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.     

Simultaneous multivessel coronary artery spasm demonstrated by quantitative analysis of thallium-201 single photon emission computed tomography

Thallium-201 myocardial scintigraphy with quantitative analysis of emission computed tomography was performed during episodes of angina in 19 patients with variant angina and nearly normal coronary arteriographic findings. Eleven patients (group I) were shown by arteriography to have spasm in 2 or more large coronary arteries. Eight patients (group II) had spasm in only 1 coronary artery. In 7 patients in group I, significant diffuse perfusion defects simultaneously appeared in multiple coronary artery regions on the scintigram (group IA). The extent and severity of the perfusion defect as measured by thallium-201 tomography were significantly greater in group IA than in group II (p less than 0.001 and p less than 0.01, respectively). The duration of transient ST-segment elevation during the attack in group IA was significantly longer than in group II (p less than 0.001). The incidence of ventricular arrhythmias, including ventricular tachycardia, or complete atrioventricular block during the anginal attack was significantly higher (p less than 0.05) in group IA than in group II. In all study patients, neither attack nor scintigraphic perfusion defect appeared on the repeat test after oral administration of nifedipine. In conclusion, multivessel coronary artery spasm simultaneously appears and causes the attack in many patients with variant angina and nearly normal coronary arteriographic findings, and myocardial ischemia due to simultaneous multivessel coronary spasm is likely to be more extensive and severe, persist longer and have a higher frequency of potentially dangerous arrhythmias than that due to spasm of only 1 coronary artery.     

Pure arrhythmic form of the pre-infarction syndrome or spasm responsible for myocardial necrosis

A 74 years old man was admitted as an emergency for syncopal attacks due to recurrent ventricular fibrillation (VF). These attacks were observed at the height of myocardial ischaemia as shown by ST elevation in Leads II, III and RV without associated anginal pain. Inferior myocardial infarction occurred during recurrent VF on the 4th day; the outcome was favourable. Coronary angiography was performed on the 10th day and showed double vessel disease; ergometrine (0.2 mg) induced anginal pain and ST elevation in Leads II, III and AVF. A good clinical result was obtained by calcium antagonists with an 18 months follow-up. Coronary spasm, documented in this case by the ergometrine provocation test, is now recognised as a cause of resting angina, effort angina and also some cases of myocardial infarction. This report suggests that coronary spasm may also induce apparently isolated severe ventricular arrhythmias without associated chest pain, which raises the question as to whether arrhythmias induced by spasm could play a primary role in aggravating myocardial ischaemia, leading to myocardial infarction.     

Newly developed stenocardia: lack of ventricular electrical instability in the absence of acute myocardial ischemia

A total of 130 patients with angina of new onset were examined within first 3 months of the disease. Macrofocal myocardial infarction survivors were not admitted to the study. The investigation included selective coronaro-angiography and ventriculography, Holter's ECG monitoring over 24 to 48 hours and bicycle ergometry. Programmed right-ventricular electric stimulation was conducted in 41 patients. Only one major coronary artery was affected in 78% of patients. Left-ventricular ejection fraction nearly always exceeded 50%. Groups of ventricular extrasystoles were detected by ECG monitoring in 10.8% and by bicycle ergometry in 2.5%. No signs of electrical instability were ever detected at programmed stimulation, done in the absence of anginal attacks. Groups of ventricular extrasystoles were more common, as compared to single extrasystoles (p less than 0.001), in acute myocardial ischemia, being more frequently associated with unstable rather than stable angina of new onset (p less than 0.05). In early coronary heart disease, signs of electric ventricular instability are not detectable in the absence of myocardial ischemia.     

