Role of coronary artery revascularization and aneurysmectomy in ventricular arrhythmias in the chronic phase of myocardial infarction

INTRODUCTION AND OBJECTIVES: The influence of coronary artery revascularization on the control of ventricular arrhythmias in patients with chronic myocardial infarction is uncertain. However, ablation of the arrhythmogenic circuit in these patients by aneurysm resection is useful for controlling ventricular arrhythmias. We made a prospective analysis of our clinical strategy in patients who were candidates for coronary artery revascularization and/or aneurysmectomy to determine its influence on the recurrence of ventricular arrhythmias. PATIENTS AND METHOD: Prospective study of 17 consecutive patients with chronic myocardial infarction and ventricular arrhythmias unrelated with an acute ischemic event, who had coronary artery disease and/or ventricular aneurysm susceptible to aggressive treatment. We evaluated our clinical strategy and the recurrence of ventricular arrhythmias during a mean follow-up period of 33.64 months. RESULTS: Two groups of patients were studied: patients with ventricular aneurysm (group I: 12 patients) and patients without ventricular aneurysm (group II: 5 patients). Seven patients of group I underwent endoaneurysmorrhaphy and endocardial resection (4 of these patients had associated revascularization procedures). Three patients were not candidates for aneurysmectomy or revascularization procedures. Two patients underwent only revascularization procedures. All the patients in group II were revascularized. The patients who underwent aneurysmectomy did not have recurrence of arrhythmias. In 5 of the 6 patients who underwent programmed electrophysiological stimulation after aneurysmectomy, no sustained arrhythmia could be induced. Patients who were only revascularized had a high rate of recurrence of ventricular arrhythmias (57%), which were inducible after revascularization. CONCLUSION: Aneurysmectomy and endocardial resection constituted, in our experience, an effective tool for controlling ventricular arrhythmias associated with left ventricular aneurysm. Coronary artery revascularization in patients with ventricular arrhythmias and chronic myocardial infarction probably does not prevent the recurrence of ventricular arrhythmias.     

Ventricular Tachycardia in Coronary Artery Disease

Ventricular arrhythmias are important contributors to morbidity and mortality in patients with coronary artery disease. Ventricular fibrillation accounts for the majority of deaths occurring in the acute phase of ischemia, whereas sustained, monomorphic ventricular tachycardia due to reentry generated in the scar tissue develops most often in the setting of healed myocardial infarction, especially in patients with lower left ventricular ejection fraction. Despite determinant advances in population education and myocardial infarction management, the ventricular tachycardia risk in the overall population with coronary artery disease continues to be a major problem in clinical practice. The initial evaluation of a patient presenting with ventricular tachycardia requires a 12-lead electrocardiogram, which can be helpful to confirm the diagnosis, suggest the presence of potential underlying heart disease, and identify the location of the ventricular tachycardia circuit. An invasive electrophysiologic study is usually crucial to determine the mechanism of the arrhythmia once induced and to provide guidance for ablation. The approach for ventricular tachycardia ablation depends on several factors, including inducibility, sustainability, and clinical tolerance of ventricular tachycardia. The paper also reviews other therapeutic options for patients with ventricular tachycardia associated with coronary artery disease, including antiarrhythmic drug therapy, surgical ablation, and current implantable cardioverter-defibrillator indications.     

