Determinants of inducible ventricular tachycardia in patients with clinical ventricular tachyarrhythmia and no apparent structural heart disease

Thirty-seven patients with symptomatic ventricular tachyarrhythmia and no apparent structural heart disease were evaluated with multiple cardiovascular tests to establish the relationship between the results of programmed electric stimulation and other clinical and arrhythmia variables. Of 37 patients, 12 (32%) had inducible sustained ventricular tachycardia. Factors associated with the results of programmed electric stimulation included a history of ventricular tachycardia > or = 30 seconds requiring intervention for termination and global right heart abnormality documented by echocardiography. During treatment for a mean follow-up of 50 months, 29 patients did well, 6 patients had recurrences of major arrhythmia symptoms, 1 was lost to follow-up and 1 had a noncardiac death. Those patients with an adverse outcome were more likely to have inducible ventricular tachycardia. Thus certain clinical and echocardiographic data are associated with the results of programmed electric stimulation, which in turn have important prognostic value in this group of patients. Sustained ventricular tachycardia is unlikely to be induced in patients with no evidence of structural heart disease and clinical nonsustained ventricular tachycardia.     

Results and efficiency of programmed ventricular stimulation with four extrastimuli compared with one, two, and three extrastimuli

BACKGROUND: Conventional programmed ventricular stimulation protocols are inefficient compared with more recently proposed protocols. The purpose of the present study was to determine if additional efficiency could be derived from a 6-step programmed ventricular stimulation protocol that exclusively uses four extrastimuli. METHODS AND RESULTS: The subjects were 209 consecutive patients with coronary artery disease and documented sustained monomorphic ventricular tachycardia, nonsustained ventricular tachycardia, aborted sudden death, or syncope. These patients underwent 159 electrophysiological tests in the absence of antiarrhythmic drug therapy and 105 electrophysiological tests in the presence of antiarrhythmic therapy. Programmed stimulation was performed with two protocols in random order in each patient. Both protocols used an eight-beat drive train, 4-s intertrain pause, and basic drive cycle lengths of 350, 400, and 600 ms. The 6-step protocol started with coupling intervals of 290, 280, 270, and 260 ms, which were shortened simultaneously in 10-ms steps until S2 was refractory. The 18-step protocol used one, two and three extrastimuli in conventional sequential fashion. The end points were 30 s of sustained monomorphic ventricular tachycardia, two episodes of polymorphic ventricular tachycardia requiring cardioversion, or completion of the protocol at two right ventricular sites. There was no significant difference in the yield of sustained monomorphic ventricular tachycardia using the two protocols, regardless of the clinical presentation or treatment with antiarrhythmic drugs. Polymorphic ventricular tachycardia occurred with the 18-step protocol twice as frequently as with the 6-step protocol (6% versus 3%, P < .001). The duration of the 18-step protocol was significantly longer than that of the 6-step protocol in patients with inducible ventricular tachycardia (5.5 +/- 7 versus 2.3 +/- 2 minutes, P < .001), as well as in patients without inducible ventricular tachycardia (25.4 +/- 7 versus 6.9 +/- 2 minutes, P < .001). CONCLUSION: A stimulation protocol that exclusively uses four extrastimuli improves the specificity and efficiency of programmed ventricular stimulation without compromising the yield of monomorphic ventricular tachycardia in patients with coronary artery disease.     

Syncope and ventricular arrhythmias in hypertrophic cardiomyopathy are not related to the derangement of coronary microvascular function

Non-sustained ventricular tachycardia on Holter and syncope have been considered risk factors for sudden death in hypertrophic cardiomyopathy. AIMS: In these patients the coronary vasodilator reserve is impaired despite normal coronaries, so we evaluated the correlation between the severity of coronary vasodilator reserve impairment and the occurrence of syncope and non-sustained ventricular tachycardia. METHODS AND RESULTS: Eighty-four patients with hypertrophic cardiomyopathy (62 males, age 43 +/- 12 years) had a two-dimensional echocardiographic study and a 48-h Holter. Myocardial blood flow was measured by positron emission tomography, at baseline and after dipyridamole, and the coronary vasodilator reserve was computed as dipyridamole myocardial blood flow/baseline myocardial blood flow. In 27 patients, subendocardial and subepicardial myocardial blood flow was measured in the septum and the subendocardial/subepicardial ratio was computed. Twenty of 84 patients had at least one syncopal episode, and 26 had at least one run of non-sustained ventricular tachycardia on Holter. Baseline and dipyridamole myocardial blood flow, coronary vasodilator reserve, and baseline and dipyridamole subendocardial/subepicardial myocardial blood flow ratio were similar in patients with and without syncope and with and without non-sustained ventricular tachycardia on Holter. However, patients with non-sustained ventricular tachycardia had larger left ventricular end-diastolic (47 +/- 6 vs 44 +/- 5 mm, P < 0.05) and end-systolic diameters (30 +/- 6 vs 27 +/- 4 mm, P < 0.05). CONCLUSIONS: (1) Coronary vasodilation is not more severely impaired in patients with hypertrophic cardiomyopathy and syncope or non-sustained ventricular tachycardia. (2) The left ventricle is more dilated in hypertrophic cardiomyopathy with non-sustained ventricular tachycardia.     

