Background-Although the short-term and long-term beneficial effects of early coronary revascularization by primary PTCA or thrombolytic therapy have been established for acute myocardial infarction, thrombolytic therapy Ͼ24 hours after the onset of acute myocardial infarction has not been shown to improve clinical outcome. The purpose of this study was to assess the effect of late revascularization by primary PTCA over a 5-year period. Methods and Results-Eighty-three patients with initial Q-wave anterior myocardial infarction Ͼ24 hours after onset were randomized into a PTCA group (nϭ44) and a no-PTCA group (nϭ39). Long-term follow-up was conducted with regard to end points, which included cardiac death, nonfatal recurrence of myocardial infarction, and development of congestive heart failure. Left ventricular ejection fraction and regional wall motion at 6 months after myocardial infarction were similar in the 2 groups. Left ventricular end-diastolic and end-systolic volume indexes were significantly smaller in the PTCA group than in the no-PTCA group (PϽ0.0001). With cardiac events as end points, a 5-year Kaplan-Meier event-free survival analysis revealed that the no-PTCA group had a worse prognosis than the PTCA group (PϽ0.0001). Patency of the infarct-related artery, left ventricular ejection fraction, end-diastolic volume index, and end-systolic volume index were significantly associated with cardiac events by a Cox proportional hazards analysis (hazard ratios 0.120, 0.845, 1.065, and 1.164, respectively). Conclusions-In initial Q-wave anterior myocardial infarction, we conclude that even with late reperfusion, PTCA had beneficial effects on cardiac events over the 5-year period after myocardial infarction, with the prevention of left ventricular dilation after myocardial infarction being a possible mechanism. (Circulation. 1998;98:2377-2382.)

Intracoronary infusion of BK stimulates tPA release without causing any change in PAI-1 levels in the human coronary circulation. In addition, this effect of BK is augmented by an ACE inhibitor.

Perindopril and losartan similarly augment BK-induced coronary vasodilation. Perindopril may have a greater potential to enhance the BK-induced coronary release of t-PA than losartan.

We hypothesized that plasma brain natriuretic peptide, like plasma atrial natriuretic peptide, may reflect hemodynamic changes elicited by different cardiac pacing modes. The aim of this study was to investigate whether plasma brain natriuretic peptide could be influenced by different pacing modes or electrical stimulation. The subjects consisted of 164 patients with permanent pacemakers (52 VVI, 30 AAI, 82 DDD pacemakers) and unimpaired heart function. Patients with atrial fibrillation or spontaneous beats were excluded. Plasma atrial natriuretic peptide and brain natriuretic peptide levels were measured at a rate of 70 beats/min after 45 minutes in the supine position. Under ECG monitoring, the pacing mode was switched from DDD to VVI in 12 patients and from DDD to AAI in 4 patients with a dual chamber pacemaker. Plasma atrial natriuretic peptide and brain natriuretic peptide levels were also measured 30 minutes, 60 minutes, and 1 week after mode switching. Plasma atrial natriuretic peptide and brain natriuretic peptide levels were significantly higher in the nonphysiological pacing group than in the physiological pacing group, whereas these values were similar in the DDD and AAI pacing groups. One week after switching from DDD to VVI, plasma atrial natriuretic peptide and brain natriuretic peptide levels were significantly increased, however no significant changes were observed after switching to AAI. Based on a multivariate regression analysis of noninvasive clinical parameters, only a low plasma brain natriuretic peptide was significantly correlated with physiological pacing. We conclude that: (1) plasma brain natriuretic peptide, like atrial natriuretic peptide, is influenced by the pacing mode, but is not influenced by electrical stimulation; and (2) low plasma brain natriuretic peptide is important in relation to physiological pacing.