Incidence of ventricular arrhythmias during transient myocardial ischemia in patients with stable coronary artery disease

To determine the incidence of ventricular arrhythmias related to episodes of transient myocardial ischemia during ambulatory electrocardiographic (ECG) monitoring, 97 patients with stable angina pectoris, angiographically proved coronary artery disease and an abnormal exercise test were studied. A total of 573 episodes with ST segment depression were documented: in 118 episodes (21%) the patients were symptomatic and in 455 (79%) they remained asymptomatic. Ventricular arrhythmias (greater than 5 premature ventricular beats/min, bigeminy, couplets or salvos of premature ventricular beats) occurred during 27 (5%) ischemic episodes in a subset of 10 patients (10%) (group A). The other 87 patients (90%) (group B) showed exclusively ischemic episodes without ventricular arrhythmias. Comparison of patients in group A and group B showed no differences in hemodynamic, angiographic, exercise testing and ambulatory ECG monitoring data. Ischemic episodes with and without ventricular arrhythmias showed a similar duration and amplitude of ST segment depression and a comparable heart rate at the onset of ischemia. Both types of ischemic episodes, with and without arrhythmias, occurred predominantly during the morning hours between 6:00 AM and noon, and both types remained asymptomatic to within similar percentages. The data demonstrate that ventricular arrhythmias are related to transient myocardial ischemia in only a few patients with stable angina pectoris; these arrhythmias are related neither to the degree of ischemia during ambulatory ECG monitoring nor to the occurrence of anginal symptoms.     

Comparative sensitivity of intracoronary injection of acetylcholine for the induction of coronary spasm in patients with various types of angina pectoris

To elucidate the possible contribution of coronary artery spasm to the pathogenesis of angina pectoris, coronary arterial responses to intracoronary injection of acetylcholine were examined in patients with various types of angina pectoris. Coronary artery spasm with chest pain and/or electrocardiographic ischemic changes was angiographically demonstrated in 50 (85%) of 59 patients with angina pectoris. The sensitivity for coronary spasm was 92% (24 of 26) in patients with rest angina, 100% (16 of 16) in patients with both rest and effort angina, and 59% (10 of 17) in patients with effort angina, while it was only 6% (1 of 16) in patients without coronary artery disease. When patients with effort angina were subdivided according to the variability of anginal threshold for exertional angina, the sensitivity for coronary spasm was as high as 90% (9 out of 10) in patients with variable-threshold angina. In contrast, coronary spasm was less frequently (p less than 0.05) induced in patients with fixed-threshold angina (1 of 7, 14%). These results suggest that coronary arteries in patients with angina pectoris are quite susceptible to acetylcholine except in those patients with stable exercise tolerance or anginal threshold. Thus coronary artery spasm appears to play a significant role for the pathogenesis of angina pectoris in a large proportion of patients with effort angina as well as in patients with rest angina.     

A case of unstable angina pectoris associated with an active phase of polymyositis]

We report a case of unstable angina in an active phase of polymyositis. A 51 year-old man was admitted with a diagnosis of polymyositis and unstable angina with ST elevation on prolonged rest chest pain. Rest anginal attack which had been refractory to conventional antianginal medications was controlled by high dose of glucocorticosteroid. Electrocardiography revealed multifocal premature ventricular contraction. Since silent ischemia on exercise persisted, percutaneous transluminal coronary angioplasty (PTCA) was performed on a stenotic lesion in the left anterior descending artery. Since there was recurrent anginal attack, re-PTCA was carried out at the same site. He was discharged in a good condition. This case is considered to be associated with cardiac involvement of polymyositis because of ventricular arrhythmia, persistent increased serum levels of CPK-MB, and the marked benefits of corticosteroid against unstable angina. In addition, clinical manifestations, coronary arteriographic findings, and increased plasma levels of thrombin-antithrombin III complex suggest that cardiac involvement in polymyositis accelerates intracoronary thrombus formation and/or coronary spasm.     

