These results suggest that aggressive lipid-lowering therapy using the combination of LDL-A and lipid-lowering drugs may induce regression of coronary atherosclerotic plaque in FH patients.

oronary spasm provokes the myocardial ischemia associated with angina pectoris, acute myocardial infarction and sudden death. 1,2 Calcium channel antagonists, nitrates or a combination of both drugs have been used effectively to prevent coronary spasm. [3][4][5][6] Indeed, the overall cardiac mortality is relatively low and the prognosis seems to be good for medically treated patients with coronary spasm. [7][8][9] Coronary spasm frequently occurs in minimally narrowed coronary segments, 10,11 suggesting a pathophysiologic correlation between coronary spasm and atherosclerosis, which has been demonstrated in an experimental animal model. 12 Several studies have examined the relationship between the clinical characteristics and prognosis of this type of angina, and demonstrated that preexistCirculation Journal Vol.67, December 2003 ing atherosclerosis could be an important risk factor for cardiac death and myocardial infarction during the relatively early phase. 5-9 However, there is little information regarding the long-term prognosis of medically treated coronary spasm with or without atherosclerotic risks, such as underlying coronary artery stenosis (CAS) and intrinsic hyperlipidemia. Such data should be important for not only preventing vasospasm, but also preventing the development of atherosclerosis. The purpose of this study was, first, to determine the event-free survival rate in patients with angiographically documented coronary spasm, and second, to identify the clinical predictors of cardiac events, particularly in patients with and without significant CAS. Methods Patient PopulationOf 2,740 patients who underwent diagnostic coronary angiography for suspected ischemic heart disease between 1977 and 1987, 284 consecutive patients with coronary spasm were enrolled and followed. During the follow-up, 21 patients went missing. Patient enrollment was completed in 1987 when 3-hydroxy-3-methyleglutaryl coenzyme A (HMG-CoA) reductase inhibitor, which might have altered the long-term prognosis, 13 was not generally available. Therefore, no patient had been given HMG-CoA reductase Although patients with medically treated vasospastic angina have a good outcome, few data exist regarding the role of underlying lesion severity associated with or without hyperlipidemia in the prognosis. Therefore, the aim of the present study was to assess the relationship between the long-term outcome of vasospastic angina and the factors influencing its prognosis. A total of 256 patients (219 men, 37 women; mean age, 54.1±9.2) who had coronary spasm with or without underlying lesions and were being treated with calcium channel antagonists were enrolled and followed for 13.6±3.7 years. Cardiac events consisted of cardiac death and ischemic events, which included acute myocardial infarction and unstable angina. Cox analysis selected coronary artery stenosis (CAS, ≥50%) and risk factors such as age, hypertension, diabetes mellitus, low-density lipoprotein-cholesterol (LDL-C), sex and smoking. There were 19 cases of cardiac death (7...

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We studied the effects of right ventricular ischemia on left ventricular three-dimensional geometry Received Dec. 31, 1984; revision accepted July 5, 1985. Presented in part at the 56th Scientific Sessions of The American Heart Association, Anaheim, CA, 1983. evaluated left ventricular geometry nor measured left ventricular volume.The goal of the present study was to elucidate the effects of right ventricular ischemia on left ventricular geometry and the end-diastolic pressure-volume relationship in dogs, and to consider the importance of the intact pericardium. To this end, we measured septallateral, anterior-posterior, and apical-basal dimensions of the left ventricle with three pairs of ultrasonic dimension gauges, during right coronary artery (RCA) occlusions with the pericardium intact and open. MethodsAnimal preparation and instrumentation. Sixteen mongrel dogs weighing 13 to 24 kg (average 16.9) were anesthetized with ketamine hydrochloride (5 to 7 mg/kg im) followed by intravenous a-chloralose (50 mg/kg) and urethane (500 mg/kg). After endotracheal intubation, ventilation was maintained, by a volume respirator, with room air. A bilateral thoracotomy was performed in each dog in the fifth intercostal space with transection of the sternum. The electrocardiogram was continuously monitored in a limb lead (lead II). Arterial blood was repeatedly sampled for measurements of pH, Po2, and Pco2 with a blood gas analyzer (Acid-Base Laboratory, ABL2d), and supplemen-

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Transient cortical blindness, an uncommonly recognized complication of cerebral angiography, is an exceedingly rare event after cardiac catheterization and angiography. This report describes a sixty-two-year-old patient who had transient cortical blindness following bypass graft angiography. In this case, the authors showed that cortical blindness was associated with the breakage of the blood-brain barrier (BBB) and an increase in vascular permeability rather than with primary cerebral circulatory insufficiency. When the possibility exists that an excess volume of contrast medium may enter the cerebral circulation as in this case, that is, following a coronary artery bypass graft (CABG) using the internal mammary artery (IMA), precautionary measures may be necessary such as changing the type of contrast medium to be used or decreasing the volume injected. When cortical blindness occurs, it is a serious clinical problem whether transient or permanent. Therefore, the circumstances leading to this complication should be understood to determine suitable treatment and management.

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Rifampicin, an antituberculosis agent, is known to be a potent inducer of microsomal drug-metabolizing enzymes in the liver. Elimination or clearance of many drugs has been reported to be enhanced, and their effectiveness reduced; however, no report in the literature has dealt with the interaction between rifampicin and dihydropiridine calcium entry-blocking drugs such as nifedipine. We present here evidence for the possible interaction between rifampicin and nifedipine in a patient with angina pectoris, which was exacerbated during coadministration or rechallenge with rifampicin. The peak plasma level and area under the curve were reduced and the apparent oral clearance of nifedipine was increased by rifampicin, suggesting that rifampicin enhanced the elimination of nifedipine via induction of a hepatic microsomal drug-metabolizing enzyme, as has been reported on other drugs widely metabolized in the liver.