Résumé
Hepatitis C disease burden is substantially increasing in Egyptian community, it is estimated that prevalence of Hepatitis C virus [HCV] in Egyptian community reach 22% of total population. Recently there is a global alert of HCV cardiovascular complications. To evaluate LV diastolic functions of HCV patients using tissue Doppler Imaging and NTPBNP. 30 HCV patients of 30 years, sex and BMI matched controls were evaluated by PCR, ECG, Echocardiography "conventional Doppler, pulsed wave tissue Doppler [PW-TD], strain rate imaging" and NTPBNP to assess LV diastolic functions. Mean age was 32.8 years +/- 5.1 in HCV group, 29.8 years +/- 6.6 in control group. Cardiovascular anomalies and predisposing factors were excluded. HCV group has shown significant increase in QTc interval, significant statistical increase in A wave, deceleration time; [p < 0.05], highly significant decrease in tissue Doppler E[a] [p < 0.001], highly significant decrease in A[a] [p < 0.001], highly significant increased E/E[a] ratio [p value < 0.001], significant decrease in E[a]/A[a] ratio and significant increase in SR[a] [p < 0.05]. NTPBNP levels showed highly significant increase with mean value 222 pg/ml +/- 283 in HCV group and 32.7 pg/ml +/- 21.2 in control group [p value < 0.001]. The best cut-off value of NTPBNP to detect diastolic dysfunction in HCV group was 213 pg/ml. No statistical differences in SRe/SRa and E/SRe ratios were observed, however they had significant correlation with NTPBNP level and tissue Doppler parameters. The best cut-off value of E/SRe ratio to detect diastolic dysfunction in HCV group was 0.91, with 75% sensitivity and 100% specificity. This data show the first direct evidence that HCV infection causes diastolic dysfunction without any other predisposing factors, probably due to chronic inflammatory reaction with mild fibrosis in the heart. Previous studies did not follow strict inclusion and exclusion criteria that confirm the independent role of HCV to cause diastolic dysfunction. Tissue Doppler was more sensitive to diagnose diastolic dysfunction than conventional Doppler
Résumé
Coronary collateral blood vessels formation helps to preserve myocardial function in coronary artery disease as their presence reduces the degree of myocardial ischemia and functional deficit. Vascular endothelial growth factor [VEGF] plays a significant role in this adaptive process. Diabetes mellitus decreases the expression of messenger ribodeoxy nucleic acid [mRNA] and protein for VEGF and its receptors in the myocardium, so diabetes mellitus is one of the first negative predictors of collateral vessel formation. The aim of this work is to estimate the level of serum VEGF in a group of non diabetic patients complaining of coronary artery disease and another group of non insulin dependent diabetic patients complaining of coronary artery disease and to evaluate the relation between diabetes mellitus and the level of VEGF in patients complaining of coronary artery disease in comparison to control group and to assess the relation of VEGF level to systolic and diastolic functions of the heart and to resting wall motion abnormalities in ischemic heart disease patients. In this study we measured the serum level of VEGF in 30 non diabetic patients with coronary artery disease, 30 non insulin dependent diabetic patients with coronary artery disease and 20 apparently healthy subjects matched for age and sex using enzyme immunoassay methods. The study revealed that as in non diabetic patients with coronary artery disease, there was a significant increase in the level of serum VEGF while in diabetic patients there was a significant decrease of the serum level of VEGF, so diabetes mellitus is considered a major risk factor for patients with coronary artery disease as it decreases the level of VEGF induced by myocardial ischemia which is very important for the formation of coronary collaterals. This effect was reflected on systolic and diastolic functions and wall motion abnormalities which were more significantly affected in type 2 diabetic patients and could be explained by reduced collateral vessel formation