Malignant arrhythmia in relation to serum potassium in acute myocardial infarction

Several studies of patients with acute myocardial infarction have shown an association between hypokalemia, including mild hypokalemia, and increased occurrence of cardiac arrhythmia. Hypokalemia in acute myocardial infarction is significantly associated with diuretic therapy before or during the infarction. In a study of 1,074 patients with acute myocardial infarction, ventricular fibrillation occurred in 17.2% of 122 hypokalemic patients and in 7.5% of 952 normokalemic patients (p less than 0.01). The association of hypokalemia and ventricular fibrillation was not specifically related to poor left ventricular function. Recent studies indicate that hypokalemia is an independent risk factor of ventricular arrhythmia early in acute myocardial infarction, but a definite causal role of potassium remains to be shown. The importance of catecholamines versus serum potassium levels in occurrence of arrhythmia has not been clarified.     

Suppressant effects of conventional beta blockers and sotalol on complex and repetitive ventricular premature complexes.

Beta-blocking drugs have been shown to reduce the overall mortality and risk of sudden cardiac death in survivors of acute myocardial infarction. It is not known whether such an effect is mediated by suppression of ventricular premature complexes (VPCs). The circadian rhythmicity of ventricular arrhythmia can also be suppressed by beta-blocking drugs, and this may help reduce the risk of sudden cardiac death during the morning hours. Recent studies have also shown that beta blockers can provide a safe and effective combination with class IA antiarrhythmic agents when arrhythmias cannot be controlled with class IA agents alone. Sotalol, a nonselective beta antagonist, has unique electrophysiologic properties, and several studies have shown it to be more effective than conventional beta blockers in suppressing ventricular arrhythmias. However, direct comparative studies of the suppression of VPCs are lacking. In a recent double-blind, placebo-controlled, parallel study, the antiarrhythmic effects of sotalol and propranolol were compared in 172 patients with greater than 30 VPCs/hour. After the initial 1-week washout and 1-week placebo period, patients were randomly assigned to either 160 mg of sotalol administered twice daily (76 patients) or 40 mg of propranolol administered 3 times daily (91 patients). Those responding to therapy (decreases greater than 75% VPCs) continued to take these doses, but nonresponders were given higher doses, 320 mg of sotalol twice daily or 80 mg of propranolol 3 times daily, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)     

Occurrence of hypokalemia in suspected acute myocardial infarction and its relation to clinical history and clinical course

In 1350 patients with suspected acute myocardial infarction, serum potassium levels during the first 3 days in hospital was correlated to clinical history and clinical course. A higher incidence of hypokalemia was observed in women, in patients with hypertension, and in those on chronic diuretic treatment. Patients with anterior infarction had a higher incidence of hypokalemia than those with inferior infarction, as did patients with large as compared with small infarcts. No clear difference was observed between patients whose infarction was confirmed and those in whom the diagnosis was not confirmed. Independent predictors for hypokalemia were treatment with diuretics before admission to hospital, infarct size, and female sex. Hypokalemia during the first 3 days of hospitalization was associated with the occurrence of severe ventricular arrhythmias during hospitalization, but not with survival during a 5-year follow-up.     

低钾血症对急性心肌梗死患者预后的影响

目的探讨急性心肌梗死(AMI)患者低钾血症的发生情况及其对预后的影响。方法对929例ST段抬高的AMI患者于入院时抽血测定血钾、肌酸激酶(CK)、肌酸激酶同工酶(CK-MB)、肌钙蛋白I(cTnI),根据血钾水平分为低血钾组(血钾<3.5 mmol/L)和正常血钾组(血钾3.5~5.5 mmol/L),同时观察住院期间严重不良事件(室性心动过速、心室颤动和猝死)的发生情况。结果低钾血症的发生率为13.7%,下壁+后壁AMI的发生率最低(10.4%),明显低于下后壁+右心室、前间壁和广泛前壁心肌梗死;发病至抽血时间≤3 h的低钾血症发生率为17.3%,明显高于发病时间>3 h者;低血钾组的CK、CK-MB和cTnI峰值明显高于正常血钾组;低血钾组总的严重不良事件发生率(23.8%)明显高于正常血钾组(15.8%)。结论低钾血症与AMI患者的梗死时间、部位和面积相关,并严重影响患者的预后。     

Frequency of hypokalemia after successfully resuscitated out-of-hospital cardiac arrest compared with that in transmural acute myocardial infarction

