This study shows that stress echo in patients with hypertension yields a satisfactory diagnostic accuracy for identifying significant epicardial CAD. Our results indicate that dobutamine might be superior to dipyridamole. The low specificity of myocardial scintigraphy probably relates to the fact that this method traces perfusion abnormalities, not necessarily caused by epicardial CAD, possibly due to microvascular disease and not causing obvious wall motion abnormalities.

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Background —The possibility that enoximone, a nonglycoside, noncatechol, positive inotropic agent, in combination with 2-dimensional echocardiography may predict recovery of myocardial dysfunction after revascularization has not been yet evaluated. Methods and Results —Forty-five patients with chronic coronary artery disease and left ventricular dysfunction underwent dobutamine (DE, 5 to 10 μg · kg −1 · min −1 ) and enoximone (EE, 1.5 mg/kg, over 10 minutes) echocardiography. Myocardial wall motion was scored from 1 (normal) to 4 (dyskinesia): an asynergic segment was considered to have contractile enhancement when the score decreased by ≥1 grade. Of 478 asynergic segments, 216 (45%) exhibited functional recovery after revascularization. Dobutamine- and enoximone-induced contractile enhancement was observed in 41% and 46% of segments, respectively. Compared with DE, EE had higher sensitivity (88% versus 79%, P <0.01) and negative predictive value (90% versus 84%, P <0.05) in predicting functional recovery. The specificity (89% versus 90%) and positive predictive value (87% for both EE and DE) were similar. Concordant interpretation of EE and DE findings was found in 85% (406 of 478) of affected segments. Prerevascularization coronary angiography showed that stenosis severity of vessels supplying areas which only improved with enoximone was significantly greater (89.9%) than that of vessels (77.7%) supplying areas that responded to both agents ( P <0.02). Both dobutamine and enoximone increased heart rate (16% and 10%, respectively), whereas enoximone did not cause changes in systolic blood pressure that increased by 14% with dobutamine. Conclusions —Enoximone echocardiography provides a novel and reliable approach for the prediction of functional recovery after revascularization. Compared with dobutamine echocardiography, the test yields higher sensitivity and induces lesser hemodynamic alterations.

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.

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In patients with single-vessel disease without coronary occlusion or previous myocardial infarction, coronary lesion morphology of the complex type is associated with a higher DSE sensitivity and with a greater prevalence of low-dose, positive responses. Presence of irregular plaque contours, not only plaque geometry, is important in modulating stress responses in the presence of angiographically assessed coronary artery disease.

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We have recently shown that in patients with single vessel disease and no myocardial infarction, a complex plaque morphology makes myocardium more vulnerable to ischaemia during dipyridamole echocardiography testing. Whether coronary lesion morphology in the infarct-related artery in a chronic phase may also modulate prevalence of ischaemia in the same territory remains unknown. In order to determine the possible relationship between culprit lesion morphology in the infarct-related artery and the prevalence of homotopic ischaemia during stress tests, data from high dose dipyridamole echocardiography tests (up to 0.84 mg.kg-1 over 10 min), exercise electrocardiography and coronary angiography from 73 in-hospital patients with a previous myocardial infarction and patent infarct-related single-vessel disease (> or = 50% diameter reduction) were analysed. An angiographic culprit lesion was considered complex (Ambrose classification) when irregular borders, ulcers, thrombus and/or intraluminal lucencies were present. According to angiographic lesion morphology, two groups were identified: Group I, with simple-type culprit lesions; Group II, with complex type culprit lesions. Number of patients (I = 36; II = 37), age (I = 57 +/- II vs II = 55 +/- 9 years), ejection fraction (I = 58.8 +/- II 3 vs II = 56.5 +/- 10.2%), number of Q or non-Q wave myocardial infarctions, prevalence of rest angina (I = 9; II = II) or effort angina (I = 10; II = 10), culprit lesion stenosis severity (I = 57.9 +/- 7.2% vs II = 57.7 +/- 6.2% by computer analysis) and degree of infarct artery anterograde flow (I = 2.64 +/- 0.48 vs II = 2.56 +/- 0.50 by Thrombolysis in Myocardial Infarction definition) did not differ between the two groups (P = ns for all intergroup differences). Dipyridamole echocardiography test-induced ischaemia (considered as new or worsening abnormal wall motion) in the infarct-related artery territory was 25% in Group I and 59% in Group II (P < 0.01). Among positive dipyridamole echocardiography tests, low dose (0.56 mg.kg-1 over the 4 min) positivity occurred in two out of nine Group I patients and in 16 out of 22 Group II patients (22 vs 73%, P < 0.05). Exercise electrocardiography was positive in seven out of 32 Group I patients, and in 16 out of 35 Group II patients (22 vs 46%, P < 0.05). The peak rate pressure product tended to be higher in Group I than in Group II patients (282 +/- 65 vs 257 +/- 65 mmHg x beats.min x 10(2), P = 0.07). Thus, in patients with previous myocardial infarction and a patent infarct-related artery, complex culprit lesion morphology is associated with a higher prevalence of ischaemia and a lower ischaemic threshold during both exercise and dipyridamole stress testing. The morphology of culprit stenosis is important in modulating different stress responses in the chronic phase of myocardial infarction.