OBJECTIVE: 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.
Ventricular function; ventricular dilatation; ventricular hypertrophy
