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In this study, the authors examined relations between coronary and carotid atherosclerosis and between coronary atherosclerosis and silent cerebral infarction. They ascertained the risk factors for carotid atherosclerosis and silent cerebral infarction complicating coronary heart disease (CHD) in 77 Japanese subjects. As coronary atherosclerosis progressed, the carotid ultrasonographic score and the brain computed tomographic score increased. Multivariate analyses showed that the significant and independent risk factors for carotid atherosclerosis in patients with CHD were age (p < 0.01) and apolipoprotein (apo) B (p < 0.05) and the factors for silent cerebral infarction were age (p < 0.05) and hypertension (p < 0.05). Their study confirms a positive relation between coronary atherosclerosis and carotid atherosclerosis and between coronary atherosclerosis and silent cerebral infarction in patients with CHD. Their data suggest that carotid atherosclerosis should be looked for in patients with CHD who are old and have a high value of apo B, and silent cerebral infarction should be looked for in those who are old and have hypertension, to prevent complicating symptomatic cerebral vascular disease (CVD). If severe carotid atherosclerosis or silent cerebral infarction are detected, antithrombotic medication should be given.

A 28-year-old man with acute myocardial infarction after carbon monoxide poisoning is reported. He had chest pain after the exposure to carbon monoxide. The electrocardiogram, serum enzymes, and technetium-99m pyrophosphate scintigrams showed anterior myocardial infarction. The coronary angiogram, which was performed one month after the onset, showed no visible atherosclerotic lesion. As to the cause of myocardial infarction, it is assumed that carbon monoxide reduced the oxygen supply to the myocardium and might induce coronary artery spasm with or without accompanying coronary thrombosis.

A forty-four-year-old woman with Takayasu's arteritis and involvement of the aortic arch and its main branches complained of precordial pain on effort. Exercise electrocardiograms revealed significant ST segment depression in leads II, III, aVF, and V. Coronary arteriograms demonstrated no stenosis. However, the right coronary arteriogram revealed collateral circulation arising from the sinus node artery to the bilateral vertebral arteries and the left internal carotid artery. The collateral circulation was considered to be an important route of blood flow supply to the brain and, at the same time, a cause of coronary steal syndrome and, consequently, of angina pectoris.