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[Cigarette smoke exposure intensifies ventricular remodeling process following myocardial infarction].

Arquivos Brasileiros de Cardiologia

Ventricular Remodeling, Animals, ultrasonography, etiology, Ventricular Dysfunction, Left, adverse effects, Tobacco Smoke Pollution, physiology, Systole, Statistics, Nonparametric, Rats, Wistar, Rats, physiopathology, Myocardial Infarction, Male, Hypertrophy, Left Ventricular, Echocardiography

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      Abstract

      To evaluate the role of cigarette smoke exposure (CSE) on ventricular remodeling following acute myocardial infarction (AMI). 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). 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 microm2, F = 253.9 +/- 7.9 microm2; p = 0.01). Cigarette smoke exposure intensifies ventricular remodeling following acute myocardial infarction.

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      /S0066-782X2006000400007
      16680292

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