Different clinical and prognostic aspects of angina pectoris in unstable phase

The purpose of this study was to focus on the clinical and angiographic characteristics of 113 patients with crescendo angina (Group I) as compared to 187 patients with angina of new onset (Group II), selected from a series of 474 consecutive subjects, admitted to our clinic between January 1976 and July 1983 because of recurrent episodes of spontaneous angina, who underwent cardiac catheterization and coronary angiography within one month of hospitalization. Group I patients showed a greater incidence of prior transmural myocardial infarction (p less than 0.01), arterial hypertension (p less than 0.01), multivessel disease (p less than 0.01) and a lower value of left ventricular ejection fraction (p less than 0.01) than Group II patients. In the latter group of patients anginal episodes were more frequently associated with S-T segment elevation than with S-T segment depression (p less than 0.001), while the opposite was found in patients with crescendo angina. Survival curves up to five years showed that medically treated patients with crescendo angina had a worse long-term prognosis than patients with unstable angina of new onset (p less than 0.01). On the contrary no difference was found between the surgically treated patients of the two groups. Our data suggest that the more diffuse involvement of the coronary tree associated with a more depressed left ventricular function may result in an unfavorable long-term prognosis in patients with crescendo angina as compared to those with unstable angina of new onset. Such a difference between the two groups was abolished by surgical treatment.     

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.

In contrast to findings in patients manifesting only typical exertional angina, the hemodynamic findings during spasm were those of a hypodynamic state. Left ventricular systolic pressure decreased from 138.9 ± 6.0 (mean ± standard error of the mean) to 113.2 ± 6.2 mm Hg; left ventricular end-diastolic pressure did not change significantly. Myocardial lactate extraction during spasm was invariably markedly reduced: −53.19 percent ± 15.44 (P < 0.001). However, the effect of coronary sinus pacing on myocardial lactate extraction was not significantly abnormal: +15.74 percent ± 6.66.

The respective roles of medical and surgical intervention are uncertain. Only 3 patients had a completely satisfactory pharmacologic response to nitrates alone or in combination with propranolol, and the condition of 5 others was partially improved; the remaining 21 patients were judged intractable to medical management. Coronary bypass surgery was performed as the ultimate recourse in 18 patients. However, short-term results reveal that only nine (50 percent) showed improvement, four (22 percent) had myocardial infarction during or after surgery and four (22 percent) died.

These studies confirm that coronary arterial spasm is a definite pathogenetic factor in a variety of acute myocardial ischemic syndromes. The incidence and full clinical significance of this functional disorder remain to be determined.     

Early exercise testing after stabilization of unstable angina: correlation with coronary angiographic findings and subsequent cardiac events

To evaluate the safety and diagnostic use of exercise testing in patients with unstable angina, 78 patients underwent submaximal exercise testing and diagnostic cardiac catheterization early after stabilization of their pain. Thirty-six patients (46%) had a positive exercise test manifested as angina or ST segment depression of greater than or equal to 0.1 mV during or immediately after exercise. Thirty-three of 36 patients (92%) with a positive exercise test had multivessel coronary disease compared to 18 of 42 patients (43%) with a negative exercise study (p less than 0.001). Twenty-two of 36 patients (61%) with a positive exercise test had three-vessel disease compared to 12 of 42 patients (29%) with a negative test (p = 0.004). The sensitivity of exercise testing in detecting multivessel disease was 65%, specificity 89%, predictive value of a positive test 92%, predictive value of a negative test 57%, and overall accuracy 73%. When the 42 patients taking beta blockers were examined, these values were essentially unchanged. Ventricular arrhythmias during exercise testing were associated with a lower ejection fraction, 61.1 +/- 12.5%, compared to 67.9 +/- 11.1% in patients without ventricular arrhythmias (p less than 0.05). Submaximal exercise testing after stabilization of patients with unstable angina is safe and useful in evaluating patients for the presence of multivessel coronary artery disease.     

Accelerated coronary atherosclerosis revealed by arrhythmogenic coronary spasm

Coronary artery spasm is sometimes associated with life-threatening ventricular arrhythmias. Based on intravascular ultrasound findings, it appears that coronary artery spasm promotes negative arterial remodeling, suggesting that patients with coronary artery spasm might be at higher risk of accelerated coronary atherosclerosis. We report the cases of 3 patients with ventricular arrhythmia secondary to coronary artery spasm complicated by accelerated coronary atherosclerosis. Consequently, coronary disease progression should be considered in the case of angina pectoris recurrence in patients with coronary artery spasm, especially in those with coronary artery spasm complicated by ventricular arrhythmia.     

