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Premature Coronary Artery Disease (premature + coronary_artery_disease)
Selected AbstractsThe Effect of Ethnicity on the Relationship Between Premature Coronary Artery Disease and Traditional Cardiac Risk Factors Among Uninsured Young AdultsPREVENTIVE CARDIOLOGY, Issue 3 2009Amit P. Amin MD Prior studies of premature coronary artery disease (CAD) in young adults did not address the association of race/ethnicity and risk factors. Therefore, the authors conducted a study of 400 patients 40 years and older undergoing coronary angiography at a large, urban public hospital that serves predominately minority, uninsured populations. The prevalence of risk factors and their association with premature CAD varied markedly by ethnic group. Among blacks, dyslipidemia, diabetes, and smoking were independently associated with premature CAD. Among Hispanics, dyslipidemia, male sex, and family history of CAD were independently associated with premature CAD. Smoking was the only risk factor in whites, and no independent risk factor was identified in Asian Indians. Whites and Asian Indians had a higher prevalence of disease than blacks or Hispanics,before and after adjusting for risk factor imbalances across ethnic groups. In this ethnically diverse population, the authors' findings underscore the importance of identifying distinctive risk factors in various ethnic groups. [source] Congenital Cardiovascular Disease in Turner SyndromeCONGENITAL HEART DISEASE, Issue 1 2008Carolyn A. Bondy MD ABSTRACT Turner syndrome (TS), or monosomy X, occurs in ,1/2000 live born females. Intelligence is normal and short stature is the most obvious and consistent feature of the syndrome. Congenital cardiovascular disease affects ,50% of individuals and is the major cause of premature mortality in adults. Unfortunately, this most important aspect of the syndrome has received little attention outside of pediatric medicine, and adult cardiological follow-up is seriously lacking. This review describes the spectrum of cardiovascular defects with particular attention to identifying risk factors for aortic dissection/rupture. X-chromosome genetic pathways implicated in Turner cardiovascular disease, including premature coronary artery disease, are discussed. Recent guidelines for diagnosis and treatment of girls and women with TS are reviewed. [source] CD31+/Annexin V+ microparticles in healthy offsprings of patients with coronary artery diseaseEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 1 2009D. Bulut ABSTRACT Background, First-degree relatives of patients with premature coronary artery disease (CAD) develop endothelial dysfunction even in the case they are apparently healthy. In this study we wanted to clarify whether reduced blood levels of circulating endothelial progenitor cells (EPCs), an endogenous repair mechanism to replace dysfunctional endothelium, or elevated endothelial-derived microparticles (EMPs), an indicator and a mediator of increased endothelial cell damage/apoptosis, are an initial step in the pathogenesis of endothelial dysfunction in genetically predisposed subjects. Materials and methods, Fifty-six healthy young men (aged 23 to 31 years) from a fire brigade were enrolled, of which 20 subjects had a positive family history (FH) for premature CAD. Subjects with or without a positive FH did not differ with respect to age, body mass index, risk factors and C-reactive protein. Endothelial function was assessed by hyperaemia-mediated relaxation of the brachial artery, blood levels of EPCs (VEGFR2+CD34+ cells) and number of EMPs (CD31+(bright)/Annexin V+ particles) were analysed by flow cytometry. Results, Hyperaemia-mediated relaxation of the brachial artery was similar in both groups, and the blood levels of EPCs were comparable. However, the number of EMPs were significantly increased in subjects with a positive FH compared to those with a negative FH (neg. FH: 55·31 ± 4·88 vs. pos. FH: 70·37 ± 6·32 particles µL,1 platelet poor plasma; P < 0·05). Number of EMPs correlate inversely with the FMD response. Conclusions, These results suggest that increased plasma levels of EMPs may be an initial step in the development of endothelial dysfunction in genetically predisposed subjects. [source] LDL-receptor mutations in Europe,HUMAN MUTATION, Issue 6 2004George V.Z. Dedoussis Abstract Familial hypercholesterolemia (FH) is a clinical definition for a remarkable increase of cholesterol serum concentration, presence of xanthomas, and an autosomal dominant trait of either increased serum cholesterol or premature coronary artery disease (CAD). The identification of the low-density lipoprotein (LDL)-receptor (LDLR) as the underlying cause and its genetic characterization in FH patients revealed more insights in the trafficking of LDL, which primarily transports cholesterol to hepatic and peripheral cells. Mutations within LDLR result in hypercholesterolemia and, subsequently, cholesterol deposition in humans to a variable degree. This confirms the pathogenetic role of LDLR and also highlights the existence of additional factors in determining the phenotype. Autosomal dominant FH is caused by LDLR deficiency and defective apolipoprotein B-100 (APOB), respectively. Heterozygosity of the LDLR is relatively common (1:500). Clinical