To evaluate the prevalence of hypokalemia in out-of-hospital cardiac arrest, the initial serum potassium and arterial pH values were reviewed from 138 consecutive patients resuscitated from cardiac arrest. For comparison, the same variables were reviewed for 62 consecutive patients who had transmural acute myocardial infarction (AMI) without cardiac arrest. The mean serum potassium level was lower after resuscitation from cardiac arrest (3.6 +/- 0.6 mEq/liter) than during AMI (3.9 +/- 0.5 mEq/liter) (p less than 0.005). The incidence of hypokalemia (potassium less than 3.5 mEq/liter) was greater in patients sustaining cardiac arrest (41%) than in patients who had AMI without cardiac arrest (11%) (p less than 0.001). Hypokalemia was common after cardiac arrest regardless of the occurrence of AMI at the time of arrest. Hypokalemia after cardiac arrest was independent of arterial pH, epinephrine or bicarbonate therapy during resuscitation, or prior therapy with diuretic drugs, digoxin or propranolol. In 10 patients with marked hypokalemia, the serum potassium level returned to normal rapidly (16 hours) during the hospitalization even though only 29% of the predicted potassium requirement was infused before its normalization. Thus, hypokalemia is prevalent immediately after out-of-hospital cardiac arrest, whereas it is uncommon in AMI in the absence of cardiac arrest. The cause and electrophysiologic consequences of this hypokalemia are unknown; in most cases, it is apparently caused by a shift of potassium from the intravascular compartment rather than a total body depletion of potassium.     

Serum magnesium and potassium in acute myocardial infarction. Influence on ventricular arrhythmias

Over a 13-month period, serum potassium and magnesium levels were measured in 590 patients admitted to a coronary care unit. Hypokalemia, often in the absence of diuretic use, occurred in 17% of the 211 patients with acute myocardial infarction. Patients with acute myocardial infarction and a potassium level of less than 4.0 mEq/L (4.0 mmol/L) had an increased risk of ventricular arrhythmias (59% vs 42%). Because hypokalemia is common in acute myocardial infarction and is associated with ventricular arrhythmias, routine measurement of serum potassium levels and prompt correction are recommended. Hypomagnesemia occurred in only 4% of the patients, but it was more common in the group with acute myocardial infarction than in the group without myocardial infarction (6% vs 3%). Ventricular arrhythmias occurred in ten of the 13 patients with both acute myocardial infarction and hypomagnesemia, but eight of these patients also had low serum potassium levels. This low incidence of hypomagnesemia does not justify routine measurement of serum magnesium levels. However, the mean level (2.5 +/- 0.4 mg/dL [1.03 +/- 0.16 mmol/L]) in a reference population of healthy volunteers was unexpectedly high and suggests that the low incidence of hypomagnesemia in our population may not be applicable to other centers and may reflect a higher magnesium content in our geographic area of southeastern Ontario.     

The heart in hypertension and arrhythmias

Antihypertensive management reduces the incidence of congestive heart failure, malignant hypertension and stroke; however, the overall incidence of events due to ischemic heart disease was not influenced by antihypertensive treatment. One of the possible explanations might be some negative metabolic effects of antihypertensive drugs. Hypokalemia develops in 20 to 50% patients who receive a thiazide diuretic. An association between hypokalemia and malignant arrhythmias (including ventricular fibrillation), in acute myocardial infarction, has been observed. 24-hour ambulatory electrocardiographic monitoring demonstrated a higher frequency of ventricular ectopic beats in hypertensive patients taking thiazides. There is, however, no convincing evidence of a simple causative relation between ventricular extrasystoles and low concentrations of serum potassium. Hypertensives with left ventricular hypertrophy (ECG criteria) had significantly more premature ventricular contractions than patients with established hypertension without left ventricular hypertrophy or normotensive subjects. These data could provide an electrophysiologic substrate for the epidemiologic findings of increased morbidity and mortality in patients with left ventricular hypertrophy.     

Hypokalemia,Arrhythmias and Early Prognosis in Acute Myocardial Infarction

ABSTRACT Serum potassium concentration was estimated on admission to hospital in 289 women and 785 men with acute myocardial infarction. The proportion of women in potassium subgroups was inversely related to serum potassium concentration, increasing from 8% at serum potassium ≥5.2 mmol/1 to 58% at ≤3 mmol/1. The frequency of diuretic therapy was also higher in women (35%) than in men (23%). The mortality rate was high at 3 months in patients with one or more arrhythmias (atrioventricular block grade 2, complete heart block, bundle branch block, atrial fibrillation, premature ventricular contractions, ventricular tachycardia) detected by conventional methods during the first 48 hours after admission. Hypokalemia (serum potassium ≤3.5 mmol/1) did not significantly predict increased occurrence of any of these arrhythmias. Small inhomogeneities of arrhythmias between the potassium groups may have been caused by digitalis therapy prior to admission. Hypokalemia on admission did not predict altered prognosis during the first 3 months.     

