Comparison of exercise electrocardiography, technetium-99m sestamibi single photon emission computed tomography, and dobutamine and dipyridamole echocardiography for detection of coronary artery disease in hypertensive women.

To assess the performance of currently used stress tests for the detection of coronary artery disease (CAD) in a series of female hypertensive patients. We performed exercise electrocardiography (ECG), technetium-99m sestamibi (MIBI) single photon emission computed tomography, dobutamine and dipyridamole echocardiography, and coronary angiography in 76 hypertensive women. Of the 76 study patients, 31 (41%) had significant CAD. The sensitivity of exercise ECG (81%), MIBI scanning (90%), and dobutamine echocardiography (87%) was greater than that of dipyridamole echocardiography (61%). This finding resulted from the lower sensitivity of dipyridamole echocardiography in the detection of single-vessel CAD (47% vs 76%, 88%, and 82% for the other 3 methods). In contrast, the sensitivity of the 4 tests was similar in the detection of multivessel CAD. The specificity of exercise ECG (56%) and MIBI scanning (53%) was less than that of dobutamine (82%, both p <0.01) and dipyridamole (91%, both p <0.001) echocardiography. This finding related to the lower specificity of exercise ECG in patients with either left ventricular hypertrophy or ST-T abnormalities at rest compared to the specificity in patients without these disorders (33% vs 89%, p <0.01). A lower MIBI scan specificity was found only in patients with left ventricular hypertrophy (31% vs 66%, p <0.05). The overall accuracy of dobutamine echocardiography reached 84% compared to exercise ECG (66%, p <0.01), MIBI scan (68%, p <0.05), and dipyridamole echocardiography (79%, p <0.05). In conclusion, dobutamine echocardiography yielded satisfactory diagnostic accuracy for identifying CAD in hypertensive women. Although dipyridamole echocardiography had the greatest specificity, it might be limited in detecting mild CAD. Both exercise ECG and MIBI scanning had fare sensitivity; however, our findings limit the usefulness of these 2 tests in unselected patients.

Assessment of residual viability by enoximone echocardiography in patients with previous myocardial infarction correlation with positron emission tomographic studies and functional follow-up.

BACKGROUND: The aim of this study was to evaluate enoximone echocardiography (EE) for the identification of residual myocardial viability in postinfarction patients. Findings obtained during EE were compared with those acquired by myocardial uptake of fluorine-18 fluorodeoxyglucose ((18)F-FDG) positron emission tomography (PET) and functional follow-up results. METHODS: Twenty-five patients underwent EE and PET (18)F-FDG studies. An asynergic segment was considered as having contractile enhancement when the wall motion score decreased by > or = 1 grade during EE and was defined as viable if (18)F-FDG uptake score was > or = 2 grade on PET. RESULTS: Of 293 dysfunctional segments at baseline, 139 (47%) were viable by PET criteria; 117 (40%) had contractile enhancement induced by enoximone (P = 0.07). Agreement between EE and PET was found in 75% of involved segments (K = 0.46, P < 0.001). The majority of discrepancies (65%, P < 0.01) were mainly due to discordant segments in which PET revealed evidence of (18)F-FDG uptake but EE showed no change in wall motion. In 179 revascularized segments, negative predictive value for functional recovery of both tests reached the same value (89% for both), whereas positive predictive value was 82% for EE and 68% for PET, respectively (P < 0.05). Sensitivity was 85% for EE and 88% for PET (P = ns); specificity was 87% and 70%, respectively (P < 0.01). CONCLUSIONS: EE yields a fair concordance with PET study. Compared with PET, despite a similar negative accuracy, EE shows a greater specificity for prediction of function recovery after revascularization. (Echocardiography 2010;27:544-551).

Acute effects of heparin administration on the ischemic threshold of patients with coronary artery disease: evaluation of the protective role of the metabolic modulator trimetazidine.

OBJECTIVES: We sought to assess the effects of heparin and the potential protective effects of trimetazidine (TMZ) on exercise performance, plasma nitric oxide (NO), endothelin-1 (ET-1) and free fatty acid (FFA) release in patients with stable coronary artery disease (CAD). BACKGROUND: Heparin has been shown to reduce the ischemic threshold in patients with CAD. Trimetazidine may affect myocardial substrate utilization by shifting energy production from FFA to glucose oxidation. METHODS: In four consecutive days, nine patients with CAD each received one of the following four regimens: 1) one tablet of placebo the evening before and at 8 AM and 4 PM on the day of the study, 10 ml of saline in a bolus 10 min before exercise, followed by an infusion of the same preparation; 2) placebo at the same times as in the first regimen, 5,000 IU of heparin 10 min before exercise, followed by 1,000 IU/h; 3) 20 mg TMZ at the same times as in the first regimen, 5,000 IU of heparin 10 min before exercise, followed by 1,000 IU/h; or 4) TMZ at the same times as in the first regimen, 10 ml of saline 10 min before exercise, followed by an infusion of the same preparation. RESULTS: During placebo (test 2), heparin reduced the time to 1-mm ST-segment depression and prolonged the recovery time, as compared with the results of test 1. When heparin was administered after TMZ (test 3), the time to 1-mm ST-segment depression and the recovery time were similar to those recorded during saline (test 1). Finally, compared with all study phases, TMZ during saline (test 4) prolonged the time to 1 mm. No changes in NO release were found, whereas ET-1 was decreased at peak exercise and during recovery, when the patients were receiving TMZ (tests 3 and 4). Free fatty acids increased after heparin, both with placebo and TMZ. CONCLUSIONS: In patients with CAD, heparin reduces the ischemic threshold. Trimetazidine reduces the effects of heparin, probably by inhibiting FFA oxidation and enhancing glucose metabolism. The concomitant novel observation of reduced ET-1 release is likely to be also dependent on TMZ-induced improvement of endothelial metabolism or reduction of myocardial ischemia.