Dobutamine echocardiography in predicting improvement in global left ventricular systolic function after coronary bypass or angioplasty in patients with healed myocardial infarcts.

The aim of this study was to determine whether low-dose dobutamine echocardiography (DE) could predict quantitative improvement in global left ventricular (LV) systolic function after coronary revascularization. Low-dose DE was performed in 71 consecutive patients with coronary artery disease and LV dysfunction. Successful coronary bypass surgery or angioplasty was performed in 44 patients, 37 of whom had a resting echocardiogram 1 to 3 months afterward. Group A consisted of 20 patients with contractile reserve during DE, and group B consisted of 17 patients without contractile reserve. As expected, regional wall motion score index (mean +/- SD) improved in group A (1.62 +/- 0.39 to 1.38 +/- 0.31, p < 0.01) but not group B (1.56 +/- 0.42 to 1.57 +/- 0.41, p = NS). In addition, LV ejection fraction (LVEF) improved after bypass surgery or angioplasty in group A (38 +/- 5% to 42 +/- 5%, p < 0.01), but not in group B (38 +/- 7% to 39 +/- 8%, p = NS). In group A, a significant linear correlation was observed between the number of segments with contractile reserve and the improvement in LVEF (r = 0.91, p < 0.0001). A good correlation also existed between the improvement in regional wall motion score index during dobutamine infusion and the improvement in LVEF after bypass surgery or angioplasty (r = 0.90, p < 0.0001). In conclusion, low-dose DE can be used to predict quantitative improvement in global LV systolic function after coronary bypass or angioplasty.

Racial differences in the prevalence of left ventricular hypertrophy among chronic cocaine abusers.

There are racial differences in the prevalence and pattern of left ventricular (LV) hypertrophy in hypertension. This study was performed to determine whether racial differences also exist in LV hypertrophy among chronic cocaine users. We studied 112 chronic cocaine abusers < 45 years old in whom normal blood pressures (< or = 140/90 mm Hg) were recorded 3 times daily for 3 weeks. LV wall thickness and mass were measured echocardiographically. Technically adequate studies were obtained in 79 blacks and 33 whites. Self-reported cocaine use was higher in whites than in blacks (688 +/- 516 vs 431 +/- 468 $/week, p = 0.03). There were no group differences in terms of duration of cocaine use, age, height, weight, blood pressure, LV dimensions, or left atrial size. However, posterior wall thickness (1.13 +/- 0.17 vs 1.03 +/- 0.14 cm, p = 0.0035) and LV mass index (113 +/- 25 vs 94 +/- 19 g/m2, p = 0.0001) were significantly greater in blacks. LV hypertrophy, defined as an M-mode LV mass index > or = 134 g/m2, was present in 24 blacks (30%) and 2 whites (6%) (p = 0.011). When defined as a posterior wall thickness > or = 1.2 cm and a 2-dimensional echocardiographic LV mass index > or = 105 g/m2, LV hypertrophy was present in 37 of 79 blacks (47%) and in 6 of 33 whites (18%) (p = 0.0086). Cocaine-related LV hypertrophy is more prevalent in black men than in white men.(ABSTRACT TRUNCATED AT 250 WORDS)

Time course of improvement in left ventricular function, mass and geometry in patients with congestive heart failure treated with beta-adrenergic blockade.

OBJECTIVES: We examined the time course of ventricular functional improvement in patients with dilated cardiomyopathy who received beta-blockade and the long-term effects of beta-blockade on ventricular mass and geometry in these patients. BACKGROUND: Previous studies have shown that beta-adrenergic blocking agents when administered long term improve ventricular function in patients with heart failure. However, the time course of improvement in ventricular function and the long-term effects of beta-blockade on ventricular mass and geometry are not known. METHODS: Twenty-six men with dilated cardiomyopathy underwent serial echocardiography on days 0 and 1 and months 1 and 3 of either metoprolol (n = 16) or standard therapy (n = 10). At 3 months all patients on standard therapy were crossed over to metoprolol, and late echocardiograms were obtained after 18 +/- 5 (mean +/- SD) months of metoprolol therapy. All echocardiograms were read in blinded manner. RESULTS: Patients treated with metoprolol had an initial decline (day 1 vs. day 0) in ventricular function (increase in end-systolic volume and decrease in ejection fraction). Ventricular function improved between months 1 and 3 (p = 0.013, metoprolol vs. standard therapy). Left ventricular mass regressed at 18 months (333 +/- 85 to 275 +/- 53 g, p = 0.011) but not at 3 months. Left ventricular shape became less spherical and assumed a more normal elliptical shape by 18 months (major/minor axis ratio 1.5 +/- 0.2 to 1.7 +/- 0.2, p = 0.0001). CONCLUSIONS: Patients with heart failure treated with metoprolol do not demonstrate an improvement in systolic performance until after 1 month of therapy and may have a mild reduction in function initially. Long-term therapy with metoprolol results in a reversal of maladaptive remodeling with reduction in left ventricular volumes, regression of left ventricular mass and improved ventricular geometry by 18 months.