低血钾与急性心肌梗死的梗死部位冠状动脉病变及预后的关系

目的探讨低血钾与急性心肌梗死的梗死部位、冠状动脉病变及预后的关系。方法根据心肌梗死早期血钾水平把110例患者分为低血钾组、正常血钾组,对比两组的梗死部位、冠状动脉病变特征、并发症和预后情况。结果急性心肌梗死患者低血钾36例(占32.7%),其中广泛前壁心肌梗死(57.1%)与下壁(23.9%)相比更易合并低血钾(P<0.01)。低血钾组的梗死相关血管更多为前降支(55.6%)和近段病变(55.6%),与对照组差异有统计学意义(分别为P=0.01,P=0.03)。低血钾组心力衰竭、严重心律失常、梗死后心绞痛等并发症发生率显著高于正常血钾组(均为P<0.05)。结论急性心肌梗死合并低血钾的梗死相关血管多为近段病变,多为前降支,预后相对较差。     

Do endothelin receptor antagonists have an antiarrhythmic potential during acute myocardial infarction? Evidence from experimental studies

Sudden cardiac death constitutes a major health-related problem. In the majority of cases, sudden cardiac death is due to ventricular tachyarrhythmias secondary to acute myocardial infarction. The pathophysiologic chain of events leading to ventricular tachyarrhythmias after acute coronary occlusion is complex and incompletely understood. Experimental and clinical studies have indicated that endothelin-1 production rises markedly very early in the course of myocardial infarction. Endothelin-1 exerts significant electrophysiologic actions on ventricular cardiomyocytes and participates in the genesis of ischemic ventricular tachyarrhythmias. Endothelin-1, acting via two G-protein-coupled receptors (ETA and ETB), prolongs the action potential duration and increases the occurrence of spontaneous calcium transients, resulting in early afterdepolarizations and ventricular tachyarrhythmias via triggered activity. Moreover, endothelin-1 enhances sympathetic stimulation, a well established contributor to ventricular arrhythmogenesis during acute myocardial infarction. Despite these considerations, the therapeutic potential of endothelin receptor antagonists as antiarrhythmic drugs during myocardial ischemia/infarction is still under investigation. To date, a number of endothelin-1 receptor antagonists are available, presenting different degrees of selectivity for ETA and ETB receptors. The arrhythmogenic effects of endothelin-1 are exerted mainly via stimulation of the ETA receptors, but the role of ETB receptors remains controversial, as previous studies have produced conflicting results. This review summarizes the current state-of-the-art on the role of endothelin-1 in the genesis of ventricular arrhythmias during acute myocardial infarction and raises some hypotheses that could be explored in future studies.     

Effect of beta blockade on ventricular fibrillation- and ventricular tachycardia-induced circulatory arrest in acute myocardial infarction

The risk of developing circulatory arrest secondary to ventricular fibrillation or tachycardia in acute myocardial infarction (AMI) is greatly increased in patients with hypokalemia, whether diuretic induced or not. In a retrospective study of 5,877 infarctions during an 8-year period, hypokalemia was more common (22.5%) in diuretic-treated AMI patients than in those not treated with diuretics (12.9%). Thus, hypokalemia should be avoided in diuretic-treated patients with increased risk of myocardial infarction. Circulatory arrest occurred in 13% of hypokalemic patients treated with nonselective beta blockers on admission compared with 26% in those treated with selective beta blockers. No difference was found in normokalemic patients. The mean serum potassium value was 4.07 mM/liter in the patients treated with nonselective beta blockers compared with 4.0 and 4.01 in those treated with selective and no beta blockade, respectively. In a separate study, adrenaline infusion in healthy volunteers produced a decrease not only in serum potassium but also in serum magnesium, although the latter occurred later. Pretreatment with verapamil exaggerated the decrease in serum potassium. When starting beta-blocker treatment in patients at risk of developing AMI, consideration should be given to commencing with a nonselective instead of a selective beta blocker.     

