Percutaneous transluminal coronary angioplasty in vasospastic angina. Results and technical problems in 13 cases.
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Biomedical subjects
Publications and source records attributed to E Bramucci.
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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.
In order to clarify the role of coronary arterial spasm in the pathogenesis of angina at rest, coronary arteriography was perforned during spontaneous chest pain or following intravenous administration of ergonovine maleate in 40 patients with angina at rest. Coronary vasospasm was demonstrated in 23 patients with ST-segment elevation during chest pain (group I), in 7 with ST-segment depression (group II), and in 4 with both ST-segment depression and elevation (group III). Complete spastic occlusion of the proximal or of the midportion of the left anterior descending artery was always associated with ST-segment elevation in anterior leads. In contrast, transient ST-segment depression in anterior leads was associated with diffuse narrowing of the left anterior descending artery with slow progression of the contrast medium, or complete occlusion of a small branch or of the distal segment of the left anterior descending artery. ST-segment elevation in inferior leads was associated with complete spastic occlusion or with significant spastic narrowing of the right coronary artery or of the circumflex artery. We conclude that coronary spasm can be demonstrated in a selected cohort of patients with angina at rest associated with transient ST-segment changes. In some cases the site and the severity of the spasm may produce varying degrees of ischemia, thus determining the direction of the ST-segment shift.
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.
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The effects of isometric exercise on left ventricular function in 16 patients with chronic coronary heart disease were assessed by measuring left ventricular pressures and volumes under basal conditions and during a sustained effort of 2 minutes 30 seconds at 50% of the maximal effort. In 7 patients (Group I) with abnormal elevation of left ventricular end diastolic pressure (LVEDP) (over 4 mmHg) the end diastolic volume remained unchanged and the diastolic pressure-volume curve was displaced upwards. The ejection fraction fell together with the percentage filling during the first part of diastole with 50% filling occurring after 61% instead of 45% of diastole. The time constant T also increased showing abnormal relaxation. In 9 patients without abnormal elevation of LVEDP on exercise no changes in the other parameters studies were observed. Our results show that pathological elevation of LVEDP during isometric exercise is associated with a decreased ejection fraction and an abnormality of left ventricular relaxation with a reduced rate of filling during protodiastole and an upward displacement of the diastolic pressure-volume curve. The LVEDP alone is therefore an important index of the haemodynamic behaviour of the left ventricle during isometric exercise.
107 patients suffering from angina at rest associated with ST segment changes underwent coronary arteriography. 46 patients showed ST segment elevation during ischemic attacks (group I) while 61 patients exhibited ST segment depression during chest pain (group II). Non-significant coronary artery disease was more frequent in group I patients (group I 15%, group II 5%) as well as one vessel disease (group I 33%, group II 15%) while multivessel disease and left main involvement were more frequent in group II patients (group I 28%, group II 60%). Depression of left ventricular function was found in similar percentage of cases in both groups. During hospitalization all patients were treated with calcium antagonists (Nifedipine 10/20 mg every six hours) and/or nitrates (2% nitroglycerin ointment 2 inches every six/four hours) with one death (occurring after coronary arteriography) and eleven non-fatal myocardial infarctions. 50 patients underwent coronary bypass grafting with four perioperative deaths and six nonfatal myocardial infarctions. Most of the surgically treated patients were poorly responsive to medical treatment and had multivessel disease or left main involvement. Since these features are known to be related to a poor prognosis with medical treatment, surgical results in such patients seem satisfactory.
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Four patients with variant angina pectoris exhibited reproducible exercise-induced chest pain and ST-segment elevation. Coronary arterial spasm was documented with arteriography during exercise-induced 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 and ST-segment elevation.
31 patients presenting with Prinzmetal variant angina were divided into three groups according to their angiographic appearances. Group I comprised 9 patients with normal or coronary arteries with lesions less than 50% narrowing. Group II comprised 12 patients with single vessel disease. Group III comprised the other 10 patients with significant lesions on two or all three principal arteries. No clinical or electrocardiographical differences were found between the groups as to age, sex or the clinicapresentation of the chest pain. Most patients with normal or nearly normal coronary arteries had normal electrol cardiogrammes between attacjs (8 out of 9) and electrical changes mainly over the inferior wall (8 out of 9). Exercise electrocardiography reproduced ST elevation in 4 of the 9 patients but, in contrast to the patients in the other two groups, never ST depression. However, these features are not specific for patients in Group I as they were observed in 4 patients in the other two groups. Spontaneous or induced coronary spasm were observed in 27 patients, confirming its role as the mechanism of Prinzmetal angina, whatever the anatomical appearance of the coronary tree.
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The effects of atrial pacing (A.P.) on the myocardial balance of inorganic phosphate (Pi) were studied in 11 patients with coronary atherosclerosis and pacing-induced angina (Group C) and in 5 normal subjects (Group N). During A.P. in group C 64% of patients had myocardial loss of Pi, statistically significant (p less than 0,025) always with concomitant reduced myocardial extraction or production of lactate, but only 70% of patients with reduced myocardial extraction or production of lactate had myocardial loss of Pi. In only 1 p. of group N myocardial loss of Pi with normal lactate extraction was observed. These data show that during pacing-induced ischemia there is a negative myocardial balance of Pi, that can be used as a metabolic indicator of ischemia, but less reliable than lactate reduced extraction or production.
We have seen a case with spasm of the right coronary artery coming on during exercise ergometry in the course of a coronary arteriogram. The patient had angina pectoris spontaneously and on exercise. Bicycle ergometry was repeated four times by the same method, and was positive in three; in two of these there was angina and ST elevation in II, III, aVF, and ST depression in I, aVL and V2 to V5. On one occasion the test was negative, the patient having taken a trinitrin tablet one hour before the test. Repeating the exercise test during coronary arteriography showed spasm of the right coronary artery and elevation of the segment ST in II, III and aVF; this disappeared after trinitrin treatment.