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Coronary Atherosclerosis (coronary + atherosclerosis)

Distribution by Scientific Domains

Medical Sciences	97%

Distribution within Medical Sciences

Cardiovascular Disease	23%
Diabetes	8%

Selected Abstracts

Inflammatory Cytokine Imbalance after Coronary Angioplasty: Links with Coronary Atherosclerosis

JOURNAL OF INTERVENTIONAL CARDIOLOGY, Issue 4 2007
NATALE DANIELE BRUNETTI M.D., Ph.D.
Aim:To investigate release of some inflammatory cytokines (Cys) after coronary angioplasty and its links with coronary atherosclerosis. Methods:Twenty-seven consecutive subjects with acute coronary syndrome (ACS) who underwent percutaneous coronary intervention (PCI) were enrolled in the study: serial blood samples were taken in order to evaluate plasma concentrations of Interleukin (IL)-2, IL-10, IL-18, TNF,, and IFN, just before PCI at 12 and 24 hours. Patients were then divided, considering balance between each inflammatory Cy and IL-10, an antiinflammatory Cy, into four groups, ranging from a prevalent antiinflammatory response (stable inflammatory Cy,increasing IL-10 values) to a marked inflammatory imbalance (increasing inflammatory Cy,stable IL-10 values). Results:All Cys showed significant increases in plasma concentrations if compared with baseline values. Release curves were not significantly different when comparing subjects with ST-elevation myocardial infarction (STEMI) versus unstable angina,non-STEMI (UA-NSTEMI), diabetics versus controls. Subjects with marked inflammatory response showed a higher incidence of stenosis on left anterior descending (LAD) coronary artery (IL-2 ,2 and IFN, P < 0.05); Cy release was higher in patients with multivessel coronary disease (IL-2 and IFN,, ANOVA P < 0.01). Correlations were also referable between Cys and myocardial enzyme release. Subjects treated with sirolimus-eluting stents (SES) showed significantly lower Cy periprocedure ratio if compared with those treated with bare metal stents. Conclusions:A significant Cy release is detectable after PCI: inflammatory response seems to correlate with both PCI due to plaque instabilization and coronary atherosclerosis. A blunted inflammatory response is detectable in subjects treated with SES. [source]

Antioxidant Intake and Coronary Atherosclerosis: Consider a "Foods First" Approach

PREVENTIVE CARDIOLOGY, Issue 2 2006
Dianne A. Hyson PhD
No abstract is available for this article. [source]

Insulin resistance and endothelial dysfunction: the road map to cardiovascular diseases

DIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue 6 2006
Eugenio Cersosimo
Abstract Cardiovascular disease affects approximately 60% of the adult population over the age of 65 and represents the number one cause of death in the United States. Coronary atherosclerosis is responsible for the vast majority of the cardiovascular events, and a number of cardiovascular risk factors have been identified. In recent years, it has become clear that insulin resistance and endothelial dysfunction play a central role in the pathogenesis of atherosclerosis. Much evidence supports the presence of insulin resistance as the fundamental pathophysiologic disturbance responsible for the cluster of metabolic and cardiovascular disorders, known collectively as the metabolic syndrome. Endothelial dysfunction is an important component of the metabolic or insulin resistance syndrome and this is demonstrated by inadequate vasodilation and/or paradoxical vasoconstriction in coronary and peripheral arteries in response to stimuli that release nitric oxide (NO). Deficiency of endothelial-derived NO is believed to be the primary defect that links insulin resistance and endothelial dysfunction. NO deficiency results from decreased synthesis and/or release, in combination with exaggerated consumption in tissues by high levels of reactive oxygen (ROS) and nitrogen (RNS) species, which are produced by cellular disturbances in glucose and lipid metabolism. Endothelial dysfunction contributes to impaired insulin action, by altering the transcapillary passage of insulin to target tissues. Reduced expansion of the capillary network, with attenuation of microcirculatory blood flow to metabolically active tissues, contributes to the impairment of insulin-stimulated glucose and lipid metabolism. This establishes a reverberating negative feedback cycle in which progressive endothelial dysfunction and disturbances in glucose and lipid metabolism develop secondary to the insulin resistance. Vascular damage, which results from lipid deposition and oxidative stress to the vessel wall, triggers an inflammatory reaction, and the release of chemoattractants and cytokines worsens the insulin resistance and endothelial dysfunction. From the clinical standpoint, much experimental evidence supports the concept that therapies that improve insulin resistance and endothelial dysfunction reduce cardiovascular morbidity and mortality. Moreover, interventional strategies that reduce insulin resistance ameliorate endothelial dysfunction, while interventions that improve tissue sensitivity to insulin enhance vascular endothelial function. There is general agreement that aggressive therapy aimed simultaneously at improving insulin-mediated glucose/lipid metabolism and endothelial dysfunction represents an important strategy in preventing/delaying the appearance of atherosclerosis. Interventions that 1 correct carbohydrate and lipid metabolism, 2 improve insulin resistance, 3 reduce blood pressure and restore vascular reactivity, and 4 attenuate procoagulant and inflammatory responses in adults with a high risk of developing cardiovascular disease reduce cardiovascular morbidity and mortality. Whether these benefits hold when the same prevention strategies are applied to younger, high-risk individuals remains to be determined. Copyright © 2006 John Wiley & Sons, Ltd. [source]