Ventricular arrhythmias initiated by programmed stimulation in four groups of patients with healed myocardial infarction

Programmed electrical stimulation of the heart was prospectively used in 160 patients with healed myocardial infarction to study the incidence and characteristics of ventricular arrhythmias induced. Thirty-five patients had neither documented nor suspected ventricular arrhythmias (Group A); 37 patients had documented nonsustained ventricular tachycardia (Group B); 31 patients had been resuscitated from ventricular fibrillation (Group C); and 57 patients had documented sustained monomorphic ventricular tachycardia (Group D). No electrophysiologic differences were found between patients in Group A and Group B, but patients in both groups differed significantly from patients in Group C and Group D. In the last two groups, sustained monomorphic ventricular tachycardia was more frequently induced, the cycle length of the induced ventricular tachycardia was slower and a lesser number of premature stimuli was required for induction. No differences were found in the incidence, rate or mode of induction of nonsustained monomorphic ventricular tachycardia, but nonsustained polymorphic ventricular tachycardia and ventricular fibrillation were more frequently induced in Groups A and B. It is concluded that the substrate for sustained ventricular arrhythmia is present in at least 42% of patients after myocardial infarction. The electrophysiologic characteristics of the substrate for ventricular tachycardia seem to be the major determinant of the clinical occurrence of sustained ventricular arrhythmia. Changes in the electrophysiologic properties of the substrate of ventricular tachycardia, either spontaneously with time or induced by ischemia or antiarrhythmic drugs, can contribute to the clinical occurrence of sustained ventricular arrhythmias in patients with an old myocardial infarction.     

Spontaneous variability of ventricular arrhythmias in patients at increased risk for sudden death after acute myocardial infarction: consecutive ambulatory electrocardiographic recordings of 88 patients

The Cardiac Arrhythmia Pilot Study, sponsored by the National Heart, Lung, and Blood Institute, is a multicenter, prospective, randomized, double-blind trial designed to identify patients having 10 or more ventricular premature complexes (VPCs) per hour within 6 to 60 days of acute myocardial infarction. The present investigation selected patients after acute myocardial infarction who had ambulatory electrocardiographic qualifying arrhythmia for CAPS. An additional baseline electrocardiogram was recorded before enrollment in the study to assess baseline spontaneous variability of VPCs. A total of 88 patients (15 women, 73 men, aged 57 +/- 10 years) were studied. The 43 patients (49%) receiving beta-blocking drugs were included because the dose was not altered between the 2 consecutive electrocardiographic recordings. This investigation shows that a 95% reduction in VPCs is required to document a significant drug effect rather than variability alone if 1 day of control and 1 day of treatment electrocardiographic recording are compared. Similarly, based on 1 day of electrocardiographic recording before and after antiarrhythmic therapy, 1,780% increase in VPC frequency is required to establish "arrhythmia aggravation" from an antiarrhythmic drug rather than from variability alone based on a 95% confidence interval. Variability of ventricular arrhythmias is independent of left ventricular function, whereas patients taking beta-blocking therapy tend to have greater VPC variability (p = 0.052), even though VPC frequencies were lower (59 +/- 19 vs 138 +/- 31 VPCs/hour, p less than 0.006) than those not taking beta-blocking drugs.     

急性心肌梗死早期血钾浓度与冠状动脉造影相关罪犯血管及室性心律失常的关系

目的 探讨急性心肌梗死患者早期血钾浓度与冠状动脉造影相关罪犯血管及室性心律失常的关系.方法 选择136例符合“急性心肌梗死诊断标准”,且发病时间＜12 h的患者.入院后立即采静脉血3ml,测血钾浓度,做18导联心电图.患者均同意做急诊介入治疗,给予冠状动脉造影,确定急性心肌梗死的罪犯血管.观察急性心肌梗死患者早期血钾浓度与冠状动脉造影确定罪犯血管及室性心律失常的关系,并进行统计学分析.结果 急性心肌梗死罪犯血管为左前降支的血钾浓度最低,左回旋支血钾浓度最高,右冠状动脉的血钾浓度位于左前降支及左回旋支之间.左前降支病变与左回旋支病变血钾浓度对比差异有统计学意义（P＜0.01）.右冠状动脉病变与左回旋支病变血钾浓度对比差异有统计学意义（P＜0.05）.急性心肌梗死低血钾组与正常血钾组室性心律失常发生率对比差异有统计学意义（P＜0.01）.结论 急性心肌梗死患者,罪犯血管是左前降支的发病早期最容易合并低血钾,预后普遍较差.急性心肌梗死早期合并低血钾易发生室性心律失常.     

