Multivessel coronary spasm as a cause of ischemic syncope in angina at rest.
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Biomedical subjects
Publications and source records attributed to P Bobba.
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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.
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Presence of rate-dependent (RD) intraventricular conduction defects (IVCD) was documented by inducing variations in heart rate in 30 acute myocardial infarction (AMI) patients (10 right bundle branch block, six left bundle branch block, 13 left anterior hemiblocks, and two left posterior hemiblocks). Five IVCDs were tachycardia-dependent (TD), 20 were bradycardia-dependent (BD), and six were both TD and BD. In TD blocks shortest cycles showing normal intraventricular conduction ranged from 410 to 1330 msec (697 +/- 84 SE); in BD blocks longest cycles with normal intraventricular conduction ranged from 450 to 1450 msec (962 +/- 52). In 60% of cases intermittent incomplete RD blocks were also present. In one patients RD-IVCD intermittency remained until discharge; in the others it lasted from 4 minutes to 10 days. Afterwards 19 RD-IVCDs disappeared and four became stable; six patients died during RD-IVCD intermittency period. Disappearance of RD block was preceded by gradual reduction in cycle length showing TD block and lengthening of cycles stopped beats with BD block. Serial observation of RD-IVCDs provides information about sequence of electrophysiologic effects on the intraventricular conduction system in clinical AMI.
The effectiveness of nitroglycerin ointment in vasospastic angina pectoris at rest was evaluated in 10 patients selected for study. The study was performed after a 24 hour control period, and a randomized single-blind crossover experimental design was followed. Two percent nitroglycerin ointment (15 mg) or placebo ointment was administered every 6 hours for a period of 48 hours each; the first treatment period was followed by a second in which each preparation was used for a 24 hour period. All patients were hospitalized in the coronary care unit; an objective evaluation was carried out using a multichannel electrocardiographic recording to assure recognition of the painless ischemic episodes. Coronary angiography showed critical stenosis of one or two vessels in 9 of the 10 patients; spasm was demonstrated in 3. Results of the ergonovine test were positive in nine of nine patients. Nitroglycerin ointment produced a significant reduction in the mean daily number of episodes during the first (12.5 +/- 3.9 versus 0.5 +/- 0.4, p less than 0.02) as well as the second treatment period (10.6 +/- 3.8 versus 0.6 +/- 0.4, p less than 0.02). These results demonstrate that nitroglycerin ointment provides effective, long-lasting protection against angina due to coronary spasm.
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.
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.
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. Exercise-induced 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.
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A patient admitted for evaluation of repeated episodes of faintness not associated with chest pain is presented. The episodes were caused by marked sinus bradyarrhythmias secondary to ischemic attacks with inferior ST-segment elevation, no accompanied by anginal pain. Medical treatment with nifedipine was able to prevent both the ischemic attacks and cardiac rhythm disturbances associated with acute ischemia. This case shows that ischemic pathogenesis of syncopal attacks should not be ruled out even in the absence of chest pain and that the attacks may be prevented by treating their primary cause.
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