Long-term efficacy of d/l sotalol in patients with sustained ventricular tachycardia refractory to class I antiarrhythmic drugs

The efficacy of d/l sotalol was investigated in 50 patients (43 men, seven women; 33 with coronary artery disease, 15 with dilated cardiomyopathy; ejection fraction 33 +/- 10%) with inducible sustained ventricular tachycardia. Before d/l sotalol a mean of 2 +/- 1 (1 to 4) class I antiarrhythmic drugs were ineffective. In 24 patients (48%) oral d/l sotalol (320 +/- 47 mg.day-1) prevented induction of the ventricular tachycardia; in 23 patients the ventricular tachycardia remained inducible (d/l sotalol 326 +/- 50 mg.day-1). The electrophysiological effects of d/l sotalol did not differ between patients in whom d/l sotalol prevented induction of ventricular tachycardia and those in whom the ventricular tachycardia remained inducible. In two patients, torsade des pointes developed after oral application of d/l sotalol; one patient suffered from severe hypotension even with 80 mg of sotalol per day. During long-term follow-up (27 +/- 12 months) 5/24 patients (21%) had a non-fatal recurrence of ventricular tachycardia (1 week to 21 months), one patient died suddenly and another from progressive heart failure. In patients in whom the ventricular tachycardia could be induced despite oral application of d/l sotalol, control of the ventricular tachyarrhythmia was attempted by the use of sotalol in combination with mexiletine (n = 2), amiodarone (n = 9), catheter ablation (n = 2), antitachycardia surgery (n = 1) or the implantation of an automatic cardioverter defibrillator (n = 12). Recurrence of ventricular tachycardia was observed in four patients without an implanted cardioverter defibrillator. Seven out of 12 patients with an implanted cardioverter defibrillator received appropriate shocks or successful antitachycardia pacing. Although no patient died suddenly, overall mortality was 17% in this group. It is concluded that d/l sotalol is highly effective in the suppression of sustained monomorphic ventricular tachycardia inducible by programmed electrical stimulation. However during a mean follow-up of 27 +/- 12 months a recurrence of ventricular tachycardia was seen in 21% of patients, and one patient died suddenly.     

Electrocardiographic patterns relative to initiating mechanisms of exercise-induced ventricular tachycardia

The initiating mechanisms of exercise-induced ventricular tachycardia were studied in a population of 5842 patients who performed 9064 bicycle exercise tests. Sixty (1%) patients had 194 episodes of ventricular tachycardia during the test. Forty-two percent of these occurred during exercise and 58% during recovery. Two different initiating electrocardiographic patterns were observed. In 17 (28%) patients ventricular tachycardia was initiated by a short-long-short sequence of R-R intervals (group 1). Thirty-eight (63%) patients did not have this pattern of interval changes preceding ventricular tachycardia (group 2). Five (8%) other patients showed both patterns. The clinical characteristics of the groups were different for angina and cardiomyopathy but not for previous myocardial infarction. In group 1 ventricular tachycardia was related to recovery (76%; p < 0.05). In group 2 tachycardia occurrence was equally divided between exercise and recovery. The electrocardiographic differences suggest that different initiating mechanisms are involved in the development of exercise-induced ventricular tachycardia. The present findings may enhance aimed drug therapy in ventricular tachycardia.     

