9% (p < 0.001) compared with the pre-ischemic value (n = 8). When the hearts were reperfused after 10 min of ischemia, the amplitude of the Ca2+ transient and LVP recovered to 79.0+/-7.2% and 73.2+/-7.5 mmHg, respectively. Whereas diastolic [Ca2+]i decreased to the preischemic value. In the hearts exposed to 30 min of ischemia (n = 10), diastolic [Ca2+]i increased even further by 32.7+/-5.3% at the end of ischemia and continued increasing during the 10 min of reperfusion by 42.6+/-15.6%. Six of 10 hearts developed ventricular fibrillation (VF) and intracellular Ca2+ overload after reperfusion. Recovery of LVP after reperfusion was significantly smaller in the hearts exposed to 30 min of ischemia than in the hearts exposed to 10 min of ischemia (58.9+/-11.7 vs. 97.2+/-3.0% of pre-ischemic value, p < 0.05). Diastolic [Ca2+]i also increased under hypoxic conditions (N2 bubbling) in this model. These results suggest that increases in diastolic [Ca2+]i might play an important role in myocardial contractile dysfunction and viability in ischemia-reperfusion injury. |
4,116 | Risk stratification for sudden cardiac death in dilated cardiomyopathy using microvolt-level T-wave alternans. | Predicting sudden cardiac death (SCD) in patients with dilated cardiomyopathy (DCM) is difficult, so the present study evaluated the efficacy of microvolt-level T-wave alternans (TWA) and compared it with conventional parameters for prospective risk stratification of SCD in patients with DCM. Eighty-two patients with DCM (53+/-15 years old, 67M/15F) underwent assessment of TWA, left ventricular end-diastolic diameter (LVDd), left ventricular ejection fraction (LVEF), signal-averaged ECG, and analysis of 24-h Holter monitoring and QT dispersion (QTd). The endpoint of the study was defined as either SCD or documented sustained ventricular tachycardia/ventricular fibrillation (SVT/VF) during the follow-up period. During an average follow-up period of 24 months, 1 patient died suddenly and 9 patients had SVT/VF. Kaplan-Meier survival analysis showed that TWA, LVEF (< or =35%), nonsustained ventricular tachycardia, and QTd (>90ms) were significant univariate risk stratifiers (p<0.005, p<0.005, p<0.005, and p<0.05, respectively). Multivariate Cox regression analysis showed that TWA and the LVEF were statistically significant independent risk stratifiers (p<0.05 and p<0.01, respectively). A combination of TWA and LVEF identified high risk DCM patients (p<0.01); TWA for the electrical substrate and the LVEF for the hemodynamic function. |
4,117 | Choice of venous cannulation for bypass during repair of traumatic rupture of the aorta. | Choices for venous cannulation for left heart bypass, to assist repair of traumatic rupture of the thoracic aorta, are between the left atrial appendage and pulmonary veins.</AbstractText>A retrospective chart review was performed of patients who underwent operative repair of ruptured aorta.</AbstractText>Over a 15-year period between March 1985 and February 2000, 133 patients were admitted to a level I trauma center with aortic rupture. Of the 50 procedures performed with left heart bypass, the left atrial appendage was cannulated in 19 and pulmonary veins in 31 (four superior, 27 inferior). Complications occurred in 7 of the 19 patients who underwent venous cannulation via the atrial appendage (two ventricular fibrillation, three atrial fibrillation, one pericardial effusion leading to tamponade, and one phrenic nerve injury). Complications occurred in 2 patients who underwent cannulation via pulmonary vein (one atrial fibrillation, one pericardial effusion requiring tapping) (p = 0.02).</AbstractText>Cannulation via the pulmonary veins is associated with a decrease in complication rates compared with cannulation of the atrial appendage.</AbstractText> |
4,118 | Ischemia-induced ventricular fibrillation in isolated perfused rat heart: role of alpha1A-adrenoceptor mediated activation of protein kinase C. | It previously has been reported in ischemic rat hearts that local release of noradrenaline triggers ventricular fibrillation via alpha1A-adrenoceptor stimulation. In order to elucidate the intracellular pathway mediating ventricular fibrillation in this setting, we used inhibitors or activators of protein kinase C in the absence or presence of the alpha1A-adrenoceptor antagonist WB 4101. Regional ischemia was induced in isolated perfused rat heart byligature of the left coronary artery. Pharmacological interventions were tested by addition of drugs to the perfusate 10 min prior to ligature and throughout 30 min of ischemia while the epicardial electrocardiogram was continuously monitored. Blockade of protein kinase C by polymyxin B (1 micromol/l) significantly reduced ventricular fibrillation to 40% (from 87% in controls). Similar effects were seen with the protein kinase C inhibitors staurosporine 10 nmol/l (46% vs. 91%) and cremophor RH 40 100 micromol/l (33% vs. 77%). Activation of protein kinase C by 1,2-dioctanoyl-sn-glycerol (DOG, 10 micromol/l) or phorbol 12-myristate 13-acetate (PMA, 10 nmol/l) did not affect ventricular fibrillation. In the presence of the alpha1A-adrenoceptor antagonist WB 4101 (0.1 micromol/l), which per se suppressed ventricular fibrillation to 17%, both DOG and PMA increased the occurrence of ventricular fibrillation to 73% and 75%, respectively, whereas the inactive phorbol ester 4alpha-phorbol 12,13-didecanoate (4alpha-PDD, 10 nmol/l) revealed no proarrhythmic effect. In summary, during regional ischemia in the isolated perfused rat heart, alpha1A-adrenoceptor stimulation induces ventricular fibrillation mainly by activating protein kinase C. |
4,119 | Effect of long-term application of Crataegus oxyacantha on ischemia and reperfusion induced arrhythmias in rats. | The effect of long-term application of Crataegus oxyacantha on ischemia and reperfusion induced arrhythmias was investigated in Wistar rats on the heart in situ and on Langendorff preparations. Seventeen rats were fed for 8 weeks with 0.5 g/kg b.w. Crataegus extract per day, standardised to 2.2% flavonoids. Twenty age-matched untreated rats served as controls. In the hearts in situ as well as in the Langendorff preparations the left anterior descending coronary artery (LAD) was ligated for 20 min and subsequently reperfused for 30 min. ECG was continuously recorded and the time spent between start of ischemia and onset of arrhythmias was measured. In addition, during ischemia and reperfusion the number of ventricular premature beats and bigemini and the duration of salvos and ventricular flutter and fibrillation were determined. The ischemic area was evaluated in all experiments and coronary flow was measured in Langendorff preparations. In the present experiments, no cardioprotective effects of Crataegus oxyacantha could be detected, neither in the heart in situ nor in the Langendorff preparations. Although the ischemic areas were identical, arrhythmias occurred even earlier in the Crataegus collectives than in the controls. Also the number and duration of ischemia and reperfusion induced arrhythmias tended to occur longer and more frequently in the Crataegus collectives, whilst coronary flow remained unchanged. The phenomenon that Crataegus rather aggravates than prevents arrhythmias may be reduced to a Crataegus induced increase in intracellular Ca(2+)-concentration proven true for the positive inotropic effects of Crataegus. |
4,120 | [A case of rhabdomyolysis after open heart surgery in a child]. | Rabdomyolysis usually occurs after trauma and release of myoglobin from the damaged muscle, i.e.; after ishchemic myopathy due to arterial occlusion or malignant hyperthermia. We encountered a pediatric case of rhabdomyolysis after Ross-Konnos' operation in an 8-yr-old girl with aortic regurgitation. After the first weaning from cardiopulmonary bypass (CPB), ventricular fibrillation occurred due to an insufficiency in coronary blood flow and CPB was resumed with rapid cooling of body temperature. The total CPB lasted for 5 hr 43 min. After the second weaning from CPB, myoglobinuria was found. Furthermore, blisters and abrasions appeared on her back and CPK levels were abnormally elevated (maximum 19,132 IU.l-1) without any elevation of body temperature in the postoperative course. Rhabdomyolysis due to intraoperative hypoperfusion was suspected and diuretics were administrated with a large amount of crystalloid to maintain urine output. The patient showed a good clinical course without acute renal failure. The course of this case suggests that rhabdomyolysis is one of rare complications of CPB and an early correct diagnosis of rhabdomyolysis and forced diuresis at an early stage are important to avoid acute renal failure. |
4,121 | [Arrhythmogenic right ventricular dysplasia]. | Arrhythmogenic right ventricular dysplasia (ARVD), disease of uncertain etiology, is characterized by fibrofatty collections in the right ventricular myocardium, premature ventricular complexes with left bundle branch block (LBBB) morphology, ventricular tachycardia and fibrillation.</AbstractText>To point out diagnostic methods for this progressive disease and to analyze differential diagnosis and significance of arrhythmogenic right ventricular dysplasia in young, active athletes.</AbstractText>Arrhythmogenic right ventricular disease can be asymptomatic or manifested (syncope). It is not uncommon that the first evidence of the disease is ventricular tachycardia/fibrillation or sudden cardiac death. Results of electrocardiography, echocardiography, invasive and other methods can, even after few years, be negative for ARVD. The most significant ECG features are inverese T wave in precordial V1-V3 leads and widened QRS complex (> 120 ms) in V1 lead. Significant echocardiographic features and data obtained by invasive hemodynamic examinations are: dilated right ventricle, left and right ventricular end-diastolic diameter ratio less then 0.5, hypokinetic/akinetic areas involving the wall of the right ventricle, predominantly inferobasal, apical and wall of the left ventricular outflow tract. Findings may also include deep fissures among hypertrophied trabeculae. Biopsy may reveal fibrofatty tissue in hypo/akinetic regions of the right ventricular myocardium.</AbstractText>Since arrhythmogenic right ventricular dysplasia is diagnosed in predominantly young population, not uncommonly athletes, and since it may be cause of sudden cardiac death, there must be a high degree of suspicion in cases with activity related VT/VF and positive family history (it is proposed that it is a hereditary disease).</AbstractText> |
4,122 | [Echocardiography and sonography of the carotid arteries in diabetics with cerebrovascular stroke]. | The incidence of cerebrovascular attacks (CVA) in diabetics is 2-3 times higher as compared with the non-diabetic population. The objective of the present work was to evaluate etiological factors by means of echocardiography and sonography of the carotid arteries. The authors evaluated retrospectively findings of these examinations in 253 patients with CVA in a group of diabetic and non-diabetic patients as well as in a group of patients with atrial fibrillations or sinus rhythm. In patients with a sinus rhythm the presence of diabetes was associated with a more frequent finding of atherosclerotic changes, significant stenoses of the carotid vessels (2% as compared with 8%, p < 0.05) as well as thickness of the intima in the carotid bulbus (0.78 as compared with 0.96 mm, p < 0.05). Conversely when evaluating signs of thromboembolic risk, i.e. the size of the left ventricle (42 vs. 40 mm, n.s.) and ejection fraction of the left ventricle (55% vs. 50%, n.s.) no statistical significance in the difference of parameters was found. In the sub-group of patients with atrial fibrillation, who accounted for 28% of the group, the authors did not find when comparing diabetic and non-diabetic patients, any difference as regards the presence of significant stenoses in the carotid arteries nor in the thickness of the intima. There was no statistically significant difference in the size of the left atrium and left ventricular function. The findings suggest the possibility that the increased risk of ischaemic CVA in diabetic patients is caused by the atherosclerotic process in the carotid vessels and not a higher risk of embolism of cardiac origin. |
4,123 | Arterial hypertension and cardiac arrhythmias. | PURPOSE AND DATA IDENTIFICATION: One of the main clinical problems of patients with arterial hypertension is the presence of arrhythmias, especially if left ventricular hypertrophy exists. Recent results from our group and all data available via Med-Line-search have been analysed. The analysis was focused on atrial and ventricular arrhythmias and arrhythmic risk prediction, using non-invasive markers. RESULTS OF ANALYSIS AND CONCLUSION: Arterial hypertension is a major cause of non-rheumatic atrial fibrillation and other supraventricular arrhythmias. The prevalence of ventricular arrhythmias is increased in hypertensive patients without left ventricular hypertrophy, compared to normotensives. If left ventricular hypertrophy is present, the risk for ventricular tachycardias is quadrupled. The presence of left ventricular hypertrophy is associated with an increase in all-cause mortality by a factor of seven in men and nine in women. In particular, patients with hypertrophy, increased rate of ventricular extrasystoles up to non-sustained ventricular tachycardia and ST-depression in long-term ECG are threatened by sudden cardiac death. At present, it is not possible to safely identify patients with increased risk. Regression of hypertrophy exists along with a decreased rate of ventricular extrasystoles. We hypothesize that by the regression of hypertrophy, the prevalence of sustained ventricular tachycardia decreases and therefore the prognosis of those patients can be improved, although controlled studies are not yet available. |
4,124 | [Anesthesia for a patient with cardiac sarcoidosis]. | Anesthesia for a 49-year-old man with cardiac sarcoidosis is reported. Preoperative cardiac examination showed left ventricular dysfunction (ejection fraction = 27%) and myocardial conduction defects. In addition, his previous history included atrial fibrillation and cerebral infarction. Transesophageal echocardiography showed thrombus in the left appendage. Anesthesia was induced with fentanyl and diazepam and maintained with fentanyl and isoflurane. Perioperative hemodynamic monitoring included direct arterial pressure, central venous and pulmonary artery pressure and continuous cardiac output. In addition, transesophageal echocardiography was useful for watching thrombus in the left appendage. His hemodynamic condition was stable and no neurological complication was noted after anesthesia. |
4,125 | The feasibility of a porcine model of acute coronary occlusion and reperfusion using off-pump coronary artery bypass grafting. | We developed an open-chest porcine model of acute coronary occlusion and surgical reperfusion, and attempted to prevent intra-operative ischaemic ventricular fibrillation (VF) by a Retrograde Intracoronary Glyceryl trinitrate (RIG) infusion into the occluded vessel. Five Yorkshire pigs (weight 50 +/- 1.1 kg), randomized into 3 groups, underwent median sternotomy under general anaesthesia. One pig (Group 1, control) underwent sternotomy and pericardiotomy only. Four pigs underwent acute left anterior descending (LAD) coronary occlusion. Two pigs were not reperfused (Group 2). Two pigs underwent surgical reperfusion (Group 3) via left internal mammary artery (LIMA) grafting to the LAD using the Off-Pump Coronary Artery Bypass (OPCAB) technique. Ischaemic injury was assessed using 7-lead electrocardiography (ECG) and transthoracic/epimyocardial echocardiography (ECHO). Group 1: transient intraoperative hypotension and VF occurred. Successful resuscitation and 10-week survival (until sacrifice) with normal left ventricular (LV) function was achieved. Group 2: there were ECG and ECHO evidence of acute LV ischaemic dysfunction in both pigs. The surviving pig had persistent anterior hypokinesis at 8 1/2 months. The other died intra-operatively following progressive ischaemic LV dysfunction despite resuscitative attempts. Group 3: the surviving pig had normal LV function at 8 months. Initial anterior LV akinesis normalized within 7 days. The other developed post-occlusion haemodynamic instability and died intra-operatively despite reperfusion. In this porcine model, acute LAD artery occlusion modified by the novel RIG infusion technique, followed by surgical reperfusion (OPCAB) is feasible. This model would facilitate further development of OPCAB surgical expertise and understanding of the pathophysiology of ischaemia-reperfusion injury. |
