Evidence of abnormal vasodilator reserve in coronary spasm.

A 60-year-old man was referred for cardiac catheterization because of increasingly frequent episodes of chest pain occurring mainly at rest but also with exertion. He had a history of mild systemic hypertension and esophagitis due to gastroesophageal reflux. A treadmill test performed shortly after the onset of his symptoms 3 years earlier was negative at a pressure rate product of 264 X IO2 mm Hg X beats/min. Medications included propranolol 120 mg/day, topical nitrates 20 mg/day, hydrochlorothiazide 50 mg/day and cimetidine 400 mg/day. The blood pressure was lSO/SS mm Hg and the heart rate was 56 beats/min. The remainder of the examination was entirely normal as was the electrocardiogram at rest, the chest roentgenogram and an M-mode echocardiogram. No evidence for left ventricular hypertrophy was present. A repeat treadmill exercise test was stopped after 7 minutes of the standard Bruce protocol because of fatigue. The pressure-rate product achieved was 224 X lo2 mm Hg X beats/min. The patient had no chest pain, but there was 2 mm of horizontal ST depression in leads VJ, V5 and Vg, and concomitant thallium-201 scintigraphy revealed a reversible anteroseptal perfusion defect. A11 medications were withheld the night before catheterization. Left ventriculography and coronary arteriography were performed using the