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

• Published in: Clinical cardiology (Mahwah, N.J.) N.J.), 2001-10, Vol.24 (10), p.656-662
• Main Authors: Tikz, H., Balbay, Y., Atak, R., Terzi, T., Gençl, Y., Utüuk, E. Kü
• Format: Article
• Language: English
• Subjects: Adult; Biological and medical sciences; Blood. Blood coagulation. Reticuloendothelial system; Collateral Circulation; Coronary Aneurysm - etiology; Coronary Aneurysm - prevention & control; Coronary Angiography; Coronary Circulation; Female; Fibrinolytic Agents - therapeutic use; Humans; left ventricular aneurysm; Male; Medical sciences; Middle Aged; myocardial infarction; Myocardial Infarction - complications; Myocardial Infarction - physiopathology; Myocardial Reperfusion; Pharmacology. Drug treatments; Prospective Studies; Streptokinase - therapeutic use; successful reperfusion; Thrombolytic Therapy; Tissue Plasminogen Activator - therapeutic use; Ventricular Function, Left; vessel patency
• ISSN: 0160-9289; 1932-8737
• DOI: 10.1002/clc.4960241005

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 thrombolytic therapy on the incidence of left ventricular aneurysm (LVA) formation and its relationship to clinical and angiographic determinants are limited. Hypothesis: The study aimed to determine the independent factors involved in the development of LVA and to evaluate whether thrombolytic therapy has any 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 symptoms received thrombolytic therapy (thrombolytic group) and the remaining 145 patients served as control group. All patients received aspirin and maximal‐dose anticoagulation with intravenous heparin therapy. Early successful reperfusion was assessed by enzymatic and electrocardiographic evidence, and late vessel patency was evaluated according to Thrombolysis in Myocardial Infarction (TIMI) classification. Patients with TTMI grade 2 or 3 flow were considered to have vessel patency. Results: The overall incidence of LVA was 11.7% (41/350), and no statistical 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 therapy 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 left anterior descending artery (LAD) stenosis, total LAD occlusion, multivessel disease, and hypertension were found to be important factors in LVA formation after AMI. After adjustment for other clinical and angiographic variables, 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 = 0.0037) 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 thrombolytic therapy, but only those with PIRA had evidently reduced the incidence of LVA. Patients with total LAD occlusion, with proximal LAD stenosis, and without PIRA were found to have increased risk for formation of LVA after AMI. These findings