4,126 | Ventricular preexcitation in children and young adults: atrial myocarditis as a possible trigger of sudden death. | Sudden death (SD) in ventricular preexcitation (VP) syndrome is believed to be the result of atrial fibrillation with rapid ventricular response over the accessory pathway. Previous reports are anecdotal and often lack autopsy validation.</AbstractText>Prevalence and clinicopathological features of VP were investigated in a series of 273 SDs in children and young adults (aged <or=35 years). Site of accessory atrioventricular (AV) connection was predicted by 12-lead ECG. Right and left AV ring together with the sinoatrial and AV septal junction were studied in serial histological sections. Ten patients (3.6%; male, mean age 24+/-7 years) had VP: 8 had Wolff-Parkinson-White (WPW) and 2 had Lown-Ganong-Levine (LGL) syndrome. Six patients had previous symptoms, and SD occurred at rest in all but 1. Pathological substrates of LGL consisted of AV-node hypoplasia and right-sided atrio-Hisian tract, respectively. In the 8 WPW patients, 10 total accessory AV pathways consisting of ordinary myocardium were found (7 left lateral, 2 right posterolateral, and 1 septal). These pathways were close to the endocardium (mean distance, 750+/-530 microm) and 310+/-190 microm thick. In 4 WPW patients (50%), isolated acute atrial myocarditis was found, which was polymorphous in 1 and lymphocytic in 3.</AbstractText>VP accounted for 3.6% of SD in young people and was not preceded by warning symptoms in 40%. A left accessory pathway was the most frequent substrate, and its subendocardial location supports the feasibility of catheter ablation. Isolated atrial myocarditis may act as a trigger of paroxysmal atrial fibrillation that leads to SD.</AbstractText> |
4,127 | Chemical cardioversion of atrial fibrillation or flutter with ibutilide in patients receiving amiodarone therapy. | Ibutilide is a class III drug that is used for the cardioversion of atrial arrhythmias, but it can cause torsade de pointes. Amiodarone also prolongs the QT interval but rarely causes torsade de pointes. There are no studies in which the concomitant use of the 2 agents was examined. The purpose of the present study was to assess the efficacy and safety of cardioversion with combination therapy in patients with atrial fibrillation or flutter.</AbstractText>The study included 70 patients who were treated with long-term oral amiodarone and were referred for elective cardioversion of atrial fibrillation (57 of 70, 81%) or flutter (13 of 70, 19%). Patients were taking amiodarone (153+/-259 days, mean+/-SD) and were administered 2 mg intravenous ibutilide. Left ventricular ejection fraction was measured with echocardiography. The QT intervals were measured on 12-lead ECG. Fifty-five patients (79%) had structural heart disease. Patients were in arrhythmia for 196+/-508 days before cardioversion, with a left ventricular ejection fraction of 50+/-11%. In patients with atrial fibrillation, 22 (39%) of 57 and 7 (54%) of 13 patients with flutter converted within 30 minutes of infusion. Thirty-nine patients who did not convert after ibutilide were treated with electrical cardioversion, and 35 (90%) of 39 patients were successfully converted. The QT intervals were further prolonged after ibutilide for the group from 371+/-61 to 479+/-92 ms (P:<0.001). There was 1 episode of nonsustained torsade de pointes (1 of 70, 1.4%) after ibutilide.</AbstractText>The use of ibutilide converted 54% of patients with atrial flutter and 39% of patients with atrial fibrillation who were treated with long-term amiodarone. Despite QT-interval prolongation after ibutilide, only 1 episode of torsade de pointes occurred. Our observations suggest that combination therapy may be a useful cardioversion method for chronic atrial fibrillation or flutter.</AbstractText> |
4,128 | Effectiveness of high resolution ECG spectral analysis in discrimination of patients prone to ventricular tachycardia and fibrillation. | To improve the diagnostic power of high resolution electrocardiography for discriminating patients at risk of ventricular arrhythmias, new methods based on spectral analysis have been used in recent years. The purpose of this study was to evaluate the effectiveness of these methods for predicting the risk of ventricular tachycardia and ventricular fibrillation in patients after myocardial infarction.</AbstractText>High resolution ECG were recorded in 129 post-infarction patients and 23 healthy volunteers. Of the post-infarction patients: 62 presented with ventricular tachycardia, 23 with ventricular fibrillation, while 44 had no clinically relevant arrhythmias. The ECG signals were recorded in three orthogonal X, Y, Z leads and averaged using cross-correlation method. Spectral analysis was performed by fast Fourier transform and the parametric modeling method with autoregressive model. Spectral analysis data were evaluated quantitatively by computing normality factor for FFT and spectral factor for AR.</AbstractText>Both methods were found to be useful for evaluating the risk of arrhythmias. The sensitivity of ventricular tachycardia risk evaluation was higher (81%--FFT, 73%--AR) than that of evaluating the risk of ventricular fibrillation (30%--FFT, 48%--AR). The specificity in post-infarction patients without arrhythmias (93%--FFT, 84%--AR) was as high as that in healthy subjects (96%--FFT, 87%--AR).</AbstractText>Spectral analysis of HRECG is an effective method for evaluating the risk of VT and VF in patients after myocardial infarction.</AbstractText> |
4,129 | Diagnosis and long-term follow-up of the Brugada syndrome in patients with idiopathic ventricular fibrillation. | Some patients with idiopathic ventricular fibrillation may suffer from the Brugada syndrome. The diagnostic criteria for the Brugada syndrome are uncertain and arbitrarily set. Therefore, we studied the prevalence of the Brugada syndrome using various diagnostic criteria and long-term follow-up in 37 idiopathic ventricular fibrillation patients.</AbstractText>Idiopathic ventricular fibrillation was diagnosed after thorough clinical evaluation in 37 survivors of an out-of-hospital cardiac arrest referred to our institute (UMC Utrecht). Retrospectively, nine patients (24%, group I) were classified as potentially having the Brugada syndrome based on the presence of (in)complete right bundle branch block and ST-segment elevation in leads V(1)-V(3)of > or =1 mm. Only three patients (8%, group II) showed (in)complete right bundle branch block and > or =2 mm ST-segment elevation. With the intermittent presence of these ECG features and/or their (re)appearance with class I antiarrhythmic drugs included as criteria, the percentage of the Brugada syndrome was attenuated in group I (2/37; 5%) and group II (1/37; 3%). Sixteen (43%) of all idiopathic ventricular fibrillation patients (mean follow-up 77+/-41 months) had a recurrent episode of syncope, ventricular tachyarrhythmias or sudden death. Recurrence rate was 3/9 (33%) in Brugada patients group I, 2/3 (66%) in group II and 13/28 (46%) in patients without the Brugada syndrome (P=ns).</AbstractText>Depending on the diagnostic criteria used, the Brugada syndrome was observed in 3% to 24% of patients with idiopathic ventricular fibrillation, underlining the importance of defining the precise diagnostic criteria in these patients. For all idiopathic ventricular fibrillation patients, the ventricular tachyarrhythmia recurrence rate was substantial during an average follow-up of more than 6 years.</AbstractText>Copyright 2001 The European Society of Cardiology.</CopyrightInformation> |
4,130 | Possible role of nitric oxide and mast cells in endotoxin-induced cardioprotection. | The present study is designed to investigate the role of nitric oxide (NO) and cardiac mast cells in the cardioprotective effect of endotoxin in isolated rat heart subjected to 30 min of global ischaemia and 30 min of reperfusion. Endotoxin (2.5 mg kg(-1); i.p.) was administered 8 h before subjecting the heart to global ischaemia. Endotoxin pretreatment markedly reduced the release of lactate dehydrogenase (LDH) and creatine kinase (CK), markers of cardiac injury, in coronary effluent and the percentage incidence of ventricular premature beats (VPBs) and ventricular tachycardia/fibrillation (VT/VF) during the reperfusion phase. Endotoxin pretreatment significantly increased the release of nitrite prior to and after global ischaemia. On the other hand, endotoxin pretreatment decreased the release of mast cell peroxidase (MPO) during the reperfusion phase. The cardioprotective and antiarrhythmic effect of endotoxin pretreatment was abolished by dexamethasone (3 mg kg(-1); i.p.) or l -canavanine (20 mg kg(-1); i.p.) given 1 h before the administration of endotoxin. It is proposed that the cardioprotective and antiarrhythmic effect of the endotoxin may be ascribed to the induction of nitric oxide synthase (NOS) and subsequent increase in the release of NO. NO may stabilize cardiac mast cells and consequently decrease the release of cytotoxic mediators from these cells. Prevention of degranulation of cardiac mast cells may be responsible for the cardioprotective and antiarrhythmic effects of the endotoxin. |
4,131 | O-[2-hydroxy-3-(dialkylamino)propyl]ethers of (+)-1,7,7-trimethyl bicyclo[2.2.1]heptan-2-one oxime (camphor oxime) with analgesic and antiarrhythmic activities. | A novel series of O-[2-hydroxy-3-(dialkylamino)propyl]ethers of (+)-camphor oxime was prepared and tested for its cardiovascular, analgesic and anti-inflammatory properties. No significant anti-inflammatory and hypotensive activities were displayed by any of the compounds, whereas several of them are reasonably active as antiarrhythmic and analgesic agents. |
4,132 | [Multiple organ failure following inhalation of butane gas: a case report]. | Most cases of acute poisoning by butane and other volatile compounds occur in young people as a consequence of substance abuse by inhalation. Clinical symptoms are caused by asphyxia and mainly affect the cardiovascular, respiratory and central nervous system. There are also reported deaths from intoxication of butane inhalation, mostly by cardiac arrhythmia. We report the case of a healthy 14 year-old boy who inhaled butane gas from an aerosol can for refilling cigarette lighters. Despite successful resuscitation and defibrillation, he died two days later from multiple organ failure involving the central nervous system, cardiovascular system, pulmonary system and the liver. Although such incidents are rare in middle European countries, emergency and intensive care medicine staff should be instructed on the consequences and management of butane gas poisoning. |
4,133 | Pacing during ventricular fibrillation: factors influencing the ability to capture. | Recent studies showed that pacing atrial and ventricular fibrillation (VF) is possible. The studies presented here determined which parameters influence the efficacy of a pacing train to capture fibrillating ventricular myocardium. Electrode type, current strength, order of pacing trains, polarity, and VF morphology preceding the pacing trains were investigated.</AbstractText>A 504-electrode recording plaque sutured to the right ventricle of pig hearts was used to record the activations of VF and those resulting from the pacing stimulation. Capture of VF by pacing was determined by observing an animated display of the first temporal derivative of the electrograms. A series of electrodes in a line captured the heart more frequently during VF than did a point electrode. Increasing the current strength to 10 x diastolic pacing threshold increased the incidence of capture, but increasing this strength further did not. The second or third train of 40 stimuli had greater capture rates than did the first train during the same VF episode. Anodal and cathodal unipolar, and bipolar stimulation were equally efficacious in capturing VF. VF activation during the 1-second interval preceding pacing was more organized for pacing trains that captured than those that did not. The highest incidence of capture, 46% to 61% of pacing trains, occurred with a line of electrodes at 10 x diastolic pacing threshold delivered by the second or third train.</AbstractText>The probability of a pacing train capturing fibrillating myocardium can be influenced by the pacing protocol parameters.</AbstractText> |
4,134 | Role of structural complexities of septal tissue in maintaining ventricular fibrillation in isolated, perfused canine ventricle. | It is unclear how the patterns of wavelet propagation during ventricular fibrillation (VF) vary between structurally different tissues. We hypothesized that the structural complexities of septal tissue influence the maintenance of reentrant wavelets in the ventricle.</AbstractText>Endocardial activation patterns during VF were analyzed in the isolated, perfused canine right ventricular (RV) free wall (n = 9), interventricular septum (n = 5), and left ventricular (LV) free wall (n = 6) using a computerized mapping system (2-mm resolution) with 120-msec consecutive windows. Each tissue sample was cut progressively to reduce the tissue mass until the VF was terminated. More wavelets were seen in the septa than in the RV and LV free walls at baseline (P = 0.004), and VF in the septa displayed a shorter cycle length than in the RV and LV free walls (P = 0.017). As the tissue mass decreased, VF became successively more organized in all regions: the number of wavelets decreased and the cycle length of VF lengthened. Single and "figure-of-eight" stationary, reentrant wavelets often were mapped after tissue mass reduction in the RV free walls and rarely in the LV free walls, but they were not observed in the septa. Less critical mass was required to maintain VF in the septa than in the RV and LV free walls (P = 0.0006). Gross anatomic and histologic examinations indicated that the tissue structure of the septa is more complex than that of the RV and LV free walls.</AbstractText>VF activation patterns with progressive reduction of tissue mass differ for the septum and the ventricular free walls. The structural complexities of the septal tissue influence the maintenance of fibrillation in the ventricle.</AbstractText> |
4,135 | Differential modulation of electrocardiographic indices of ventricular repolarization dispersion depending on the site of pacing during premature stimulation. | Dispersion of ventricular repolarization has been shown to increase with premature stimulation. Moreover, a straight correlation between the amount of dispersion of repolarization and the vulnerability to ventricular fibrillation was reported. On the other hand, differences between right ventricular (RV) and left ventricular (LV) fibrillation threshold have been reported. However, no data exist regarding the influence of the site of stimulation on modulation of dispersion of repolarization.</AbstractText>In the present study, several ECG indices of dispersion of repolarization, as a function of the coupling interval and the site of stimulation, were evaluated in a modified Langendorff-perfused rabbit heart (n = 12), with a 5 x 8 array of a simulated body surface unipolar lead system. As the coupling interval was shortened, a biphasic modulation of dispersion of repolarization was found when stimuli were elicited at the LV. In contrast, when the heart was paced from the RV, the dispersion increased monotonically as coupling interval was shortened.</AbstractText>A differential behavior of the modulation of dispersion of repolarization was found as a function of the site of stimulation.</AbstractText> |
4,136 | Relatively benign clinical course in asymptomatic patients with brugada-type electrocardiogram without family history of sudden death. | The incidence of sudden death or ventricular fibrillation (VF) in asymptomatic Brugada syndrome patients with a family history of sudden death is reported to be very high. However, there are few reports on the prognosis of asymptomatic Brugada syndrome patients without a family history of sudden death.</AbstractText>Eleven patients (all male; mean age 40.5 +/- 9.6 years, range 26 to 56) with asymptomatic Brugada-type ECG who had no family history of sudden death were evaluated. The degrees of ST segment elevation and conduction delay on signal-averaged ECG (SAECG) before and after pilsicainide were evaluated in all 11 patients. VF inducibility by ventricular electrical stimulation also was evaluated in 8 of 11 patients. Patients were followed for a period of 9 to 84 months (mean 42.5 +/- 21.6). The J point level was increased (V1: 0.19 +/- 0.09 mV to 0.36 +/- 0.23 mV; V2: 0.31 +/- 0.12 mV to 0.67 +/- 0.35 mV) by pilsicainide. Conduction delay was increased (total QRS: 112.2 +/- 6.3 msec to 131.7 +/- 6.3 msec; under 40 microV: 42.0 +/- 8.5 msec to 52.7 +/- 12.7 msec; last 40 msec: 17.4 +/- 5.9 microV to 10.4 +/- 6.1 microV) on SAECG by pilsicainide. VF was induced in only 1 of 8 patients. None of the patients had syncope or sudden death during a mean follow-up of 42.5 +/- 21.6 months.</AbstractText>This study suggests that asymptomatic patients with Brugada-type ECG who have no family history of sudden death have a relatively benign clinical course.</AbstractText> |