Taquicardia ventricular en la enfermedad coronaria

Ventricular arrhythmias are important contributors to morbidity and mortality in patients with coronary artery disease. Ventricular fibrillation accounts for the majority of deaths occurring in the acute phase of ischemia, whereas sustained, monomorphic ventricular tachycardia due to reentry generated in the scar tissue develops most often in the setting of healed myocardial infarction, especially in patients with lower left ventricular ejection fraction. Despite determinant advances in population education and myocardial infarction management, the ventricular tachycardia risk in the overall population with coronary artery disease continues to be a major problem in clinical practice. The initial evaluation of a patient presenting with ventricular tachycardia requires a 12-lead electrocardiogram, which can be helpful to confirm the diagnosis, suggest the presence of potential underlying heart disease, and identify the location of the ventricular tachycardia circuit. An invasive electrophysiologic study is usually crucial to determine the mechanism of the arrhythmia once induced and to provide guidance for ablation. The approach for ventricular tachycardia ablation depends on several factors, including inducibility, sustainability, and clinical tolerance of ventricular tachycardia. The paper also reviews other therapeutic options for patients with ventricular tachycardia associated with coronary artery disease, including antiarrhythmic drug therapy, surgical ablation, and current implantable cardioverter-defibrillator indications.     

Sympathetic influences in myocardial ischemia: possible mechanisms of arrhythmogenesis

The large-scale trials of beta-adrenergic receptors have indicated a clear-cut benefit in patients having survived an acute myocardial infarction. At present, we do not understand the mechanism for these results, which impairs our ability to totally prevent mortality from myocardial infarction with beta blockade therapy. This review was aimed at the considerable recent experimental and clinical observations in adrenergic influences on the myocardial ischemia. Based on these and future studies, other manipulations of the sympathetic nervous system may prove helpful in preventing ventricular arrhythmias associated with coronary artery disease.     

Echocardiography in ischemic heart disease.

Echocardiographic findings in patients with ischemic heart disease are described; their correlations with clinical, hemodynamic and angiographic data are presented and discussed. Regional abnormalities of left ventricular wall motion and/or thickening during systole are detected in 84 per cent of patients with acute myocardial infarction and in a high percentage of patients with larger than or equal to 75 per cent narrowing of a major coronary artery. These abnormalities may occur with stress and may be reversible. Left ventricular wall thinning during systole indicates acute ischemia or infarction and thin, dense myocardial echoes indicate scar. Echocardiographic evidence of left ventricular dysfunction is useful in predicting heart failure and mortality in patients with acute myocardial infarction and in predicting surgical mortality for patients undergoing aneurysmectomy and/or coronary artery bypass surgery. Echocardiography has not proved useful in determining graft patency following coronary artery bypass surgery. Technical difficulties and limitations of echocardiography in patients with coronary artery disease are discussed.     

The incidence, significance and prognosis of arrhythmias in acute myocardial infarction.

Concepts of the incidence, significance and prognosis of almost all cardiac arrhythmias during acute myocardial infarction have changed greatly in the last 15 years. In some cities facilities are available to reach patients in the very earliest phases of ischaemia or infarction. As previously suspected but now confirmed, ventricular fibrillation occurs commonly at this time and depending on whether ischaemia or infarction is the basis of its occurrence, has a variable long-term prognosis. In the coronary care unit ventricular arrhythmias are more frequent than was originally believed and current research suggests that they have little if any predictive value in defining individuals who would develop ventricular fibrillation. Such events, however, appear related to the severity of myocardial or coronary artery disease. Similarly, asystole and heart block in acute myocardial infarction are important causes of mortality through their association with severe underlying disease. Other cardiac arrhythmias are not infrequent in acute myocardial infarction. They may carry an immediate prognostic implication for the patient but rarely have long-term implications. Autonomic nervous system disturbances may underlie many arrhythmias occurring particularly in the earliest phases of infarction.     

急性心肌梗死直接冠状动脉成形术后再灌注心律失常分析

目的 分析急性心肌梗死直接冠脉成形术后严重再灌注心律失常发生的状况，探讨其预防和紧急治疗方法。方法 行直接经皮冠状动脉成形术的急性心肌梗死患者245例，根据梗死相关动脉分成三组，LAD组：126例；RCA组：97例；LCX组：22例。统计各组经皮冠状动脉成形术后再灌注心律失常发生的状况。结果 共151例患者发生严重的再灌注心律失常，发生率为61．6％；加速性室性自主心律发生率最高(22．0％)，与梗死相关动脉无关；其次是室性早搏(19．2％)，以LAD组最高(27．8％)。RCA组缓慢性心律失常(窦缓、窦性停搏、高度房室传导阻滞)发生率(35．1％)显著高于LAD组(3．9％)和ICX组(22．7％)：LCX组各种再灌注心律失常发生率界于LAD组和RCA组之间。结论 急性心肌梗死直接冠脉成形术后严重心律失常总的发生率较高，心律失常的类型与梗死相关动脉有明确的相关性。     

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.     

