Original ArticleOriginal Article 276 Cigarette Smoke Exposure Intensifies Ventricular Remodeling Process following Myocardial Infarction

To evaluate the role of cigarette smoke exposure (CSE) on ventricular remodeling following acute myocardial infarction (AMI). METHODS Rats were submitted to myocardial infarction and divided into two groups: C (control, n = 31) and F (CSE: 40 cigarettes/day, n = 22). After 6 months, the survivors were submitted to echocardiogram, functional study with isolated heart, and morphometric analysis. For comparison purposes, we used the t test (mean ± standard deviation) or the Mann-Whitney test (with median and 25th and 75th percentiles). RESULTS The CSE animals tended to have larger diastolic (C = 1.5 ± 0.4 mm2, F = 1.9 ± 0.4 mm2; p = 0.08) and systolic (C = 1.05 ± 0.3 mm2, F = 1.32 ± 0.4 mm2; p = 0.08) left ventricular(LV) areas. The systolic function of the LV, assessed according to the fractional area change, tended to be impaired in CSE animals (C = 31.9 ± 9.3%, F = 25.5 ± 7.6%; p = 0.08). The- dp/dt values for CSE animals were statistically lower (C = 1474 ± 397 mmHg, F = 916 ± 261 mmHg; p = 0.02) than for control animals. The CSE animals presented higher right ventricle (RV) weight adjusted for body weight (C = 0.8 ± 0.3 mg/g, F = 1.3 ± 0.4 mg/g; p = 0.01), higher content of water in lungs (C = 4.8 (4.3-4.8)%, F = 5.4 (5.1-5.5); p = 0.03), and larger LV myocyte cross-sectional areas (C = 239.8 ± 5.8 µm2, F = 253.9 ± 7.9 µm2; p = 0.01). CONCLUSION Cigarette smoke exposure intensifies ventricular remodeling following acute myocardial infarction. KEY WORDS Ventricular function, ventricular dilatation, ventricular hypertrophy