The implantable cardioverter-defibrillator

Ventricular arrhythmias remain a major cause of cardiovascular mortality. Therapy for serious ventricular arrhythmias has evolved over the past decade, from treatment primarily with antiarrhythmic drugs to implanted devices. The implantable cardioverter-defibrillator (ICD) is the best therapy for patients who have experienced an episode of ventricular fibrillation not accompanied by an acute myocardial infarction or other transient or reversible cause. It is also superior therapy in patients with sustained ventricular tachycardia (VT) causing syncope or hemodynamic compromise. Controlled clinical trials have confirmed the utility of these devices. As primary prevention, the ICD is superior to conventional antiarrhythmic drug therapy in patients who have survived a myocardial infarction and who have spontaneous, nonsustained ventricular tachycardia, a low ejection fraction, inducible VT at electrophysiologic study, and whose VT is not suppressed by procainamide. The effect of the ICD on survival of other patient populations remains to be proven. The device is costly, but its price is generally accepted to be reasonable. The ICD has been a major advance in the treatment of ventricular arrhythmias.     

Out-of-hospital pleomorphic ventricular tachycardia and resuscitation: association with acute myocardial ischemia and infarction.

Pleomorphic ventricular tachycardia is characterized by QRS complexes with repeated variation in polarity, amplitude, and regularity. When associated with prolongation of the QT interval, the term torsades de pointes is used to describe the arrhythmia. It usually is seen clinically in association with class IA antiarrhythmic drugs such as quinidine and procainamide, bradycardia, hypokalemia, and, much less often, other drugs and electrolyte disorders as well as a result of congenital and neurogenic causes. It also may accompany acute myocardial infarction or ischemia. We describe four patients in whom pleomorphic ventricular tachycardia was observed as the presenting rhythm or during the course of resuscitation in out-of-hospital cardiac arrest. In all four patients, acute myocardial ischemia appeared to be the provocative mechanism. Therapeutic implications include an awareness of the unusual behavior of this arrhythmia, especially its propensity to terminate spontaneously. Such awareness may prevent the delivery of unnecessary defibrillatory shocks.     

Evaluation and treatment strategies in patients at high risk of sudden death post myocardial infarction

Over 50 percent of deaths in patients who survive an acute myocardial infarction are due to fatal ventricular tachyarrhythmias. Patients who survive an episode of sustained ventricular arrhythmia are at highest risk of recurrent cardiac arrest. Electrophysiologic studies have been found to be useful in guiding therapy and reducing mortality in these patients and in patients with syncope due to arrhythmic etiology. Evaluation and treatment of nonsustained ventricular tachycardia post infarction remains somewhat controversial. A recently published trial (MADIT), however, showed improved survival with an implanted defibrillator in patients with coronary disease and asymptomatic nonsustained ventricular tachycardia. Asymptomatic patients post infarction at high risk include those who have significant left ventricular dysfunction, late potentials, high-grade ventricular ectopy, and abnormal heart rate variability. These tests individually, however, have a low positive predictive accuracy. This, combined with the fact that antiarrhythmic drugs are frequently not effective and can be proarrhythmic, leaves the best treatment for these patients uncertain. It is known, however, that beta-adrenoreceptor blocking agents do reduce mortality after an acute myocardial infarction. Early studies have shown mixed results relating to sudden death and total mortality with amiodarone. To date, no other antiarrhythmic drug has shown benefit, while several have been shown to be harmful. Recent studies have also shown some beneficial effects of angiotensin-converting enzyme inhibitors, carvedilol, a third-generation beta-blocking agent with vasodilator properties, and the angiotensin II receptor antagonist losartan. However, their precise role in reducing sudden death needs to be defined further.     

