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ith their marked antianginal and blood pressure lowering effects, calcium antagonists have been widely used since the 1970s for the treatment of cardiovascular disease, particularly myocardial infarction (MI). 1 However, in 1984 the short-acting calcium antagonist nifedipine was shown to be ineffective for preventing MI; 2 indeed, a 1995 report showed that short-acting nifedipine actually increased the total mortality associated with MI when its daily dose reached 80 mg. 3 Similarly, a study carried out in Japan showed that short-acting nifedipine did not reduce the incidence of cardiac events among patients with a healed MI. 4 Finally, in 1999 the American Heart Association 5 and then researchers in Japan 6 announced that short-acting nifedipine was contraindicated for treatment of acute MI, and it was suggested that the cause of nifedipine's failure to improve the prognosis of MI was an increase in sympathetic nerve activity associated with the rapid reduction in blood pressure elicited by the drug. 7,8 But if a rapid decrease in the blood pressure was the cause of the problem, perhaps long-acting calcium antagonists, which reduce blood pressure slowly and are less likely to stimulate sympathetic nervous system activity, would more effectively prevent cardiac events following MI. The purpose of the present study, therefore, was to analyze retrospectively the effect of short-and long-acting calcium antagonists on the secondary prevention of MI and whether those drugs exert any preventative effect. MethodsWe retrospectively analyzed the effects of calcium antagonists on secondary prevention of MI in inpatients and outpatients treated at the Department of Cardiology, Kinki University School of Medicine. The subjects and methods of the study are described in detail in a previous report 4 and briefly below. Study Population and Inclusion CriteriaWe enrolled all patients (n=6,428) with MI treated in the Department during the study period, including those hospi- Methods and ResultsThe present study was a retrospective analysis of the incidences of cardiac events among patients with a healed MI treated with 3 times-a-day type nifedipine (half-life 1.8 h; n=617), twice-a-day type nifedipine (half-life 4.0 h; n=527) and those not taking calcium antagonists (n=1,593) from 1986 to 1993, and the incidences of those on once-a-day type calcium antagonists (half-life 11.0 h; n=903) and those not taking calcium antagonists (n=2,788) from 1994 to 2001. Cardiac events included cardiac death and nonfatal recurrent MI. Single and multivariate analyses using the Cox-Hazard model were performed. From 1986 to 1993 cardiac events occurred in 38 patients with 3-times-a-day nifedipine (6.2%, hazard ratio and 95% confidence interval: 1.45 and 0.93-2.27), in 18 patients with twice-a-day nifedipine (3.4%: 0.68 and 0.39-1.20), 57 patients without calcium antagonists (3.6%). Cardiac events also occurred in 11 patients with once-a-day type nifedipine (1.2%: 0.72 and 0.37-1.42) and 48 patients without calcium antagonists (1.7%). Of the once-a...

The capacity of beta-blockers to prevent cardiac events in post-myocardial infarction (MI) patients was investigated. Among 1,483 study participants, a beta-blocker was included in the therapeutic regimens of 833 (beta-blocker group) and was omitted from the regimens of 650 (control group). The incidence of cardiac events (recurrent MI, sudden death and death by congestive heart failure) during a follow up period of 17.4 +/- 20.9 months was retrospectively compared between the two groups. Cardiac events occurred in 27 (3.2%) members of the beta-blocker group and in 44 (6.8%) controls, which represents a significant decline in the incidence of cardiac events among patients administered beta-blockers (p < 0.01, odds ratio 0.46, 95 % confidence intervals 0.28-0.75). Subgroup and multivariate analyses showed beta-blockers to be as efficacious in Japanese post-MI patients as was previously shown in Western patients. While these findings are compelling, it is clear that confirmation in a large, multicenter, placebo - controlled, randomized clinical trial, analogous to those that have been carried out in Western countries, is necessary.

bicuspid aortic valve is a relatively common congenital abnormality and is recognized as a major cause of aortic stenosis. 1,2 It sometimes accompanies other cardiovascular abnormalities, such as coarctation of aorta and aortic aneurysm. 1,3 Renal hypoplasia, which is rarely unilateral, has been reported as a complication with malformation of other organs, including the central nervous system, 4 but to our best knowledge, however, the coincidence of renal hypoplasia with a bicuspid aortic valve has not been reported. Case ReportA 20-year-old man was admitted to hospital for investigation of exertional dyspnea and edema. He was diagnosed elsewhere as having hypertension (HT) and proteinuria, for which he was given amlodipine and furosemide. None of his family had aortic stenosis, renal hypoplasia, electrocardiogram (ECG) abnormalities, periodic paralysis or skeletal abnormalities. On physical examination, his height was 167 cm, body weight was 98 kg (body mass index =31.7), pulse rate 106 beats/min and blood pressure 185/120 mmHg; the external jugular vein was slightly dilated. A systolic murmur (Levine 3/6) was audible over the aortic area, and there were moist rales were in both lower lung fields. An abdominal bruit was also audible in the epigastrium. The liver was palpable below the right costal margin and there was pretibial pitting edema. Chest X-ray on admission revealed cardiac enlargement with a cardiothoracic ratio of 0.61, and mild pulmonary congestion. The ECG showed sinus tachycardia, left atrial overload and counterclockwise rotation. Laboratory tests showed proteinuria (3+), which soon reduced to 0.4 g/day, indicating that the edema was A 20-year-old man with congestive heart failure (CHF) and hypertension (HT) was admitted to hospital. Ultrasonic echocardiography showed that he had aortic stenosis caused by a bicuspid aortic valve. The plasma renin concentration was slightly elevated, and enhanced magnetic resonance imaging and renography revealed a hypoplastic kidney that had almost lost its normal function. It is postulated that the increased afterload and preload of the left ventricle induced by both of these abnormalities contributed to the onset of CHF and HT. Pharmacological therapy alone failed to control the CHF and HT, but surgical removal of the hypoplastic kidney was effective in reducing the plasma renin concentration and treating the CHF and HT. (Circ J 2005; 69: 359 -361)

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