4,137 | Vasospastic angina accompanied by Brugada-type electrocardiographic abnormalities. | Brugada Syndrome and Vasospastic Angina. We present two patients with vasospastic angina and Brugada-type ECG abnormalities. The first patient complained of chest pain, and transient ST segment elevation was confirmed on ECG. Coronary angiogram showed no organic stenosis. The second patient had syncopal episodes following anginal chest pain, and the same symptoms were reproduced by intracoronary acetylcholine injection that induced vasospasm. In both patients, ECG at rest showed ST segment elevation in leads V1 and V2 and a right bundle branch block pattern that were accentuated by a Class I antiarrhythmic drug. Ventricular fibrillation also was induced by programmed electrical stimulation. Susceptibility to ventricular fibrillation can be modulated by the interaction of coronary vasospasm with Brugada syndrome or vice versa; therefore, it is important to study the clinical implications of the coexistence of the two diseases in such patients. |
4,138 | [Left atrial myxoma. Clinical and surgical features in 26 surgically treated cases]. | Left atrial myxomas are the most common benign intracardiac tumors. The aim of this study was to compare our experience with the data reported in the literature.</AbstractText>Between May 1985 and August 1999, 26 patients (8 males, 18 females) with left atrial myxomas underwent surgical resection of these tumors at the Department of Cardiac Surgery, Ospedali Riuniti of Bergamo (Italy). Symptoms included congestive heart failure, dyspnea, arrhythmias, chest pain and syncope. Diagnosis was established preoperatively in all patients by echocardiography and angiocardiography was performed in 8 cases. All tumors were excised with a wide margin of uninvolved atrial septum. Two patients underwent concomitant coronary artery bypass.</AbstractText>There was 1 early death due to irreversible ventricular fibrillation. Follow-up was completed for the 25 late survivals. Three patients died, years after operation, due to extracardiac causes. One patients had recurrence of the tumor, which was successfully removed 4 years after initial operation. All other patients are asymptomatic and free from disease.</AbstractText>Operation for left atrial myxoma can be undertaken solely on the basis of echocardiographic findings, but coronary angiography should be performed in older patients who are at risk for coronary artery disease. Surgical excision of left atrial myxomas must be performed as soon as possible after diagnosis is established because of the high risk of valvular obstruction or systemic embolization. Biatrial approach allows for the inspection of the four cardiac chambers, limits manipulation of the mass, and facilitates the complete excision of the tumor. Thus, surgical intervention can be curative for patients with left atrial myxomas and most of these can expect an excellent outcome. Since late recurrence, although rare, has been reported, especially in familial myxomas, long-term clinical and echocardiographic follow-up is recommended.</AbstractText> |
4,139 | [Long-term clinical assessment of single-lead VDD electric stimulation]. | During the last decade single lead VDD pacing has been progressively affirmed as an electrotherapy of choice in patients with advanced atrioventricular block without alterations of the sinus function. It combines the benefits of P-synchronous ventricular pacing with an easy implant procedure when compared to the conventional DDD approach. The aim of this study was to evaluate the validity of such an approach in a large population of patients, all implanted in a single center.</AbstractText>From 1987 up to now, 317 patients, all affected by advanced atrioventricular block and without sinus node dysfunction, were implanted in our center with a single lead VDD pacemaker. During follow-up the persistence of a proper atrioventricular synchronization was assessed and evaluated.</AbstractText>The mean follow-up was 3.9 +/- 2.7 years/patient (range 6-138 months). The 94.6% of implanted systems maintained the normal VDD pacing function. Permanent reprogramming in VVI mode was necessary in 17 patients (5.36%); in 12 (3.78%) because of chronic atrial fibrillation and in 5 (1.63%) for loss of atrial sensing. The percentage of atrial synchronization was optimal (> 98%) and acceptable (> 95%) in 81% and 19% of patients, respectively. Episodes of paroxysmal atrial fibrillation occurred in 3 patients. Neither inhibition by myopotentials nor occurrence of sinus node disease was observed during follow-up. These results are in accordance with those reported by previous studies, performed on a smaller population or on a multicenter basis, and are comparable with the results reported for conventional DDD pacemaker.</AbstractText>Our results confirm the high reliability of the single lead VDD pacing system concerning the long-term persistence of a proper atrioventricular synchronization. Data showed above enforce our opinion that this pacing approach should be considered the treatment of choice in patients with advanced atrioventricular block and preserved sinus node function.</AbstractText> |
4,140 | [3-year-survival and quality of life after out-of-hospital heart arrest]. | Although the long- and short-term aspects of the outcome of advanced cardiopulmonary resuscitation on patients have been studied to evaluate the percentage of survival up to the moment of discharge from hospital, little information has been published concerning the patients' long-term quality of life. In order to verify the efficiency of our group we retrospectively evaluated 468 subjects admitted to the Emergency Room of Rho Hospital (Milan, Italy) for out-of-hospital cardiac arrest that had occurred over a 90-month period. We studied the correlations between some variables: epidemiological (sex and age), objective (time required for advanced cardiopulmonary resuscitation and type of arrhythmias in the Emergency Room) and instrumental (left ventricular ejection fraction) and post-discharge survival. We also considered the state of health of the survivors by means of a questionnaire on their quality of life. Our data show that: a) 10.25% of the patients were discharged alive; b) younger men (< 65 years old) admitted with a ventricular fibrillation (p = 0.01) and those who had undergone advanced cardiopulmonary resuscitation for less than 25 min (p = 0.001) had a better survival rate at 3 years from discharge; c) 64% of the survivors have a satisfactory quality of life; d) younger age (p = 0.01) and cardiac left ventricular ejection fraction (> 40%) (p = 0.05) are positive predictors for future work capacity. In conclusion, we believe that the critical moment following advanced cardiopulmonary resuscitation is hospitalization because after discharge survival percentage abruptly increased from 10.25 to 65%. |
4,141 | [Effect of the sympathetic nervous system activation on the antifibrillatory efficacy of various anti-arrhythmia agents]. | Experiments with a 7-min occlusion followed by reperfusion of the left coronary artery in narcotized rats showed that antiarrhythmic drugs of various classes--ethacizin (class I), AL-275 (class III), and CM-345 (class V)--produce pronounced antifibrillatory and antiarrhythmic effects. AL-275 and CM-345, in contrast to ethacizin, retained their efficacy under the conditions of isoproterenol-induced stimulation of beta-adrenoceptors. This difference in behavior is probably explained by dissimilar effects of the antiarrhythmics on the ion channels of cardiomyocite membranes. |
4,142 | A comparative study on the behavior of three different automatic mode switching dual chamber pacemakers to intracardiac recordings of clinical atrial fibrillation. | Automatic mode switching (AMS) allows patients with dual chamber pacemakers who develop paroxysmal AF to have a controlled ventricular rate. The aim of this study was to (1) compare the rate-controlled behavior of three AMS algorithms in response to AF, in terms of speed and stability of response and resynchronization to sinus rhythm, and (2) compare the influence of pacemaker programming on optimal mode switching. We studied 17 patients (12 men, 5 women; mean age 59 +/- 15 years) who developed AF during electrophysiological study. Unfiltered bipolar atrial electrograms during sinus rhythm and AF were recorded onto high fidelity tapes and replayed into the atrial port of three dual chamber pacemakers with different mode switching algorithms (Thera, Marathon, Meta). The Thera pacemaker uses rate smoothing, and mode switches occur when mean sensed atrial rate exceeds the predefined AMS rate (MR). Marathon mode switches after a programmable number of consecutive rapid atrial events (NR). Meta DDDR monitors the atrial rate by a counter for atrial cycles faster than the programmed AMS rate. It increases or decreases the counter if the atrial cycle length is shorter or longer than the programmed AMS interval, respectively. Mode switch occurs when the AF detection criteria are met (CR). A total of 260 rhythms were studied. NR was significantly faster than MR and CR (latency 2.5 +/- 3 s vs 26 +/- 7 s vs 15 +/- 22 s, respectively, P < 0.0001). During sustained AF, MR resulted in the most stable and regular ventricular rhythm compared to NR or CR. In CR, ventricular rate oscillated between AMS and atrial tracking (cycle length variations: 44 +/- 2 s vs 346 +/- 109 s vs 672 +/- 84 s, P < 0.05). At resumption of sinus rhythm, MR resynchronized after 143 +/- 22 s versus 3.4 +/- 0.7 s for NR and 5.9 +/- 1.1 s for CR, resulting in long periods of AV dissociation when a VVI/VVIR mode is used after AMS. Programming of atrial refractory periods did not affect AMS response, although the speed of AMS onset can be adjusted by programming of onset criteria in the Meta DDDR. AMS algorithms differ in their ability to handle recorded clinical atrial arrhythmias. The rapid-responding algorithm exhibits rate instability, whereas slow responding algorithm shows a long delay in response and risk of AV dissociation. Thus different instrumentation of AMS may have clinical implications in patients with dual chamber pacemakers who develop AF. |
4,143 | [Mechanism of induction and termination of ventricular fibrillation--significance of dispersion of ventricular repolarization]. | It has been known for many years that ventricular fibrillation may be induced and terminated by electrical field stimuli. Recent experimental studies have shown that both fibrillation and defibrillation have a common electrophysiologic mechanism that is based on the interaction between the electrical field stimulus and ventricular repolarization. Ventricular fibrillation will be induced if the field stimulus is applied with the area of vulnerability, this area of vulnerability is defined two dimensionally by the shock coupling interval and shock strength, and is modified by the configuration of the shock. A field shock that is applied within the area of vulnerability causes heterogeneity of ventricular repolarization immediately after the shock (postshock dispersion), thereby enabling the development of circuit movements and reentry, and resulting in ventricular fibrillation. High energy shocks, however, that are applied above the area of vulnerability (i.e., above the upper limit of vulnerability) will not induce ventricular fibrillation due to homogeneous prolongation of repolarization and a resulting small postshock dispersion. In analogy, ventricular fibrillation will continue after unsuccessful low-energy defibrillation shocks due to high postshock dispersion, whereas a high-energy shock will synchronize ventricular repolarization, thereby causing small postshock dispersion and termination of ventricular fibrillation. This paper describes the relation between fibrillation, defibrillation and ventricular repolarization based on experimental findings. A possible clinical application of these findings is that the upper limit of vulnerability may be used as a surrogate for the defibrillation threshold. Thus, defibrillation threshold testing may not be necessary during future implantations of automatic cardioverter defibrillators. |
4,144 | [Effects of cilostazol in patients with bradycardiac atrial fibrillation]. | Cilostazol, an antithrombotic agent, directly and indirectly increases the heart rate. This study investigated whether cilostazol increases the heart rate, and whether it has chronotropic effects on cardiac failure in patients with bradycardiac atrial fibrillation.</AbstractText>Twelve patients (6 males and 6 females) with bradycardiac atrial fibrillation underwent Holter monitoring (24-hour total heartbeat counts and frequency of pause), echocardiography (left ventricular end-diastolic diameter, percentage fractional shortening), chest roentgenography (cardiothoracic ratio), and measurements of brain natriuretic peptide and atrial natriuretic peptide before and 6 months after daily oral administration of 100-200 mg cilostazol.</AbstractText>Cilostazol administration increased the 24-hour total heartbeat counts from 69,685 +/- 1,690 (mean +/- SE; mean heart rate: 48 beats/min) to 87,352 +/- 3,123 (60), and decreased the frequency of pause from 362.3 +/- 72.9 to 112.3 +/- 41.0. Cardiothoracic ratio decreased from 55.8 +/- 1.1% to 52.5 +/- 1.1%, left ventricular end-diastolic diameter from 56.1 +/- 0.9 to 52.9 +/- 0.8 mm, but percentage fractional shortening was not significantly changed (from 33.0 +/- 2.2% to 33.7 +/- 2.1%). Brain natriuretic peptide decreased from 97.9 +/- 20.5 to 33.5 +/- 4.8 pg/ml, and atrial natriuretic peptide from 69.5 +/- 12.1 to 46.7 +/- 8.3 pg/ml.</AbstractText>Cilostazol has beneficial effects in patients with bradycardiac atrial fibrillation. The increase of heart rate may be mediated by improvement of conductivity in the atrioventricular node and increase of coronary blood supply caused by dilation of vessels.</AbstractText> |
4,145 | Arrhythmias in acute pericarditis. An endomyocardial biopsy study. | It is still controversial whether the arrhythmias in acute pericarditis are of myocardial or pericardial origin. The aim of the present study was to investigate the occurrence of arrhythmias and conduction disorders in patients with acute pericarditis with no endomyocardial biopsy evidence of myocarditis (group 1: 40 patients, 65% males, mean age 45.6 +/- 15.7 years, mean heart rate [HR] 98.7 +/- 22.2 beats per minute) in comparison to endomyocardial biopsy proven acute myocarditis/perimyocarditis (group 2: 10 patients, 3/10 with perimyocarditis, 70% males, mean age 46.1 +/- 15.8 years, mean heart rate 76.7 +/- 33.1 beats per minute). At the initial assessment all patients underwent comprehensive clinical work-up including echocardiography, cardiac catheterization, and endomyocardial biopsy. In all patients biventricular endomyocardial biopsy was performed using standard femoral approach and Schikumed 7 F or 8 F bioptomes. Tissue samples were stained by H & E, v. Gieson and independently reviewed by two cardiac pathologists. In addition immunohistochemistry and immunocytochemistry were performed, and only patients fulfilling Dallas and World Heart Federation criteria were selected for group 2. Comparative analysis of electrocardiograms and 24-hour Holter recordings at initial presentation revealed in group 1 vs group 2 significantly less frequent paroxysmal supraventricular tachyarrhythmias (5% vs 40%), and ventricular fibrillation (0 vs 20%), in contrast to atrial fibrillation that occurred more often (20% vs 0) (all p < 0.05). Furthermore, in the group 2 one patient died due to VF and two patients underwent ICD implantation. Low voltage (40% vs 30%) and ST/T wave changes (47.5% vs 30%), as well as the incidence of the II degree AV block (5% vs 0) and complete AV block (2.5% vs 10%) were not significantly different between the groups. In conclusion, patients with pericarditis and no endomyocardial biopsy indications of myocarditis had significantly less often life threatening rhythm disorders in contrast to patients with endomyocardial biopsy proven acute myocarditis/perimyocarditis. On the contrary, incidence of transitory atrial fibrillation was higher in acute pericarditis, than in myocarditis. |
4,146 | [Acute ethanol and drug poisoning in alcohol abusers]. | In the period from 1997 to 1999 one hundred twenty one alcohol abusers were admitted to the clinic with acute ethanol and drug poisoning, including 95 men and 26 women from 18 to 69 (mean 36) years old. Fifty eight persons were poisoned by ethanol, in remaining 63 cases intoxications were mixed e.g. including benzodiazepines, tricyclic antidepressants, carbamazepine, amphetamine, phenothiazines, barbiturates, theophylline, salicylates. In the mixed poisonings group two men (3.2%) died at the age above 50 years old suffering from congestive heart failure, bronchopneumonia and ventricular fibrillation. In the ethanol intoxication group there was no fatal case. |
