We studied six patients who suffered from angina pectoris but had angiographically patent major coronary arteries. Two of the patients suffered also from congestive heart failure. Three patients had supraventricular tachyarrhythmias. Three patients had conduction disturbances. During coronary angiography the patients had significantly reduced flow velocity of angiographic contrast medium compared with that in a control group. Echocardiographic and Doppler flow studies showed a tendency for symmetrical thickening of the left ventricular wall, enlargement of the right ventricle, and reduced compliance of both ventricles. Right ventricular endomyocardial biopsy revealed pathologic small coronary arteries with fibromuscular hyperplasia, hypertrophy of the media, myointimal proliferation, and endothelial degeneration. Capillaries had swollen endothelial cells encroaching on the lumen. Myocardial hypertrophy, lipofuscin deposition, and patchy fibrosis were also observed. These cases show that small-vessel coronary artery disease can cause classic angina pectoris. The diagnosis can be suspected when the coronary angiogram shows large patent arteries with slow flow of the angiographic contrast medium and it can be confirmed by endomyocardial biopsy. Circulation 74, No. 5, 964-972, 1986. ANGINA PECTORIS associated with widely patent epicardial coronary arteries is a well-recognized but poorly understood clinical entity. One pathogenetic mechanism is thought to be disease of small coronary arteries. Anatomic evidence was derived from histologic findings in autopsy studies but these were not correlated with clinical angina pectoris.' Physiologic studies showed a decreased coronary vasodilator reserve in patients with angina pectoris and patent epicardial coronary arteries. This was attributed to smallvessel disease but formal histologic proof was lacking.2'3 We have been unable to find reports of small-vessel disease in myocardial biopsy specimens taken from patients with typical angina.4 In this study we describe six patients with angina pectoris and widely patent large coronary arteries in whom endomyocardial biopsy revealed histologically and electron microscopically evident disease in the small coronary arteries. 964 MethodsIn 1985 we performed coronary angiography for the investigation of chest pain in 769 patients. Fifty-four patients did not have disease of the major epicardial arteries. Nine of them had slow flow of contrast medium in the coronary arteries. Biopsy specimens were taken from six of the patients with slow flow. Four showed changes in small arteries and capillaries (light and electron microscopy). In two patients insufficient large vessels were present in the histologic sections and the capillaries showed no pathologic changes on electron microscopy.In this report we describe these four patients with changes in their small arteries as well as another two patients (Nos. 2 and 3) in whom prior angiographic studies showed slow flow of contrast medium and in whom changes in the small arteries ...

SUMMARY The left anterior descending coronary artery of four dogs and the right common carotid artery of 15 rabbits were subjected to 40-60% reduction in transluminal diameter for 1 hour by partial ligation with suture thread. Scanning electron microscopic examination of the luminal surface of these vessels revealed endothelial craters and balloons, fragmentation and desquamation on the proximal slope of the constriction. Platelet attachment to exposed subendothelial tissues was clearly evident, and microthrombi were seen at the point of maximum constriction. Blood flow, as measured by electromagnetic flow probe, was virtually unchanged upon partial ligation. In control studies, where a second ligature was placed proximal to and before the first to reduce blood flow to the distal constriction site substantially or totally, endothelial desquamation was found in only one of 14 animals, and the number of craters and balloons was significantly reduced. We suggest that endothelial damage and thrombus formation may occur at the site of focal arterial constriction even when the reduction in transluminal diameter is insufficient to alter substantially the rate of flow.THE THREAT posed by coronary vasospasm for the initiation of myocardial ischemia or infarction is assumed to depend on the degree to which the reduction in transluminal diameter results in the interference with coronary blood flow. Further, it is thought that the thrombosis that may accompany vasospasm is a result of the grossly reduced blood flow secondary to a critical vascular constriction and that the interaction of platelets with a damaged vascular wall, with the ensuing release reaction, may further potentiate the coronary spasm." 2 In the present report we present evidence from scanning electron microscopic (SEM) studies that indicates that marked endothelial damage, extensive platelet deposition and thrombus formation may occur at the site of a focal arterial constriction even when the reduction in transluminal diameter is insufficient to alter flow substantially. MethodsFifteen New Zealand white rabbits (3.1 ± 0.4 kg, mean ± SD) were anesthetized with sodium pentobar- The RCCA of five rabbits and the LAD of two dogs were focally constricted 1 cm proximal to the probe by partial ligation with suture thread (0-cotton) to achieve a 50% reduction in transluminal diameter ( fig. 1). The desired degree of luminal constriction was achieved by the apposition of two points on the suture thread; the distance between these points was calculated from the vascular circumference, with the wall thickness (0.1 mm) considered negligible. The diameters were confirmed during SEM examination and varied from 40-60% luminal reduction. Group 2In a second group of five rabbits and two dogs, a second ligature was placed 1 cm proximal and immediately before the first ( fig. 1)

Enlarged capillaries and a normal ratio of capillaries to myocytes appear to be features of DCM. Of the patients with SVD, there was both a relative lack of capillaries and capillary lumen narrowing from swollen endothelium. These changes may induce ischemia and angina and may result in mild fibrosis.

Myocardial bridge is a not uncommon finding in routine diagnostic coronary angiography or pathological examination of the heart. It is almost always confined to the left ventricle and the left anterior descending coronary artery. This report describes a patient with chronic lung disease, severe left ventricular dysfunction, and pulmonary hypertension in whom coronary angiography revealed bridging of the right ventricular branch of the right coronary artery.

This report describes a case with double hepatic venous drainage into the right atrium. The right hepatic veins, the inferior cava, and the pulmonary veins drained normally. The