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Diseased Vessels (diseased + vessel)

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Medical Sciences	100%

Selected Abstracts

Apolipoprotein E Polymorphism and the Characteristics of Diseased Vessels in Male Chinese Patients With Angiographic Coronary Artery Disease: A Case-Case Study

CLINICAL CARDIOLOGY, Issue 6 2010
Shao-Sheng Li MD
Background Variations in the apolipoprotein E (apo E) gene may predict the incidence of coronary artery disease (CAD). However, the correlation between apo E polymorphism and the severity of CAD is still unclear. Hypothesis Apolipoprotein E polymorphism can predict CAD. Methods Used a case-case study of 213 Chinese angiographically-defined CAD patients who were screened for apo E genotypes. The characteristics of their diseased vessels were recorded. Results Apolipoprotein E4 carriers had > 75% stenosis, more wide-ranging and longer vessel disease, a greater number of diseased vessels, and a higher Gensini score than apo E2 carriers or individuals with the apo E3/3 genotype. Apolipoprotein E2 carriers had ,75% stenosis and a shorter length of vessel disease than individuals with the apo E3/3 genotype or apo E4 carriers. The severity of stenosis, length of vessel disease, and number of diseased vessels were affected by the interaction between genotype and body mass index, family history of CAD, total plasma cholesterol level, smoking history, and hypertension history. Conclusion The apo E4 allele may serve as an independent genetic marker predicting severity of CAD. Other CAD risk factors may accelerate the process of pathogenesis. The apo E2 allele may play a protective role. Copyright © 2010 Wiley Periodicals, Inc. [source]

Comparison of Hospital Mortality With Intra-Aortic Balloon Counterpulsation Insertion Before vs After Primary Percutaneous Coronary Intervention for Cardiogenic Shock Complicating Acute Myocardial Infarction

CONGESTIVE HEART FAILURE, Issue 5 2010
Scott Harris DO
We hypothesized that the insertion of the IABP before primary PCI might result in better survival of patients with cardiogenic shock compared with postponing the insertion until after primary PCI. We, therefore, retrospectively studied 48 patients who had undergone primary PCI with IABP because of cardiogenic shock complicating acute myocardial infarction (26 patients received the IABP before and 22 patients after primary PCI). No significant differences were present in the baseline clinical characteristics between the 2 groups. The mean number of diseased vessels was greater in the group of patients treated with the IABP before primary PCI (2.8±0.5 vs 2.3±0.7, P=.012), but the difference in the number of treated vessels was not significant. The peak creatine kinase and creatine kinase-MB levels were lower in patients treated with the IABP before primary PCI (median, 1077; interquartile range, 438,2067 vs median, 3299; interquartile range, 695,6834; P=.047 and median, 95; interquartile range, 34,196 vs median, 192; interquartile range, 82,467; P=.048, respectively). In-hospital mortality and the overall incidence of major adverse cardiac and cerebrovascular events were significantly lower in the group of patients receiving the IABP before primary PCI (19% vs 59% and 23% vs 77%, P=.007 and P=.0004, respectively). Multivariate analysis identified renal failure (odds ratio, 15.2; 95% confidence interval, 3.13,73.66) and insertion of the IABP after PCI (odds ratio, 5.2; 95% confidence interval, 1.09,24.76) as the only independent predictors of in-hospital mortality. In conclusion, the results of the present study suggest that patients with cardiogenic shock complicating acute myocardial infarction who undergo primary PCI assisted by IABP have a more favorable in-hospital outcome and lower in-hospital mortality than patients who receive IABP after PCI. Abdel-Wahab M, Saad M, Kynast J, et al. Comparison of hospital mortality with intra-aortic balloon counterpulsation insertion before versus after primary percutaneous coronary intervention for cardiogenic shock complicating acute myocardial infarction. Am J Cardiol. 2010;105:967,971. [source]

Plasma matrix metalloproteinase-3 level is an independent prognostic factor in stable coronary artery disease

EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 9 2005
T. C. Wu
Abstract Background, Recent evidence suggests the important role of matrix metalloproteinases (MMPs) in the progression of atherosclerosis and development of clinical events. We assessed the prognostic value of different plasma MMPs in patients with stable coronary artery disease (CAD). Materials and methods, A total of 165 consecutive nondiabetic patients with angiographically significant CAD (n = 150) or normal coronary angiograms despite exercise-induced myocardial ischemia (cardiac syndrome X, n = 15) and 17 normal subjects were evaluated. In each subject, plasma inflammatory markers including high sensitivity C-reactive protein (hsCRP) and MMP-2, 3 and 9 were measured. In CAD patients, major cardiovascular events including cardiac death, nonfatal myocardial infarction, unscheduled coronary revascularization and hospitalization as a result of unstable angina were prospectively followed up for more than 6 months. Results, Plasma levels of MMPs were significantly higher in CAD patients than in those with cardiac syndrome X and in normal subjects (MMP-2: 914·76 ± 13·20 vs. 830·79 ± 31·95 vs. 783·08 ± 28·40 ng mL,1, P = 0·002; MMP-3: 129·59 ± 4·21 vs. 116·86 ± 8·09 vs. 91·71 ± 9·55 ng mL,1, P = 0·011; MMP-9: 31·42 ± 2·84 vs. 11·40 ± 5·49 vs. 6·71 ± 2·89 ng mL,1, P = 0·006). In CAD patients, there were 48 major cardiovascular events during a mean follow-up period of 17·74 ± 0·85 months. The numbers of diseased vessels (HR = 2·19, 95% CI 1·20,1·02, P = 0·011), plasma hsCRP (HR = 2·21, 95% CI 1·18,4·11, P = 0·013) and MMP-3 level (HR = 2·46, 95% CI = 1·15,5·28, P = 0·021) were associated with the development of cardiovascular events. However, only the plasma MMP-3 level was an independent predictor of the adverse events in CAD patients (HR = 2·47, 95% CI 1·10,5·54, P = 0·028). Conclusions, Plasma MMP levels were increased in CAD patients. Plasma MMP-3 level, rather than hsCRP, was an independent prognostic marker for future cardiovascular events, suggesting its potential role in risk stratification and clinical management of stable CAD. [source]

