The effect of thrombolytic therapy on left ventricular aneurysm formation in acute myocardial infarction: Relationship to successful reperfusion and vessel patency

Background: Although there is increasing evidence for the beneficial effect of thrombolytic therapy on global left ventricular (LV) function in acute myocardial infarction (AMI), the data concerning the early effect of thromb olytic therapy on the incidence of left ventricular aneurysm (LVA) formatio n and its relationship to clinical and angiographic determinants are limite d. Hypothesis: The study aimed to determine the independent factors involved i n the development of IVA and to evaluate whether thrombolytic therapy has a ny preventive effect on the development of LVA in AMI. Methods: In all, 350 consecutive patients suffering from a first attack of AMI were included, Of these, 205 who arrived within 12 h of onset of sympto ms received thrombolytic therapy (thrombolytic group) and the remaining 145 patients served as control group. All patients received aspirin and maxima l-dose anticoagulation with intravenous heparin therapy. Early successful r eperfusion was assessed by enzymatic and electrocardiographic evidence, and late vessel patency was evaluated according to Thrombolysis in Myocardial Infarction (TIMI) classification. Patients with TIMI grade 2 or 3 flow were considered to have vessel patency. Results: The overall incidence of IVA was 11.7% (41/350), and no statistica l difference was found between the incidence of LVA between the two groups (11.7 vs. 11.7%, p>0.05). However, the patients receiving thrombolytic ther apy and exhibiting a patent infarct-related artery (PIRA) (n=125, 61%), had a significantly reduced incidence of LVA compared with those who did not ( 7.2 vs. 18.8%, p=0.015). In univariate analysis, vessel patency, proximal l eft anterior descending artery (LAD) stenosis, total LAD occlusion, multive ssel disease, and hypertension were found to be important factors in LVA fo rmation after AMI. After adjustment for other clinical and angiographic var iables, total LAD occlusion (odds ratio [OR] 3.62, 95% confidence interval [CI] 2.45-8.42, p=0.0014), absence of PIRA (OR 2.92, 95% CI 1.41-09, p=0.00 37) and proximal LAD stenosis (OR 2.11, 95% CI 1.05-4.71, p=0.045) remained the independent determinants of LVA formation after AMI. Conclusion: Our data indicate that not all patients who received thrombolyt ic therapy, but only those with PIRA had evidently reduced the incidence of LVA. Patients with total LAD occlusion, with proximal LAD stenosis, and wi thout PIRA were found to have increased risk for formation of LVA after AMI . These findings indicate that the presence of vessel patency has a prevent ive effect on LVA formation in AMI.