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Haptoglobin genotypic distribution in Iranian patients with coronary heart disease  [cached]
Bahram Kazemi,Ensieh Khalkhal,Ashraf Shabani
Journal of Paramedical Sciences , 2011,
Abstract: Haptoglobin is a plasma protein with hemoglobin binding capacity. Haptoglobin has important biological functions such as binding to free hemoglobin and removes it from the circulation, thus preventing iron loss and kidney damage during intravascular hemolysis, superior antioxidant capacity, protection against free radicals. Studies on the distribution of Hp show that the gene frequencies of Hp dependent on geographical and genetic family. In the other, several authors have showed the correlation between HP types and different diseases, such as inflammation, infection, cardiovascular diseases and malignant tumors.Smoking, hypertention,diabetes mellitus and serum lipid concentrations are risk factors for developing cardiovascular diseases. In addition, Hp polymorphism has been proposed as a risk factor for developing atherosclerotic vasculare disease. In this study, the association between Haptoglobin genotypic distribution and the incidence of coronary heart disease investigated. 50 Iranian patients with coronary heart disease were randomly selected. Genomic DNA extracted from peripheral blood leukocytes. In PCRs with primers A and B, amplification products of 1757 and 3481 bp were amplified from genomic DNA containing alleles Hp1 and Hp2, respectively. In the population studied, the distribution of haptoglobin polymorphism was 36% (n = 18) for the Hp1-1 type, 62% (n =31) for the HP1-2 type, and 2% (n = 1) for the HP2-2 type. The trend in this study showing a lower frequency of 3-vessel disease and less severe coronary artery stenosis in patients with the HP1-1 phenotype than in patients with the HP1-2 phenotypes may be indicative of a protective effect of the HP1-1 phenotype against the development of atherosclerotic coronary artery disease.
Heart and diabetes consensus: Physical exercise in diabetic patients with cardiovascular diseases.
Eduardo Rivas-Estany,José D. Barrera Sarduy,Rolando Rogés Machado,Maricela Nuez Vilar
Revista Cubana de Cardiología y Cirugía Cardiovascular , 2011,
Abstract: Cardiovascular diseases are the leading cause of death in the world, some are preventable through the control of risk factors, but the prevalence of obesityand diabetes are increasing in many countries. The current behavior for the control of diabetes includes nutritional and drug treatment, systematic physicalexercises and patient education. Physical exercise has proven to be beneficial for diabetic patients, particularly for type 2, suffering for ischemic heartdisease with high frequency, because it can provide favorable metabolic and endocrine responses. The reduction of the insulin-resistance is one of themost important effects of the exercises by its direct effect on the metabolism of glucose, insulin and own muscle metabolism. It should therefore be includedin the ideal strategy for treatment of diabetic people to prevent and reduce hyperglycemia in acute and chronic form, avoiding their long-termcomplications. Exercise in diabetics with heart disease should be carried out individually and with special care, after proper ergometric assessment; it hassimilar effects than in non-diabetic individuals.