QT dispersion, daily variations, QT interval adaptation and late potentials as risk markers for ventricular tachycardia

AIMS: The aim of the study was to determine the value and correlation between QT dispersion, daily variations in the QT interval and late potentials as risk markers for ventricular tachycardia. METHODS AND RESULTS: QT dispersion was defined as the difference between the longest and the shortest QT interval in 12 electrocardiographic leads, QTc variability as the difference between the maximal and minimal QTc interval during 24-h Holter monitoring and QT interval adaptation as the regression line between heart rate and the uncorrected QT interval. One hundred and forty-five patients, 3 months after myocardial infarction were included in the study. QT dispersion significantly increased with the severity of arrhythmia (modified Lown's classification; P< 0.001). The level of 80 ms was associated with ventricular tachycardia with a sensitivity of 72.7% and a specificity of 86.4%. The greater daily variability of the QTc interval in patients with ventricular tachycardia was insignificant (P > 0.05). QT interval adaptation did not discriminate between patients with ventricular tachycardia from those in other groups. Late potentials were associated with ventricular tachycardia with a sensitivity of 50% and a specificity of 90.3%. CONCLUSION: Large QT dispersion and late potentials were risk markers for ventricular tachycardia, but there was no correlation between QT dispersion, daily variations in the QT interval and late potentials in patients 3 months after myocardial infarction.     

Usefulness of sotalol for life-threatening ventricular arrhythmias

Two trial designs have been used in evaluating sotalol in patients with sustained tachyarrhythmias: open-label dose escalation and randomized comparison with reference agents. At least 7 open-label studies (n = 16-65) have been reported from single centers in patients in whom trials of numerous other antiarrhythmic agents were unsuccessful. At the doses used, usually 320-640 mg/day, plasma concentrations were in the range associated with both beta blockade and class III antiarrhythmic activity (2-3 micrograms/mL). These concentrations produced electrophysiologic changes that were consistent across studies: 10-16% increase in right ventricular effective refractory period (ERP), 4-8% increase in corrected QT interval (QTc), and 17-30% increase in sinus cycle length (corresponding to a 15-23% decrease in heart rate). In these open-label trials, sotalol suppressed inducible ventricular tachyarrhythmias in 20-72% of patients; the higher degrees of efficacy were reported when induction protocols were confined to double extrastimuli. Side effects leading to discontinuation of sotalol in patients with sustained ventricular tachycardia or fibrillation include fatigue (4.0%), marked bradycardia (3.0%), torsades de pointes (3.0%), and heart failure or pulmonary edema (1.0%). A multicenter randomized trial compared intravenous sotalol with intravenous procainamide in a double-blind prospective fashion. Sotalol suppressed ventricular tachyarrhythmias inducible with triple extrastimuli in 15 (30%) of 50 patients, whereas procainamide was effective in 10 (20%) of 50. In this and other series, responsiveness to sotalol was prospectively identified by a particularly fast tachycardia at baseline (e.g., cycle length of < 270 msec), but not by the extent of changes in global indices of repolarization (QTc, ERP).(ABSTRACT TRUNCATED AT 250 WORDS)     

Abnormal coronary flow dynamics at rest and during tachycardia associated with impaired left ventricular relaxation in humans: implication for tachycardia-induced myocardial ischemia

OBJECTIVES: This study attempted to clarify the effect of ventricular relaxation abnormalities on coronary flow dynamics at rest and during tachycardia in humans. BACKGROUND: Ventricular relaxation abnormality has been demonstrated in animals to have an adverse impact on early diastolic coronary flow dynamics. However, this relation has not been established in humans. Even if the adverse effect were latent at rest, it might become evident during tachycardia because tachycardia reduces coronary flow reserve and facilitates the production of myocardial ischemia. METHODS: Doppler phasic left coronary flow velocity pattern was obtained at rest and during tachycardia in 23 patients without coronary stenosis. The time constant of left ventricular isovolumic pressure (tau) was used to assess ventricular relaxation. RESULTS: The time to peak flow velocity of the diastolic coronary flow wave was longer, and the fraction of the first third of diastolic coronary flow was smaller, in patients with a longer tau (r = 0.58, p < 0.01; r = -0.44, p < 0.05), indicating a close relation between early diastolic coronary flow dynamics and ventricular relaxation. Although rapid atrial pacing yielded an increase in the coronary flow velocity integral per minute in all patients, diastolic coronary flow velocity integral per minute increased in 9 patients with a normal (< or = 40 ms) tau at rest but decreased in 14 patients with a longer (> 40 ms) tau at rest. CONCLUSIONS: Impaired left ventricular relaxation was associated with decreased coronary flow in early diastole at rest and decreased coronary flow throughout diastole during tachycardia in patients without coronary stenosis. These findings may provide more insight into the mechanism of tachycardia-induced subendocardial ischemia in patients with impaired ventricular relaxation but without concomitant coronary stenosis.     