Predictors of survival and sudden death in patients with stable severe congestive heart failure due to ischemic and nonischemic causes: a prospective long term study of 200 patients

This prospective study of 200 stable outpatients with New York Hospital Association (NYHA) class III congestive heart failure on maximal medical therapy was done to determine which factors affect survival, to record the incidence of sudden death, and to identify prognostic features which characterize patients at high risk of sudden death. Congestive heart failure was due to coronary artery disease in 151 patients (76%). After an average follow-up of 40 months, 96 patients (48%) had died: 30 (15%) suddenly, 41 (22%) of low output, and 25 (13%) of other causes. Of the 30 patients dying suddenly 12 had autopsies, and acute myocardial infarction was found in nine. Of the 41 patients dying of low output 15 had autopsies, and recent myocardial infarction was found in five. Nine of the 25 patients dying of other causes died of acute myocardial infarction. Multivariate stepwise analysis revealed that severity of ventricular arrhythmias (modified Lown classification), exercise tolerance and left ventricular ejection fraction were the most important determinants of survival. In patients with coronary artery disease, complex ventricular arrhythmias detected by ambulatory Holter monitoring were frequent in all groups and were not clinically useful in predicting which of these patients were at a higher risk of dying suddenly. In contrast, patients without coronary artery disease who died suddenly had a higher incidence of nonsustained ventricular tachycardia and a tendency towards more frequent ventricular arrhythmias in general. The authors conclude that in ambulatory patients with stable NYHA class III heart failure, the severity of ventricular arrhythmias is a predictor of survival.(ABSTRACT TRUNCATED AT 250 WORDS)     

Early treadmill testing after myocardial infarction: Angiographic and hemodynamic correlations.

Twenty-eight patients who were two weeks post acute myocardial infarction walked on a motorized treadmill at 1 MPH 0 percent grade for five minutes (group 1) or to an end-point of symptoms, ST-T wave changes or arrhythmias (group 2). At subsequent cardiac catheterization, 73 percent in group 1 had single vessel coronary artery disease whereas 82 percent group 2 had three or four vessel coronary artery disease. Ejection fraction was better in group 1 as was the slope of a modified left ventricular function curve. We conclude that limited exercise treadmill testing soon after acute myocardial infarction may be useful in predicting the extent of coronary artery disease and the amount of left ventricular dysfunction.     

Coronary artery revascularization in patients with sustained ventricular arrhythmias in the chronic phase of a myocardial infarction: effects on the electrophysiologic substrate and outcome

OBJECTIVES: The objective of this study was to analyze the influence of coronary artery revascularization in patients with ventricular arrhythmias. BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.     

Relation of silent myocardial ischemia to ventricular arrhythmias and sudden death

Silent myocardial ischemia is common in the clinical spectrum of coronary disease. Ambulatory electrocardiographic monitoring has provided the most objective evidence of silent ischemia, but the phenomenon has also been detected in patients with coronary artery disease through analysis of exercise-induced ischemic ST-segment alterations, scintigraphic myocardial perfusion defects and left ventricular wall motion abnormalities. Silent myocardial ischemia frequently occurs in patients with stable angina, unstable angina, myocardial infarction and completely asymptomatic coronary artery disease. In each of these groups, silent ischemia has been associated with an increased risk of subsequent cardiac events. However, it remains unclear whether silent ischemia is directly involved in the occurrence of these events, possibly by provoking ventricular arrhythmias. Only limited data are available on the relation between silent ischemia and arrhythmias in myocardial infarction, vasospastic angina, coronary angioplasty, exercise testing and ambulatory electrocardiography. However, fortuitous ambulatory monitoring coincident with sudden death has detected ischemia associated with lethal arrhythmias in some individual cases. This suggests that an ischemia-arrhythmia association may be important in certain patients at certain times, possibly in combination with other factors.     