A search for cyclophilin-A gene (PPIA) variation and its contribution to the risk of atherosclerosis and myocardial infarction

INTERNATIONAL JOURNAL OF IMMUNOGENETICS, Issue 2 2008
M. Palacín
Summary Cyclophilin A is secreted by vascular smooth muscle cells in response to inflammatory stimuli, and could thus contribute to atherosclerosis. We hypothesized that the genetic variation at the cyclophilin A gene (PPIA) could affect the risk for developing atherosclerosis and myocardial infarction. This study included 250 myocardial infarction patients (all male and < 60 years; 95% are smokers). All these cases had at least one atherosclerotic diseased coronary vessel. DNA was obtained from patients and from 250 healthy controls. The variation at the PPIA gene was determined in the patients through single-strand conformation analysis and direct sequencing of seven polymerase chain reaction fragments. Allele and genotype frequencies were compared between patients and controls. The effect of a promoter polymorphism (,11 G/C) on gene expression was in vitro analysed with luciferase-reporter assays. We found two common polymorphisms in the PPIA promoter (,11 G/C) and the 5, non-translated (+36 G/A) regions. Cells transfected with luciferase-plasmids containing the ,11 G had significantly higher luciferase activity. Genotype frequencies for these polymorphisms did not differ between patients and controls. In conclusion, we reported a functional variant in the PPIA promoter. However, the PPIA variation did not significantly contribute to the risk of suffering from myocardial infarction among patients with atherosclerotic diseased vessels. [source]

The Effects of Ethanol Consumption on Vasculogenesis Potential in Nonhuman Primates

ALCOHOLISM, Issue 1 2008
J. Koudy Williams
Background:, Vasculogenesis is essential to the preservation and repair of damaged or diseased vessels. Alcohol is the most commonly abused drug among young adults, but its effects on vessel growth and repair are unknown. The basis of vascular repair is endothelial progenitor cell (EPC) recruitment to assist in the formation of new vascular network (vasculogenesis). Therefore, the objective of this study was to measure the effects of ethanol consumption on the production, mobilization and vasculogenesis potential EPCs in nonhuman primates. Methods:, Four to five year-old (young adult) male rhesus monkeys consumed monkey chow and water (Control, n = 7), or chow and water + ethanol (Alcohol, 2.45 g/d, n = 7) for 12 months. Peripheral blood (PB) and bone marrow (BM) samples were collected for fluorescence-activated cell-sorting analysis of cell surface antigens (CD45, CD31, CD44, CD133, VEGF-R2 , or KDR); and for capillary formation on Matrigel-coated plates. Results:, There were greater numbers of nonhematopoeitic stromal cells (CD45,) and putative mesenchymal progenitor cells (CD45,/CD44+) in the PB and BM of Alcohol versus Control monkeys (p < 0.05). Additionally, there were greater numbers of EPCs (CD45,/CD133+/KDR+) in the BM and PB of Alcohol versus Control monkeys (p < 0.05). However, the EPCs of Alcohol monkeys were less likely to form capillaries on matrigel-coated plates than Control monkeys (p < 0.05). Conclusions:, Ethanol consumption in monkeys markedly increased the production and mobilization of EPCs, but decreased their ability to form capillaries. The pathophysiologic consequences of such effects are unclear, but may represent an ethanol-induced chronic stress on the BM, resulting in EPC. [source]

Apolipoprotein E Polymorphism and the Characteristics of Diseased Vessels in Male Chinese Patients With Angiographic Coronary Artery Disease: A Case-Case Study

Lipoprotein(a) Is Related to the Extent of Lesions in the Coronary Vasculature and to Unstable Coronary Syndromes

CLINICAL CARDIOLOGY, Issue 12 2000
B.Sc., John D. Zampoulakis M.D.
Abstract Background: Lp(a) is a highly atherogenic particle with a prothrombotic effect. Until now its relation to the extent and severity of the atheromatic lesions had not been established by standard procedures. Hypothesis: This study examined the correlation of Lp(a) to the extent and severity of coronary artery disease (CAD) and its relation to unstable clinical events (not including sudden death). Methods: In 202 patients undergoing coronary angiography, plasma lipids were measured with the usual procedures and Lp(a) with the enzyme-linked immunosorbent assay. The extent of CAD was expressed in the number of diseased vessels and its severity in terms of the severity coefficient and the obstruction coefficient. Results: A very strong relationship between LP(a) and the number of diseased vessels (p = 0.0007) signifying diffuse atherosclerosis, but no relation with the severity of the lesions, was found. However, it was the only lipid that correlated significantly with the number of totally occluded vessels (p = 0.0003). The thrombogenic ability of Lp(a) was manifested by increased incidence of myocardial infarction and unstable angina episodes in patients with elevated Lp(a) (p = 0.0157). Conclusion: Elevated Lp(a) predisposes to the extent of CAD and total occlusions but not to the severity of lesions. Patients with increased Lp(a) levels and unstable angina are at increased danger of suffering myocardial infarction. Thus, Lp(a) may predispose to plaque destabilization and thrombosis of noncritical lesions. [source]