DOBUTAMINE STRESS ECHOCARDIOGRAPHY FOR THE IDENTIFICATION OF MULTIVESSEL CORONARY-ARTERY DISEASE AFTER UNCOMPLICATED MYOCARDIAL-INFARCTION - THE IMPORTANCE OF TEST END-POINT

Our aim was to verify whether the sensitivity of pharmachological stre ss echocardiography for multivessel disease after acute myocardial inf arction may be improved by a more aggressive protocol, i.e. not consid ering the appearance of the first wall motion abnormality as the absol ute end-point if it occurs in the infarcted area without clinical or i nstrumental markers of extensive ischemia or left ventricular dysfunct ion. One-hundred twenty-one consecutive patients (age 32-71 years) pro spectively underwent dobutamine-atropine stress echo (dobutamine infus ion up to 40 mu g/kg/min with additional atropine 1 mg) 11.8 +/- 4.8 d ays after uncomplicated myocardial infarction and coronary angiography within 6 weeks. Criteria for stopping the test were: significant ST d epression or elevation, typical chest pain, major arrhythmias and left ventricular dysfunction. The test was considered as positive if a det erioration of basal wall motion pattern was observed: it was defined h omozonally positive (the deterioration occurred in the myocardial area fed by the culprit vessel) or heterozonally positive (the deteriorati on occurred in a different vascular area). A coronary stenosis > 70% o f vessel lumen was defined as critical. Thirty-four patients showed a negative test result. Among the 87 patients with positive test, 65 had no further wall motion deterioration from the first-induced wall moti on abnormality (WMA) to peak test (Group A), whereas nine patients sho wed further homozonal (Group B) and 13 further heterozonal (Group C) a synergies. Sensitivity, specificity and accuracy of dobutamine stress echocardiography for multivessel disease were, respectively, 63%, 96% and 82% using the first-induced wall motion abnormality as test end-po int, whilst they were 84%, (P < 0.01), 93% and 89% according to the ag gressive approach previously described. Dobutamine stress time of pati ents with multivessel disease was higher in Groups B and C (13.1 +/- 3 .6 min) than in Group A (9.8 +/- 3.7 min, P < 0.01) and, finally, the mean obstruction of non-culprit vessel was higher in Group A. (62.2%) than in Group C (47.4%, P < 0.05). No major complications were found. We conclude that the sensitivity of dobutamine stress echocardiography for multivessel disease following recent myocardial infarction is cri tically dependent on the test end-point. It may be improved by a more aggressive approach capable to identify less severe heterozonal corona ry lesions.