Association of liver X receptor α (LXRα) gene polymorphism and coronary heart disease, serum lipids and glucose levels.

BACKGROUND: To explore the relationship between the liver X receptor α gene (LXRα) rsl2221497 polymorphism and the susceptibility of coronary heart disease (CHD) and serum lipids and glucose levels. METHODS: The single fluorescently labeled probes technique was used to detect the genotype of rsl2221497 in LXRα gene in 240 CHD patients and 250 healthy control subjects. The difference of genotype distribution between the two groups was analyzed using of Chi-square test. The serum lipids and glucose levels between the different genotypes were also compared. RESULTS: The risk of CHD in carriers with (AA + GA) genotype was 1.76 times as that in the GG genotype carriers (OR = 1.76, 95% CI: 1.18-2.87, P <0.05), and the risk of CHD in carriers with A allele increased 0.88 times compared to that in G allele carriers (OR = 1.88, 95% CI:1.21-3.43, P <0.01). Logistic regression analysis showed that after adjusting for other confounding factors, A allele was an independent risk for CHD. However, there were no differences in serum lipids and glucose levels between each genotype. CONCLUSIONS: The rsl2221497 polymorphism in LXRα gene was associated with susceptibility of CHD in Han population.

Association study of angiotensin converting enzyme gene polymorphism with elderly diabetic hypertension and lipids levels.

OBJECTIVE: To investigate the relationship between angiotensin converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism and diabetic essential hypertension in elderly population. METHODS: Polymerase chain reaction (PCR) technique was used in 260 elderly normal control patients, 205 elderly hypertensive patients and 138 elderly diabetic hypertensive patients to detect the I/D polymorphism in ACE gene. RESULTS: DD genotype frequency (0.352) and D allele frequency (0.543) in elderly hypertensive patients were higher than those in the normal control patients. DD genotype (0.421) and D allele frequency (0.579) in elderly diabetic hypertensive patients were significantly higher than those in the control patients (0.133 and 0.250). The differences of DD genotype and D allele frequency between the elderly hypertensive patients and the elderly diabetic hypertensive patients were not significant (P > 0.05). CONCLUSION: ACE gene deletion is a risk factor for hypertension but is not a risk factor for diabetes in elderly population.

Modification of atrioventricular node in a special condition treating paroxysmal supraventricular tachycardia.

Modification of atrioventricular node is a usual and necessary operation to cure atrioventricular nodal reentrant tachycardia (AVNRT). In this operation, atrioventricular block is the most severe complication and its prevention is of our great concern. This complication always occurs under some special circumstances with potential risk. So, it is very important to realize such conditions, as in this paper. A patient with paroxysmal palpitation for 10 years, aggravating to shortness of breath with chest distress for 1 year; cardiac electrophysiological examination found slow conduction in both antegrade and retrograde paths of reentrant loop, and typical AVNRT could be induced. During effective ablation there was no junctional rhythm. In some special cases, modification of atrioventricular node should not only rely on the junctional rhythm to determine the ablation effect, but also on the time of cardiac electrophysiological examination, as such to avoid the severe complication of atrioventricular block caused by excessive ablation.

[Brain natriuretic peptide and left ventricular remodeling after emergency percutaneous coronary intervention in acute myocardial infarction patients].

OBJECTIVE: To investigate the effect of emergency percutaneous coronary interventional (PCI) treatment on plasma brain natriuretic peptide (BNP) levels and left ventricular remodeling in patients with acute myocardial infarction (AMI). METHODS: This study included 118 patients with AMI and 20 healthy volunteers (their results were regarded as normal reference). Fifty-two patients who underwent successful emergency PCI 6-12 hours after onset were named as PCI group, and 66 patients rejected or in whom emergency PCI failed served as the control group. Plasma BNP levels were determined with Triage rapid assay at admission,at 12, 24, 48, 72 hours and 7, 14, 28 days after admission for both groups. Left ventricular ejection function (LVEF) was assessed by echocardiography with the modified Simpson's equation on 3-5 days and 28 days. Same assay was performed for 20 healthy volunteers. RESULTS: Plasma BNP levels of both groups were significantly higher at admission than those of volunteers. There was significant difference in BNP levels between two groups at corresponding time points (all P<0.01). In PCI group, BNP level peaked during 12-24 hours after admission, whereas two peaks of elevation of BNP levels were detected in control group, the first peak appeared during 12-24 hours and the second peak on 7 days after admission. Plasma BNP levels in PCI group were significantly lower than those of control group at corresponding time points (all P<0.01). There was no difference in LVEF level between two groups on 3-5 days after admission. LVEF level after emergency PCI was significantly higher than that of control group on 28 days after admission (P<0.01). CONCLUSION: Emergency PCI lowers plasma BNP level and improve LVEF level in patients with AMI, and it may reverse ventricular remodeling.

Intracardiac basic fibroblast growth factor and transforming growth factor-beta 1 mRNA and their proteins expression level in patients with pressure or volume-overload right or left ventricular hypertrophy.

OBJECTIVES: The aim of the study was to investigate the pathogenic role of intracardiac basic fibroblast growth factor (bFGF) and transforming growth factor beta-1 (TGF beta-1) mRNA and their protein expression level in patients with ventricular volume or pressure-overload. BACKGROUND: Myocardial hypertrophy is responsiveness of cardiomyocytes and interstitial cells to ventricular stress produced by ventricular preload or/and afterload and a series of growth factors. However, the molecular mechanism by which the changes of bFGF and TGF beta-1 mRNA and their protein expression level in patients with volume or pressure-overload lead to distinct forms of cardiac hypertrophy is unclear. METHODS: 32 patients were divided into two groups: 16 patients with cardiac volume overload leading to left ventricular hypertrophy (VG) and 16 patients with pressure overload leading to right ventricular hypertrophy (PG), respectively, as compared with 5 unexpected deaths of noncardiac disease (CG), which is determinated by echocardiography and/or pathologic examination following operation; intracardiac bFGF and TGF beta-1 mRNA and their protein expression level were determined by immunohistochemistry and in situ hybridization as well as image analysis; cardiomyocytes and fibril collagen of type I and III were examined by haemotoxylin and eosin (HE) staining or sirius-red staining. RESULTS: Cardiocyte transverse diameter and fibril collagen of extracellular matrix, intracardiac bFGF and TGF beta-1 mRNA and their protein expression level in patients with volume or pressure-overload were significantly increased in both VG and PG, as compared with CG. CONCLUSION: This is the first paper to suggest that intracardiac bFGF and TGF beta-1 play a pivotal role in patients with pressure or volume-overload leading to right or left ventricular hypertrophy, composed of cardiomyocyte hypertrophy and extracellular matrix proliferation.