Catheter ablation of incessant ventricular tachycardia: acute and long-term results

SUBJECTS: Seventeen patients with incessant ventricular tachycardia refractory to anti-arrhythmic therapy underwent catheter ablation between 1987 and 1993. Fifteen patients had coronary heart disease and two had dilated cardiomyopathy. The mean age of the patients was 65 +/- 8 and the mean left ventricular ejection fraction was 31 +/- 9%. METHODS: Ablation sites were selected on the basis of endocardial activation mapping, concealed entrainment or bundle branch mapping. Catheter ablation was performed with direct current in nine patients and with radiofrequency energy in eight patients. Incessant ventricular tachycardia was terminated by catheter ablation in all 17 patients. RESULTS: One patient died after the ablation procedure due to pericardial tamponade. During electrophysiological testing 5-14 days later, 7 of 16 patients (44%) had inducible sustained or non-sustained ventricular tachycardia. Five of them underwent implantation of an automatic cardioverter/defibrillator, and three of these experienced discharges of the device during a mean follow-up of 30 +/- 12 months. another patient underwent implantation of a cardioverter/defibrillator after spontaneous recurrence of ventricular tachycardia. Out of the nine patients without inducible ventricular tachycardia, one died as a result of sudden cardiac death, and another had spontaneous ventricular tachycardia. Thus, ventricular tachycardia recurred clinically in 6 of 16 patients (38%), in whom ventricular tachycardia with the same morphology as that of the ablated ventricular tachycardia could be determined only in one patient. CONCLUSION: Catheter ablation is the method of choice for the emergency treatment of patients with incessant ventricular tachycardia. Due to the high risk of recurrence, additional anti-arrhythmic management, such as the implantation of a cardioverter/defibrillator, has to be considered.     

Analysis of the immunoglobulin heavy-chain gene rearrangement providing molecular evidence of second lymphoma in a patient in apparent relapse after autotransplantation

Thirteen consecutive patients with idiopathic ventricular tachycardia underwent radiofrequency catheter ablation. This group included 9 idopathic left ventricular tachycardia (ILVT) and 4 idiopathic right ventricular tachycardia (IRVT). Five ILVT patients with left axis deviation and one with right axis deviation were ablated successfully. By pace mapping, two IRVT patients with ventricular tachycardia originating from right ventricular out-flow tract were ablated. No complications occured. By means of follow-up of 3-22 months one case showed recurrence with successful reablation. It indicates that radiofrequency catheter ablation therapy is an effective and safe procedure in patients with idiopathic ventricular tachycardia.     

Update on implantable cardioverter-defibrillators. New, safer devices have led to changes in indications

The safety and efficacy of ICDs have improved significantly in the past few years. Recent evidence supports the value of these devices not only for secondary prevention of sudden cardiac death, but also for primary prevention in post-myocardial infarction patients with poor left ventricular function, unsustained ventricular tachycardia, and inducible ventricular tachycardia on electrophysiologic study. Transvenous defibrillation using the defibrillator case as the high-voltage electrode and a biphasic shock is currently the procedure of choice. Implantation is simple, and the defibrillation thresholds are acceptably low. However, the possibility of interactions must be considered in patients with cardiac pacemakers.     

Distinction between arrhythmic and nonarrhythmic death after acute myocardial infarction based on heart rate variability, signal-averaged electrocardiogram, ventricular arrhythmias and left ventricular ejection fraction

