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The diagnostic accuracy of dobutamine stress echocardiography is limited in patients with poor transthoracic acoustic windows. Transesophageal echocardiography (TEE) overcomes these limitations and thus may increase the clinical usefulness of dobutamine stress echocardiography. The present study was designed to compare the diagnostic accuracies of transesophageal and transthoracic dobutamine stress echocardiography for the identification of coronary artery disease (CAD) in a cohort of patients with a higher incidence of poor acoustic windows. Forty-two male patients (mean age, 66 +/- 9 years) underwent dobutamine stress echocardiography with simultaneous transesophageal and transthoracic imaging. Coronary arteriography was performed in 28 patients (67%). Transesophageal imaging adequately visualized 99.6% of left ventricular segments compared with 76.2% visualized by transthoracic imaging (P < 0.0001). There was substantial agreement between the two techniques for segmental wall motion analysis at baseline (kappa 0.76; 95% CI, 0.70-0.82); however, at peak dobutamine dose, agreement was significantly reduced (kappa 0.62; 95% CI, 0.55-0.69). The sensitivity (88% vs 75%), specificity (100% vs 75%), and positive predictive value (100% vs 80%) for the identification of CAD were all superior for transesophageal imaging. Transesophageal imaging correctly identified 11 of the 12 patients (92%) with multivessel disease compared with 5 patients (42%) identified by transthoracic imaging (P < 0.03). There were no major complications. Transesophageal dobutamine stress echocardiography is a safe, feasible, and accurate technique for the identification and risk stratification of patients with CAD. Transesophageal imaging appears to be superior to transthoracic imaging for identifying both the presence and extent of CAD, specifically in patients with poor acoustic windows.

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OBJECTIVES: This study was performed to assess the prognostic implications of myocardial contractile reserve (MCR) in patients with coronary artery disease (CAD) and left ventricular (LV) dysfunction. BACKGROUND: MCR during dobutamine stress echocardiography (DSE) identifies viable myocardium that may improve in function after revascularization. Whether revascularization influences prognosis of patients with MCR has not been determined. METHODS: We performed DSE in 80 patients with CAD and LV dysfunction (ejection fraction < or =40%). Viable myocardium was defined in dysfunctional myocardial segments as enhanced thickening and contraction during low-dose dobutamine (5 to 10 mcg/kg/min). Serial prospective follow-up was obtained in all patients (mean follow-up 2.2 +/- 1.1 years). RESULTS: Among 52 patients treated medically, there were 20 cardiac deaths. By multivariate analysis, the number of dysfunctional segments demonstrating MCR was the strongest predictor of survival (p < 0.03). Patients with MCR had better initial survival during medical therapy than did those without MCR, but this survival advantage was not maintained beyond three years. In contrast, survival was excellent in patients with MCR who underwent myocardial revascularization. Among 58 patients with MCR in > or =5 myocardial segments, survival at three years was 93 +/- 6% in the 24 patients who were revascularized but only 49 +/- 15% in the 34 treated medically (p < 0.02). CONCLUSIONS: Myocardial contractile reserve is a significant predictor of survival in patients with CAD and LV dysfunction undergoing medical therapy. Although patients with MCR have an initial survival advantage, this advantage is lost over the course of three years. In contrast, survival in patients with significant MCR is enhanced by revascularization.

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OBJECTIVE: To determine the prognostic significance of creatine kinase (CK) elevation following elective percutaneous transluminal coronary angioplasty (PTCA). DESIGN: Retrospective cohort study. SETTING: Tertiary care referral center. SUBJECTS: A total of 253 consecutive patients with total CK and CK-MB fraction (CK-MB) elevation (case patients) and 120 patients without CK elevation (controls). Control patients had undergone interventions during the same month and year using the same devices. MAIN OUTCOME MEASURES: In-hospital and late cardiac mortality, subsequent myocardial infarction, and the combined end point of cardiac mortality or myocardial infarction. RESULTS: Patient groups were similar with respect to age, sex, extent of coronary artery disease, left ventricular function, number of lesions treated by PTCA, and mean duration of follow-up (>3.5 years). Cardiac mortality was significantly greater (P=.02) for patients with CK elevation after PTCA. When patients were categorized according to peak CK elevation, cardiac mortality differed significantly among patient groups (P=.007), with increased cardiac mortality observed for patients with high (>3.0 times normal) and intermediate (1.5 to 3.0 times normal) CK elevations. In multivariate analyses, higher peak CK and lower ejection fraction were the most important predictors of increased cardiac mortality (both, P<.001); the relative risk for cardiac mortality was 1.05 (95% confidence interval, 1.03-1.08) per 100-U/L increment increase in CK. CONCLUSIONS: Creatine kinase elevation following elective PTCA is associated with increased late cardiac mortality. This increase in cardiac mortality is independent of clinical variables, severity of heart disease, coronary artery lesion characteristics, interventional devices, and procedural outcomes. Even patients with lesser degrees of CK elevation are at significantly increased risk for late cardiac death.

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