4,147 | [Aortic root replacement after operation for the ascending aorta and/or aortic valve]. | We reviewed ten cases who underwent aortic root replacement after operation for the ascending aorta and/or aortic valve. As initial operation, aortic valve replacement (AVR) was performed in five patients, replacement of the ascending aorta in two, original Bentall operation in two, and entry closure and suspension of the aortic valve in one. At reoperation, three patients were diagnosed as aneurysm of the ascending aorta, two were annulo-aortic ectasia, and one was acute aortic dissection, chronic dissecting aneusym, pseudoaneurysm of the ascending aorta, prosthetic valve endocarditis, and massive aortic regurgitation. Aortic root replacement was performed using mechanical valved composite graft in all cases. One patient who underwent repeat aortic root replacement for prosthetic valve endocarditis was died of septemia and ventricular fibrillation. Five patients had nine complications (two low output syndrome, respiratory failure and cerebral infarction, one gastrointestinal bleeding, septemia and ventricular fibrillation). In conclusion, aortic root replacement after operation for the ascending aorta and/or aortic valve was performed with acceptable morbidity and mortality. |
4,148 | Termination of spiral waves with biphasic shocks: role of virtual electrode polarization. | This simulation study seeks to extend the virtual electrode polarization (VEP) theory for defibrillation to explain the success and failure of biphasic shocks. The goals of the study are to (1) provide insight into why optimal biphasic shocks have a lower voltage defibrillation threshold than monophasic shocks, (2) examine the mechanisms of biphasic shock failure and to determine whether they differ from those of monophasic shocks, and (3) study how the timing of biphasic shock delivery to a spiral wave affects voltage defibrillation threshold.</AbstractText>A spiral wave is initiated in a bidomain representation of a 2-cm x 2-cm sheet of ventricular myocardium. The model incorporates nonuniform fiber curvature, membrane kinetics suitable for high-strength shocks, and electroporation. A spatially uniform extracellular field is delivered by line electrodes. The shock establishes VEP that dictates the postshock activity in the tissue. Our results demonstrate that the second phase of biphasic shocks leaves the tissue with substantially smaller postshock excitable gap, thus eliminating the majority of the substrate for reinitiation of reentrant activity. Further, the occurrence of break excitations for weaker biphasic shocks indicates that the mechanisms for biphasic shock failure are more complex than for monophasic shocks. Biphasic voltage defibrillation thresholds range from 8 to 16 V/cm, depending on the position of the spiral wave. An increase in the amount of preshock excitable gap leads to an increase in voltage defibrillation threshold.</AbstractText>This study demonstrates the importance of VEP and its interaction with preshock activity in the success and failure of biphasic defibrillation shocks.</AbstractText> |
4,149 | Profibrillatory effects of verapamil but not of digoxin in the goat model of atrial fibrillation. | Verapamil and digoxin have been shown to modulate tachycardia-induced atrial electrical remodeling. The goal of the present study was to determine the direct effects of verapamil and digoxin on atrial fibrillation (AF), before and after electrical remodeling.</AbstractText>In six goats we measured the AF cycle length (AFCL) and duration of AF (DurAF) of 50 consecutive induced paroxysms, before (t = 0) and after 24 hours (t = 24) of electrical remodeling. During AF, conduction velocity (CV(AF)), refractory period (RP(AF)), and type of AF (I, II, III) were determined. Verapamil was administered at a loading dose of 0.1 mg/kg, followed by a continuous (2-hour) infusion of 5 microg/kg/min. Digoxin was given intravenously as a single 0.02 mg/kg bolus. At t = 0 and t = 24, digoxin and verapamil caused a significant slowing of the ventricular rate of >40%. Digoxin had no effect on DurAF, AFCL, CV(AF), or RP(AF). Infusion of verapamil had a direct proarrhythmic effect. Both at t = 0 and t = 24, AFCL and RP(AF) were shortened by about 15%. During acute AF, verapamil prolonged the average duration of AF paroxysms from 7 to 16 seconds. After 24 hours of AF, the proarrhythmic effect was much stronger. Shortly after starting infusion (6 +/- 2 min), verapamil converted paroxysmal AF into sustained AF. As long as verapamil infusion was maintained, AF no longer terminated in any of the goats. This effect was associated with an increase in AF fragmentation from type I to type II-III.</AbstractText>Verapamil shortens AFCL and RP(AF) in the presence and absence of electrical remodeling. After 24 hours, it exerted a marked proarrhythmic effect and converted paroxysmal (type I) into sustained (type III) AF. In contrast, digoxin had no effect on the rate or stability of AF.</AbstractText> |
4,150 | Fibrillation is more complex in the left ventricle than in the right ventricle. | The mechanisms that maintain ventricular fibrillation (VF) are not completely understood. It has been proposed that increased ventricular wall thickness destabilizes VF wavefronts and therefore is an important determinant of VF activation patterns. We hypothesized that if this is the case, then VF patterns on the thin-walled right ventricle (RV) should be simpler than those on the thick-walled left ventricle (LV).</AbstractText>In seven open chest pigs, we mapped VF simultaneously from two epicardial recording arrays, one on the RV and one on the LV. Each array contained 504 unipolar electrodes (in a 21 x 24 grid) spaced by 2 mm. We used specialized pattern analysis methods to compute quantitative descriptors of RV and LV activation patterns. Our data show that VF is more organized in the RV than the LV, containing fewer, larger wavefronts that follow fewer distinct pathways and are less likely to fragment or collide with other wavefronts. The incidence, size, and cycle length of reentrant circuits were similar in the two ventricles, but RV reentry persisted for more cycles. These results are not predicted by the differences in electrophysiologic properties between LV and RV that have been reported in mammalian hearts.</AbstractText>The geometry of the ventricular wall, particularly wall thickness, is an important determinant of VF activation patterns.</AbstractText> |
4,151 | Is all ventricular fibrillation the same? Influence of mode of induction on characteristics of ventricular fibrillation. | Little information is available on the relationship between the mode of induction of ventricular fibrillation (VF) to VF characteristics.</AbstractText>VF was induced from the anterior left ventricle by programmed electrical stimulation, burst pacing, alternating current (AC), high current S2 at a site remote from S1, T wave shock, and intersecting wavefronts in seven normal dogs and seven dogs with chronic myocardial infarction. Using two electrode arrays, 112 electrograms were recorded from the anterior and lateral wall. Cycle lengths were analyzed and activation vectors were created by summing orthogonally recorded bipolar electrograms. The magnitude of the vector loops was integrated over time to produce an "ensemble vector" index (EVI) whose magnitude is high when beat-to-beat activation direction is consistent and low when activation direction is variable. T wave shock-induced VF had a significantly longer cycle length 1 to 5 seconds after VF onset than other modes of induction (P < 0.05). The frequency-corrected EVI was significantly larger for AC current and T wave shock-induced VF as opposed to all other modes of VF induction in early VF (P < 0.0001). After 10 seconds of VF, these differences persisted only on the anterior wall.</AbstractText>VF induced in animals by T wave shock and AC current had different characteristics than VF induced by other methods. These findings may have implications for our understanding of VF pathophysiology.</AbstractText> |
4,152 | Continuous telemetry from a chronic canine model of sudden cardiac death. | We sought to develop a continuously telemetered animal model of sudden cardiac death (SCD) to study the role of existing infarcts and acute ischemia in fatal arrhythmias.</AbstractText>A telemetry system capable of recording eight channels of electrophysiologic data continuously and chronically has been developed. To demonstrate the use of this technology in an animal model of sudden death, 12 anesthetized dogs were instrumented with eight electrodes located in endocardium of the right side of the heart, epicardium of the left ventricle (LV), or in the subcutaneous tissues. The left anterior descending (LAD) coronary artery was occluded for 90 minutes and reperfused to produce LV infarction. A copper wire was placed in the left circumflex (LCX) coronary artery to cause intimal injury in a second arterial bed. The telemetry unit recorded deaths in seven animals between 19 to 64 hours after surgery. Five animals that did not experience SCD by the fifth postoperative day served as controls. There were three modes of SCD: complex ventricular ectopy that degenerated into ventricular fibrillation (VF, n = 4); normal sinus rhythm that suddenly degenerated into VF (n = 1); and bradycardia (RR intervals >1,000 msec) that lasted >3 minutes and preceded VF (n = 2). ST segment changes were significantly greater in the LCX-bed electrograms for tachyarrhythmic compared to bradyarrhythmic deaths (mean +/- SD; 4.0 +/- 3.4 mV and 0.2 +/- 0.8 mV, respectively). Fast Fourier transform showed the peak frequency of VF 10 seconds after onset was significantly higher in the five dogs with initial tachyarrhythmias compared with the VF that followed profound bradycardia (6.5 +/- 3.1 Hz and 3.7 +/- 0.6 Hz, respectively). Computer-assisted planimetry of postmortem heart slices revealed that infarcts in the two dogs with bradycardic events were larger (19.7% +/- 2.2% of the LV and septal mass) than in the five dogs with tachyarrhythmias (7.7% +/- 2.4%) or in the five control dogs (11.9% +/- 8.1%).</AbstractText>It is possible to record via telemetry the events leading to SCD in an animal model. Continuous telemetry monitoring demonstrated that both tachyarrhythmias and bradyarrhythmias ultimately resulted in VF in an animal model of SCD. Animals with tachyarrhythmic deaths had greate ischemia in the LCX bed, smaller preexisting infarcts, and higher VF peak frequency than animals with bradyarrhythmic deaths.</AbstractText> |
4,153 | Effect of sodium channel blockers on ST segment, QRS duration, and corrected QT interval in patients with Brugada syndrome. | Brugada syndrome is characterized by an ST segment elevation in leads V1-V3 and a high incidence of ventricular fibrillation (VF). A mutation in a cardiac Na+ channel gene, SCN5A, has been linked to Brugada syndrome, and sodium channel blockers have been shown to be effective in unmasking the syndrome when concealed. The aim of this study was to examine the effects of Na+ channel blockers on ST segment elevation, QRS, corrected QT (QTc) interval, and ventricular arrhythmias in patients with Brugada syndrome.</AbstractText>We examined the effects of three different Na+ channel blockers (flecainide, disopyramide, and mexiletine) on the amplitude of the ST segment 20 msec after the end of QRS (ST20), QRS duration, QTc interval measured from 12-lead ECG, and ventricular arrhythmias in 12 Brugada and 10 control patients. Maximum ST20 observed in the V2 or V3 leads under baseline conditions was greater in the Brugada patients than in control patients, whereas QRS duration and maximum QTc interval were no different between the two groups. Flecainide and disopyramide, but not mexiletine, significantly increased maximum ST20 and QRS duration in both groups, although these effects were much more pronounced in the Brugada patients. The increases in ST20 and QRS duration with flecainide were significantly larger than those with disopyramide. An increase of 0.15 mV in ST20 with flecainide separated the two groups without overlap. Ventricular premature complexes developed only with flecainide in Brugada patients (3/12) displaying a marked ST elevation but not widening of QRS.</AbstractText>Our findings suggest that Na+ channel blockers amplify existing I(Na) and possibly other ion channel defects, with a potency inversely proportional to the rate of dissociation of the drug from the Na+ channel, thus causing a prominent elevation of the ST segment and, in some cases, prolongation of QRS duration in patients with Brugada syndrome.</AbstractText> |
4,154 | Influence of extracellular potassium on the antiarrhythmic effect of global preconditioning in isolated perfused rat hearts. | The objective of this study was to investigate if a variation in extracellular-K+ concentrations alters the effects of global pre-conditioning on ischemia-induced arrhythmias. Rat hearts were Langendorff-perfused with Krebs-Henseleit solution and randomised in 8 groups (n = 12/group): four control groups (K+: 2, 4, 6, or 8 mmol/L) which underwent 30-min coronary artery occlusion and four preconditioned groups (K+: 2, 4, 6, or 8 mmol/L) in which the 30-min regional ischemia was preceded by 2 cycles of 3 min global ischemia. In the presence of low K+ (2 mmol/L), there were no differences between control and preconditioning groups in the number of ventricular premature beats (VPBs): 194 +/- 64 vs. 217 +/- 81, the incidence of ventricular tachycardia (VT): 100% vs. 100% and of ventricular fibrillation (VF): 100% vs. 100%. In the presence of normal K+ concentration (4 mmol/L), ischemic preconditioning reduced the number of VPBs from 88 +/- 26 to 25 +/- 10, (p < 0.05), the incidence of VT from 100 to 50% (p < 0.05), and of VF from 67 to 16% (p < 0.05). In the condition of higher K+ concentration (6 mmol/ L), VPBs (34 +/- 8 vs. 11 +/- 4), the incidence of VT (100% vs. 25%; p < 0.05 ) and VF (25% vs. 8%) were further reduced in preconditioned hearts. In the condition of K+ concentration (8 mmol/L), there were no differences in VPBs (11 +/- 3 vs. 7 +/- 2), the incidence of VT (8% vs. 0%) and VF (8% vs. 0%) between control and preconditioned hearts. Our data show that ischemic preconditioning affords protection against arrhythmias during coronary artery occlusion in the isolated rat heart and that hypokalemia abolishes the antiarrhythmic effects of global preconditioning. |
4,155 | Protein kinase C is involved in cardioprotective effects of ischemic preconditioning on infarct size and ventricular arrhythmia in rats in vivo. | Protein kinase C (PKC) has been known to play an important role in ischemic preconditioning (IP). This study was designed to examine whether the translocation of PKC is associated with the cardioprotective effects of IP in vivo on infarct size and ventricular arrhythmias in a rat model. Using anesthetized rats, heart rate, systolic blood pressure, infarct size and ventricular arrhythmias during 45 min of coronary occlusion were measured. PKC activity was assayed in both the cytosolic and cell membrane fraction. Brief 3-min periods ofischemia followed by 10 min ofreperfusion were used to precondition the myocardium. Calphostin C was used to inhibit PKC. Infarct size was significantly reduced by IP (68.1 (2.5)%, mean (S.E.) vs. 45.2 (3.4)%, p < 0.01). The reduction in infarct size by IP was abolished by pretreatment with calphostin C. The total number of ventricular premature complex (VPC) during 45 min of coronary occlusion was reduced by IP (1474 (169) beats/45 min vs. 256 (82) beats/45 min, p < 0.05). The reduction the total number of VPC induced by IP was abolished by the administration of calphostin C before the episode of brief ischemia. The same tendency was observed in the duration of ventricular tachycardia and the incidence of ventricular fibrillation. PKC activity in the cell membrane fraction transiently increased immediately after IP (100 vs. 142%, p < 0.01) and returned to baseline 15 min after IP. Pretreatment with calphostin C prevented the translocation of PKC. The translocation of PKC plays an important role in the cardioprotective effect of IP on infarct size and ventricular arrhythmias in anesthetized rats. |
4,156 | Influence of age on left atrial appendage function in patients with nonvalvular atrial fibrillation. | Age is an independent risk factor for thromboembolism in nonvalvular atrial fibrillation (NVAF). An association between low left atrial appendage (LAA) Doppler velocities and thromboembolic risk in NVAF has been reported.</AbstractText>The study was undertaken to identify age-related differences in LAA function that may explain the higher thromboembolic rates in older patients with NVAF.</AbstractText>Forty-two consecutive patients (age 69+/-2 years [range 42-92], 24 [57%] men) with NVAF underwent transthoracic and transesophageal echocardiography. The following were compared in 22 patients younger and 20 older than 70 years: left ventricular (LV) diameter, mass and ejection fraction, left atrial (LA) diameter and volume, LAA area and volume, LAA peak emptying (PE) and peak filling (PF) velocities, presence and severity of spontaneous echo contrast (SEC) and mitral regurgitation (MR).</AbstractText>Left atrial diameter (4.6+/-0.1 vs. 4.5+/-0.2 cm), LA volume (105+/-10 vs. 92+/-8 ml), LAA area (6.8+/-0.6 vs. 5.2+/-0.8 cm2), and LAA volume (5.6+/-0.9 vs. 3.9+/-1.0 ml) were similar (p>0.05) in both groups. Older patients had lower LAA PE (26+/-2 vs. 34+/-3 cm/s, p = 0.02) and PF (32+/-2 vs. 41+/-4 cm/s, p = 0.04) velocities, lower LV mass (175+/-13 vs. 234+/-21 gm, p = 0.02), higher relative wall thickness (0.52+/-0.02 vs. 0.43+/-0.03, p = 0.02), smaller LV diastolic diameter (4.3+/-0.1 vs. 5.2+/-0.2 cm, p < 0.001), and higher LV ejection fraction (62+/-2 vs. 55+/-2%, p = 0.025). Frequency and severity of SEC and MR were similar in both groups. Multivariate analysis identified older age as the only significant predictor of reduced LAA velocities.</AbstractText>Compared with younger patients, older patients with NVAF have lower LAA velocities despite higher LV ejection fraction, smaller LV size, and similar LA and LAA volumes. These findings may explain the higher thromboembolic rates in older patients with NVAF.</AbstractText> |