OBJECTIVES: We investigated whether heart rate variability, the signal-averaged electrocardiogram (ECG), ventricular arrhythmias and left ventricular ejection fraction predict the mechanism of cardiac death after myocardial infarction. BACKGROUND: Postinfarction risk stratification studies have almost exclusively focused on predicting the risk of arrhythmic death. The factors that identify and distinguish persons at risk for arrhythmic and nonarrhythmic death are poorly known. METHODS: Heart rate variability, the signal-averaged ECG, ventricular arrhythmias and left ventricular ejection fraction were assessed in 575 survivors of acute myocardial infarction. The patients were followed up for 2 years; arrhythmic and nonarrhythmic cardiac deaths were used as clinical end points. During the follow-up period, 47 cardiac deaths occurred, 29 (62%) arrhythmic and 18 (38%) nonarrhythmic. RESULTS: All risk factors were associated with cardiac mortality in univariate analysis. With the exception of left ventricular ejection fraction, they were also predictors of arrhythmic death. Depressed heart rate variability (p < 0.001), ventricular ectopic beats (p < 0.001) and low ejection fraction (p < 0.001) were related to nonarrhythmic death. In multivariate analysis, depressed heart rate variability (p < 0.001) and runs of ventricular tachycardia (p < 0.05) predicted arrhythmic death. Nonarrhythmic death was associated with depressed heart rate variability (p < 0.001), ventricular ectopic beats (p < 0.001) and low ejection fraction (p < 0.01). By selecting patients with depressed heart rate variability, long filtered QRS duration or ventricular arrhythmias and excluding patients with the lowest ejection fraction, we identified a group in which 75% of deaths were arrhythmic. Similarly, by selecting patients with a low ejection fraction and excluding patients with the lowest heart rate variability, we identified a group in which 75% of deaths were nonarrhythmic. CONCLUSIONS: Arrhythmic death was associated predominantly with depressed heart rate variability and ventricular tachycardia runs, and nonarrhythmic death with low ejection fraction, ventricular ectopic beats and depressed heart rate variability. A combination of risk factors identified patient groups in which a majority of deaths were either arrhythmic or nonarrhythmic.     

Radiofrequency ablation in the therapy of supraventricular and ventricular arrhythmias

We summarize our experience with RF-ablation in 70 patients with symptomatic tachycardia (38 females and 32 males, age 25-73 years). 19 patients with AV reentry tachycardia in WPW-syndrome, 28 patients with node reentry tachycardia (AVNRT), 10 patients with ventricular tachycardia, 9 patients with atrial fibrillation and 4 patients with atrial flutter were treated. The primary success rate in the whole patient group is 87% and the longterm success rate (up to 1 year) 81%. RF-ablation of tachycardia is a highly effective therapy. The patients are free of symptoms and need no further medication. In patients with AVNRT in WPW-syndrome and ventricular tachycardia (structurally normal heart), RF-ablation is the therapy of choice. 32/70 patients were treated on an outpatient basis.     

Predictors of arrhythmic death and cardiac arrest in the ESVEM trial. Electrophysiologic Study Versus Electromagnetic Monitoring

BACKGROUND: The purpose of this study was to determine if the presenting ventricular arrhythmia (ventricular tachycardia or ventricular fibrillation/cardiac arrest) predicted the type of arrhythmia recurrence in patients treated with antiarrhythmic drugs. METHODS AND RESULTS: In the previously reported Electrophysiologic Study Versus Electrocardiographic Monitoring (ESVEM) trial, there were 486 patients who were randomized to antiarrhythmic drug testing guided by electrophysiological study or by ambulatory ECG monitoring. Use of a defibrillator (implantable cardioverter-defibrillator, ICD) without stored electrograms among 81 patients precluded determination of the type of arrhythmia recurrence; thus these patients were censored at the time of ICD implantation. Of the 486 patients, 381 presented with ventricular tachycardia and 105 with cardiac arrest. Over a 6-year follow-up period, 285 of the 486 patients had an arrhythmia recurrence; of these, 97 had an arrhythmic death or cardiac arrest as a first recurrence. In the current analysis, all 129 arrhythmic deaths/cardiac arrests that occurred any time during follow-up were evaluated as end points. CONCLUSIONS: Although univariate analysis suggested that there was an association between the presenting arrhythmia and outcome, multivariate analysis failed to substantiate the predictive value of the presenting arrhythmia. Left ventricular ejection fraction was the single most important predictor of arrhythmic death or cardiac arrest. This information may be an important factor in deciding whether to advise ICD therapy.     

Spectrum of coronary arterial spasm. Clinical, angiographic and myocardial metabolic experience in 29 cases

A relationship of coronary arterial spasm to variant angina pectoris, subendocardial ischemia, major ventricular arrhythmias and myocardial infarction has been demonstrated. In 29 patients, spasm was angiographically observed in normal-appearing coronary arteries (7 patients) as well as superimposed on various degrees of coronary atherosclerotic obstruction (22 patients). All patients experienced an atypical anginal syndrome;16 patients also experienced typical exertional angina. Coronary spasm appeared to be a major contributory factor in eight occurrences of myocardial infarction and in 11 incidents of ventricular tachycardia, ventricular fibrillation and heart block. Coronary spasm in the 29 cases was distributed in the following fashion: left main trunk, 6 cases; right main trunk, 12 cases; proximal left anterior descending artery, 13 cases; proximal circumflex artery, 1 case; distal left anterior descending artery, 1 case; and distal circumflex artery, 2 cases. In 5 cases coronary spasm was noted at multiple sites.     

