[In patients with coronary artery disease and left ventricular contractile insufficiency the pathogenicity of smoking associates with imbalance in metabolism of homocysteine]

Abstract

Development of the systolic left ventricular insufficiency in patients with coronary artery disease (CAD) markedly decreases the survival rates, so the factors affecting the clinical status of these patients should be reevaluated. The left ventricular contractile function has been assessed by measurements of the left ventricular ejection fraction (LVEF) values. The studied group of 160 males comprised 102 CAD patients diagnosed by coronarography, and 58 persons without CAD and left ventricular systolic insufficiency. The CAD patients were divided into 2 subgroups according to the LVEF values: 53 patients qualified to have normal left ventricular contractile function (with LVEF > 40%), and 49-patients, with LVEF < or = 40%, were considered as subgroup with the left ventricular contractile insufficiency. In the case-control set up the effects of smoking, concentrations of homocysteine (Hcy) and folic acid (FA) and of the known risk factors of the vascular diseases in the development of the left ventricular contractile insufficiency were assessed. Moreover, analysis was performed of the association between LV insufficiency and the statin therapy and the number of infarcts. LV insufficiency in CAD patients associated with increased diastolic pressure (p = 0.006) and with increased uric acid concentrations in plasma (p = 0.02). The smoking, decrease in HDL-C and increased index TC/HDLC were the risk factors of CAD, independent of the LV insufficiency. In comparison to the CAD patients with the preserved systolic function, in the group of CAD patients with LV systolic insufficiency, more persons had recurrent infarcts (34.7% vs. 5.7%), and less persons had no infarct (8.2% vs. 20.8%, p < 0.05). In CAD patients with LV systolic insufficiency smoking associated with the higher values of HC/FA index (p = 0.01), younger age of the patients (p = 0.01), the number of persons not treated with statins (0.01) and the number of persons not having had heart infarct before (p < 0.05). These findings confirm both the effects of infarcts on the development of LV insufficiency, and the presumed association between the pathogenicity of smoking in LV insufficiency and the unbalanced metabolism of Hcy. The straight of the effect of smoking on the development of LV insufficiency in susceptible persons is shown also by the findings of the younger age of the smoking CAD patients as compared to the nonsmoking patients with LV insufficiency.