Influence of nifedipine on left ventricular systolic and diastolic function: Relationships to manifestations of ischemia and congestive failure

In addition to the favorable effects of calcium antagonists on symptoms related to coronary spasm, we recently documented preclusion of ergonovine-induced coronary spasm angiographically in four patients with proved Prinzmetal's angina.To determine whether nifedipine has similar “relaxing” or negative inotropic actions on left ventricular myocardial function, we studied 19 patients with various degrees of left ventricular dysfunction before and after nifedipine (20 mg sublingually) during cardiac catheterization. Left ventricular afterload was reduced, with a significant (13 percent) decline in arterial pressure; left ventricular diastolic pressures were unchanged. Left ventricular ejection function was augmented, with significant increases in ejection fraction (14 percent), mean velocity of circumferential fiber shortening (41 percent), systolic ejection rate (25 percent), and end-systolic $\text{pressure}\text{volume}$ ratio (19 percent). Cardiac index increased significantly by 16 percent. Early diastolic relaxation, diastolic pressure-volume relations and end diastolic stiffness remained unchanged after nifedipine. When patients were categorized (Group I: left ventricular end-diastolic volume ≤ 90 ml/m², end-diastolic pressure ≤ 20 mm Hg; Group II: end-diastolic volume > 90 ml/m², end-diastolic pressure > 20 mm Hg), highly pertinent differences were apparent. Nifedipine significantly reduced left ventricular preload and end-diastolic pressures in Group II but not in Group I patients. Enhancement of left ventricular ejection function in Group II patients was significantly more prominent than that in patients with normal baseline function. Although diastolic properties were insignificantly changed overall, the left ventricular diastolic pressure-volume relation was displaced downward by nifedipine in Group II, but not in Group I patients. Both systemic and pulmonary vascular resistance declined significantly more in Group II patients, whereas cardiac index was increased 25 percent compared with a negligible change in group I patients. These results indicate beneficial effects of nifedipine on myocardial oxygen requirements, particularly in patients with impaired left ventricular function in whom left ventricular preload and afterload were both significantly reduced, cardiac index augmented and the pressure-volume relation shifted downward.To confirm predicted symptomatic benefits in 13 other patients with fixed coronary, disease, incremental atrial pacing to anginal threshold was performed before and 30 minutes after nifedipine (20 mg sublingually). Mean paced heart rate at onset of angina increased 19.3 percent after nifedipine. Concomitantly, aortic pressure decreased significantly by 22.1 percent at the onset of angina; double product was unchanged at the anginal threshold. Thus, although left ventricular afterload was reduced by nifedipine, the anginal threshold was unchanged in terms of myocardial oxygen requirements.In concert, these results indicate that therapeutically effective influences of nifedipine in patients with fixed coronary disease are attributable basically to hemodynamic alterations consequent upon left ventricular afterload reduction. Nevertheless, such effects imply therapeutic benefit, the reduced afterload concomitantly permitting greater exercise-induced tachycardia before the anginal threshold is reached.     

Reproducibility of functional classification in patients with stable angina pectoris

Diagnostic indices based on various sets of signs were developed to define functional classes of angina pectoris. At the same simultaneous application of clinical parameters (age, conditions for onset of anginal episodes and their arrest, the number of weekly anginal episodes, the level of daily exercise, over 1-mm ST segment depression, resting ECG signs of left ventricular hypertrophy, etc.) and bicycle ergometer testing data (cardiac output, peak exercise heart rate, etc.) augmented the accuracy and reliability of identification of a functional class in patients with stable angina. The diagnostic indices are highly reproducible and may be useful in the assessment of the course of the disease and its prognosis in patients with coronary heart disease.     

