Copyright © 1997 by the European Society of Cardiology.
© 1997 The European Society of Cardiology
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
Institute of Clinical Physiology, CNR and Medical School, University of Pisa Pisa, Italy
revised 30 May 1996; accepted 5 June 1996.
Correspondence: Alessandro Distante, MD, Istituto di Fisiologia Clinica, CNR, Institute of Cardiology, Pisa University, Via Paolo Savi, 8, 56126 Pisa, Italy
Abstract
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 myocar dial infarction and patent infarct-related single- vessel disease (
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 ± 11 vs II=55 ± 9 years), ejection fraction (I=58·8 ± 11·3 vs II=56·5 ± 10·2%), number of Q or non-Q wave myocardial infarctions, prevalence of rest angina (I=9; II=11) 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 102, 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.
Key Words: Myocardial infarction • ischaemia • stress echocardiography • exercise • lesion