Myocardial infarction in young people with normal coronary arteries

Myocardial infarction occurring in young people with angiographically normal coronary arteries is well described but the pathophysiology of this condition remains unknown. Coronary artery spasm in association with thrombus formation and minimal atheromatous disease or spontaneous coronary artery dissection are possible causes. Two young men presented with severe chest pain after acute alcohol intoxication and each sustained an extensive anterior myocardial infarction. Investigations including intravascular ultrasound showed no evidence of atherosclerotic coronary artery disease. Coronary artery spasm associated with acute alcohol intoxication as well as a prothrombotic state and endothelial damage related to cigarette smoking may be mechanisms leading to acute myocardial infarction in these cases. Acute myocardial infarction occurs in young persons with normal coronary arteries and the diagnosis should be considered in young patients presenting with severe chest pain, particularly those abusing cocaine or alcohol, so that reperfusion therapy can be initiated promptly.

Keywords: myocardial infarction;  coronary vasospasm;  alcohol;  intravascular ultrasound     

Surgical management of life-threatening ventricular arrhythmias in patients with coronary artery disease.

Twenty-one patients with coronary artery disease and severe, symptomatic ventricular arrhythmias underwent cardiac surgery after failure of medical managememt. All had coronary artery disease and either localized areas of severe hypokinesis (three patients), or ventricular aneurysms (18 patients) documented angiographically prior to surgery. Operation within one month after acute infarction resulted in an 80% in-hospital mortality, whereas operation more than one month postinfarction showed a 20% mortality. Operative treatment that included myocardial resection had a significantly lower mortality (P less than 0.05) than that which did not. With an average of 36.5 months of follow-up, 13 of the 21 patients were long-term survivors, despite the persistence of ventricular arrhythmias. Surgical treatment which includes myocardial resection and occurs more than one month after infarction should be considered in patients with symptomatic ventricular arrhythmias and severe, well-localized left ventricular wall motion abnormalities.     

The nature of ventricular arrhythmias during ergonovine-induced vasospastic angina pectoris

The peak incidence of ventricular fibrillation in acute myocardial infarction usually occurs during the first hours after the onset. Electrophysiological changes immediately after the onset have been studied in animal models, but are still incompletely understood in humans. For clarification of the characteristic features of ventricular arrhythmias during acute myocardial ischemia, ventricular arrhythmias were studied in 81 patients with vasospastic angina pectoris induced by ergonovine. Ventricular arrhythmias occurred in 45 of these patients, including ventricular tachycardia in 15, and ventricular fibrillation requiring repeated DC defibrillation in two patients. Most ventricular extrasystoles occurred before the ST segment reached maximum elevation, while reperfusion arrhythmias were less common. In many patients the coupling intervals varied, and the configuration was multiform. It is concluded that ventricular arrhythmias occurring during ergonovine-induced coronary spasm show different characteristics from those occurring during chronic ischemia. As the arrhythmias in this study seem, in some ways, to resemble arrhythmias occurring at the onset of myocardial infarction, the results might provide useful information on ventricular arrhythmias in myocardial ischemia in humans.     