Increased QT dispersion in patients with Prinzmetal's variant angina and cardiac arrest

OBJECTIVES: We sought to compare QT dispersion in patients presenting with Prinzmetal's variant angina complicated by cardiac arrest or syncope and patients with uncomplicated variant angina. BACKGROUND: Despite the usually benign course of treated Prinzmetal's variant angina, a proportion of vasospastic angina patients develop ventricular arrhythmias and sudden death in association with coronary spasm. Increased QT dispersion has been suggested to increase susceptibility to ventricular arrhythmias in patients with coronary artery spasm. METHODS: We studied 25 consecutive patients (mean age 58 years; 14 men) with classical Prinzmetal's variant angina and documented coronary artery spasm. None of the patients had coronary artery stenoses < or =40%. Five patients had suffered a documented cardiac arrest, two had recurrent syncope and 18 had no arrhythmic events or syncopal episodes. In all patients QT dispersion (QT maximum-QT minimum in every ECG lead) was measured on the baseline 12-lead electrocardiogram at study entry using a digitising board. RESULTS: Mean (+/-S.D.) QT dispersion of study patients was 62.3+/-19.5 ms. QT dispersion in patients with cardiac arrest and syncope (79.4+/-17.3 ms) was significantly higher compared to patients with no such events (56.3+/-16.9 ms), (95% CI 7.5-38.8, P=0.005). No significant clinical, biochemical or angiographic differences were found between patients with and those without cardiac arrest or syncope. CONCLUSION: QT dispersion is increased in patients with Prinzmetal's variant angina complicated by cardiac arrest and syncope compared to patients without such events. Increased QT dispersion may be both a substrate for sudden cardiac death and a marker of risk in patients with Prinzmetal's variant angina.     

Ventricular arrhythmias in patients with rest angina: correlation with ST segment changes and extent of coronary atherosclerosis

Major ventricular arrhythmias occurring concurrently with myocardial ischemia are presumed to be the most frequent mechanism for sudden cardiac death. Two hundred eighteen catheterized patients with angina pectoris at rest were reviewed to identify clinical, ECG, and arteriographic features that might correlate with the presence of serious ventricular arrhythmias occurring during episodes of rest pain. Ventricular arrhythmias during episodes of rest pain were significantly more common in patients who manifested transient ST segment elevation in the anterior leads and in patients with marked transient ST segment shifts (greater than 5 mm). Ventricular arrhythmias during episodes of rest pain were not more common in patients with extensive coronary artery disease.     

Disorders of cardiac rhythm and conduction during attacks of stenocardia

Heart rhythm and conductivity disorders, developing during anginal attacks, and their relation to the pattern of myocardial ischemia have been studied, using 24-hour ECG monitoring, in 60 patients with stable angina, and in 67 patients with unstable angina. Heart rhythm and conductivity disorders at the ventricular level were much more common in Prinzmetal's angina (73%), as compared to the attacks involving ST depression (10%). Their incidence depended both on the direction and magnitude of ST displacement. The probability of supraventricular arrhythmias was unrelated to the magnitude and direction of ST displacement. They tended to develop during the attacks, accompanied by slanting ST depressions (43%) rather than flat ones (8%). Arrhythmias were considerably more common as a complication of the attacks of unstable angina (42%) rather that stable angina (15%) owing to more severe myocardial ischemia.     

Ventricular arrhythmias during unstable angina pectoris.

In order to study the occurrence and frequency of ischemia-induced ventricular arrhythmias, we analyzed 105 episodes of spontaneous angina pectoris occurring at rest in 28 hospitalized patients with unstable angina pectoris and proved coronary artery disease. Of 24 patients with serious ventricular arrhythmias during pain, 17 (57%) were arrhythmia-free during monitoring. In the other four patients, 17 of 29 (59%) pain episodes were associated with serious ventricular arrhythmias, and three of these four had serious ventricular arrhythmias during pain-free periods. Each patient tended to manifest the same type of arrhythmia during repeat episodes of pain. It appears that continuous electrocardiogram (ECG) monitoring is important during the initial hospitalization of the patient with unstable angina. The presence of ventricular arrhythmias during pain-free periods indicates a high risk for serious ventricular arrhythmias during episodes of spontaneous pain. These patients should be considered for continued ECG monitoring and antiarrhythmic therapy.     

