Effect of Different Styles of Coronary Heart Disease and Its Risk Factors on Cardiac Remodeling and Dysfunction

Objectives To evaluate the effect of different styles of coronary heart disease （CHD）, different regions of acute myocardial infarction （AMI）, its risk factors and branches of coronary stenosis on left ventricular remodeling and dysfunction by applying echocardiography. Methods 251 patients with CHD and 96 patients without CHD （NoCHD） were verified by selective coronary angiography. CHD patients were divided into stable angina pectoris （SAP） 26, unstable angina pectoris（UAP） 53, acute myocardial infarction （AMI） 140 and old myocardial infarction （OMI） 30 based on clinical situation, cTnT, cardiac enzyme and ECG. AMI patients were further divided into subgroups including acute anterior myocardial infarct （Aa,n = 53）, acute inferior myocardial infarction （Ai, n=54） and Aa＋Ai （n=33） based on ECG. Cardiac parameters： end-diastolic interventricular septum thickness（IVSd）, end-diastolic left ventricular internal diameter （LVd）, left ventricular mass （LM）, end-diastolic left ventricular volume （EDV）, end-systolic left ventricular volume （ESV） and left ventricular ejection fraction（LVEF） were measured by ACUSON 128XP/10 echocardiography. Multiples linear regression analyses were performed to test statistical associations between LVEF and the involved branches of coronary stenosis, blood pressure, lipids, glucose and etc after onset of myocardial infarction. Results EDV and ESV were increased and LVEF decreased on patients with AMI,OMI and UAP （P〈0.05-0.0001）. LM was mainly increased in patients with OMI （P〈0.01） and LVd was mainly enlarged in patients with AMI. EF was significantly decreased and EDV, ESV, LM and LVd were remarkably increased in AMI patients with Aa and Aa＋Ai. With the multiple linear regression analyses by SPSS software, we found that LVEF was negatively correlated to the involved branches of coronary stenosis as well as to systolic blood pressure after onset of myocardial infarction while there was no significant correlation between LVEF and other factors. LVEF was significantly decreased, and LVd and LM increased in AMI patients with antecedent hypertension, compared to patients without hypertension （P〈0.001）. Conclusions Effects of different styles of CHD and different regions of AMI on left ventricular remodeling and cardiac function are different. Myocardial infarction, especially Aa and Aa＋Ai, is one of the most important causes of left ventricular remodeling and cardiac dysfunction. Multiple vessel stenosis and systolic blood pressure at the onset of myocardial infarction reduce LVEF in AMI patients. Antecedent hypertension may accelerate the effect of AMI on cardiac remodeling and dysfunction. Therefore primary and secondary preventions of CHD are critical for protecting heart from remodeling and dysfunction.

The Study on the Correlation Between Plasma Adiponectin Level and Coronary Heart Disease

Objectives To investigate the relationship between plasma adiponectin level and coronary heart disease （CHD）, and some established cardiovascular risk factors and to probe its probable pathogenesis which adiponectin results in CHD. Methods The levels of plasma adiponectin, fasting plasma insulin （FINS）, C-reactive protein （CRP） and P-selectin were measured by ELISA, plasma ET-1 was measured by radioimmunoassay （RIA） in 75 male patients with CHD and 30 healthy male people. Body mass index （BMI）, waist / hip ratio （WHR） and insulin resistance index （Homa-IR） were calculated respectively. Results （1）The plasma adiponectin levels in CHD group were lower compared with control group[（5.18±2.57）mg / L vs（8.94±2.59）mg / L, P〈 0.001 ], there was no significant difference of plasma adiponectin levels in CHD sub-groups （P 〉 0.05）.（2） Based on multinominal stepwise logistic regression analysis, adiponectin was one of significant and independent risk factors for CHD. （3） Multivariate liner stepwise regression analysis showed that adiponectin had significant correlation with BMI and TG, BMI and TG were independent factors influencing on plasma adiponectin levels. （4） Pearson correlation analysis indicated plasma adiponectin levels were inversely related to FINS levels , Homa-IR, CRP, P-selectin and ET-1. Conclusions （ 1 ）Plasma adiponectin levels are lower in CHD patients compared the control subjects, there are no significant difference of plasma adiponectin levels in patients with SAP, UAP and AMI. （2） Plasma adiponectin levels are relative with CHD. Hypoadiponectinemia is an independent risk factor for CHD. （3）Established cardiovascular risk factors such as BMI and TG have an obvious influence on adiponectin. （4）The probable pathogenesis by which adiponectin involves in CHD is suggested that adiponectin relates to insulin resistance, inflammatory reaction and dysfunction of vessel endothelium.

Hyperhomocysteinemia and hyperlipidemia in coronary heart disease

bjective To examine the relationship between coronary heart disease (C HD) and serum lipid, plasma homocysteine (HCY) as well as the factors related to HCY metabolisms Methods The mutation of the 677CT transition of 5,10methylenetetrah ydrofolate reductase(MTHFR) was determined by PCRbased assay Wholeblood an d plasma folate and plasma vitamin B12, as cofactors of MTHFR, were determi ned by radioimmunologic assay Plasma HCY was determined by HPLC Results Patients with CHD had elevated plasma HCY concentrations (173 8 194?mol/L vs 1025157?mol/L, P <001) In patients w ith my ocardial infarction (MI) and family history (FH) of CHD, plasma HCY were elevate d even higher ( P <005) Plasma HCY concentrations had significant no nlinear inverse correlation with plasma folate and B12 concentrations, i e the lower the serum folate or B12 concentrations, the higher the plasma HC Y co ncentrations ( P <001) Patients with homozygous mutants had higher p lasma HCY concentrations Patients with CHD had increased serum Chol and LDLC and ApoB levels ( P <001, P <005 and P <0 05 respectively) But plasma HCY concentrations had no correlation with serum lip i d levels 241% of the patients had high lipid and high HCY level, 259% had hig h lipid level and normal HCY level, 204% had normal lipid and high HCY level, and 296% had normal lipid and HCY level Conclusions HCY may have strong association with the genesis of CHD L o w plasma folate and B12 concentrations may induce Hyperhomocysteinemia Plasma HCY concentrations have no correlation with serum lipid lev els, so H C Y may be an independent risk factor CHD may be induced by different mechanisms and can be classified into hyperlipidemia, HH(e) and normolipidemia, and normoho mocysteinemia