diagnosis is highly important and genetic diagnosis may be helpful, since treatment is usually effective for this otherwise fatal disease. Very recently, mutations in PCSK9 have been also shown to cause autosomal dominant hypercholesterolemia. For autosomal recessive hypercholesterolemia, mutations within the so-called ARH gene encoding a cellular adaptor protein required for LDL transport have been identified. These insights emphasize the crucial importance of LDL metabolism intra- and extracellularly in determining LDL-cholesterol serum concentration. Herein, we focus on the published European LDLR mutation data that reflect its heterogeneity and phenotypic penetrance. Hum Mutat 24:443,459, 2004. © 2004 Wiley-Liss, Inc. [source] Heritability of platelet function in families with premature coronary artery diseaseJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 8 2007P. F. BRAY Summary.,Background:,Variations in platelet function among individuals may be related to differences in platelet-related genes. The major goal of our study was to estimate the contribution of inheritance to the variability in platelet function in unaffected individuals from white and African American families with premature coronary artery disease.Methods:,Platelet reactivity, in the absence of antiplatelet agents, was assessed by in vitro aggregation and the platelet function analyzer closure time. Heritability was estimated using a variance components model.Results:,Both white (n = 687) and African American (n = 321) subjects exhibited moderate to strong heritability (h2) for epinephrine- and adenosine diphosphate-induced aggregation (0.36,0.42 for white and >0.71 for African American subjects), but heritability for collagen-induced platelet aggregation in platelet-rich plasma was prominent only in African American subjects. Platelet lag phase after collagen stimulation was heritable in both groups (0.47,0.50). A limited genotype analysis demonstrated that the C825T polymorphism of GNB3 was associated with the platelet aggregation response to 2 ,M epinephrine, but the effect differed by race.Conclusions:,Considering the few and modest genetic effects reported to affect platelet function, our findings suggest the likely existence of undiscovered important genes that modify platelet reactivity, some of which affect multiple aspects of platelet biology. [source] The Effect of Ethnicity on the Relationship Between Premature Coronary Artery Disease and Traditional Cardiac Risk Factors Among Uninsured Young AdultsPREVENTIVE CARDIOLOGY, Issue 3 2009Amit P. Amin MD Prior studies of premature coronary artery disease (CAD) in young adults did not address the association of race/ethnicity and risk factors. Therefore, the authors conducted a study of 400 patients 40 years and older undergoing coronary angiography at a large, urban public hospital that serves predominately minority, uninsured populations. The prevalence of risk factors and their association with premature CAD varied markedly by ethnic group. Among blacks, dyslipidemia, diabetes, and smoking were independently associated with premature CAD. Among Hispanics, dyslipidemia, male sex, and family history of CAD were independently associated with premature CAD. Smoking was the only risk factor in whites, and no independent risk factor was identified in Asian Indians. Whites and Asian Indians had a higher prevalence of disease than blacks or Hispanics,before and after adjusting for risk factor imbalances across ethnic groups. In this ethnically diverse population, the authors' findings underscore the importance of identifying distinctive risk factors in various ethnic groups. [source] Elevated Lp(a) with a small apo(a) isoform in children: risk factor for the development of premature coronary artery diseaseACTA PAEDIATRICA, Issue 12 2008Albert Dirisamer Background: levels of Lp(a) and low-molecular-weight apolipoprotein(a) isoform are strongly associated with the development of early cardiovascular disease. Certain types of apo(a) isoforms in combination with elevated levels of Lp(a) may be important in the determining of premature coronary artery disease. Therefore, we investigated the association of familial history of premature coronary artery disease and apo(a) size and Lp(a) levels in children and adolescents with hypercholesterolemia using a novel method determining apo(a) isoforms. Methods and results: Isoforms were classified in six phenotype patterns: S1,S4, B, F and according to their K-IV repeats. Apo(a) isoforms were divided into two groups: low-molecular- and high-molecular apo(a) isoforms. In subjects with double-banded apo(a) isoforms containing a small- and a large-isoform Lp(a) each contribution was based on the intensity of staining of the two bands. The percentage of patients with elevated levels of Lp(a) and a small apo(a) isoform (i.e. elevated small-isoform Lp(a)) was 46% in the risk group and 20% in the control group, p < 0.05. The percentage number of children and adolescents with elevated Lp(a) levels was higher in the risk group, reaching statistical significance (p < 0.05). Conclusion: Elevated levels of small-isoform Lp(a) might be a strong and independent risk factor for the development of premature coronary artery disease in children and adolescents with hypercholesterolemia. [source] | ||||||||||