Nonsustained ventricular tachycardia in patients with coronary artery disease: role of electrophysiologic study

Sixty-two consecutive patients with chronic coronary artery disease referred for evaluation of nonsustained ventricular tachycardia (VT) underwent electrophysiologic studies. Sustained VT was induced by one to three ventricular extrastimuli in 28 patients (45%). Therapy was guided by the results of electrophysiologic testing in 44 patients: 19 patients without inducible sustained VT received no antiarrhythmic therapy, and 25 patients with inducible sustained or symptomatic nonsustained VT received therapy guided by the results of electrophysiologic studies. The results of electrophysiologic studies were ignored by physicians for a second group of 18 patients: four had inducible sustained VT but received no antiarrhythmic therapy, and 14 had inducible sustained or nonsustained VT and received antiarrhythmic therapy not guided by results of electrophysiologic testing. After a mean follow-up period of 28 months, 11 patients had died suddenly. Seven of the 11 patients who died suddenly had inducible sustained VT. Three of 44 patients in the group receiving therapy guided by electrophysiologic studies died suddenly versus eight of 18 in the group receiving therapy not guided by electrophysiologic studies (p = .001). Only one of 19 patients without inducible sustained VT who were not treated experienced sudden death. Two of four patients with inducible sustained VT who did not receive antiarrhythmic therapy died suddenly. Multivariate analysis of the relationship of induced arrhythmias, left ventricular ejection fraction, site of myocardial infarction, history of syncope, or type of antiarrhythmic therapy to outcome revealed a greater than twofold increased risk for sudden cardiac death in patients whose therapy was not guided by results of electrophysiologic study.(ABSTRACT TRUNCATED AT 250 WORDS)     

Carvedilol's antiarrhythmic properties: therapeutic implications in patients with left ventricular dysfunction

Carvedilol is a beta- and alpha-adrenergic-blocking drug with clinically important antiarrhythmic properties. It possesses anti-ischemic and antioxidant activity and inhibits a number of cationic channels in the cardiomyocyte, including the HERG-associated potassium channel, the L-type calcium channel, and the rapid-depolarizing sodium channel. The electrophysiologic properties of carvedilol include moderate prolongation of action potential duration and effective refractory period; slowing of atrioventricular conduction; and reducing the dispersion of refractoriness. Experimentally, carvedilol reduces complex and repetitive ventricular ectopy induced by ischemia and reperfusion. In patients, carvedilol is effective in controlling the ventricular rate response in atrial fibrillation (AF), with and without digitalis, and is useful in maintaining sinus rhythm after cardioversion, with and without amiodarone. In patients with AF and heart failure (HF), carvedilol reduces mortality risk and improves left ventricular (LV) function. Large-scale clinical trials have demonstrated that combined carvedilol and angiotensin-converting enzyme inhibitor therapy significantly reduces sudden cardiac death, mortality, and ventricular arrhythmia in patients with LV dysfunction (LVD) due to chronic HF or following myocardial infarction (MI). Despite intensive neurohormonal blockade, mortality rates remain relatively high in patients with post-MI and nonischemic LVD. Recent trials of implantable cardioverter-defibrillators added to pharmacologic therapy, especially beta blockers, have shown a further reduction in arrhythmic deaths in these patients.     

Rationale of therapy in the patient with acute myocardial infarction and life-threatening arrhythmias: a focus on bretylium

Experimental evidence suggests a number of pathologic and electrophysiologic mechanisms that may help initiate ventricular arrhythmias accompanying myocardial ischemia and infarction. Early and late phase events are associated with reentry or an enhancement of focal mechanisms, or both. These can initiate ventricular tachycardia (VT) or ventricular fibrillation (VF), or both. The presence of distinct mechanisms that may initiate and maintain life-threatening dysrhythmias early in myocardial ischemia suggest different pharmacologic approaches for their prevention or suppression. Another consideration concerns patients subjected to coronary artery angioplasty or thrombolytic therapy and the development of arrhythmias associated with reperfusion of the once ischemic myocardium. The electrophysiologic mechanisms associated with reperfusion arrhythmias are unknown, and little is known about appropriate therapy for each episode of cardiac dysrhythmia. Ventricular extrasystoles or VT usually precedes VF. These premonitory arrhythmias are poor criteria for the institution of antiarrhythmic drug therapy, because VF develops within 1 to 10 minutes after the appearance of the rhythmic disturbances. Some authorities suggest that all patients with acute myocardial infarction should receive prophylactic antiarrhythmic therapy, because warning arrhythmias either do not occur at all or provide insufficient time to intervene pharmacologically. Many of the new class I antiarrhythmic agents effectively reduce the frequency of premature ventricular depolarizations, but lack specific antifibrillatory activity. However, the recent introduction of bretylium into clinical cardiology opens a new approach to preventing life-threatening ventricular dysrhythmias. Along with other members of class III, bretylium exerts different cardiac electrophysiologic effects than do the other 3 classes of drugs.(ABSTRACT TRUNCATED AT 250 WORDS)