P. Bobba

Coronary arterial spasm as a cause of exercise-induced ST-segment elevation in patients with variant angina.

Four patients with variant angina pectoris exhibited reproducible exercise-induced chest pain ST-segment elevation. Coronary arterial spasm was documented with arteriography during exerciseinduced ST-segment elevation (three patients) or after intravenous administration of ergonovine maleate (one patient). Our observations show that in patients with variant angina exercise can trigger coronary arterial spasm, thus inducing anginal pain ST-segment elevation.

Treatment of angina at rest with nifedipine: A short-term controlled study

The effectiveness of nifedipine in treating angina pectoris at rest was evaluated in 14 patients with frequent ischemic episodes associated with S-T segment elevation or depression. The trial consisted of (1) a 48 hour control period; (2) a placebo period and a period of treatment with nifedipine of 48 hours each; and (3) a second placebo period and a second period of treatment with nifedipine of 24 hours each. The efficacy of treatment was evaluated by continuous electrocardiographic recording to detect painless ischemic episodes. During coronary angiography coronary spasm was demonstrated in five patients. The ergonovine maleate test was positive in seven of eight patients. No statistically significant difference was found in the mean daily number of ischemic episodes between the control period and the first placebo period, or between the control and the second placebo periods. Nifedipine produced a highly significant reduction in the mean daily number of episodes compared with the response to placebo during the first as well as the second period. Nifedipine is effective in angina at rest caused by coronary arterial spasm. The prevention of ischemia may be related to the ability of nifedipine to decrease calcium-dependent coronary muscle tone and to prevent coronary spasm.

Ventricular tachyarrhythmias in prinzmetal's variant angina: Clinical significance and relation to the degree and time course of S-T segment elevation

Fifty-six patients with active Prinzmetals variant angina were studied to determine the incidence and clinical significance of ventricular tachyarrhythmias and the correlation between arrhythmias and degree and time course of S-T segment changes during the ischemic attacks. Twenty-nine patients (Group I) had no ventricular arrhythmias in any of the 1,083 recorded episodes, while 27 patients (Group II) developed arrhythmias in 18% of the attacks. No significant differences in clinical, electrocardiographic, angiographic, or hemodynamic findings could be found between the 2 groups. In 23 of the 27 Group II patients, ventricular arrhythmias developed during maximal S-T segment elevation (occlusion arrhythmias), while in 10 they occurred during resolution of S-T segment changes (reperfusion arrhythmias); 6 of the latter patients also had occlusion arrhythmias. Eight of the 23 patients with occlusion arrhythmias and 6 of the 10 with reperfusion arrhythmias had ventricular fibrillation or ventricular tachycardia. Maximal S-T segment elevation was significantly greater (p less than 0.001) in patients with occlusion arrhythmias than in those without arrhythmias. The episodes with reperfusion arrhythmias were significantly longer (p less than 0.001) and showed a significantly greater S-T segment elevation (p less than 0.001) than those without arrhythmias in Group I patients. This study shows that significant ventricular tachyarrhythmias develop during ischemic attacks in about 50% of patients with active variant angina; clinical and angiographic features are not useful in distinguishing patients with arrhythmias from the others. Our findings suggest that in variant angina ventricular arrhythmias may be due to the effects of both coronary artery occlusion and reperfusion; both types of arrhythmias are correlated with the severity of ischemia, as measured by the degree of S-T segment elevation. Reperfusion arrhythmias also appear to be correlated with the duration of ischemia.

The exercise test in variant angina: results in 114 patients.

One hundred fourteen patients with variant angina performed bicycle exercise stress tests, and were divided into three groups. Group 1 included 37 patients with a normal exercise test. Coronary arteriography revealed absence of significant coronary stenoses in 18 patients, one‐vessel disease in 17 and involvement of two or more vessels in two. Group 2 consisted of 40 patients who had ST‐segment elevation during or just after exercise. Coronary arteriography in these cases revealed absence of significant coronary stenoses in nine patients, one‐vessel disease in 18 and disease of two or more vessels in 13. Group 3 included 37 patients who had ST‐segment depression during exercise. Absence of coronary artery disease was found in only two patients, one‐vessel disease was found in 19 and disease of two or more vessels was found in 16. Sixty‐one patients repeated the exercise test after a mean of 18 months after hospital discharge. Exerciseinduced ST‐segment elevation was no longer present in surgically or medically treated patients; ST‐segment depression was still evident in all the medically treated patients, but was absent in eight of 13 patients who underwent aortocoronary bypass surgery. Exercise testing can be useful in the follow‐up of patients with variant angina and in selecting patients most likely to be helped by bypass surgery.

Significance of exercise-induced ST-segment elevation in patients without myocardial infarction.