Antihypertensive therapy. Angiotensin-converting enzyme inhibitors, angiotensin II receptor antagonists, and calcium antagonists

ACEIs, angiotensin II receptor antagonists, and calcium antagonists are effective and well-tolerated antihypertensive agents but, except in special situations, should be considered alternative drugs for first line therapy until randomized trials show that they are at least as effective as diuretics and beta-blockers in preventing cardiovascular morbidity and mortality for a broad spectrum of hypertensive patients. ACEIs are particularly indicated for managing patients with congestive heart failure due to systolic dysfunction and patients with diabetic nephropathy, especially in Type I diabetes. Theoretically, the AII receptor antagonists will be equally effective for these indications, and randomized trials are now underway to demonstrate this. Special indications for calcium antagonists in the management of hypertension include angina pectoris, and for the non-dihydropyridine calcium antagonists, paroxysmal supraventricular tachycardia, and atrial fibrillation with rapid ventricular rate. Isolated systolic hypertension in the elderly is a special indication for long-acting dihydropyridine calcium antagonists, although diuretics are preferred. Calcium antagonists have been particularly effective in managing hypertension induced by cyclosporine. They are contraindicated in CHF due to systolic dysfunction and in the management of acute myocardial infarction. The long-term cardioprotective effect of calcium antagonists after a myocardial infarction has been demonstrated only for verapamil and diltiazem in patients with no evidence of LV dysfunction during their infarction. Calcium antagonists should be prescribed for this purpose only when beta-blockers are poorly-tolerated or contraindicated.     

Dispersion of repolarization following double and triple programmed stimulation. A clinical study using the monophasic action potential recording technique

To study the dispersion of ventricular repolarization following double and triple programmed stimulation and its correlation with the inducibility of ventricular arrhythmias, monophasic action potentials were simultaneously recorded from the right ventricular apex and outflow tract during programmed stimulation in 12 patients with ventricular arrhythmias and a normal QT interval. The time difference between the ends of the two monophasic action potentials were used as a measure of the dispersion of ventricular repolarization, which consists of the activation time difference and the monophasic action potential duration difference. During double and triple programmed stimulation, the dispersion of ventricular repolarization increased significantly with the shortening of the coupling interval but decreased slightly with the shortening of the preceding interval. The induction of the ventricular arrhythmias in these patients was invariably associated with a marked increase in the dispersion of ventricular repolarization. The maximal dispersion of ventricular repolarization was significantly larger in the seven patients with polymorphic ventricular tachycardia and/or ventricular flutter/fibrillation induced than in the four patients with monomorphic ventricular tachycardia induced. Analysis of the two components of the dispersion of ventricular repolarization revealed that the increased dispersion of ventricular repolarization was mainly caused by an increase in the activation time difference in the monomorphic ventricular tachycardia subgroup, and by increases in both the activation time difference and monophasic action potential duration difference in the polymorphic ventricular tachycardia/fibrillation subgroup. These findings suggest that increased dispersion of ventricular repolarization is one of the underlying mechanisms accounting for the myocardial vulnerability to ventricular arrhythmias and that repolarization disturbance is important for the genesis of polymorphic ventricular tachycardia/fibrillation.     

Fish, fish oils, arrhythmias and sudden death

Cardiovascular morbidity and mortality is relatively low in individuals with a high consumption of fish oils containing omega-3 fatty acids (eicosapentaenoic acid and docosahexaenoic acid). This has been mainly attributed to the anti atherogenic and anti thrombotic effects of these oils. However, recent evidence suggests that fish and fish oils may also prevent malignant ventricular arrhythmias and sudden cardiac death. Several animal experiments have shown that fish oils can reduce the incidence of ischaemia induced ventricular tachycardia and fibrillation. Observational studies in humans have shown that there is a connection between the intake of omega-3 fatty acids and a lower risk of sudden cardiac death. Some trials suggest that fish oils can prevent ventricular arrhythmias in humans. It is possible that the effect of fish oils on arrhythmias is independent of their anti atherogenic and anti thrombotic activities. There is also some evidence that these oils affect ion fluxes in cardiomyocytes.     