Myocardial infarction, severe reversible ischemia, and shock following excess thyroid administration in a woman with normal coronary arteries

In the absence of fixed coronary artery disease, thyrotoxicosis is rarely associated with acute myocardial infarction and/or ischemia. There are no known reports on the association of acute myocardial infarction with iatrogenic or factitious thyrotoxicosis in the absence of fixed coronary artery stenosis or coronary artery spasm. A 68-year-old woman, clinically in a state of thyrotoxicosis as a result of taking 0.3 g/d of exogenous thyroid replacement, sustained a severe, reversible myocardial ischemic event. Echocardiographic and scintigraphic evaluations demonstrated a large apical dyskinetic region. Subsequently, after the original dose of levothyroxine sodium was reduced to 0.15 mg and the patient became euthyroid, two-dimensional echocardiography and scintigraphic and cardiac catheterization studies demonstrated normal left ventricular contractility and normal coronary anatomy. Coronary artery spasm was not induced by ergonovine maleate therapy. Exogenous thyroid administration may directly influence myocardial oxygen supply and demand, exclusive of coronary artery disease and coronary spasm. A critical imbalance may then result in acute myocardial ischemia and reversible left ventricular segmental wall motion abnormalities.     

Are coronary patients at higher risk with digoxin therapy? An ongoing controversy

Previous reports have yielded contradictory conclusions regarding the safety of digoxin therapy in patients with acute myocardial infarction. The purpose of our study was to determine whether digoxin therapy is associated with increased mortality in patients with chronic coronary artery disease. We analyzed data from 8173 patients who were screened for participation in the Bezafibrate Infarction Prevention (BIP) trial and who survived an acute myocardial infarction at least 6 months prior to the study. Three-year overall mortality of the 451 (15.5%) patients receiving digoxin (according to the judgement of their treating physician) at the time of screening for BIP participation, was 22.4% compared to 8.3% in the patients who did not receive digoxin. Cardiac mortality was 16.2% in the digoxin-treated group, compared to 4.9% in the non-treated patients. The increased risk associated with digoxin remained statistically significant when patients were stratified according to sex, age groups, functional capacity and the presence of hypertension, diabetes or angina. The administration of digoxin to survivors of an acute myocardial infarction in the chronic phase of their disease, is statistically associated with a 30-50% increase in the risk of overall and cardiac mortality during long-term follow-up. A propensity of increased risk of arrhythmias in ischemic coronary patients may explain this finding.     

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)     

Hypertrophic cardiomyopathy and transmural myocardial infarction without significant atherosclerosis of the extramural coronary arteries

Clinical and morphologic features of transmural myocardial infarction (associated with insignificant or absent atherosclerosis of the extramural coronary arteries) are described in seven patients with hypertrophic cardiomyopathy. Marked chronic congestive heart failure associated with supraventricular arrhythmias occurred in six of the seven patients, each of whom had no or mild left ventricular outflow tract obstruction under basal conditions. No patient had typical angina pectoris, and only one patient had clinically evident acute myocardial infarction. Infarction may have caused cardiac arrest in one other patient, but was “silent” in the remaining five patients.

At necropsy, six of the seven patients had extensive myocardial scarring involving the ventricular septum, left ventricular free wall and one or both left ventricular papillary muscles; in four patients portions of the right ventricular wall were also scarred. Six patients had dilated ventricular cavities, including two who were known to have nondilated ventricular cavities earlier in their clinical course.

It is concluded that transmural myocardial infarction in the absence of significant coronary atherosclerosis is a not uncommon finding (prevalence rate 15 percent) in a population of patients who had died from hypertrophic cardiomyopathy. Although transmural infarction is possibly a secondary event, it more likely contributes causally to the clinical deterioration of some patients with hypertrophic cardiomyopathy, leading to ventricular dilatation and progressive fatal cardiac failure.     

Acute myocardial infarction due to vasospasm induced by prostaglandin

Prostaglandin E (PGE) is the preferred agent for second-trimester pregnancy termination. Hypotension, bradycardia, ventricular arrhythmias, myocardial infarction, cardiac arrest and death associated with PGE have been reported. A case of acute myocardial infarction due to coronary vasospasm induced by PGE is described in the present report. The diagnosis was confirmed by electrocardiography and coronary angiography.