4,157 | Prevention of recurrent ventricular fibrillation by ventricular rate stabilization. | This report describes a post-infarct patient with recurrent ventricular fibrillation in the absence of acute ischaemia, in whom arrhythmia recurrences could be prevented by ventricular rate stabilization of a third-generation cardioverter defibrillator. Review of the literature and clinical implications are discussed. |
4,158 | Ventricular fibrillation induced by rapid atrial rates in patients with hypertrophic cardiomyopathy. | To describe the mechanisms of induction of ventricular fibrillation (VF) by rapid atrial rates in patients with hypertrophic cardiomyopathy (HCM).</AbstractText>Electrophysiological studies, management and follow-up in three patients with HCM with VF induced by atrial pacing.</AbstractText>In one patient, spontaneous sinus tachycardia triggered VF. In another patient, VF occurred after verapamil infusion during rapid atrial fibrillation, and in the remaining patient there was no clinical VF. In all three patients, short runs of atrial pacing (cycle length 272-380 ms) induced VF, and QRS widening preceded fibrillation in all patients. Marked ventricular electrogram fragmentation was documented in one patient during atrial pacing and in another patient during late ventricular extra-stimuli. Hypotension was associated with sinus tachycardia in one patient. The two patients developing clinical VF underwent atrioventricular (AV) junctional ablation; a ventricular defibrillator was implanted in one, and a mode-switching dual-chamber pacemaker in the other. No arrhythmic events occurred during 34- and 35-month follow-up, respectively. In the other patient, postatrial fibrillation pauses caused syncope, and he is asymptomatic 52 months after implantation of a dual-chamber pacemaker.</AbstractText>Rapid atrial rates can trigger VF in some patients with HCM, probably through a combination of electrophysiological and ischaemic mechanisms. AV junctional ablation may prevent VF in selected cases.</AbstractText> |
4,159 | Brain natriuretic peptide predicts chronic atrial fibrillation after ventricular pacing in patients with sick sinus syndrome. | Chronic atrial fibrillation (AF) is one of the main complications of sick sinus syndrome (SSS). As previously reported, plasma brain natriuretic peptide (BNP), reflects hemodynamic changes in different pacing modes, as does plasma atrial natriuretic peptide (ANP), so the present study investigated whether plasma BNP or ANP can predict chronic AF after single-chamber ventricular (VVI) pacemaker implantation in patients with SSS. Plasma ANP and BNP levels were measured before and 1-3 months after implantation in 99 SSS patients. Long-term follow-up was conducted with chronic AF as an endpoint. Chronic AF occurred in 19 patients during a mean follow-up of 5.1 years. Plasma ANP and BNP were significantly higher in the patients who developed chronic AF after implantation than in those who did not, despite similar ANP and BNP levels between the 2 groups before implantation. Post-implant high BNP and a history of paroxysmal AF were independent predictors of chronic AF by a multivariate Cox proportional hazards analysis. Plasma BNP can predict the development of chronic AF after VVI pacemaker implantation in patients with SSS because increased levels may reflect latent hemodynamic abnormalities, which may contribute to the development of AF after VVI pacemaker implantation. |
4,160 | Effects of BIIB513 on ischemia-induced arrhythmias and myocardial infarction in anesthetized rats. | Na+/H+ exchange (NHE) plays an important role in the regulation of the intracellular pH (pHi) and in cardiac cell injury induced by ischemia and reperfusion. In the present study, we investigated the effects of BIIB513, a selective NHE-1 inhibitor on myocardial ischemia induced arrhythmias and myocardial infarction, provoked by 30 minutes of left main coronary artery occlusion followed by 2 hours of reperfusion in an anesthetized rat model. Intravenous administration of BIIB513 (0.01-3.0 mg/kg) did not induce changes in blood pressure or heart rate. BIIB513 (0.01, 0.1, 0.3, 1.0, 3.0 mg/kg) given prior to the coronary artery occlusion dose-dependently reduced ventricular premature beats, ventricular tachycardia, and a complete suppression of ventricular fibrillation down to the dose of 0.1 mg/kg. BIIB513 (0.01, 0.1, 0.3, 1.0, 3.0 mg/kg) given prior to the coronary artery occlusion dose-dependently reduced the infarct size with an ED50 value of 0.16 mg/kg. BIIB513 (1.0 mg/kg) given prior to reperfusion also reduced infarct size by 47.3 +/- 13.1%. The reduction in infarct size was accompanied by a decrease in circulating levels of creatine phosphokinase (CPK). In conclusion, the present study demonstrates the cardioprotective ability of NHE-1 inhibition during myocardial ischemia and reperfusion by reducing serious ventricular arrhythmias and myocardial infarct size in anesthetized rats. |
4,161 | Cardioprotection with beta-adrenoceptor blockers. Does lipophilicity matter? | Beta-blockers have several beneficial cardiovascular effects in patients with hypertension, angina pectoris, myocardial infarction, and congestive heart failure. In patients with myocardial infarction and congestive heart failure some beta-blockers have been found to reduce mortality and morbidity. The beta-blockers with a proven effect on prognosis include timolol, metoprolol, propranolol, bisoprolol, and carvedilol. One important question is whether all cardiovascular effects obtained by beta-blockers can be considered to be class effects. The beta-blockers with favorable effects on prognosis include two with more selective beta1-receptor blockade (metoprolol and bisoprolol) and three non-selective (timolol, propranolol and carvedilol). One non-selective beta-blocker, which also has a more pronounced class III effect, sotalol, has been studied in a large postinfarction study without a significant effect on mortality. However, sotalol reduced the incidence of reinfarction similarly to the other beta-blockers with proven effect on mortality after myocardial infarction. Sotalol had no influence at all on sudden cardiac death, while all the other beta-blockers referred to above have a very marked effect on sudden cardiac death, in fact more marked than on overall mortality. The beta-blockers with proven effect on mortality and on sudden death have one property in common and that is some degreee of lipophilicity. Sotalol and atenolol are hydrophilic. From animal experimental data it has been suggested that beta-bockers with some degree of lipophilicity penetrate into the brain and have an indirect effect on vagal activity, which is of importance for prevention of ventricular fibrillation and sudden cardiac death. It can be summarized that some beta-blockers have been found to reduce mortality and sudden cardiac death in patients after myocardial infarction and in congestive heart failure, while others have not. It seems that the major properties of the beta-blockers with proven effects on mortality and sudden cardiac death are beta1-receptor blockade and some degree of lipophilicity. Until we know more about the mechanisms behind prevention of death and especially sudden cardiac death by beta-blockers, only drugs with proven effects on prognosis should be used. |
4,162 | The management of heart failure--an overview. | National and international societies have issued guidelines on the management of heart failure: The European Society of Cardiology, WHO, ACC/AHA Task Force Report, US Department of Health and Human Services, German Society of Cardiology. The therapeutic approaches to heart failure have undergone considerable changes during the last few years. The guidelines have to be updated almost yearly due to new results from prospective randomized studies. Although an agreement could be reached with respect to general measures and drug treatment, no agreement on mechanical devices, pacemakers and surgical interventions has been reached. The basis for medical treatment of chronic heart failure depends on diuretics, digitalis, ACE inhibitors, and beta-blockers. Calcium antagonists and other positive inotropic drugs, other than digitalis, should be avoided as far as possible. Thiazides, loop diuretics and aldosterone antagonists are needed for acute and chronic treatment of heart failure, alone or in combination (diuretic resistant heart failure!). Digitalis glycosides are needed in patients with atrial fibrillation with a fast ventricular rate or atrial flutter and in patients with systolic dysfunction, large hearts and symptomatic failure class NYHA III and IV. However, digitalis does not convert atrial fibrillation to sinus rhythm. Today there is no question that ACE inhibitors improve the prognosis of all patients with heart failure in all stages, if ejection fraction is reduced. Therefore, most patients after myocardial infarction or after having experienced pump failure due to myocarditis or cardiomyopathy are treated with ACE inhibitors and diuretics. The beneficial effects of ACE inhibitors seem to be most pronounced the worse the situation is. Relative risk reductions (mortality!) between 10% and 40% have been published depending on the severity of symptomatic left ventricular dysfunction. Those patients with high absolute risk have more to gain than those with low risk for any given "risk reduction", of course. Recent studies also indicate that most high risk cardiac patients profit from ACE inhibitors even if pump function is normal (i.e., patients with coronary heart disease, diabetes mellitus, cerebral vascular disease, hypertension) (15). AT1 antagonists can substitute for ACE inhibitors, if the latter are not tolerated due to cough. Up to now, beta-blocking agents apart from diuretics seem to be the best investigated drugs in heart failure. Large controlled studies with bisoprolol, carvedilol and metoprolol in addition to diuretics, digitalis and ACE inhibitors convincingly yielded positive results in chronic left ventricular failure patients. Reduction of mortality by 35% and even of sudden cardiac deaths by 40% have been proven beyond doubt. Thus, heart failure patients today should also receive beta-blocking agents in all stages of the disease. In the era of controlled prospective studies (evidence-based medicine), physicians are well advised to use only drugs that have been proven beneficial in large controlled studies. |
4,163 | Clinical trial data on the cardioprotective effects of beta-blockade. | In most patients with heart failure the underlying cause is coronary artery disease (CAD). They have a poor prognosis and die slowly from deteriorating cardiac function or suddenly from ventricular fibrillation or atheromatous plaque rupture. Two key aims of treatment, therefore, are to slow the progression of the underlying CAD and the resulting heart failure and to reduce the risk of sudden death. The impact of drugs on CAD and sudden death can be assessed most effectively in patients who have recovered from a myocardial infarction (post-MI patients). Beta-blockers have been studied in at least 25 trials in post-MI patients and their capacity to reduce mortality and re-infarction has been well documented. About 50% of those who die in post-MI trials die suddenly and beta-blockers particularly propranolol, timolol and metoprolol have been shown to reduce the risk of sudden death significantly. Further evidence that beta-blockers are cardioprotective in post-MI patients can be obtained from trials of other drugs by noting the mortality rates in those patients who were also on a beta-blocker. In three trials of antiarrhythmic drugs and two trials of ACE inhibitors, those on beta-blockers had a better prognosis. There is therefore good evidence that in a patient population known to have serious CAD, beta-blockers can effectively reduce the risk of major coronary events and are particularly effective in reducing the risk of sudden death. |
4,164 | Susceptibility to ischemia-induced arrhythmias and the effect of preconditioning in the diabetic rat heart. | Diabetic heart is suggested to exhibit either increased or decreased resistance to ischemic injury. Ischemic preconditioning suppresses arrhythmias in the normal heart, whereas relatively little is known about its effects in the diseased myocardium. Our objective was to investigate whether development of diabetes mellitus modifies the susceptibility to ischemia-induced arrhythmias and affects preconditioning in the rat heart. Following 1 and 9 weeks of streptozotocin-induced (45 mg/kg, i.v.) diabetes, the hearts were Langendorff-perfused at constant pressure of 70 mm Hg and subjected to test ischemia induced by 30 min occlusion of the left anterior descending (LAD) coronary artery. Preconditioning consisted of one cycle of 5 min ischemia and 10 min reperfusion, prior to test ischemia. Susceptibility to ischemia-induced arrhythmias was lower in 1-week diabetics: only 42 % of diabetic hearts exhibited ventricular tachycardia (VT) and 16 % had short episodes of ventricular fibrillation (VF) as compared to VT 100 % and VF 70 % (including sustained VF 36 %) in the non-diabetics (P<0.05). Development of the disease was associated with an increased incidence of VT (VT 92 %, not significantly different from non-diabetics) and longer total duration of VT and VF at 9-weeks, as compared to 1-week diabetics. Preconditioning effectively suppressed arrhythmias in the normal hearts (VT 33 %, VF 0 %). However, it did not provide any additional antiarrhythmic protection in the acute diabetes. On the other hand, in the preconditioned 9-weeks diabetic hearts, the incidence of arrhythmias tended to decrease (VT 50 %, transient VF 10 %) and their severity was reduced. Diabetic rat hearts are thus less susceptible to ischemia-induced arrhythmias in the acute phase of the disease. Development of diabetes attenuates increased ischemic tolerance, however, diabetic hearts in the chronic phase can benefit more from ischemic preconditioning, due to its persisting influence. |
4,165 | Cardiopulmonary resuscitation and medical ethics. | This paper presents an overview of the ethical issues involved in creating policy regarding the use of cardiopulmonary resuscitation. Cardiopulmonary resuscitation was introduced in 1965 as a method to revive victims of acute cardiac insult from near-death conditions. The procedure is intended to prevent premature death; to be effective it must be initiated at the very latest within 12 minutes of cardiac arrest (ventricular fibrillation). Since the introduction of CPR, the scope of its use has widened such that it is often used in situations for which it has shown little, if any, benefit, and also in situations where it is contraindicated. This paper uses the issue of CPR to show how the bioethical principles of beneficence, non-maleficence, autonomy, and justice can be used to analyze issues in medical ethics. |
4,166 | [Clinical characteristics of ventricular tachycardia and ventricular fibrillation in exercise stress testing]. | Ventricular tachycardia (VT) and ventricular fibrillation (Vf) induced in exercise stress testing should be treated urgently, although the occurrence of arrhythmia is rare. The conditions for the onset of arrhythmia and the clinical characteristics of VT and Vf patients in exercise stress testing were studied.</AbstractText>Fifty-nine patients (mean age 54 +/- 17 years, 41 males, 18 females) with VT (succession of 3 or more ventricular premature beats) or Vf induced in exercise stress testing were selected from 7,594 patients with consecutive treadmill stress testing in our hospital from January 1993 to February 1998.</AbstractText>The incidence of exercise-induced VT or Vf was 0.8%, and there were no fatal accidents in all tests. Among the 59 patients with exercise-induced VT or Vf, 52 patients had non-sustained VT, 5 had sustained VT, and 2 had Vf. Of the 59 patients, 23 had rhythm or conduction disturbances, 14 had coronary artery disease, 13 had cardiomyopathy, and 9 had valvular heart disease. The VT or Vf incidence in coronary artery disease was 0.2%, and in valvular heart disease was 10.8%. VT or Vf occurred at over 80% of maximum heart rate exercise intensity in 40 patients, including 4 with sustained VT and 2 with Vf, of the 59 patients. Also, in 9 VT patients including the 4 sustained VT patients, VT occurred in the exercise recovery period within 2 min after the exercise. Although VT disappeared spontaneously in 52 non-sustained VT and 3 sustained VT patients, intravenous injection of lidocaine was needed in 2 sustained VT patients and direct current defibrillator was needed in 2 Vf patients. Furthermore, only one non-cardiac death was observed in the follow-up period of average 42 months.</AbstractText>Our results showed clinical characteristics and incidence of VT or Vf similar to past reports. Furthermore, all sustained VT and Vf patients, who should be treated urgently, had a past history of ventricular premature beats or VT. Our data suggest that VT and Vf could occur during the recovery period, especially in patients with documented ventricular tachyarrhythmias when the stress intensity has reached the critical level in the exercise tolerance test.</AbstractText> |