Genetic polymorphisms of angiotensin-2 type 1 receptor and angiotensinogen and risk of renal dysfunction and coronary heart disease in type 2 diabetes mellitus
Julie Lin, Frank B Hu, Lu Qi, Gary C Curhan
BMC Nephrology , 2009, DOI: 10.1186/1471-2369-10-9
Abstract: Study participants were diabetics from the Health Professionals Follow-Up Study (HPFS) and the Nurses' Health Study (NHS). We analyzed single nucleotide polymorphisms (SNPs) associated with cardiovascular pathophysiology (including AGT1R T573C, AGT1R A1166C, and AGT M235T) and presence of renal dysfunction (eGFR<60 ml/min/1.73 m2) or history of CHD.The AGT1R 1166 C-allele was associated with eGFR<60 ml/min/1.73 m2 (multivariable OR 1.63 [1.01, 2.65]) in the HPFS men (n = 733) and in the combined dataset (n = 1566) (OR 1.42 [1.02, 1.98]). The AGT1R 1166 C-allele was also associated with CHD in men (OR 1.57 [1.10, 2.24]). In NHS women (n = 833), AGT 235T-allele was associated with CHD (OR 1.72 [1.20, 2.47]). Removal of hypertension from the fully adjusted models did not influence results, suggesting that the associations may not be mediated by hypertension. There were significant interactions between sex and AGT1R 1166 C-allele (p = 0.008) and AGT M235T (p = 0.03) in models for CHD. No significant associations were seen between AGT1R T573 C-allele and renal dysfunction or CHD.Polymorphisms in AGT1R and AGT genes are associated with renal dysfunction and CHD in type 2 diabetes and further support the important role of the RAS in these complications. Sex may modify associations between AGT1R 1166 C-allele and AGT 235T and CHD in type 2 diabetes.Increased activation of the renin-angiotensin system (RAS) has been postulated to play a central role in the progression of chronic kidney disease (CKD) and coronary heart disease (CHD). This theory is supported by randomized clinical trials that have shown beneficial clinical effects of the blockade of production of angiotensin-II (AII) by angiotensin converting enzyme inhibitor (ACE-I) medications or antagonism of AII action through angiotensin receptor blockade (ARBs). For example, among diabetics, the ARB losartan significantly slowed progression of CKD [1], whereas the ACE-I medication ramipril significantly reduced CHD morb
The role of autonomic cardiovascular neuropathy in pathogenesis of ischemic heart disease in patients with diabetes mellitus  [PDF]
Popovi?-Peji?i? Snje?ana,Todorovi?-?ilas Ljiljana,Pantelinac Pavle
Medicinski Pregled , 2006, DOI: 10.2298/mpns0604118p
Abstract: Introduction. Diabetes is strongly associated with macrovascular complications, among which ischemic heart disease is the major cause of mortality. Autonomic neuropathy increases the risk of complications, which calls for an early diagnosis. The aim of this study was to determine both presence and extent of cardiac autonomic neuropathy, in regard to the type of diabetes mellitus, as well as its correlation with coronary disease and major cardiovascular risk factors. Material and methods. We have examined 90 subjects, classified into three groups, with 30 patients each: those with type 1 diabetes, type 2 diabetes and control group of healthy subjects. All patients underwent cardiovascular tests (Valsalva maneuver, deep breathing test, response to standing, blood pressure response to standing sustained, handgrip test), electrocardiogram, treadmill exercise test and filled out a questionnaire referring to major cardiovascular risk factors: smoking, obesity, hypertension, and dyslipidemia. Results. Our results showed that cardiovascular autonomic neuropathy was more frequent in type 2 diabetes, manifesting as autonomic neuropathy. In patients with autonomic neuropathy, regardless of the type of diabetes, the treadmill test was positive, i.e. strongly correlating with coronary disease. In regard to coronary disease risk factors, the most frequent correlation was found for obesity and hypertension. Discussion Cardiovascular autonomic neuropathy is considered to be the principal cause of arteriosclerosis and coronary disease. Our results showed that the occurrence of cardiovascular autonomic neuropathy increases the risk of coronary disease due to dysfunction of autonomic nervous system. Conclusions. Cardiovascular autonomic neuropathy is a common complication of diabetes that significantly correlates with coronary disease. Early diagnosis of cardiovascular autonomic neuropathy points to increased cardiovascular risk, providing a basis for preventive and therapeutic measures. .
