Vasodilator therapy has been shown to improve ventricular function in patients with left ventricular failure complicating acute myocardial infarction. Sublingual nitroglycerin also improves ventricular function in these patients but its effects are transient and variable. Infusion of intravenous nitroglycerin in 12 patients with acute infarction resulted in a decrease in left ventricular filling pressure from a mean of 22 plus or minus 2 mm Hg to 12 plus or minus 1 mm Hg (P less than 0.001) associated with a 7 mm Hg decrease in mean arterial pressure (P less than 0.05). Since stroke work index did not change significantly, this represents and improvement in ventricular performance and/or an alteration in ventricular compliance. All six patients in whom serial precordial mapping studies were performed showed a decrease in sigma ST (P less than 0.001). These findings suggest that intravenous nitroglycerin improved left ventricular function and decreased the extent of myocardial ischemia. Longer infusion may act to preserve borderline ischemic myocardium and thus limit infarct size.

Six patients who had documented coronary spasm and no coronary artery with organic obstruction greater than 50% developed angina and ST-segment elevation on exercise testing. Oral verapamil, 160-480 mg/day, prevented exercise-induced ischemia in all patients and increased maximal work capacity from 611+/- 250 kpm to 808 +/- 160 kpm (p less than 0.02). In two patients, a relationship between the prevention of exercise-provoked ischemia and the plasma concentration of verapamil was demonstrated, and in one of these, the relationship had a diurnal pattern. Patients with variant angina may develop coronary spasm on effort and often respond to verapamil.

SUMMARY Exercise-induced ST-segment elevation in leads V1 and/or aVL in the absence of anterior Q waves occurred in 46 We conclude that during 12-lead exercise electrocardiography, ST-segment elevation in V and/or aVL in the absence of anterior Q waves predicts anterior myocardial ischemia and LAD disease.ST-SEGMENT ELEVATION during exercise electrocardiography in patients without resting Q waves is uncommon,'13 but when present, it indicates a region of severe myocardial ischemia. 1, 4The site of STsegment elevation during exercise, in contrast to the site of ST-segment depression,5 appears to predict the site of myocardial ischemia and associated coronary artery obstruction.1 2, 4, 6In a previous study in patients with one-vessel disease and no resting Q waves, we found that although ST-segment elevation during exercise was infrequent in most leads, 52% of the patients with LAD disease showed ST elevation in leads V1 and/or aVL.' The purpose of this study was to determine the significance of ST-segment elevation during exercise in leads V1 or aVL in the total population of patients undergoing 12-lead exercise electrocardiography, exercise thallium-201 myocardial perfusion scanning and coronary arteriography to assess coronary artery disease. Exercise-induced ST-segment elevation in V1 and/or aVL in the absence of ECG evidence of previous anterior myocardial infarction (defined by Q waves in leads V1-V3) was found in 46 patients (44 men and two women); these patients form the study group. Of the remaining 192 patients, 144 (126 men and 18 women) had no ECG evidence of previous anterior myocardial infarction and form the comparison group. Methods Exercise ElectrocardiographyThe patients were exercised maximally on an upright bicycle ergometer using a graded multistage continuous protocol7 until they experienced chest pain, breathlessness or fatigue. Leads were placed in the standard location recommended by Mason et al.8 and a 12-lead ECG was recorded before and during each minute of exercise and recovery using an Avionics three-channel Exerstress 400 unit.The ECGs were interpreted by two independent observers according to the criteria of the American Heart Association.9 During and after exercise, each lead of the ECG was analyzed for ischemic STsegment changes: 1 mm or greater horizontal or downsloping ST-segment depression below the baseline, lasting 0.08 second and present in three consecutive beats; and 1 mm or greater horizontal or upsloping ST-segment elevation above baseline, lasting 0.08 second and present in three consecutive beats in any lead without a Q wave other than V1 or aVL. Patients without exercise-induced ischemic ST-

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1 New knowledge of the pathophysiology of coronary disease has helped determine the therapy for angina pectoris. Calcium antagonists have the advantage of being direct coronary vasodilators as well as decreasing overall demand by systemic vasodilatation. 2 Verapamil has the same anti-anginal effect during exercise as 0-adrenoceptor blockers but has the advantage of increasing rather than decreasing the cardiac output and so fatigue both at rest and exercise commonly seen with P-adrenoceptor blockers is not found with verapamil. The longterm incidence of side-effects with verapamil are few and it can be used as a single anti-anginal therapy in a three times daily dosage. Left ventricular function where normal and near-normal is not depressed. Tolerance to therapy has not been recorded. The anti-anginal effects have been shown to remain effective over at least a 5 year period. Verapamil should be considered as initial therapy for patients with stable angina pectoris.The pathophysiology of coronary disease can be depicted as a triad with atherosclerosis, vasospasm and thrombosis interacting to obstruct the coronary vessels. Angina occurs when the oxygen supply, impaired by the partially obstructed coronary vessels, is exceeded by oxygen demand of the heart.The anatomy of atherosclerotic segments of coronary arteries is also important. Traditionally the artery was thought to be concentrically narrowed with gradual progressive obliteration of the lumen. Much attention has been recently focused on the eccentric lesion. This is thought to be associated with vasospasm. An atherosclerosis plaque opposite the normal arterial wall may produce selective vasospasm at that site (i.e. more pronounced than that occurring in the rest of the artery) (Figure 1). The eccentric type of atherosclerosis is often ulcerative and this type of lesion progresses producing unstable angina or infarction. The specific morphology of atherosclerosis now appears to have clinical relevance (Greg Brown et al., 1984).Meyer Friedman writing on the pathology of atherosclerosis stated 'The die is cast when plaque rupture occurs, only the time of the catastrophe remains to be determined.' Atherosclerotic plaque rupture can activate all the mechanisms which promote either vasospasm or thrombosis through platelet activation, prostanoids and neurogenic amines, so that both the coagulation cascade and the factors that produce vasospasm may operate together to further narrowing or occlusion of that artery (Figure 2