Impact of culprit lesion morphology on prevalence of provoked myocardial ischaemia in patients with old myocardial infarction. A dipyridamole stress echocardiography, exercise electrocardiography and angiographic study.

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.