An activator/repressor dual system allows tight tetracycline-regulated gene expression in budding yeast

OBJECTIVES: This study sought to determine the prevalence and significance of nonsustained ventricular tachycardia (NSVT) in patients with premature ventricular contractions (PVCs) and heart failure treated with vasodilator therapy. BACKGROUND: Heart failure patients with ventricular arrhythmia and NSVT have a significantly increased risk of premature cardiac death. Recently there has been the question of whether these arrhythmias are expressions of a severely compromised ventricle or are they independent risk factors. We, therefore, determined the prevalence and significance of NSVT in patients with PVCs and heart failure and on vasodilator therapy. METHODS: Twenty-four hour ambulatory recordings were done at randomization, at 2 weeks, at months 1, 3, 6, 9 and 12 and then every 6 months in 674 patients with heart failure and on vasodilator therapy. The median period of follow-up was 45 months (range 0 to 54). RESULTS: Nonsustained ventricular tachycardia was present in 80% of all patients. Patients without (group 1) and with (group 2) NSVT were balanced for variables: age, etiology of heart disease, New York Heart Association (NYHA) functional class, use of amiodarone and diuretics and left ventricular diameter by echocardiogram. However, group 1 patients had significantly less beta-adrenergic blocking agent use and higher ejection fraction (EF) (p < 0.002 and p < 0.001, respectively). Survival analysis for all deaths showed a greater risk of death among group 2 patients (p=0.01). Similarly, sudden death was increased in group 2 patients (p=0.02, risk ratio 1.8). After adjusting for the above variables, only EF (p=0.001) and NYHA class (p=0.01) were shown to be independent predictors of survival. Nonsustained ventricular tachycardia showed a trend (p=0.07) as an independent predictor for all-cause mortality but not for sudden death. Only EF was an independent predictor for sudden death. CONCLUSIONS: Nonsustained ventricular tachycardia is frequently seen in patients with heart failure and may be associated with worsened survival by univariate analysis. However, after adjusting other variables, especially for EF, NSVT was not an independent predictor of all-cause mortality or sudden death. These results have serious implications in that suppression of these arrhythmias may not improve survival.     

Adenosine-sensitive ventricular tachycardia from the anterobasal left ventricle

OBJECTIVES: This study demonstrates that exercise-provocable tachycardia resembling right ventricular outflow tract tachycardia may originate from the anterobasal left ventricle. BACKGROUND: Reentry is the operative mechanism of idiopathic left ventricular tachycardia, with a QRS complex of right bundle branch block and superior axis that is responsive to verapamil but not adenosine. Whether some mechanism other than reentry is operative in some idiopathic left ventricular tachycardias is unclear. METHODS: In 4 of 53 consecutive patients with idiopathic left ventricular tachycardia, the tachycardia was sensitive to adenosine. These four patients were women 63, 61, 61 and 31 years old and were the subjects of the present study. RESULTS: In all four patients, spontaneous tachycardia was related to exercise or emotional stress. The tachycardia displayed atypical left (one patient) or right (three patients) bundle branch block with an inferior axis and marked variation in cycle length. An intravenous bolus of adenosine triphosphate (10 to 20 mg) terminated tachycardia in all four patients. Tachycardia was terminated or prevented in three patients given intravenous or oral verapamil. Atrial or ventricular incremental or extrastimulus testing induced tachycardia in all four patients (three with, one without isoproterenol infusion). Electrically induced tachycardia also demonstrated marked variation in cycle length, which ranged from 230 to 390 ms. Entrainment was not demonstrable with overdrive pacing from multiple sites. Endocardial mapping during tachycardia revealed that the earliest activations were registered 25, 40, 35 and 50 ms before onset of the QRS complex, respectively, from the anterior aspect of the left ventricle just below the mitral annulus, adjacent to the left ventricular outflow tract. High frequency Purkinje spikes were not recorded at this site. Radiofrequency current delivered to this site successfully ablated the tachycardia in three of the four patients. CONCLUSIONS: Exercise-provocable, catecholamine-mediated, verapamil-responsive, adenosine-sensitive ventricular tachycardia may arise from the anterobasal left ventricle adjacent to the outflow tract.