Maternal diabetes induces congenital heart defects in mice by altering the expression of genes involved in cardiovascular development
Srinivasan Kumar, S Thameem Dheen, Samuel Tay
Cardiovascular Diabetology , 2007, DOI: 10.1186/1475-2840-6-34
Abstract: We analyzed the morphological changes, the expression pattern of some genes, the proliferation index and apoptosis in developing heart of embryos at E13.5 from streptozotocin-induced diabetic mice. Morphological analysis has shown the persistent truncus arteriosus combined with a ventricular septal defect in embryos of diabetic mice. Several other defects including defective endocardial cushion (EC) and aberrant myofibrillogenesis have also been found. Cardiac neural crest defects in experimental embryos were analyzed and validated by the protein expression of NCAM and PGP 9.5. In addition, the protein expression of Bmp4, Msx1 and Pax3 involved in the development of cardiac neural crest was found to be reduced in the defective hearts. The mRNA expression of Bmp4, Msx1 and Pax3 was significantly down-regulated (p < 0.001) in the hearts of experimental embryos. Further, the proliferation index was significantly decreased (p < 0.05), whereas the apoptotic cells were significantly increased (p < 0.001) in the EC and the ventricular myocardium of the experimental embryos.It is suggested that the down-regulation of genes involved in development of cardiac neural crest could contribute to the pathogenesis of maternal diabetes-induced congenital heart defects.Maternal diabetes mellitus is associated with a five fold increase in risk of cardiovascular malformations in infants of diabetic mothers [1]. These malformations include endocardial cushion (EC) defects, persistent truncus arteriosus (PTA) and ventricular septal defects (VSD) which appear to result from aberrant cardiac neural crest development [1-3]. Several studies have used animal models to examine the diabetes-induced congenital malformations during development of brain, heart and blood vessels [4-6]. However, the molecular mechanisms by which the teratogenicity of maternal diabetes causes congenital heart defects in embryos remain undefined.During development, cells from the neural crest over the occipital somite
Gender differences of polymorphisms in the TF and TFPI genes, as related to phenotypes in patients with coronary heart disease and type-2 diabetes
Trine B Opstad, Alf Pettersen, Thomas Weiss, Harald Arnesen, Ingebj?rg Seljeflot
Thrombosis Journal , 2010, DOI: 10.1186/1477-9560-8-7
Abstract: Patients with angiographically verified CHD (n = 1001; 22% women, 20% diabetics), and 204 healthy controls (28% women), were included. The investigated SNPs were: TF -1812C/T and TF -603A/G in the 5'upstream region, TF 5466A/G in intron 2, TFPI -399C/T and TFPI -287T/C in the 5'upstream region and the TFPI -33T/C in intron 7.No significant differences in frequencies between the CHD population and the controls of any polymorphisms were observed. In the CHD population, the TF 5466 A/G SNP were significantly more frequent in women as compared to men (p < 0.001). The TF-1812C/T and the TF-603A/G SNPs were significantly more frequent in women without type-2 diabetes compared to those with diabetes (p < 0.018, both), and the heterozygous genotypes were associated with significantly lower TF plasma levels compared to the homozygous genotypes (p < 0.02, both).The TFPI-399C/T and the TFPI-33T/C SNPs were associated with lower and higher TFPI total antigen levels, respectively (p < 0.001, both).Genetic variations in the TF and TFPI genes seem to be associated with gender and type-2 diabetes, partly affecting their respective phenotypes.Tissue factor (TF) and its endogenous inhibitor, tissue factor pathway inhibitor (TFPI) are the main regulators of the initiation of the coagulation process, important in atherothrombosis. Injury of the vessel wall and rupture of an atherosclerotic plaque lead to exposure of TF to circulating blood, followed by an activation of the haemostatic system. In addition, blood-borne, or soluble TF (TF) from micro particles and monocytes may represent thrombogenic potential [1]. TFPI is the main regulator in the initial step of the coagulation cascade mediated by TF, by binding to coagulation factors Xa, VIIa and TF forming an inactive complex [2,3]. TFPI, mainly produced by the endothelium [4], is predominantly associated with lipoproteins in the blood [2,5] or is endothelial-bound [6], whereas a small portion circulates as free molecules. Enhanced TF
Síndrome metabólico y riesgo de enfermedad cardiovascular Metabolic syndrome, diabetes and heart failure
Alonso Merchán V
Acta Medica Colombiana , 2005,
Abstract: El síndrome metabólico (SM) es un conglomerardo de factores de riesgo, todos ellos asociados con un componente principal causante que es la adiposidad visceral y que identifica a quien lo posee con un riesgo de desarrollar enfermedad cardiovascular (ECV) o diabetes mellitus tipo 2 (DM-2). En los últimos a os se ha enfatizado en este síndrome por la alta prevalencia progresiva de obesidad y DM-2 a nivel mundial. Múltiples clasificaciones se han propuesto, que dificultan homologar los estudios y resultados sobre el riesgo de enfermedad cardiovascular. Recientemente la Federación Internacional de Diabetes ha propuesto una clasificación que se espera sea la aplicada a partir de la fecha en el mundo. Esta revisión enfatizará en el riesgo de ECV asociado al SM. Metabolic syndrome (MS) consists of a series of risk factors, all of them associated with visceral fat leading to a high risk of developing cardiovascular disease or type II diabetes mellitus. Emphasis has been made on this syndrome in recent years due to the increasingly high prevalence of obesity and type-II diabetes world wide. Multiple classifications have been proposed, making it difficult to standardize studies and outcomes regarding the risk of cardiovascular disease. The International Diabetes Federation has proposed recently a new classification which is expected to be implemented throughout the world. The purpose of this paper is to emphasize the risk of cardiovascular disease associated with metabolic syndrome.
