To explore the relation of angiotensin-converting enzyme (ACE) and angiotensin II type 1 receptor (AT1R) gene polymorphism with coronary heart disease (CHD) and the severity of coronary artery stenosis, 130 CHD patients who underwent coronary angiography were examined for the number of affected coronary vessels (> or = 75% stenosis) and coronary Jeopardy score. The insertion/deletion of ACE gene polymorphism and AT1R gene polymorphism (an A-->C transversion at nucleotide position 1166) were detected by using polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) in CHD patients and 90 healthy serving as controls. The results showed that DD genotype and of ACE were more frequent in CHD patients than that in control group (38.5% vs 14.4%, P<0.001). The frequency of the AT1R A/C genotypes did not differ between the patients and the controls (10% vs 13.1%, P>0.05). The relative risk associated with the ACE-DD was increased by AT1R-AC genotype. Neither the number of affected coronary vessels nor the coronary score differed among the ACE I/D genotypes (P>0.05). But the number of affected coronary vessels and the coronary score were significantly greater in the patients with the AT1R-AC genotype than in those with the AA genotype (P<0.05). In conclusion, DD genotype may be risk factor for CHD and MI in Chinese people, and is not responsible for the development of the coronary artery stenosis. The AT1R-C allele may increase the relative risk associated with the ACE-DD genotype, and may be involved in the development of the stenosis of coronary artery.
Coronary Disease/genetics ; Coronary Disease/pathology ; Coronary Stenosis/*genetics ; Coronary Stenosis/*pathology ; Peptidyl-Dipeptidase A/*genetics ; Polymorphism, Genetic ; Receptor, Angiotensin, Type 1/*genetics

OBJECTIVE: To investigate the association of CXCL12 and CXCR4 polymorphisms with the genetic risk and severity of coronary stenosis in patients with coronary artery disease (CAD). METHODS: Competitive allele specific PCR(KASP) was performed to identify the genotypes of rs2297630 and rs2322864 polymorphisms in 302 CAD patients and 302 age-and gender-matched healthy controls. The severity of CAD patients was assessed by the Gensini scoring system according to the results of coronary arteriography. The association of rs2297630 and rs2322864 polymorphisms with genetic risk of CAD and Gensini scores were analyzed by unconditional logistic regression and multivariate linear regression respectively. RESULTS: There were significant differences in the genotype and allele frequencies of both rs2297630 and rs2322864 between the CAD group and healthy control (all <0.01). Regression analysis showed that rs2297630 polymorphism was associated with genetic risk of CAD and Gensini scores (all <0.01). People who carried the AA genotype suffered higher risk of CAD susceptibility and more serious coronary stenosis (all <0.01), compared with GG genotype carriers. There was also significant association between rs2322864 polymorphism and genetic risk of CAD (<0.01); those who carried the CT genotype had higher risk of CAD (<0.01), compared with TT genotype carriers. However, rs2322864 polymorphism was not associated with the severity of coronary stenosis (>0.05). CONCLUSIONS Gene polymorphism of CXCL12 rs2297630 is associated with the genetic risk of CAD and the severity of coronary stenosis. Moreover, the gene polymorphism of CXCR4 rs2322864 is associated with genetic risk of CAD, but not with the severity of coronary stenosis.
Chemokine CXCL12 ; genetics ; Coronary Angiography ; Coronary Artery Disease ; complications ; Coronary Stenosis ; complications ; genetics ; Gene Frequency ; Genetic Predisposition to Disease ; Genotype ; Humans ; Polymorphism, Genetic ; Receptors, CXCR4 ; genetics ; Risk Factors

Aortic Valve Stenosis ; blood ; diagnosis ; etiology ; Child ; Coronary Artery Disease ; blood ; diagnosis ; etiology ; Coronary Vessels ; diagnostic imaging ; pathology ; Echocardiography ; Female ; Humans ; Hyperlipoproteinemia Type II ; blood ; complications ; diagnosis ; genetics ; Lipoproteins, LDL ; blood ; Triglycerides ; blood

