Variant angina culminating in coronary thrombosis and myocardial infarction.
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Biomedical subjects
Publications and source records attributed to E C Schick.
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The systemic, pulmonary, and limb circulatory responses to the angiotensin-converting enzyme inhibitor, captopril, were determined in 10 patients with severe, chronic heart failure. Immediate effects include sustained reductions in arterial pressure and pulmonary capillary wedge pressure and improvement in cardiac output, as reported with other vasodilator drugs. Calf vascular resistance did not change despite substantial lowering of total systemic vascular resistance, indicating that arteriolar dilatation occurred on a selective basis. Transient reduction in mean right atrial pressure paralleled slight calf venodilatation, but effects upon the resistance vasculature predominated. Plasma renin activity and norepinephrine concentrations increased after therapy in the acute phase as plasma aldosterone levels consistently fell. During maintenance oral treatment over 7 to 15 months (median, 11.5 months), patients displayed symptomatic benefit, improved functional capacity, and greater exercise tolerance. No major adverse reactions developed. These findings suggest that angiotensin converting enzyme inhibition with captopril in congestive heart failure patients improved cardiocirculatory function through selective arteriolar dilatation. The reordering of regional blood flow which appears to result from release of angiotensin-mediated vasoconstriction, as well as the suppression of aldosterone, may underlie the prolonged benefit observed in these patients. This oral vasodilator appears to represent an effective adjunct for the treatment of advanced, chronic heart failure refractory to conventional measures.
The carotid pulse method of recording systolic time intervals is limited by significant motion-induced artifact, making it unsuitable for studying patients during exercise. As an approach to overcoming this limitation, a new method utilizing the blood velocity profile of the superficial temporal artery measured by Doppler ultrasound has been developed. When compared with the values obtained from the conventional carotid pulse method, Doppler-derived left ventricular ejection time and preejection period showed excellent correlation (r = 0.99 for both) and the Doppler-derived measurements showed little intra- or interobserver variability. Studies performed during treadmill exercise showed that in 8 of 10 subjects, suitable tracing could be recorded through stage 3 of the Bruce protocol, confirming the enhanced stability of the technique compared with the carotid pulse method.
An increase in QRS amplitude with S-T elevation occurs during the acute phase of myocardial infarction, coronary ligation and variant angina. Ischemic conduction delay, postulated as the cause, has not been well characterized. Six patients with transient chest pain, S-T elevation and increase in R-wave voltage also displayed concomitant shift of the frontal QRS axis toward the locus of injury. Electrocardiographic considerations suggest that regional ischemic block, not true hemiblock as has been suggested, offers the most inclusive explanation, providing previously neglected clinical confirmation of experimental observations.
Four patients underwent exercise testing because of a history of pain in the chest; all four developed marked elevation of the S-T segment only during recovery after exercise. Three of the four patients showed ST-segment depression during exercise, but ST-segment elevation was absent until two or more minutes after cessation of exercise. ST-segment elevation after exercise was accompanied by hypotension in three patients and by ventricular arrhythmias in one. Subsequent coronary angiographic studies revealed normal or minimally diseased coronary arteries in two patients and significant coronary lesions in the other two. Review of the literature shows that contrary to the prevailing belief, over half of the patients with Prinzmetal's variant angina have electrocardiographic changes diagnostic of ischemia during exercise testing. Over half of the patients with abnormal findings on tests during exercise display ST-segment elevation as a manifestation of ischemia; however, delayed ST-segment elevation of the type seen in these four patients is distinctly uncommon, having previously been described in only three individual case reports. The pathophysiology of this response is uncertain but may relate to rapid alterations in the autonomic balance during recovery after exercise.