No abstract

Little is known of the clinical significance of myocardial bridges, which may be recognized angiographically as systolic coronary artery narrowing (SCAN). A retrospective review of a 1 year's experience (313 consecutive coronary arteriograms) revealed 5 patients with SCAN, an incidence of 1.6%. SCAN involved the proximal and/or middle segments of the left anterior descending coronary artery in all patients. It is of particular note that the administration of nitroglycerin noticeably accentuated the SCAN phenomenon in each of 3 patients to whom it was administered. Four of the 5 patients had left ventricular hypertrophy due to hypertrophic cardiomyopathy (2), aortic stenosis (1), and hypertension (1). All 5 patients with the SCAN phenomenon had anginal chest pains, and critical obstructive coronary atherosclerosis was observed in only 2 cases. The other 3 patients showed, otherwise normal coronary arteriograms. Thus, myocardial bridges appear to be angiographically manifest predominantly in patients with cardiac hypertrophy. Nitroglycerin, which accentuates SCAN, might be useful as a provocative test to enhance the angiographic recognition of this phenomenon. The possible role of myocardial bridges in the production of myocardial ischemia warrants further investigation.

In this study we attempted to determine if the cold pressor test, a known sympathetic reflexogenic stimulus, could precipitate coronary artery spasm. Thirty-five patients undergoing coronary arteriography for evaluation of chest pain syndromes were given the cold pressor test. During 1 minute of cold pressor stimulation, aortic systolic pressure increased 18.1 ± 9.7 mm Hg (mean ± SD) and heart rate did not change significantly. Focal coronary artery spasm was provoked in seven patients, each of whom had an atheromatous plaque at the site of spasm. Four of six patients with a precatheterization clinical diagnosis of variant angina (group 1) had coronary artery spasm, and two of the four had associated ischemic manifestations. Of 14 patients in whom classic angina (group 2) was diagnosed before cardiac catheterization, two manifested focal coronary spasm. One of 15 patients thought to have atypical chest pain (group 3) manifested spasm. There were no significant differences in baseline variables (aortic systolic or diastolic pressure, heart rate, double product and left ventricular end-diastolic pressure) or hemodynamic response (aortic systolic pressure, heart rate or double product) to cold pressor stimulation between patients in each group and between those who manifested spasm and those who did not. Ventricular ectopy and ventricular tachycardia developed in one patient but were readily reversed with intravenous nitroglycerin. Quantitative angiography showed that the luminal diameter of normal coronary segments significantly decreased in each group of patients in response to cold pressor stimulation, but this response was most pronounced in the variant angina group (-12.7 ± 11.5% from control in group 1, -5.1 ± 10.2% in group 2, and -7.9 ± 9.6% in group 3; p < 0.001 for each group). Patients who are prone to coronary spasm may represent one extreme of a spectrum of reactivity to a coronary vasoconstrictive stimulus. The cold pressor test can provoke focal coronary artery spasm in certain patients and may be a useful nonpharmacologic provocative screening test to aid in the diagnosis of this phenomenon.CORONARY ARTERY SPASM has become the focus of increasing attention. Its role in variant angina is well documented,'-' and it has been observed in patients with classic angina,6 7 unstable angina8 9 and myocardial infarction.10 The transience of coronary artery spasm makes it difficult to diagnose. Consequently, various interventions, primarily pharmacologic, have been used to provoke coronary artery spasm during coronary arteriography. These pharmacologic interventions include the administration of ergot aklaloids,", 12 epinephrine in combination with propranolol,13 and methacholine.14 Thirty-five patients (34 males and one female), mean age of 50.1 years (range 30-62 years), undergoing routine cardiac catheterization and coronary arteriography for evaluation of chest pain syndromes were included in this study. The patients were categorized according to their precatheterization clinical presentation. Group 1 consi...

This study suggests that amlodipine given once daily is efficacious and safe in the treatment of vasospastic angina.

The significance of exercise-induced ST-segment elevation remains unsettled. We reviewed the treadmill tests of 840 consecutive patients and exercise-induced ST-segment elevation was noted in 29 (3.5%). Only eight of these (28%) stopped because of angina. Anterior myocardial infarction (AMI) was found on the resting electrocardiogram in 25 (85%). Angiographic studies performed on 21 showed critical lesions of the left anterior descending (LAD) in 19 (90%) and left ventricular aneurysm in 18 (86%). When all the patiens who had AMI or critical LAD obstruction during the study period were reviewed, only 22% and 18% respectively showed exercise-induced ST-segment elevation, while 64% of the cases with left ventricular aneurysm displayed this phenomenon. Thus, exercise-induced ST elevation seems to reflect the presence of severe coronary artery disease most commonly with an associated left ventricular aneurysm and may relate more to the abnormal wall motion than to the myocardial ischemia per se.