SUMMARY Sixteen patients with exercise-induced ST-segment elevation and without a history of myocardial infarction or left ventricular aneurysm were studied. Fourteen complained of angina at rest, which was associated with ST-segment elevation in the same leads where it was recorded during exercise, and two patients had only exertional angina. Exercise-induced ST-segment elevation was generally reproducible in subsequent exercise tests performed in different hours of the day, but exercise tests repeated a mean of 15 months later did not induce this electrocardiographic abnormality. All patients had a marked susceptibility to coronary spasm, as shown by the response to the ergonovine test (12 positive tests in 12 patients) and by the occurrence of spontaneous spasm during coronary arteriography in two patients. In addition, coronary arteriography, performed in seven patients at the time of exercise-induced ST-segment elevation, revealed spasm of a major coronary vessel in all. In two patients we documented that exercise-induced ST-segment elevation was accompanied by a decreased coronary blood flow and increased coronary vascular resistance. We conclude that exercise-induced ST-segment elevation in patients without a history of myocardial infarction or left ventricular aneurysm is caused by coronary spasm of a major coronary vessel.

Dipyridamole Test in Angina Pectoris: Diagnostic Value and Pathophysiological Implications

The value of the dipyridamole test (0.75 mg/kg i.v.) in the diagnosis of angina pectoris was studied in 54 patients with angina pectoris (35 with angina on effort associated or not associated with rest angina and 19 with angina only at rest) and in 12 control subjects. The test induced electrocardiographic signs of ischemia (positive test) in 74% of patients with angina on effort, while it was negative in all cases with angina only at rest and in control subjects. All anginal patients with normal coronary arteries or less than 50% stenosis had a negative test; a positive response was observed in 36, 79 and 60% of cases with one-, two-or three-vessel disease, respectively. Hemodynamic changes with a marked arteriolar vasodilatation were observed both in the negative and in the positive tests. In the positive tests no significant change of double product, blood pressure and left ventricular end-diastolic pressure occurred before ischemia appeared. The results of the study show that dipyridamole as a diagnostic test in angina pectoris has a high specificity but a lower sensitivity than exercise test. The hemodynamic and eletrocardiographic findings in the positive tests suggest that dipyridamole-induced ischemia is due to a flow maldistribution with selective subendocardial ischemia secondary to the coronary arteriolar dilatation caused by the drug.

Transient Left Posterior Hemiblock Report of Four Cases Induced by Exercise Test

Four cases with transient electrocardiographic features which have been attributed to left posterior hemiblock (LPH) are reported. These features were induced by the exercise test in patients with severe coronary artery disease. In all of them the following exercise-induced changes were noted: (1) A shift of the main QRS forces inferiorly and to the right (between +90° and +120°). (2) A definite shift of the initial 0.02 QRS vectors superiorly and to the left, causing a small Q wave to appear in leads II, III, and aVF and/or to disappear from leads I and aVL. (3) A SIQIII pattern. (4) A leftward displacement of the precordial transition zone. (5) An increase of QRS duration in about 0.02 sec. Gradual disappearance of the exercise-induced axis shift was observed in all four cases and these findings were compatible with multiple degrees of “incomplete’ LPH. The occurrence of transient LPH patterns was related to the development of acute, transient injury in the posteroinferior wall of the left ventricle in the presence of segmental or widespread coronary artery disease and chronic posteroinferior damage. Before the exercise test, two patients had electrocardiographic patterns suggesting old myocardial infarction and the other two had repolarization changes related to inferior myocardial ischemia according to the angiographic findings.

Variable threshold of angina during exercise: A clinical manifestation of some patients with vasospastic angina

Two patients complained of chest pain while at rest and during physical activities. However there seemed to be no direct relation between exertional angina and an increasing level of work performed, indicating that these patients had a variable threshold of angina during exercise. In one patient spontaneous chest pain was associated with transient S-T segment changes in precordial leads, and during coronary arteriography the administration of ergonovine induced spasm of the left anterior descending coronary artery. The other patient showed S-T segment elevation in inferior leads during an ergonovine-induced anginal attack and coronary arteriography revealed a spontaneous spasm of the right coronary artery. In both patients repeated exercise tests yielded different results, because the chest pain and S-T segment depression occurred at different work loads with large differences in heart rate-systolic blood pressure product. It is concluded that a variable threshold of angina during exercise is a clinical manifestation in some patients with vasospastic angina and is probably due to the difference in coronary arterial tone at the onset of exercise.

Angiographic demonstration of different pathogenetic mechanisms in patients with spontaneous and exertional angina associated with S-T segment depression

Three patients complained of spontaneous and exertional chest pain, both associated with S-T segment depression in anterior electrocardiographic leads. In each, coronary spasm was demonstrated on coronary arteriography during a spontaneous attack of pain. Coronary arteriograms taken during exercise-induced angina did not show evidence of spastic obstruction; this suggests that exercise-induced chest pain and S-T segment depression were secondary to the increase in oxygen requirements rather than to a sudden decrease in coronary blood flow. Thus, two pathogenetic mechanisms coexisting in the same patient may cause chest pain associated with subendocardial ischemia.

Exercise-Induced RS-T Elevation

In 4 patients in which an exercise test induced an elevation of the RS-T segment and an increase of the R-wave, coronary angiography showed a localized, subocclusive stenosis of the single major coron