Haptoglobin Genotype and Risk Markers of Cardiovascular Disease in Patients with Chronic Kidney Disease  [PDF]
Charlotte Strandhave,My Svensson,Henrik Krarup,Jeppe Hagstrup Christensen
International Journal of Nephrology , 2013, DOI: 10.1155/2013/650847
Abstract: Sudden cardiac death and atherosclerosis have a major impact on cardiovascular mortality in chronic kidney disease (CKD). Inflammation with elevated high-sensitive C-reactive protein (hs-CRP) is involved in both sudden cardiac death and atherosclerosis, and decreased heart rate variability (HRV) is a predictor of both sudden cardiac death and atherosclerosis. Haptoglobin (Hp) is characterised by three genotypes (1-1, 2-1, and 2-2) with different antioxidant abilities. The aim was to examine whether HRV and hs-CRP were associated with Hp genotype in CKD patients. Fifty-six patients with CKD stage 2–5 were included. Hp genotype was determined by high-performance liquid chromatography. HRV was analysed from the 24 h Holter recordings. Hs-CRP was measured using an immunoturbidimetric assay. The results show that the HRV indices SDNN and SDANN were significantly lower in the Hp 2-2 patients ( and 0.04, resp.). In an adjusted linear regression model, Hp 2-2 was associated with both SDNN ( ) and SDANN ( ). Hs-CRP was higher in the Hp 2-2 patients ( ). In an adjusted linear regression model, the association between Hp 2-2 and hs-CRP remained significant ( ). In conclusion, a negative association was observed between Hp 2-2 and HRV, and Hp 2-2 was positively associated with hs-CRP in CKD patients. 1. Introduction Cardiovascular disease (CVD) including sudden cardiac death (SCD) [1] is a major cause of mortality in chronic kidney disease (CKD) [2]. Apart from left ventricular dysfunction [1], unique factors such as autonomic imbalance and inflammation contribute to the high incidence of SCD in CKD [3]. Traditional risk factors for atherosclerosis [4], such as hypertension and dyslipidaemia, can to some extent explain the increased risk of atherosclerosis in CKD [5]. However, nontraditional risk factors like oxidative stress and inflammation may also be of importance [6]. Heart rate variability (HRV) is a reliable, noninvasive measurement of autonomic tone of the heart [7]. A reduction in HRV reflects an autonomic imbalance towards decreased vagal tone and subsequent sympathetic overactivity [3]. Decreased HRV is a predictor of SCD in patients with CKD [8]. Furthermore, attenuated HRV is associated with atherosclerosis in CKD [9]. Chronic, low-grade inflammation is involved in the development of both SCD [10] and atherosclerosis [11]. The most extensively examined marker of inflammation is high-sensitive C-reactive protein (hs-CRP), which is a predictor of cardiovascular mortality in different populations [12, 13] including patients with CKD [14]. Hs-CRP may even
HNF1A gene polymorphisms and cardiovascular risk factors in individuals with late-onset autosomal dominant diabetes: a cross-sectional study
Fernando MA Giuffrida, Gilberto K Furuzawa, Teresa S Kasamatsu, Marcos M Oliveira, Andre F Reis, Sergio A Dib
Cardiovascular Diabetology , 2009, DOI: 10.1186/1475-2840-8-28
Abstract: eighteen LOADDM (age at onset > 40 y.o.; diabetes in 3 contiguous generations, uniparental lineage) along with 48 CT2DM patients and 42 normoglycemic controls (N group) have been evaluated for cardiovascular risk factors and SNPs of HNF1A.LOADDM showed significantly higher frequencies of SNPs A98V (22.2% vs 2.1%, p = 0.02) and S487N (72.2% vs 43.8%, p = 0.049) of HNF1A compared to CT2DM. I27L did not show significant difference (66.7% vs 45.8%), but associated with lower risk of hypertriglyceridemia (OR 0.16, 95% CI 0.04–0.65, p = 0.01). "Protective