4,167 | [Mid-term complications of automatic implantable cardiac defibrillators]. | The incidence and the nature of medium-term complications of automatic implantable cardiac defibrillators (AICD) were studied. Seventy-nine AICD were implanted in 50 consecutive patients (42 men, aged 54.5 +/- 13.7 years). Forty-six patients had spontaneous ventricular arrhythmia. These arrhythmias were resistant to treatment (N = 9), reproducible with treatment (N = 28). In 4 patients, the indication was prophylactic, in 2 a Brugada syndrome, in 2 syncope with reinducible ventricular tachycardia and in 1 patient, torsades with a short coupling interval. Forty-six patients had underlying cardiac disease (ischaemic, N = 28, primary dilated cardiomyopathy, N = 10, others, N = 8). The ejection fraction was > 40% in 32 patients. The average follow-up was 41.3 +/- 34.9 months. Eight patients died, 2 from cardiac failure. Twenty-one patients (42%) had 1 or more complications related to their AICD. These occurred: in the operative period (N = 3): 1 post-shock atrioventricular block, 1 ruptured electrode and 1 increased threshold with amiodarone; in the postoperative period (N = 6): infection in 3 cases, cerebrovascular accident in 1 case, deep venous thrombosis of the left arm in 1 case, pneumothorax in 1 case. In the medium-term, the complications were mainly inappropriate electrical shocks observed in 14 patients related to atrial arrhythmias in 7 cases, sinus tachycardia in 1 case, over-detection of myopotentials in 2 cases and electrode dysfunction in 4 cases. In addition, the authors observed complications related to the material: AICD failure in 1 case, electrode displacement in 1 case, and electrode rupture in 3 cases. The authors conclude that AICD are effective for the treatment of malignant ventricular arrhythmias which justify strict specialist follow-up given the incidence and diversity of their complications. |
4,168 | Bioavailability of amiodarone tablets administered with and without food in healthy subjects. | The tablet form of amiodarone is indicated for the treatment of recurrent ventricular fibrillation or hemodynamically unstable ventricular tachycardia. It is recommended that the tablet be taken with meals in cases of gastrointestinal intolerance. However, the effect of food on its bioavailability is unknown. The primary objective of this study was to determine the effect of food on the bioavailability of amiodarone. This was a 2-period crossover study conducted in 30 healthy male subjects. Subjects were randomly assigned to 1 of 2 sequences in which the following 2 treatments were administered: (1) a single-dose of amiodarone (three 200-mg Cordarone tablets) after an overnight fast, and (2) the same dose immediately after a standard high-fat breakfast. Plasma concentrations of amiodarone and desethylamiodarone (DEA) were measured for 6 weeks after each dose. Food enhanced the extent of absorption, resulting in a peak concentration (Cmax) and area under the curve (AUCT) 3.8 and 2.4 times the respective values under fasting conditions. Food also significantly increased the rate of absorption, reducing the time (tmax) to Cmax from 7.1 to 4.5 hours. The effect of food on DEA levels was significant but less pronounced. An in vitro dissolution study confirmed a marked difference between amiodarone release under simulated fed and fasting conditions. Thus, food significantly enhances both the rate and extent of absorption of amiodarone, which is attributed partially to the effect of food on drug release from its formulation. Therefore, it is recommended that amiodarone tablets be taken consistently with meals. |
4,169 | Importance of heart failure with preserved systolic function in patients > or = 65 years of age. CHS Research Group. Cardiovascular Health Study. | Although congestive heart failure (CHF) is a common syndrome among the elderly, there is a relative paucity of population-based data, particularly regarding CHF with normal systolic left ventricular function. A total of 4,842 independent living, community-dwelling subjects aged 66 to 103 years received questionnaires on medical history, family history, personal habits, physical activity, and socioeconomic status, confirmation of pre-existing cardiovascular and cerebrovascular disease, anthropometric measurements, casual seated random-zero blood pressure, forced vital capacity and expiratory volume in 1 second, 12-lead supine electrocardiogram, fasting glucose, creatinine, plasma lipids, carotid artery wall thickness by ultrasonography, and echocardiography-Doppler examinations. Participants with at least 1 confirmed episode of CHF by Cardiovascular Health Study criteria were considered prevalent for CHF. The prevalence of CHF was 8.8% and was associated with increased age, particularly for women, in whom it increased more than twofold from age 65 to 69 years (6.6%) to age > or = 85 years (14%). In multivariate analysis, subjects with CHF were more likely to be older (odds ratio [OR] 1.2 for 5-year difference, men OR 1.1), and more often had a history of myocardial infarction (OR 7.3), atrial fibrillation (OR 3.0), diabetes mellitus (OR 2.1), renal dysfunction (OR 2.0 for creatinine < or = 1.5 mg/ dl), and chronic pulmonary disease (OR 1.8; women only). The echocardiographic correlates of CHF were increased left atrial and ventricular dimensions. Importantly, 55% of subjects with CHF had normal left ventricular systolic function and 80% had either normal or only mildly reduced systolic function. Among subjects with CHF, women had normal systolic function more frequently than men (67% vs 42%; p < 0.001). Thus, CHF is common among community-dwelling elderly. It increases with age and is usually associated with normal systolic LV function, particularly among women. The finding that a large proportion of elderly with CHF have preserved LV systolic function is important because there is a paucity of data to guide management in this dominant subset. |
4,170 | Do patients over 40 years of age benefit from surgical closure of atrial septal defects? | To determine the value of surgical closure of atrial septal defects in patients over 40 years of age.</AbstractText>Retrospective analysis of 76 patients (63 women, 13 men), age range 40-62 years (mean (SD) 45.8 (5.1) years), who underwent surgical repair of atrial septal defect. Pre- and postoperative clinical status (New York Heart Association (NYHA) functional class) was assessed, and ECG, x ray, and echocardiographic investigations performed. Follow up was between 1 and 17 years.</AbstractText>One operative and one late death occurred during the study period. Before operation, 47 patients (61.8%) were in NYHA functional classes III and IV. After operation, 61 patients (82.4%) were in classes I and II. Four patients had atrial fibrillation before surgery versus nine after surgery. Before operation, 52 patients had intensified pulmonary vascularity compared with only seven after operation. Echocardiographic examination showed a significant reduction in right ventricular dimension (4.10 (0.91) v 2.95 (0.36) cm, p < 0.001). No residual intracardiac shunts were identified on echocardiographic follow up.</AbstractText>Surgical closure of atrial septal defects in patients over 40 years old can improve their clinical status and prevent right ventricular dilatation and insufficiency.</AbstractText> |
4,171 | Treatment of congestive heart failure: guidelines for the primary care physician and the heart failure specialist. | During the past 10 years, the philosophy of heart failure treatment has evolved from symptom control to a combined prevention and symptom-management strategy. Recent clinical trials have proved that early detection can delay progression. Treatment of asymptomatic left ventricular dysfunction is as important as treatment of symptomatic disease. The purpose of this review is to simplify recent guidelines for pharmacological management of chronic systolic heart failure for the primary care physician and the heart failure specialist. Early recognition and prevention therapies, combined with lifestyle modification, are essential in the treatment of heart failure. Therapy with angiotensin-converting enzyme inhibitors, beta-blockers, and diuretics is now standard. Digoxin is added to improve clinical symptoms, especially in patients with atrial fibrillation. Aldosterone antagonists may be recommended in select patients with stable New York Heart Association class III or IV heart failure. If angiotensin-converting enzyme inhibitors are not tolerated, angiotensin receptor blockers, hydralazine hydrochloride, and isosorbide dinitrate are recommended. The data on antiarrhythmic and anticoagulation therapies are inconclusive. |
4,172 | Cardiac arrhythmias in the athlete. | Cardiac arrhythmias in the athlete are a frequent cause for concern. Some arrhythmias may be benign and asymptomatic, but others may be life threatening and a sign that serious cardiovascular disease is present. Physicians often are consulted with regard to arrhythmias, or symptoms consistent with arrhythmias, in athletes. Sinus bradyarrhythmias are common and even expected in athletes. These bradyarrhythmias are rarely a cause for concern. Heart block is unusual and merits a thorough workup. Atrial fibrillation may be more common in the athlete. Supraventricular tachycardias other than atrial fibrillation generally warrant consideration of radiofrequency ablation for cure of the tachyarrhythmia. Ventricular arrhythmias in the athlete generally occur in the setting of structural heart disease that is genetically determined (hypertrophic cardiomyopathy, arrhythmogenic right ventricular dysplasia, anomalous coronary arteries) or acquired (coronary artery disease, myocarditis, idiopathic dilated cardiomyopathies). In these conditions, the arrhythmia generally is life threatening. Ventricular arrhythmias that occur in the athlete without structural heart disease are not thought to be life threatening. Athletes with structural heart disease and syncope and those with exertional syncope merit a complete evaluation. |
4,173 | What is the sudden death syndrome in Southeast Asian males? | Sudden unexplained death syndrome describes the death of apparently healthy individuals--usually young men--in whom postmortem examination does not reveal the cause of death. The victims are in apparently good health and usually die at night while sleeping. They die within minutes after the onset of agonal respiration. Patients who have been resuscitated were found to have ventricular fibrillation and inducible polymorphic ventricular tachycardia in the electrophysiologic laboratory. This syndrome has been most frequently described in young Southeast Asian men. In this review, the epidemiology, clinical and electrophysiologic manifestations, pathology and risk factors, prognosis, and treatments for sudden unexplained death syndrome are described. |
4,174 | Right atrial spontaneous echo contrast and thrombi in atrial fibrillation: a transesophageal echocardiography study. | Previous studies have reported the clinical and echocardiographic findings of patients with left atrial spontaneous echo contrast (SEC) and thrombi. We sought to study these characteristics in patients with right atrial SEC and thrombi.</AbstractText>We reviewed 580 consecutive patients from the ACUTE (Assessment of Cardioversion Using Transesophageal Echocardiography) Registry and found 79 patients (14%, aged 67 +/-13 years, 67 male) with transesophageal echocardiography (TEE) findings of right atrial SEC or thrombi (group 1). This group was compared with a control group of 75 consecutive patients (group 2) (aged 68 +/- 13 years, P = not significant; 49 male, P <.005) from the registry with no TEE findings of SEC or thrombi in the left or right atrium.</AbstractText>Atrial fibrillation was present in 60 of 79 group 1 patients (76%). Five right atrial (6%) and 11 left atrial (14%) thrombi were identified. Both left ventricular ejection fraction (39% +/- 16% versus 47% +/- 14%; P =.0005) and presence of right ventricular dysfunction (n = 44 versus 18; P =.0001) differed significantly between groups 1 and 2, respectively. Right atrial area (24 +/- 6 cm(2) versus 22 +/- 6 cm(2); P = .02) was larger in patients in group 1. Left atrial SEC was present in 68 of 79 group 1 patients (86%). Patients with right atrial thrombi and right atrial SEC had a longer duration of arrhythmia (524 +/-812 days versus 147 +/-368 days, P <.05) than patients with right atrial SEC only.</AbstractText>Right atrial SEC has a prevalence of 14% in patients with atrial arrhythmia who undergo TEE-guided cardioversion. Right atrial thrombi are a rare finding and were seen in fewer than 1% (5/580) of patients with atrial arrhythmia. Right atrial thrombi among patients on anticoagulation therapy were not associated with clinically significant pulmonary embolism.</AbstractText> |
4,175 | A new method describing cross-sectional blood flow velocity profiles in the left ventricular outflow tract of patients with atrial fibrillation with the use of high-frame rate 2-dimensional color flow imaging. | A new Doppler method was developed to evaluate the instantaneous cross-sectional velocity profile variability in the left ventricular outlet tract in patients with atrial fibrillation. Blood flow velocities acquired at a high frame rate (>90 frames/s) from a single heart cycle were used to display the velocity profile. In 9 patients, 2 heart cycles with different R-R interval lengths were recorded in color flow mode in a transthoracic apical 5-chamber and long-axis view. Raw digital ultrasound data were analyzed with an external personal computer. The data indicated a variable skew in the profiles with the highest velocities and velocity-time integral (VTI) most often located in the center and toward the septum. The maximum VTI overestimated the mean VTI by approximately 40%. No significant difference existed between the two heartbeats. Thus the VTI can be averaged from heartbeats of different R-R lengths in atrial fibrillation. |
4,176 | Pharmacologic management of atrial fibrillation: current therapeutic strategies. | Atrial fibrillation (AF), the most common form of sustained arrhythmia, is associated with a frightening risk of embolic complications, tachycardia-related ventricular dysfunction, and often disabling symptoms. Pharmacologic therapy is the treatment used most commonly to restore and maintain sinus rhythm, to prevent recurrences, or to control ventricular response rate.</AbstractText>This article reviews published data on pharmacologic treatment and discusses alternative systems to classify AF and to choose appropriate pharmacologic therapy.</AbstractText>AF is either paroxysmal or chronic. Attacks of paroxysmal AF can differ in duration, frequency, and functional tolerance. In the new classification system described, 3 clinical aspects of paroxysmal AF are distinguished on the basis of their implications for therapy. Chronic AF usually occurs in association with clinical conditions that cause atrial distention. The risk of chronic AF is significantly increased by the presence of congestive heart failure or rheumatic heart disease. Mortality rate is greater among patients with chronic AF regardless of the presence of coexisting cardiac disease. The various options available for the treatment of chronic AF include restoration of sinus rhythm or control of ventricular rate. Cardioversion may be accomplished with pharmacologic or electrical treatment. For patients in whom cardioversion is not indicated or who have not responded to this therapy, antiarrhythmic agents used to control ventricular response rate include nondihydropyridine calcium antagonists, digoxin, or beta-blockers. For patients who are successfully cardioverted, sodium channel blockers or potassium channel blockers such as sotalol, amiodarone, or a pure class III agent such as dofetilide, a selective potassium channel blocker, may be used to prevent recurrent AF to maintain normal sinus rhythm.</AbstractText>The ultimate choice of the antiarrhythmic drug will depend on the presence or absence of structural heart disease. An additional concern with chronic AF is the risk of arterial embolization resulting from atrial stasis and the formation of thrombi. In patients with chronic AF the risk of embolic stroke is increased 6-fold. Therefore anticoagulant therapy should be considered in patients at high risk for embolization. Selection of the appropriate treatment should be based on the concepts recently developed by the Sicilian Gambit Group (based on the specific channels blocked by the antiarrhythmic agent) and on clinical experience gained over the years with antiarrhythmic agents. For example, termination of AF is best accomplished with either a sodium channel blocker (class I agent) or a potassium channel blocker (class III agent). In contrast, ventricular response rate is readily controlled by a beta-blocker (propranolol) or a calcium channel blocker (verapamil). Alternatively, antiarrhythmic drug therapy may be chosen based on the Vaughan-Williams classification, which identifies the cellular electrophysiologic effects of the drug.</AbstractText> |
