BACKGROUND: Post-acute myocardial infarction (AMI) ventricular septal defect (VSD) is a rare but catastrophic complication. The aim of study was to delineate the incidence and risk factors of VSD in patients after AMI treated with successful primary percutaneous coronary intervention (pPCI). METHODS AND RESULTS: In the years 2004-2006, a total of 1835 patients with AMI underwent successful pPCI in our hospital. Thirteen patients (0.71%) developed VSD after pPCI. Mean time of occurrence of VSD was 24.46 ± 9.32 h. Patients with VSD had longer time from the AMI onset to pPCI vs. patients without VSD (7.77 ± 2.83 vs. 4.49 ± 4.45, P<.001). In the VSD group, most of the patients were nonsmokers, had arterial hypertension, and had no previous history of coronary artery disease (CAD). Neither group differed in administered antiplatelet therapy. According to univariate log-regression analysis, the presence of VSD was strongly associated with age >70 years (OR=4.66; P=.007), female gender (OR=5.73; P=.004), anterior infarction (OR=3.86; P=.04), single-vessel CAD (OR=3.74; P=.03), body mass index (BMI) <25 (OR=2.98; P=.04), and left ventricular wall hypertrophy (OR=3.39; P=.03). CONCLUSIONS: Our study demonstrated that the incidence of VSD after AMI appears to have declined in patients treated with pPCI. The pathomechanism of VSD in the invasive treatment era is the consequence of several processes and needs further investigation. Advanced age, female gender, anterior infarction, single-vessel CAD, left ventricular wall hypertrophy, and low BMI are strong risk factors of this complication after AMI, which remain invariable over the years.
BACKGROUND: Post-acute myocardial infarction (AMI) ventricular septal defect (VSD) is a rare but catastrophic complication. The aim of study was to delineate the incidence and risk factors of VSD in patients after AMI treated with successful primary percutaneous coronary intervention (pPCI). METHODS AND RESULTS: In the years 2004-2006, a total of 1835 patients with AMI underwent successful pPCI in our hospital. Thirteen patients (0.71%) developed VSD after pPCI. Mean time of occurrence of VSD was 24.46 ± 9.32 h. Patients with VSD had longer time from the AMI onset to pPCI vs. patients without VSD (7.77 ± 2.83 vs. 4.49 ± 4.45, P<.001). In the VSD group, most of the patients were nonsmokers, had arterial hypertension, and had no previous history of coronary artery disease (CAD). Neither group differed in administered antiplatelet therapy. According to univariate log-regression analysis, the presence of VSD was strongly associated with age >70 years (OR=4.66; P=.007), female gender (OR=5.73; P=.004), anterior infarction (OR=3.86; P=.04), single-vessel CAD (OR=3.74; P=.03), body mass index (BMI) <25 (OR=2.98; P=.04), and left ventricular wall hypertrophy (OR=3.39; P=.03). CONCLUSIONS: Our study demonstrated that the incidence of VSD after AMI appears to have declined in patients treated with pPCI. The pathomechanism of VSD in the invasive treatment era is the consequence of several processes and needs further investigation. Advanced age, female gender, anterior infarction, single-vessel CAD, left ventricular wall hypertrophy, and low BMI are strong risk factors of this complication after AMI, which remain invariable over the years.