Association of Lipoprotein-Associated Phospholipase A2 with Characteristics of Vulnerable Coronary Atherosclerotic Plaques

PURPOSE: Lipoprotein-associated phospholipase A2 (Lp-PLA2) is an inflammatory enzyme expressed in atherosclerotic plaques. We investigated the association of circulating Lp-PLA2 with characteristics of vulnerable coronary atherosclerotic plaques. MATERIALS AND METHODS: We recruited 113 patients with either unstable angina (UA, n=59) and stable angina (SA, n=54) by coronary angiography. Thirty-six healthy subjects served as controls. Intravascular ultrasound (IVUS) was used to evaluate the characteristics of coronary atherosclerotic plaque, and serum Lp-PLA2 concentration was measured as well. RESULTS: Lp-PLA2 concentration was significantly higher in both UA and SA patients [(396+/-36) microg/L and (321+/-39) microg/L, respectively] compared with the controls [(127+/-49) microg/L, p<0.01], and higher in UA than SA group. IVUS findings showed that remodeling index (RI) (0.91+/-0.15 vs. 0.85+/-0.11, p=0.005) and eccentricity index (EI) (0.73+/-0.16 vs. 0.65+/-0.22, p=0.039) were larger in UA than in SA group, and fibrous caps were thicker in SA than UA group [(0.91+/-0.23) mm vs. (0.63+/-0.21) mm, p=0.032]. Moreover, Lp-PLA2 correlated positively with EI (r=0.439, p<0.01) and RI (r=0.592, p<0.05) in UA group. There was an inverse relationship between Lp-PLA2 and fibrous cap thickness in both UA (r=-0.587, p<0.001) and SA (r=-0.318, p<0.05) groups. The independent risk factors in UA group were Lp-PLA2 (OR=1.055, 95% CI: 1.03-1.08, p=0.013), LDL-cholesterol (OR=0.032, 95% CI: 0.00-0.05, p=0.041) and fibrous cap thickness (OR=0.008, 95% CI: 0.00-0.45, p=0.019). Lp-PLA2 was strongly associated with both EI and fibrous cap thickness in both groups. CONCLUSION: Serum level of Lp-PLA2 is associated with both eccentricity index and fibrous cap thickness in both UA and SA groups. Elevated levels of circulating Lp-PLA2 might to be a strong risk factor and more serious for unstable angina than stable angina.

Plasma activated coagulation factor VII and Msp I polymorphism in elderly patients with coronary heart disease / 中华医学遗传学杂志

<p><b>OBJECTIVE</b>To investigate the association of activated coagulation factor VII(F7a) and its gene Msp I polymorphism with coronary heart disease in elderly patients.</p><p><b>METHODS</b>This was a case-control study, and the method of candidate gene was adopted. F7 genotypes were identified with polymerase chain reaction amplified genomic deoxyribonulieic acid (DNA) and Msp I restriction fragment length polymorphism analysis, and the level of plasma F7a was detected with recombinant tissue factor method for 108 elderly patients with coronary heart disease and 120 sex- and age-matched healthy control subjects.</p><p><b>RESULTS</b>(1) Plasma F7a levels was significantly higher in elderly patients with coronary heart disease than in healthy control subjects (2.88 +/- 0.62 vs 2.58 +/- 0.60 microg/L, P < 0.05), and was significantly higher in old myocardial infarction than in stable angina pectoris (3.12 +/- 0.62 vs 2.76 +/- 0.60, P < 0.05). F7a was shown to be a risk factor for coronary heart disease in elderly patients by Logistic regression analysis (OR=1.21 P < 0.05). (2) The allelic frequencies were in accordance with Hardy-Weinberg equilibrium. The results suggested that the distribution of genotype and allelic frequencies in the groups displayed no significant difference, and there was no difference between the subgroups of coronary heart disease in elderly patients, either (P > 0.05). (3) F7a level was significantly higher in RR genotype than in Q allele carriers (2.72 +/- 0.60 vs 1.98 +/- 0.59 microg/L, P < 0.05) and was associated with F7 gene polymorphism.</p><p><b>CONCLUSION</b>Plasma F7a level may be an independent risk factor of coronary heart disease in elderly patients, and it may be influenced by the Msp I polymorphism of F7 gene.</p>

The effect of physical training on insulin resistance in patients with chronic heart failure / 中华物理医学与康复杂志

Objective To investigate insulin resistance and the effect of physical training on it in the pa- tients with chronic heart failure (CHF). Methods One hundred and twenty NYHAⅡ-ⅢCHF patients were ran- domly divided into a training group( n = 65 ) and a routine therapy group (n = 55 ). Another 35 healthy subjects were recruited as control group. All the patients were treated with routine anti-CHF drugs, and the training group patients had received physical training twice a day in addition. The HOMA-IR, insulin sensitivity index (ISI) , left ventricu- lar ejection fraction (LEVF), left ventricular fractional shortening( LVFS), 6-minute walking distance, heart rate and mean blood pressure were compared between the training and routine therapy groups before and after physical ex- ercise in both groups, and a comparison was made between the patients and the controls before the intervention with regard to HOMA-IR and ISI. Results Comparing with control group, ISI was reduced while the HOMA-IR in- creased (P

Changes in NT-proBNP after physical training in patients with chronic heart failure / 中华物理医学与康复杂志

Objective To investigate the effect of physical training on plasma N-terminal pro-brain natri- uretic peptide(NT-proBNP)levels in patients with chronic heart failure(CHF).Methods Eighty NYHAⅡ-ⅢCHF patients were randomly divided into a training group(n=42)and a control group(n=38).A 6-minute walk- ing test was performed within 24 hours after the patients were admitted.The 6-minute walking distance and plasma NT-proBNP levels were determined before and after 8 weeks of programmed physical training.The patients of both groups were treated with routine drugs for heart failure.6-minute walk training was only performed in the training group twice a day for 8 weeks.Results Physical training could significantly reduce plasma NT-proBNP levels and improve performance on the 6-minute walking test.Conclusions Physical training could significantly reduce plas- ma NT-proBNP levels and improve the motor function of patients with CHF,and could be helpful in delaying the de- velopment of CHF.