4,177 | Dofetilide: a new class III antiarrhythmic agent. | Dofetilide is a new, pure class III antiarrhythmic agent that prolongs the refractory period and action potential duration without having beta-blocking or calcium channel-blocking properties, making it unique among established class III agents. Dofetilide is effective in converting atrial and ventricular arrhythmias, and in maintaining sinus rhythm after cardioversion. Interestingly, it is more effective in converting atrial flutter than atrial fibrillation. It appears to be safe in patients with left ventricular dysfunction and postmyocardial infarction. In small studies, intravenous dofetilide was superior to flecainide, procainamide and amiodarone in converting atrial fibrillation and flutter. Dofetilide can be administered orally or intravenously with no significant effect on heart rate or blood pressure, but it can prolong QT interval and cause torsade de pointes in 3% to 4% of patients receiving it intravenously and in 0.8% to 1.5% of patients receiving it orally. So far, it is recommended that therapy be initiated in hospital under electrocardiogram monitoring for at least two days, with particular care to avoid torsade de pointes in high risk patients such as women, and those with bradycardia, hypokalemia, hypomagnesia and renal dysfunction. Studies have failed to show any extracardiac side effects. |
4,178 | Arrhythmia issues in patients with renal disease. | Arrhythmia issues arise frequently in the renal disease population, spanning the spectrum from benign ectopy to sustained arrhythmias. Studies adding to our understanding of arrhythmias and advances in technology have revolutionized the way we deal with many arrhythmias. In dealing with ventricular tachyarrhythmias, risk stratification is important, class III antiarrhythmics are preferred medications, and implantable defibrillators have assumed a dominant role. Atrial fibrillation, the most common cardiac arrhythmia, presents the challenges of dosing and drug interactions in the renal disease population; established and evolving catheter ablation approaches are becoming increasingly important. Other supraventricular arrhythmias will occur in this population and will require management. Permanent pacemakers continue to have a significant role for bradyarrhythmias; newer modes and features allow tailoring of these devices to individual patients. In addition, newer types of pacemakers may allow for clinical improvement in heart failure patients. Appropriate handling of arrhythmias can enhance the survival and quality of life of patients with renal disease. |
4,179 | Acute ventricular rate control in atrial fibrillation: IV combination of diltiazem and digoxin vs. IV diltiazem alone. | To analyze the efficacy of an IV combination of diltiazem and digoxin vs IV diltiazem alone for acute ventricular rate control in patients with atrial fibrillation.</AbstractText>Prospective, randomized, open-label study.</AbstractText>Fifty-two patients with atrial fibrillation and uncontrolled ventricular rates were randomized to receive either an IV combination of diltiazem and digoxin or IV diltiazem alone and were observed for 12 h. The successful rate control was defined as a ventricular rate < 100 beats per minute (bpm) persisting for 1 h or conversion to sinus rhythm. The loss of rate control was defined as an increase in the ventricular rate to > 100 bpm persistently for > 30 min or rebound to atrial fibrillation.</AbstractText>In both treatment arms (n = 26 each), all patients achieved successful and comparable ventricular rate control at 12 h. The mean (+/- SD) time taken to achieve successful rate control was shorter in the combination arm (15 +/- 16 vs. 22 +/- 22 min). Six patients in the combination arm and 11 in the diltiazem-alone arm experienced episodes of loss of rate control. This loss in the combination arm was less than that in the diltiazem-alone arm (14 vs 39 episodes; p = 0.05). The loss of rate control per patient in the combination arm was also less than that in the diltiazem-alone arm (2.0 +/- 1.0 vs. 3.5 +/- 1.9 episodes per patient; p = 0.04).</AbstractText>This study demonstrates that in patients with atrial fibrillation who have a rapid ventricular response, the IV combination of diltiazem and digoxin results in a more efficacious ventricular rate control with fewer fluctuations than that achieved by therapy with IV diltiazem alone.</AbstractText> |
4,180 | Lethal ventricular arrhythmias following one-step pacemaker reprogramming for rapid tracking of atrial tachyarrhythmias. | An abrupt decrease in the pacing rate in patients with dual-chamber pacemakers tracking atrial tachyarrhythmias carries a high risk of malignant ventricular arrhythmia. The pacing rate should be reduced by multistep programming over several days. |
4,181 | Interval-dependent potentiation of left ventricular contractility is preserved in patients with atrial fibrillation and depressed ejection fraction. | Echocardiographic techniques were used to measure left ventricular isovolumic and ejection phase indexes of contractility in 54 patients with atrial fibrillation, and the relations between cycle lengths and contractility were compared in patients with normal and depressed ejection fractions. Data indicate that variations in contractility occur in a pattern that is consistent with postextrasystolic potentiation and that such interval-dependent potentiation is preserved in patients with atrial fibrillation and depressed ejection fraction. |
4,182 | Ibutilide: a class III rapidly acting antidysrhythmic for atrial fibrillation or atrial flutter. | Ibutilide is an intravenous Class III antidysrhythmic approved for the treatment of recent onset atrial fibrillation or atrial flutter. Pharmacological effect occurs within 30 min, and the efficacy approaches 40%. In contrast to DC electrical cardioversion, which requires anesthesia, pharmacologic cardioversion offers an alternative in which sedation can be avoided. Patients receiving ibutilide should be monitored for at least 4 h after completed drug administration because of a small chance of ventricular dysrhythmia, mainly torsades de pointes. Careful patient selection is the key to avoiding dysrhythmic complications. The purpose of this article is to review the mechanisms, clinical applications, potential complications, and appropriate use of ibutilide. |
4,183 | Angiotensin II provokes cesium-induced ventricular tachyarrhythmias. | The purpose of this study was to investigate whether angiotensin II provokes ventricular tachyarrhythmias and to clarify its mechanism using the cesium-induced arrhythmia model, which has been widely used as an afterdepolarization and triggered activity model.</AbstractText>Eighteen adult mongrel dogs of either sex weighing 9.6-23.0 kg were studied. The dogs were randomly divided into three groups. In the control group (n=6), the subjects received intravenous saline solution at a 0.45 ml/kg/h, and intravenous bolus injections of cesium (0.25, 0.5, 1.0 mmol/kg) were given at 20-min intervals. In the captopril-treated group (n=6), captopril was administered intravenously at 15 microg/kg/min, and cesium was injected as above. After the infusion of only captopril, in the captopril-treated group, angiotensin II was simultaneously infused at a dose of 0.1 ng/kg/min, and cesium was injected as above. When the dog survived, the dose of angiotensin II was increased to 1.0 ng/kg/min, and the same procedure was repeated. The remaining six dogs were simultaneously infused with captopril (15 microg/kg/min), angiotensin II (1.0 ng/kg/min), and U-73122 (10 microg/kg/min), a selective phospholipase C blocker, and injected with cesium (1.0 mmol/kg). Forty minutes after termination of U-73122 infusion, the dogs were injected with the same dose of cesium.</AbstractText>Sustained ventricular tachycardia or ventricular fibrillation was induced by cesium in all of the dogs in the control group. In the captopril-treated group, none of the dogs showed these arrhythmias when only captopril was infused. The treatment of captopril significantly reduced lethal arrhythmias (P<0.01 vs. control group). During the simultaneous infusion of captopril and angiotensin II (0.1 ng/kg/min), cesium produced sustained ventricular tachycardia in all six dogs and the arrhythmia developed into ventricular fibrillation in three dogs. By increasing the dose of angiotensin II (1.0 ng/kg/min), the surviving three dogs died following induced ventricular fibrillation. The additional infusion of angiotensin II (0.1 and 1.0 ng/kg/min) significantly increased fatal arrhythmias (P<0.01 vs. only captopril- infused period, respectively). None of the dogs in the third group exhibited ventricular tachycardia during the infusion of U-73122, and ventricular fibrillations were recorded in all six dogs in the absence of U-73122. The treatment of U-73122 significantly reduced lethal arrhythmias. (P<0.01 vs. control period).</AbstractText>These results suggest that angiotensin II provokes cesium-induced ventricular tachyarrhythmias by increasing calcium release from sarcoplasmic reticulum in myocytes via activation of a phosphatidylinositol response.</AbstractText> |
4,184 | Diagnosis of heart failure in elderly patients in primary care. | Heart failure is difficult to diagnose in a primary care setting with a reported false positive diagnosis in up to 70% of cases.</AbstractText>To use echocardiography in a large rural practice to evaluate the accuracy of diagnosis of heart failure in patients over 65 years of age.</AbstractText>Sixty patients with a previous diagnosis of heart failure were selected at random from the practice records and were invited to attend for an echocardiogram at the practice premises.</AbstractText>Fifty-eight patients attended, the age was 81+/-7 years, 29% had impaired left ventricular (LV) systolic function of whom 65% were in atrial fibrillation. A further 7% had isolated diastolic LV dysfunction. The prevalence of heart failure by clinical assessment was 29 per 1000 in this patient group and 9 per 1000 when echocardiography was used to confirm the diagnosis.</AbstractText>True heart failure in this population is less prevalent than has been estimated from practice records.</AbstractText> |
4,185 | Radial artery graft vasospasm. | We report an unusual case of vasospasm of a grafted radial artery complicated with ventricular fibrillation during the postoperative course of coronary artery bypass graft surgery. To our knowledge this is the first documented case of a radial artery graft spasm leading to a severe arrhythmia. The arrhythmia resolved spontaneously. Radial artery graft spasm was demonstrated by angiography and was successfully resolved by intravenous nitroglycerin administration. |
4,186 | Clinical events leading to the progression of heart failure: insights from a national database of hospital discharges. | To describe the sequence of clinically apparent events causing readmission and antedating death, subsequent to a first-time hospital admission for heart failure, in order to give insights into the natural history and mechanisms of progression of heart failure.</AbstractText>A national database of linked hospital discharge and mortality data for Scotland (population 5.1 million) was used. Patients with a first-time admission to hospital with heart failure in 1992 (index population) were identified and, using a record linkage system, hospital readmissions and their cause according to the hospital physician and deaths were recorded over the subsequent 3 years. A flowchart showing the sequence of events leading to death or recurrent admission was constructed.</AbstractText>12 640 patients had first-time admissions with heart failure in 1992; their mean age was 74 years and 46.2% were men. A cohort of 2922 (23%) patients died on their first admission. Among the remaining 9718 patients there were 22 747 readmissions and 4877 deaths over the subsequent 3 years; only 15% had neither event reported. Nine per cent of patients died without any readmission and a further 6% without a further readmission for cardiovascular reasons. A cohort of 5992 (61% of patients at risk) had at least one cardiovascular readmission and half of these had occurred within 6 months. Heart failure without a report of any cardiovascular precipitating event was responsible for 37% (2188 patients) of first cardiovascular readmissions and of these patients approximately 12% had evidence of renal failure or acute respiratory infection as possible triggers for readmission. Acute ischaemic events including myocardial infarction (19%), myocardial infarction alone (8%) and atrial fibrillation (11%) were associated with a substantial number of first readmissions. First readmission precipitated by acute myocardial infarction was associated with a particularly poor prognosis (40% inpatient mortality).</AbstractText>Recurrent ischaemic events and atrial fibrillation may be the predominant mechanisms leading to exacerbation of and progression of heart failure and death. A substantial proportion of readmissions appear related to heart failure alone. Whether this reflects progressive ventricular remodelling leading to worsening heart failure or other unidentified mechanisms cannot be discerned from this data.</AbstractText>Copyright 2001 The European Society of Cardiology.</CopyrightInformation> |
4,187 | Direct cardiac effects of intracoronary bupivacaine, levobupivacaine and ropivacaine in the sheep. | 1. The racemic local anaesthetic agent bupivacaine is widely used clinically for its long duration of action. Levobupivacaine and ropivacaine are bupivacaine enantiopure congeners, developed to improve upon the clinical safety of bupivacaine, especially the risk of fatal arrhythmogenesis. 2. In previous preclinical studies of the safety of these drugs with intravenous administration in conscious ewes over a wide dose range, we found that central nervous system (CNS) excito-toxicity reversed the cardiac depressant effects when doses approached the convulsant threshold and thus precluded accurate comparison of their cardiovascular system (CVS) effects. 3. To study CVS effects over a wide range of doses with minimal CNS and other influences, brief (3 min) infusions of bupivacaine, levobupivacaine or ropivacaine were administered into the left main coronary arteries of previously instrumented conscious ewes (approximately 50 Kg body weight). After dose-ranging studies, the drugs were compared in a randomized, blinded, parallel group design. Equimolar doses were increased from 8 micromol (approximately 2.5 mg) in 8 micromol increments, to either a fatal outcome or a 40 micromol (approximately 12.5 mg) maximum. 4. All three drugs produced tachycardia, decreased myocardial contractility and stroke volume and widening of electrocardiographic QRS complexes. Thirteen of 19 animals died of ventricular fibrillation: four of six with bupivacaine (mean+/-s.e.mean actual fatal dose: 21.8+/-6.4 micromol), five of seven with levobupivacaine (22.9+/-3.5 micromol), four of six with ropivacaine (22.9+/-5.9 micromol). No significant differences in survival or in fatal doses between these drugs were found. 5. The findings suggest that ropivacaine, levobupivacaine and bupivacaine have similar intrinsic ability to cause direct fatal cardiac toxicity when administered by left intracoronary arterial infusion in conscious sheep and do not explain the differences between the drugs found with intravenous dosage. |
4,188 | Na(+)/H(+) exchange inhibition reduces hypertrophy and heart failure after myocardial infarction in rats. | We investigated the effect of sodium/hydrogen exchange inhibition (NHE-1) on hypertrophy and heart failure after coronary artery ligation (CAL) in the rat. Animals were subjected to occlusion (or sham) of the left main coronary artery and immediately administered a control diet or one consisting of the NHE-1 inhibitor cariporide for 13-15 wk. Hearts were separated by small [</=30% of left ventricle (LV)] and large (>30% of LV) infarcts. CAL depressed change in left ventricular increase in pressure over time (LV +dP/dt) in small and large infarct groups by 18.8% (P < 0.05) and 34% (P < 0.01), respectively, whereas comparative values for the cariporide groups were 8.7% (not significant) and 23.1% (P < 0.01), respectively. LV end-diastolic pressure was increased by 1,225% in the control large infarct group but was significantly reduced to 447% with cariporide. Cariporide also significantly reduced the degree of LV dilation in animals with large infarcts. Hypertrophy, defined by tissue weights and cell size, was reduced by cariporide, and shortening of surviving myocytes was preserved. Infarct sizes were unaffected by cariporide, and the drug had no influence on either blood pressure or the depressed inotropic response of infarcted hearts to dobutamine. These results suggest an important role for NHE-1 in the progression of heart failure after myocardial infarction. |