Relation of thrombus in the left atrial appendage by transesophageal echocardiography to clinical risk factors for thrombus formation.

Transesophageal echocardiography provides excellent visualization of the left atrial appendage (LAA). This study was conducted to determine whether specific clinical risk factors could predict the presence of LAA thrombus as demonstrated by transesophageal echocardiography. The most recent 860 transesophageal echocardiographic studies performed at our institution were retrospectively reviewed. The LAA was adequately visualized in 778 patients (90%). For each study, the presence or absence of 5 specific clinical risk factors (mitral stenosis, severe left ventricular dysfunction, left atrial dilatation, atrial fibrillation, or a prosthetic mitral valve) and the presence or absence of LAA thrombi were assessed. One or more clinical risk factors were present in 149 patients, whereas no defined risk factors were noted in 629. Left atrial appendage thrombi were found in 20 of 149 patients with versus 6 of 629 patients without a clinical risk factor (13% vs 1%, p = 0.0001). By logistic regression analysis, mitral stenosis, severe left ventricular dysfunction, and left atrial dilatation were independent risk factors for LAA thrombus formation. Neither atrial fibrillation nor the presence of a mitral prosthetic valve achieved statistical significance as independent risk factors for LAA thrombus. Thus, LAA thrombi occur most often in patients with risk factors for thrombus formation that can be determined by clinical evaluation and transthoracic echocardiography. Transesophageal echocardiography rarely identifies LAA thrombi in patients without such clinical risk factors.

Dobutamine stress echocardiography identifies hibernating myocardium and predicts recovery of left ventricular function after coronary revascularization.

BACKGROUND: The identification of hibernating myocardium is important in selecting patients who will benefit from coronary revascularization. This study was performed to determine whether dobutamine stress echocardiography (DSE) could identify hibernating myocardium and predict improvement in regional systolic wall thickening after revascularization. METHODS AND RESULTS: DSE was performed in 49 consecutive patients with multivessel coronary disease and depressed left ventricular function. Contractile reverse during DSE was defined by the presence of two criteria: (1) improved systolic wall thickening in at least two adjacent abnormal segments and (2) > or = 20% improvement in regional wall thickening score. Postoperative echocardiograms were evaluated for improved regional wall thickening in 25 patients at least 4 weeks after successful coronary revascularization. All studies were read in blinded fashion. Contractile reserve during DSE was present in 24 (49%) of 49 patients. The presence or absence of contractile reserve on preoperative DSE predicted recovery of ventricular function in the 25 patients who underwent successful revascularization. Thus, 9 of 11 patients with contractile reserve had improved systolic wall thickening after revascularization (hibernating myocardium), whereas 12 of 14 patients without contractile reserve did not improve (P = .003). CONCLUSIONS: Dobutamine stress echocardiography provides a simple, cost-effective, and widely available method of identifying hibernating myocardium and predicting improvement in regional left ventricular wall thickening after coronary revascularization. This technique may be clinically valuable in the selection of patients for coronary revascularization.

Exaggerated pressor response to treadmill exercise in chronic cocaine abusers with left ventricular hypertrophy.

BACKGROUND: Chronic cocaine abuse has been associated with a high prevalence of left ventricular hypertrophy (LVH) in normotensive individuals at rest. This study was conducted to determine whether chronic cocaine abusers with LVH would manifest an exaggerated pressor response to treadmill exercise. METHODS AND RESULTS: Forty-nine normotensive chronic cocaine abusers underwent Bruce protocol treadmill exercise testing until they attained 85% maximum predicted heart rate. A peak exercise systolic blood pressure greater than or equal to 210 mm Hg was defined as abnormal. In addition, they underwent two-dimensional echocardiography and had left ventricular mass determined by the area-length method. LVH was defined as left ventricular mass greater than or equal to 105 g/m2 and a posterior wall thickness greater than or equal to 1.2 cm. Age- and race-matched control subjects also underwent echocardiography and exercise testing. Group differences in peak exercise blood pressure in cocaine abusers with LVH, cocaine abusers without LVH, and control subjects were assessed by ANOVA: Groups were similar concerning age, race, heart rate, resting blood pressure, body surface area, and exercise duration. LVH was present in 16 of 49 (33%) cocaine abusers and three of 30 (10%) control subjects (p = 0.02). Of the 16 cocaine abusers with LVH, 10 (63%) had peak exercise blood pressures greater than or equal to 210 mm Hg, and three others had exercise blood pressures of 200 mm Hg. Therefore, peak exercise systolic blood pressure was significantly higher in cocaine abusers with LVH than in all other groups (p = 0.0001). CONCLUSIONS: Chronic cocaine abusers with LVH manifest an exaggerated pressor response to treadmill exercise. These data suggest that chronic cocaine abuse predisposes a subset of individuals to a heightened pressor response to a given sympathetic stimulus such as exercise and that this may contribute to the pathogenesis of LVH in chronic cocaine abusers.