-
[show abstract]
[hide abstract]
ABSTRACT: To investigate whether acute atrial fibrillation (AF) creates a prothrombotic state in hypertensive patients, and to assess the evolution in research indices after cardioversion.
Plasma levels of von Willebrand factor (vWf), soluble P-selectin and fibrin D-dimers were measured in hypertensive patients with acute AF pre-cardioversion and at 1, 7, 14, and 30days post-cardioversion. The results were compared with hypertensive controls and healthy controls.
Pre-cardioversion plasma vWf levels in acute AF patients were similar to those of controls; however, post-cardioversion, the vWf levels increased significantly and only returned to baseline levels 14days later. Compared with controls, acute AF patients had higher levels of fibrin D-dimers, which lasted at least 14days after cardioversion.
This study demonstrated that hypertensive patients with acute AF have an abnormal prothrombotic state, which persists for up to 14days after cardioversion.
Clinical biochemistry 10/2010; 43(15):1212-5. · 2.02 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: MMP-2 and TIMP-2 play important roles in the pathogenesis of arrhythmogenic atrial remodeling, and may contribute to the development and persistence of atrial fibrillation (AF). Functional polymorphisms in the promoter of MMP-2 and TIMP-2 gene may modulate an individual's susceptibility to AF.
A total of 881 hypertensive heart disease patients from Chinese Han population (128 with and 753 without AF) were recruited in this study. The genotypes of the MMP2-1306C>T and -735C>T polymorphisms and TIMP-2 -418G>C polymorphisms were determined using PCR based method. The plasma concentration of TIMP-2 was measured by enzyme-linked immunosorbent assay in a subgroup with 81 patients.
Both genotype distribution and allele frequency of the TIMP-2 -418G>C polymorphism were significantly different between the AF and control group (P=0.005 and P=0.001, respectively). The C allele carriers (GC+CC) had a significantly increased risk of AF compared with the GG homozygotes (odds ratio,1.77, 95% CI 1.21-2.92, P=0.009) in a logistic regression model after adjustment for age, left atrial dimension, left ventricular mass index, and antihypertensive drugs. The C allele carriers also had reduced levels of plasma TIMP-2 levels compared with GG homozygotes in both AF patients and control subjects. No relationship was found in this cohort between the presence of the MMP-2 -1306C>T and -735C>T polymorphism and AF.
The TIMP-2 -418G>C polymorphism is significantly associated with an increased susceptibility to AF in Chinese Han patients with hypertensive heart disease. The -418C allele, which is associated with a decreased expression of TIMP-2, might be a genetic risk for the development of AF in this cohort.
Clinica chimica acta; international journal of clinical chemistry 02/2010; 411(9-10):719-24. · 2.54 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: MMP-9 plays an important role in the pathogenesis of arrhythmogenic atrial remodeling, and may contribute to the development and persistence of atrial fibrillation (AF). Functional polymorphisms in the MMP-9 gene which lead to altered MMP-9 production and/or activity may modulate an individual's susceptibility to AF.
A total of 881 hypertensive heart disease patients of Chinese Han population (128 with and 753 without AF) were recruited in this study. The MMP-9 -1562C>T and R279Q genotypes were determined using PCR-RFLP method. The plasma concentration of MMP-9 was measured by ELISA.
Both the genotype distributions and allele frequencies of the -1562C>T polymorphism were significantly different between the AF and control group (P=0.007 and P=0.002, respectively). The T allele carriers (TT + CT) had significantly increased risk of AF compared with the CC homozygotes (OR 1.94, 95% CI 1.20-3.14; adjusted P=0.006) in a logistic regression model after controlling age, left atrial dimension, and the use of angiotensin-converting enzyme inhibitors and/or angiotensin receptor blockers. The T allele carriers also had increased plasma MMP-9 levels compared with CC homozygotes in both AF patients and control subjects. No relationship between R279Q polymorphism and AF was found in this cohort.
The -1562C>T polymorphism of MMP-9 gene is significantly associated with AF risk in Chinese Han patients with hypertensive heart disease. The -1562T allele which is associated with increased expression of MMP-9 might be a genetic risk for the development of AF in this cohort.
Clinica chimica acta; international journal of clinical chemistry 09/2009; 408(1-2):105-9. · 2.54 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: The activated renin-angiotensin-aldosterone system has been reported to play an important role in the pathogenesis of atrial fibrillation (AF). We hypothesized that functional genetic variations of angiotensin-converting enzyme (ACE) and CYP11B2 genes may influence the susceptibility to AF in patients with hypertensive heart disease.
The I/D polymorphism of ACE was detected by polymerase chain reaction (PCR), and the -344C/T polymorphism of the CYP11B2 gene was detected using PCR and subsequent cleavage by HaeIII restriction endonuclease.
The overall distribution of ACE I/D genotypes in patients with and without AF was significantly different (p=0.001). The frequency of the DD genotype was significantly higher in patients with AF than in patients without AF (20.6% vs. 8.1%, OR 2.94, 95% CI 1.64-5.26, p<0.001). The frequency of the D allele was significantly higher in the AF group than in the non-AF group (p=0.001). After adjustment for age and left atrial dimension, multivariable analysis showed that the DD genotype of the ACE gene was an independent risk factor for AF in patients with hypertensive heart disease. No relationship between -344 C/T CYP11B2 polymorphism and AF was found in this cohort.
Our study suggests that ACE I/D polymorphism is associated with AF and the DD genotype may be an independent predictive factor for AF in patients with hypertensive heart disease.
Clinical Chemistry and Laboratory Medicine 02/2009; 47(1):32-7. · 2.15 Impact Factor
