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Background: Coronary flow velocity reserve (CFVR) measured by transthoracic Doppler echocardiography (TTDE) has been reported to be useful for the noninvasive assessment of coronary stenosis in the left anterior descending artery. However, the measurement of CFVR in the right coronary artery by TTDE has not yet been validated in a clinical study. Objective: The aim of this study was to evaluate whether CFVR by TTDE can detect significant stenosis in the right coronary artery. Methods: We studied 50 patients who underwent coronary angiography. Coronary flow velocity in the posterior descending branch of the right coronary artery (PD) was measured by TTDE both at baseline and during hyperemia induced by the intravenous infusion of adenosine triphosphate. CFVR was calculated as the hyperemia/baseline (average diastolic peak velocity). Results: Adequate spectral Doppler recordings in the PD were obtained in 36 patients including 26 patients who were given an echocardiographic contrast agent to improve Doppler spectral signals. The study population was divided into 2 groups with (Group A;n = 11) and without (Group B;n = 25) significant stenosis in the right coronary artery. CFVR in Group A was significantly smaller than that in Group B (1.6±0.3versus2.5±0.4; P < 0.0001). The sensitivity of a CFVR of

The peak early diastolic filling velocity/flow propagation velocity (E/FPV) by color M-mode Doppler provides a better estimate of pulmonary capillary wedge pressure (PCWP) than transmitral or pulmonary venous flow. However, the value of E/FPV for the assessment of PCWP has not been evaluated in patients with acute myocardial infarction. We investigated the correlation between E/FPV and PCWP and whether PCWP can be estimated from E/FPV in patients with acute myocardial infarction. One hundred and two patients with acute myocardial infarction were divided into two groups. The first 60 patients were used to generate an equation to estimate PCWP (retrospective group). This equation was then assessed prospectively in the remaining 42 patients (prospective group). We measured the transmitral flow velocity indices and the deceleration time of diastolic pulmonary venous flow and E/FPV by Doppler echocardiography and compared these variables with PCWP measured using a pulmonary artery catheter. E/FPV was strongly correlated with PCWP (r = 0.89) in the retrospective group. The sensitivity of an E/FPV of > or = 2.0 for predicting a PCWP of > or = 18 mmHg was 95%, and the specificity was 98%. The estimated PCWP showed a strong correlation with the measured PCWP (r = 0.84, P < 0.0001) in the prospective group. The mean difference between the measured and estimated PCWP was - 0.4 +/- 3.6 mmHg. In patients with acute myocardial infarction, E/FPV by color M-mode Doppler during early left ventricular filling provides a better estimate of PCWP than transmitral or pulmonary venous flow.

OBJECTIVES This study was conducted to evaluate: 1) the effect of adjunctive percutaneous transluminal coronary angioplasty (PTCA) after directional coronary atherectomy (DCA) compared with stand-alone DCA, and 2) the outcome of intravascular ultrasound (IVUS)-guided aggressive DCA. BACKGROUND It has been shown that optimal angiographic results after coronary interventions are associated with a lower incidence of restenosis. Adjunctive PTCA after DCA improves the acute angiographic outcome; however, long-term benefits of adjunctive PTCA have not been established. METHODS Out of 225 patients who underwent IVUS-guided DCA, angiographically optimal debulking was achieved in 214 patients, then they were randomized to either no further treatment or to added PTCA. RESULTS Postprocedural quantitative angiographic analysis demonstrated an improved minimum luminal diameter (2.88 ± 0.48 vs. 2.6 ± 0.51 mm; p = 0.006) and a less residual stenosis (10.8% vs.15%; p = 0.009) in the adjunctive PTCA group. Quantitative ultrasound analysis showed a larger minimum luminal diameter (3.26 ± 0.48 vs. 3.04 ± 0.5 mm; p CONCLUSIONS With IVUS guidance, aggressive DCA can safely achieve optimal angiographic results with low residual plaque mass, and this was associated with a low restenosis rate. Although adjunctive PTCA after optimal DCA improved the acute quantitative coronary angiography and quantitative coronary ultrasonography outcomes, its benefit was not maintained at six months.

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.

Several studies have demonstrated that the ratio of peak E wave velocity/flow propagation velocity (E/FPV) using color M-mode Doppler echocardiography and the mitral E wave deceleration time make it possible to estimate left ventricular filling pressure. Recent studies have indicated that deceleration time can predict left ventricular dilation after acute myocardial infarction. The purpose of this study was to determine whether the early assessment of deceleration time and E/FPV could predict left ventricular dilation after acute myocardial infarction. We studied 55 patients with first anterior acute myocardial infarction who underwent successful coronary angioplasty by two-dimensional (2-D) Doppler echocardiography within 12 hours and at 1 and 6 months after reperfusion. Patients were divided into three groups according to deceleration time and E/FPV immediately after reperfusion: (1). restrictive filling (deceleration time or= 2.0), (2). elevated filling pressure (deceleration time >or= 140 msec and E/FPV >or= 2.0), (3). and normal filling pressure (deceleration time >or= 140 msec and E/FPV < 2.0). The end-diastolic volume index (EDVI) was similar in the three groups immediately after reperfusion. EDVI in the groups with restrictive filling and elevated filling pressure was significantly greater than that in the group with normal filling pressure at 6 months (93 +/- 11 and 89 +/- 16 vs 59 +/- 11 ml/m(2), respectively; P < 0.0001). E/FPV shows a better correlation with the change in EDVI at 6 months than deceleration time (r = 0.77; P < 0.0001 and r = - 0.46; P < 0.001, respectively). The early measurement of E/FPV provides a simple and accurate means for predicting left ventricular dilation after acute myocardial infarction.

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 >24 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 >24 hours after onset were randomized into a PTCA group (n=44) and a no-PTCA group (n=39). 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 ( P P 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.

The Shiga Pravastatin Study (SHIPS) is a 5 center randomized, double blind placebo controlled trial to test whether pravastatin, 10 mg twice daily begun at least 10 days prior to elective PTCA in patients with total cholesterol (T-Chol) hess than 280 mg/dl can decrease restenosis. The endpoint is a between group comparison of frequency of restenosis defined as a more than 50% loss of gain at PTCA site at 3 months follow-up by automated quantitative coronary arteriography. 179 lesions (85 pravastatin. 94 placebo) in 124 patients (62 pravastatin. 62 placebo) were randomized. The two groups were comparable for baseline clinical and angiographic characteristics. T-Chol decreased from 204 to 172 mg/dl in pravastatin group (P l 0.001), but not in placebo (201 vs 202 mg/dl). Although restenosis rate was not different in the two groups (29.4% in pravastatin vs 39.4% in placebo. P = 0.16) as a whole, it was reduced to about 1/5 (8.B%) in pravastatin group compared to 44.B% in placebo (P = 0.0011) when the analysis was restricted to high grade lesions (≥ 75% diameter stenosis by automated analysis. which is equivalent to ≥90% stenosis by visual analysis; 34 lesions in pravastatin, 29 lesions in placebo). The effect of pravastatin in prevention of restenosis in high grade lesions was equally seen both in the groups with baseline T-Chol of above (10.5 vs 45.5%, P = 0.029) and below 200 mg/dl (6.7 vs 44.4%. P = 0.015). Conclusion Pravastatin prevents restenosis after PTCA of high grade lesions irrespective of baseline T-Chol level.

Alcoholics who were first admitted for alcoholism treatment at a psychiatric hospital between 23 and 32 years of age were more likely than alcoholics admitted at a later age to be the firstborn or only child in their family, to have experienced paternal death before age 10 and to have had alcoholic relatives.