4,189 | Myocardial ischemia-reperfusion damage impacts occurrence of ventricular fibrillation in dogs. | To define the relationship between ischemia-reperfusion-induced myocardial damage (IRD) and the occurrence of ventricular tachycardia (VT) and fibrillation (VF), we studied 23 dogs with a three-dimensional activation mapping system. Left anterior descending (LAD) coronary artery occlusion and reperfusion were performed while recording electrograms during VF and atrial pacing. Prior nonischemic sites showing IRD, defined as at least 10% loss of electrogram voltage after reperfusion, had the longest ventricular effective refractory periods (ERPs). IRD sites also occurred more frequently in dogs with reperfusion VF (44 +/- 2 sites, P < 0.01) compared with dogs with VT (18 +/- 5 sites) and no VT (16 +/- 3 sites). In dogs (n = 3) with 3 h of reperfusion, 95% of IRD sites still had lower voltage than those recorded during occlusion. Activation mapping of the first eight complexes of VF had Purkinje or endocardial focal origin in 57%, and complexes originated from IRD sites in 28%. In contrast, dogs with only reperfusion VT also had Purkinje or endocardial focal origin in 79%, but only 5% (P < 0.01 vs. VF dogs) of the sites of origin had IRD. Therefore, dogs with reperfusion VF had more IRD sites where the ERP was longest, and more focal ventricular complexes originated from IRD sites, indicating that IRD may be one important factor in the occurrence of VF during reperfusion. |
4,190 | Electrophysiological heterogeneity and stability of reentry in simulated cardiac tissue. | Generation of wave break is a characteristic feature of cardiac fibrillation. In this study, we investigated how dynamic factors and fixed electrophysiological heterogeneity interact to promote wave break in simulated two-dimensional cardiac tissue, by using the Luo-Rudy (LR1) ventricular action potential model. The degree of dynamic instability of the action potential model was controlled by varying the maximal amplitude of the slow inward Ca(2+) current to produce spiral waves in homogeneous tissue that were either nearly stable, meandering, hypermeandering, or in breakup regimes. Fixed electrophysiological heterogeneity was modeled by randomly varying action potential duration over different spatial scales to create dispersion of refractoriness. We found that the degree of dispersion of refractoriness required to induce wave break decreased markedly as dynamic instability of the cardiac model increased. These findings suggest that reducing the dynamic instability of cardiac cells by interventions, such as decreasing the steepness of action potential duration restitution, may still have merit as an antifibrillatory strategy. |
4,191 | Critical analysis of dual-chamber implantable cardioverter-defibrillator arrhythmia detection : results and technical considerations. | One of the perceived benefits of dual-chamber implantable cardioverter-defibrillators (ICDs) is the reduction in inappropriate therapy due to new detection algorithms. It was the purpose of the present investigation to propose methods to minimize bias during such comparisons and to report the arrhythmia detection clinical results of the PR Logic dual-chamber detection algorithm in the GEM DR ICD in the context of these methods.</AbstractText>Between November 1997 and October 1998, 933 patients received the GEM DR ICD in this prospective multicenter study. A total of 4856 sustained arrhythmia episodes (n=311) with stored electrogram and marker channel were classified by the investigators; 3488 episodes (n=232) were ventricular tachycardia (VT)/ventricular fibrillation (VF), and 1368 episodes (n=149) were supraventricular tachycardia (SVT). The overall detection results were corrected for multiple episodes within a patient with the generalized estimating equations (GEE) method with an exchangeable correlation structure between episodes. The relative sensitivity for detection of sustained VT and/or VF was 100.0% (3488 of 3488, n=232; 95% CI 98.3% to 100%), the VT/VF positive predictivity was 88.4% uncorrected (3488 of 3945, n=278) and 78.1% corrected (95% CI 73.3% to 82.3%) with the GEE method, and the SVT positive predictivity was 100.0% (911 of 911, n=101; 95% CI 96% to 100%).</AbstractText>A structured approach to analysis limits the bias inherent in the evaluation of tachycardia discrimination algorithms through the use of relative VT/VF sensitivity, VT/VF positive predictivity, and SVT positive predictivity along with corrections for multiple tachycardia episodes in a single patient.</AbstractText> |
4,192 | Effects of physiologic pacing versus ventricular pacing on the risk of stroke and death due to cardiovascular causes. Canadian Trial of Physiologic Pacing Investigators. | Evidence suggests that physiologic pacing (dual-chamber or atrial) may be superior to single-chamber (ventricular) pacing because it is associated with lower risks of atrial fibrillation, stroke, and death. These benefits have not been evaluated in a large, randomized, controlled trial.</AbstractText>At 32 Canadian centers, patients without chronic atrial fibrillation who were scheduled for a first implantation of a pacemaker to treat symptomatic bradycardia were eligible for enrollment. We randomly assigned patients to receive either a ventricular pacemaker or a physiologic pacemaker and followed them for an average of three years. The primary outcome was stroke or death due to cardiovascular causes. Secondary outcomes were death from any cause, atrial fibrillation, and hospitalization for heart failure.</AbstractText>A total of 1474 patients were randomly assigned to receive a ventricular pacemaker and 1094 to receive a physiologic pacemaker. The annual rate of stroke or death due to cardiovascular causes was 5.5 percent with ventricular pacing, as compared with 4.9 percent with physiologic pacing (reduction in relative risk, 9.4 percent; 95 percent confidence interval, -10.5 to 25.7 percent [the negative value indicates an increase in risk]; P=0.33). The annual rate of atrial fibrillation was significantly lower among the patients in the physiologic-pacing group (5.3 percent) than among those in the ventricular-pacing group (6.6 percent), for a reduction in relative risk of 18.0 percent (95 percent confidence interval, 0.3 to 32.6 percent; P=0.05). The effect on the rate of atrial fibrillation was not apparent until two years after implantation. The observed annual rates of death from all causes and of hospitalization for heart failure were lower among the patients with a physiologic pacemaker than among those with a ventricular pacemaker, but not significantly so (annual rates of death, 6.6 percent with ventricular pacing and 6.3 percent with physiologic pacing; annual rates of hospitalization for heart failure, 3.5 percent and 3.1 percent, respectively). There were significantly more perioperative complications with physiologic pacing than with ventricular pacing (9.0 percent vs. 3.8 percent, P<0.001).</AbstractText>Physiologic pacing provides little benefit over ventricular pacing for the prevention of stroke or death due to cardiovascular causes.</AbstractText> |
4,193 | Nitroglycerin to control blood pressure during endovascular stent-grafting of descending thoracic aortic aneurysms. | Temporary asystole induced with adenosine or electrically induced ventricular fibrillation has previously been proposed to prevent hypertension during transluminal placement of thoracic endovascular stent-grafts. Nitroglycerin is a safe and less invasive alternative to control blood pressure and, in contrast to the methods mentioned, can also be used during stent-grafting performed under local anesthesia. |
4,194 | Importance of rate control or rate regulation for improving exercise capacity and quality of life in patients with permanent atrial fibrillation and normal left ventricular function: a randomised controlled study. | To determine the importance of rhythm regulation or rate control in patients with permanent atrial fibrillation (AF) and normal left ventricular function.</AbstractText>Thirty six patients with a mixed fast and slow ventricular response rate to their AF were randomised to either His bundle ablation (HBA) and VVIR pacemaker (HBA group) or VVI pacemaker and atrioventricular modifying drugs (Med group). Outcomes assessed at one, three, six, and 12 months included exercise duration and quality of life.</AbstractText>Exercise duration significantly improved from baseline in both groups. There was no difference in outcome between the groups (Med +40% v HBA +20%, p = NS). The heart rate profile on exercise was similarly slowed in both groups compared to baseline. Quality of life significantly improved in both treatment arms for the modified Karolinska questionnaire (KQ) (Med +50% v HBA +50%, p = NS) and the Nottingham health profile (NHP) (Med +40% v HBA +20%, p = NS). However, for the individual symptom scores of each questionnaire more were improved in the Med group (KQ-Med 6 improved v HBA 4, NHP-Med 3 v HBA 1). Left ventricular function was equally preserved by both treatments during follow up.</AbstractText>In these patients control of ventricular response rate with either HBA + VVIR pacemaker or atrioventricular modifying drugs + VVI pacemaker will lead to a significant improvement in exercise duration and quality of life. Rhythm regulation by HBA did not confer additional benefit, suggesting rate control alone is necessary for the successful symptomatic treatment of these patients in permanent AF.</AbstractText> |
4,195 | Effects of hyperoxia on neonatal myocardial energy status and response to global ischemia. | This study examines the effect of neonatal exposure to clinically relevant hyperoxia levels on both in vivo myocardial metabolism and the subsequent metabolic response to global ischemia.</AbstractText>Three-day-old pigs were ventilated to normoxia (80 mm Hg, 2 or 5 hours, n = 11), mild hyperoxia (250 mm Hg, 2 hours, n = 9), or severe hyperoxia (500 mm Hg, 5 hours, n = 14). Ventricular biopsies obtained at the end of the ventilation period, and at early and late ischemia were analyzed for ATP, ADP, AMP, creatine phosphate, glycogen, and lactate.</AbstractText>Hyperoxia did not significantly alter in vivo metabolism. During early ischemia, hearts exposed to severe hyperoxia had better ATP and glycogen preservation (p < 0.003). These hearts exhibited almost complete (92%) creatine phosphate depletion, in contrast to incomplete creatine phosphate use in all other neonatal hearts, even in the face of 30% ATP reductions. However, hearts exposed to severe hyperoxia also had a higher incidence of fibrillation during ischemia, which accelerated ATP and glycogen degradation.</AbstractText>Although severe hyperoxia provided an energy-sparing effect during early ischemia, it also increased the incidence of ventricular fibrillation, which negated this beneficial effect.</AbstractText> |
4,196 | Right thoracotomy for mitral reoperation: analysis of technique and outcome. | This report describes technical details of the right thoracotomy approach for mitral surgery, and analyzes our experience with this procedure for patients with a prior sternotomy. Three methods for myocardial management (hypothermic cardioplegic arrest, beating heart, and fibrillating heart) are compared.</AbstractText>Records were abstracted of patients who had a right thoracotomy between January 1, 1992 and July 1, 1999 for mitral surgery after at least one prior sternotomy. Demographic, operative, and outcome data were collected for analysis. Telephone follow-up was used to measure postoperative New York Heart Association functional status.</AbstractText>Eighty-four patients (mean age 60 +/- 15 years) had reoperative mitral surgery via a right thoracotomy. Myocardial management included ventricular fibrillation in 10 patients, operation on the beating heart in 58 patients, and hypothermic blood cardioplegia arrest in 16 patients. The mean time in the operating room was 185 +/- 73 minutes, and the mean duration of cardiopulmonary bypass was 63 +/- 56 minutes. There were no perioperative strokes and the prevalence of death for patients who received cardioplegic arrest was significantly higher than the prevalence of death for patients who had mitral surgery with perfused fibrillating or beating heart techniques (p = 0.007; Fisher's exact test comparing risk-unadjusted mortality).</AbstractText>Right thoracotomy provides efficient exposure for reoperative mitral surgery. Mitral valve procedures on the fibrillating or beating heart are feasible in most patients and are at least as safe as surgery using cardioplegic arrest.</AbstractText> |
4,197 | [Hypertrophic cardiomyopathy and pregnancy]. | We report the case of a 32 years old patient, with a known diagnostic of hypertrophic cardiomyopathy; who has presented at the first trimester of pregnancy a ventricular fibrillation treated by electric shock with a favorable outcome. The risks for the mother and the foetus are discussed; The recommendations for the conduct of the delivery are reviewed. |
4,198 | Management of postoperative arrhythmias. | Arrhythmias occur commonly in patients after cardiac surgery. Atrial fibrillation is the most common arrhythmia in the postoperative period; it accounts for significant morbidity to the patient and prolonged hospital stays, and it contributes significantly to the cost of hospitalization. It occurs more commonly in elderly men and in patients undergoing valvular procedures. Beta blockers are effective agents that keep patients from developing postoperative atrial fibrillation and help maintain ventricular rate control. Prophylaxis with antiarrhythmic agents such as amiodarone and sotalol and recently with atrial pacing have shown promise in recent randomized trials. Patients with atrial fibrillation that persists for longer than 48 hours appear to be at a greater risk for cerebroembolic events and should receive anticoagulation unless a contraindication exists. Although frequent premature ventricular contractions and nonsustained ventricular tachycardia (NSVT) occur frequently in patients after cardiac surgery, sustained ventricular tachycardia and ventricular fibrillation are rare and are associated with a poor prognosis. Polymorphic ventricular tachycardia may occur in the setting of myocardial ischemia, metabolic disturbances, and drug toxicities (including antiarrhythmic agents used to treat atrial fibrillation). Poor left ventricular function is a potent risk factor for sudden death in patients with NSVT. Patients with persistent NSVT and ischemic cardiomyopathy with left ventricular ejection fractions of less than 40% should undergo electrophysiologic testing. Conduction abnormalities that may be encountered in patients after cardiac surgery are rarely life threatening. Patients who have undergone valve replacement or repair are at higher risk of developing significant bradyarrhythmias that may require temporary pacing. |
4,199 | Clinical characteristics of unexplained sudden cardiac death in Korea. | In Western countries, sudden cardiac death (SCD) is closely related to coronary artery disease, but in Korea the clinical characteristics of SCD are not well determined. Over a 4-year period (June 1995 to May 1999), 186 cases of SCD, ranging in age from 16 to 75 years, were admitted to the Chonnam National University Hospital. In 82 (44.1%) of these, neither symptoms nor evidence of structural heart disease was found and so their clinical characteristics were investigated. There were 66 (80.5%) men and 16 (19.5%) women (male/female ratio = 4.1:1). The mean age was 50 +/- 14 years: 19 (23.2%) were in their 40s, 21 (25.6%) in their 50s, and 17 (20.7%) in their 60s. The time of circulatory collapse witnessed in 68 cases of SCD showed 2 peaks: between midnight and 03.00h (n=16, 23.5%) and between 09.00h and midday (n=15, 22.1%). Unexplained SCD occurred at home in 48 (64.9%) cases and on the street in 12 (16.2%); it occurred during normal daily routine activity in 23 (39.6%) and during sleep in 15 (25.9%). Thirty-three patients (40.2%) experienced various prodromal symptoms, including chest discomfort (n=13, 15.9%) and dyspnea (n=8, 9.8%). The electrocardiogram taken on arrival recorded asystole in 65 (79.3%) and ventricular fibrillation in 17 (20.7%). Idiopathic ventricular fibrillation was diagnosed in 14 (10 men, 4 women; 45 +/- 11 years) of 21 patients who recovered spontaneous circulation. Five (6.1%) patients were discharged alive, and an implantable cardioverter-defibrillator was implanted in 2. Unexplained SCD is common in Korea and develops predominantly in middle-aged males around midnight or in the late morning usually with no prodromal symptoms (59.8%). Idiopathic ventricular fibrillation is thought to be one of the important causes. |
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