effect" was independent from other well-known predictive risk factors for hypertriglyceridemia, such as waist circumference (OR 1.09 per 1 cm increase, p = 0.01) and HDL (OR 0.01 per 1 mmol/l, p = 0.005), after logistic regression.Late onset autosomal dominant diabetes mellitus is clinically indistinguishable from classical type 2 diabetes individuals. However, LOADDM group is enriched for common HNF1A polymorphisms A98V and S487N. I27L showed "protective effect" upon hypertriglyceridemia in this sample of individuals, suggesting a role for HNF1A on diabetic individuals' lipid profile. These data contribute to the understanding of the complex interactions between genes, hyperglycemia and cardiovascular risk factors development in type 2 diabetes mellitus.Type 2 diabetes mellitus (T2DM) is a clinically and genetically heterogeneous disease. The spectrum of T2DM ranges from lean and predominantly insulin-deficient individuals, to those more obese and insulin resistant [1]. Associated clinical conditions such as dyslipidemia, hypertension and visceral obesity, components of the Metabolic Syndrome (MS), further contribute to this heterogeneity.Important advancements in the understanding of the genetic bases of T2DM have arisen in the last few years and several genes have now been associated to this disease. However, complete knowledge about the interaction among involved genes is still lacking. Curiously, most T2DM genes wit
Association of CETP TaqI and APOE polymorphisms with type II diabetes mellitus in North Indians: a case control study
Manjusha Dixit, Sandeep Bhattacharya, Balraj Mittal
BMC Endocrine Disorders , 2005, DOI: 10.1186/1472-6823-5-7
Abstract: Study subjects were 136 patients and 264 healthy controls. All polymorphisms were detected using PCR-RFLP and statistical analysis done with χ2 test and ANOVA.Although CETP TaqI B polymorphism was not associated with the T2DM, yet B1B2 genotype was significantly (p = 0.028) associated with high risk of hypertension in diabetic patients (OR = 3.068, 95% CI 1.183–7.958). In North Indians D442G variation in CETP gene was found to be absent. Frequency of APOE HhaI polymorphism was also not different between patients and controls. In diabetic patients having neuropathy and retinopathy significantly different levels of total-cholesterol [(p = 0.001) and (p = 0.029) respectively] and LDL-cholesterol [(p = 0.001) and (p = 0.001) respectively] were observed when compared to patients with T2DM only. However, lipid levels did not show any correlation with the CETP TaqI B and APOE Hha I genetic polymorphisms.CETP TaqI B and APOE HhaI polymorphism may not be associated with type II diabetes mellitus in North Indian population, however CETP TaqI B polymorphism may be associated with hypertension along with T2DM.Dyslipidemia is a major cardiovascular risk factor in type II diabetes mellitus (T2DM) with coronary heart disease being the most common cause of death. Risk relates to raised triglycerides (TG) and decreased high density lipoproteins (HDL) as well as raised low density lipoproteins (LDL). In diabetes, lipid risk thresholds are lower and interactions with other cardiovascular risk factors are more powerful, compared with general population. Hypertension is upto twice as common in diabetic patients as in general population [1]. Studies have shown that lipid abnormalities might contribute to the development and progression of diabetic nephropathy [2]. Hypercholesterolemia is a major determinant of decline of renal function in patients with diabetes [3].Genetic polymorphisms of the enzymes and proteins involved in lipid metabolism like cholesteryl ester transfer protein (CETP
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