BACKGROUND/AIMS: Underlying cardiac pathology and atrial fibrillation (AF) affect the molecular remodeling of ion channels in the atria. Changes in the expression of these molecules have not been demonstrated in Korean patients with mitral valvular heart disease. Thus, the purpose of this study was to analyze ion channel expression in patients with chronic AF and mitral valvular heart disease. METHODS: A total of 17 patients (eight males and nine females; mean age, 57 +/- 14 years [range, 19 to 77]) undergoing open-heart surgery were included in the study. Twelve patients (seven with coronary artery disease and five with aortic valvular disease) had sinus rhythm, and five patients (all with mitral valvular disease) had chronic, permanent AF. A piece of right atrial appendage tissue (0.5 g) was obtained during surgery. RT-PCR was used to evaluate the expression of L-type Ca2+ channels, ryanodine receptor (RyR2), sarcoplasmic reticular Ca2+-ATPase (SERCA2), gene encoding the rapid component of the delayed rectifier Ikr (HERG), gene encoding calcium-independent transient outward current I(to1) (Kv4.3), gene encoding the ultrarapid component of the delayed rectifier Iku (Kv1.5), K+ channel-interacting protein 2 (KChIP2), hyperpolarization-activated cation channel 2 associated with the pacemaker current If (HCN2), and gene encoding Na+ channel (SCN5A). RESULTS: Reduced L-type Ca2+ channel, RyR2, SERCA2, Kv1.5, and KChIP2 expression and borderline increased HCN2 expression were observed in the patients with AF and mitral valvular heart disease. Left atrial diameter was negatively correlated with RyR2 and KChIP2 expression. Fractional area shortening of the left atrium was positively correlated with RyR2 and KChIP2 expression. CONCLUSIONS: Alterations in ion channel expression and the anatomical substrate may favor the initiation and maintenance of AF in patients with mitral valvular heart disease.
Adult ; Aged ; Aortic Valve Stenosis/metabolism ; Atrial Fibrillation/*metabolism ; Calcium/metabolism ; Chronic Disease ; Coronary Artery Disease/metabolism ; Female ; Heart Valve Diseases/*metabolism ; Humans ; Ion Channels/*genetics ; Male ; Middle Aged ; *Mitral Valve ; Potassium Channels/genetics ; Ryanodine Receptor Calcium Release Channel/genetics ; Sodium Channels/genetics

AIM: To investigate the different effects of salvianolic acid and notoginseng triterpenes on proliferation, angiogenesis and expression of vascular endothelial growth factor in EA-hy926 cells in vitro. METHODS: EA-hy926 cells were cultured in vitro. Salvianolic acid and notoginseng triterpenes at concentrations of 0.4, 0.8 and 1.2 mg·L(-1) were used to culture EA-hy926 cells. EA-hy926 cells in a blank control group were grown in culture solution only. Viability of cells was assessed by CCK-8, and after treated for 12 h, capillary-like structures were examined. After 24 h culture, the expression of VEGF was detected by real-time PCR. RESULTS: Salvianolic acid at 0.4, 0.8 mg·L(-1), the same as notoginseng triterpenes, increased VEGF content in EA-hy926 cells. Expression of VEGF protein in the salvianolic acid at 1.2 mg·L(-1) group, was up-regulated as compared with notoginseng triterpenes group (P < 0.05). CONCLUSION Salvianolic acid and notoginseng triterpenes can promote EA-hy926 cell proliferation, angiogenesis and expression of VEGF protein. This analysis also provided evidence that salvianolic acid had the better effects as compared with notoginseng triterpenes.
Alkenes ; pharmacology ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Coronary Stenosis ; drug therapy ; genetics ; metabolism ; physiopathology ; Drugs, Chinese Herbal ; pharmacology ; Endothelial Cells ; drug effects ; metabolism ; Humans ; Neovascularization, Pathologic ; drug therapy ; genetics ; metabolism ; physiopathology ; Panax notoginseng ; chemistry ; Polyphenols ; pharmacology ; Triterpenes ; pharmacology ; Vascular Endothelial Growth Factor A ; genetics ; metabolism