Transient predominant right ventricular ischemia caused by coronary vasospasm

This study describes the clinical experience with four patients with variant angina caused by spasm of the right coronary artery who were assessed for evidence of right ventricular involvement. The patients were suspected of having predominant right ventricular ischemia on the basis of normal thallium-201 scans, left ventricular ejection fraction, regional wall motion assessed by equilibrium radionuclide angiography (RNA), two-dimensional echocardiographic findings, and left ventricular hemodynamics; all procedures were performed during transient ST segment elevation in the inferior leads. Right ventricular ischemia was documented in four patients by first-pass radionuclide studies and phase analysis of RNA, and in three patients by simultaneous right and left hemodynamic monitoring. The clinical findings from these four patients are compared with those from four other patients with similar electrocardiographic changes, coronary anatomic distribution, and documented right coronary spasm but with evidence of left ventricular involvement as documented by abnormal thallium-201 scintigraphy, RNA, two-dimensional echocardiography, and left hemodynamics during ischemic episodes. Although preliminary, these data indicate the existence of prevalent right ventricular ischemia during variant angina caused by right coronary vasospasm. This condition should be suspected whenever typical anginal symptoms and/or ischemic electrocardiographic changes are accompanied by normal thallium-201 scintigraphic findings and/or normal left ventricular function as assessed by RNA, echocardiography, and left hemodynamic monitoring. Among noninvasive procedures, first-pass radionuclide study and phase analysis of RNA represent suitable techniques for detecting transient right ventricular dysfunction.     

Vasospastic ischemic mechanism of frequent asymptomatic transient ST-T changes during continuous electrocardiographic monitoring in selected unstable angina patients

Asymptomatic episodes of ST segment and/or T wave changes are often reported during Holter monitoring in patients with angina pectoris. However, the interpretation of such changes is debated relative to silent myocardial ischemia. We studied 11 patients admitted to the CCU because of frequent episodes of unstable anginal attacks who had undergone repeated periods of Holter monitoring, characterized by predominantly occurring asymptomatic episodes of ST segment and/or T wave changes associated with less frequent typical anginal attacks. In a total of 89 days of Holter monitoring, the patients evidenced 520 episodes of transient ECG changes including 180 of ST elevation, 73 of ST depression, and 267 of T wave alterations. Only 12% of episodes were symptomatic. Coronary injection during asymptomatic ST-T changes was performed in eight patients. In six it was possible to document spontaneous coronary spasm. In seven patients ergonovine administration induced anginal pain, ST-T changes, and coronary spasm. In all patients the anginal attacks completely disappeared with medical treatment and the asymptomatic episodes were abolished in six and reduced in four. Our findings support the hypothesis that in certain selected unstable anginal patients, transient asymptomatic ECG changes are caused by acute myocardial ischemia.     

Anatomo-functional substrate of high risk arrhythmia after myocardial infarct

Ventricular arrhythmias detected in the late-hospital phase of myocardial infarction have been identified as a risk factor for sudden death, being their prognostic value independent of ventricular function. However, relations between both factors are not clarified. In order to study hypothetic associations between ventricular arrhythmias and some clinical, hemodynamic and angiographic variables, 60 patients (52 males, 8 females) underwent 24-hour Holter recordings and cardiac catheterization with left ventricular and coronary angiographies, 3-5 weeks after hospital admission. Past history data, acute phase complications and hemodynamic and angiographic results were compared between patients with and without significant ventricular arrhythmias during Holter monitoring (10 or more PVC's/hour and/or repetitive forms). No significant differences were found between both groups neither in mean age nor in the incidence of previous angina or infarction, cerebral ischemia, diabetes, lipid disorders or subjective feeling of being under psychological stress. Prior history of arterial hypertension was, however, significantly more frequent in patients with ventricular arrhythmias (53.3% vs 17.8%; p = 0.0183). No differences were observed in the localization of the infarct or in the complications during the acute phase (CPK peak, Killip's score, angina after 24 hours of evolution, intraventricular or A-V conduction disorders and supraventricular and ventricular arrhythmias). Among hemodynamic data, only left ventricular and aortic systolic pressures were different in both groups, being significantly higher in patients with ventricular arrhythmias. There were not differences in left ventricular segmentary contraction and in number of coronary vessels involved. To conclude, significant ventricular arrhythmias were recorded in 25% of patients.(ABSTRACT TRUNCATED AT 250 WORDS)