Impact of genetic defects on coronary atherosclerosis in patients suspected of having familial hypercholesterolaemia

EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 1 2003
O. S. Descamps
Abstract Background In the present study we assessed whether the presence of genetic mutations typical of familial hypercholesterolaemia (FH) was associated with greater atherosclerosis in the coronary vessels in patients with severe hypercholesterolaemia and a family history of early cardiovascular disease. Materials and methods Two hundred and thirty-five patients selected for having severe hypercholesterolaemia and a family history of cardiovascular disease were classified as FH (57 men and 38 women) or non-FH (84 men and 56 women) according to a genetic analysis of the LDL-R or ApoB genes. Coronary atherosclerosis was evaluated by performing a thoracic CT scan and exercise stress testing. Results Familial hypercholesterolaemia individuals had a significantly higher prevalence of coronary calcification than the non-FH patients from among both the men (OR = 3·90; 95% CI 1·86,8·19; P < 0·001) and the women (OR = 2·34; 95% CI 1·01,5·48; P = 0·05). In exercise stress testing, ECG abnormalities suggestive of cardiac ischaemia were found with a higher prevalence in the FH patients than the non-FH patients from among both the men (OR 6·15; 95% CI 2·16,17·5; P < 0·001) and the women (OR 4·76; 95% CI 0·91,24·6; P = 0·06). All differences were statistically significant after adjusting for age and cholesterol and for most classical risk factors that differed between the FH and non-FH groups. Conclusion Among patients with severe hypercholesterolaemia and a family history of early cardiovascular disease, the presence of a genetically ascertained FH is associated with a higher prevalence of coronary artery calcifications and a positive exercise stress test. These results suggest that despite a similar phenotype, patients carrying mutations suggestive of FH may have a greater cardiovascular risk than patients without these mutations. [source]

Cardiac anxiety in people with and without coronary atherosclerosis,

DEPRESSION AND ANXIETY, Issue 10 2008
Craig D. Marker Ph.D.
Abstract Many studies have shown that cardiac anxiety when occurring in the absence of coronary artery disease is common and quite costly. The Cardiac Anxiety Questionnaire (CAQ) is an 18-item self-report measure that assesses anxiety related to cardiac symptoms. To better understand the construct of cardiac anxiety, a factor analysis was conducted on CAQ data from 658 individuals who were self or physician-referred for electron beam tomographic screening to determine whether clinically significant coronary atherosclerosis was present. A four-factor solution was judged to provide the best fit with the results reflecting the following factor composition: heart-focused attention, avoidance of activities that bring on symptoms, worry or fear regarding symptoms, and reassurance-seeking. Factorial invariance across groups was also assessed to determine whether the factor structure of the CAQ was similar in individuals with and without clear evidence of coronary atherosclerosis. The factor structure of the CAQ did not differ between the two groups. However, the group without coronary atherosclerosis had significantly higher mean scores on their attention and worry/fear factors suggesting that people without a diagnosed cardiac condition pay more attention to and worry more about their cardiac-related symptoms than those people who have coronary atherosclerosis. Depression and Anxiety 2007. Published 2007 Wiley-Liss, Inc. [source]

Post-challenge glucose predicts coronary atherosclerotic progression in non-diabetic, post-menopausal women,

DIABETIC MEDICINE, Issue 10 2007
P. B. Mellen
Abstract Aims, We sought to determine whether fasting or post-challenge glucose were associated with progression of coronary atherosclerosis in non-diabetic women. Methods, We performed a post-hoc analysis of 132 non-diabetic women who underwent 75-g oral glucose tolerance testing. The primary outcome of interest was progression of atherosclerosis determined by baseline and follow-up coronary angiography, a mean of 3.1 ± 0.9 years apart. We analysed the association of change in minimal vessel diameter (,MD) by quartile of fasting and post-challenge glucose using mixed models that included adjustment for age, systolic blood pressure, total : high-density lipoprotein cholesterol ratio, current smoking, lipid-lowering and anti-hypertensive medication use and other covariates. Results, At baseline, participants had a mean age of 65.7 ± 6.7 years and a mean body mass index of 27.9 ± 8.5 kg/m2. Although there were no significant differences in atherosclerotic progression by fasting glucose category (P for trend across quartiles = 0.99), there was a significant inverse association between post-challenge glucose and ,MD (in mm) (Q1 : 0.01 ± 0.03; Q2 : 0.08 ± 0.03; Q3 : 0.13 ± 0.03; Q4 : 0.11 ± 0.03; P for trend = 0.02). Conclusions, In post-menopausal women without diabetes, post-challenge glucose predicts angiographic disease progression. These findings suggest that even modest post-challenge hyperglycaemia influences the pathogenesis of atherosclerotic progression. [source]

Prognostic significance of asymptomatic coronary artery disease in patients with diabetes and need for early revascularization therapy

DIABETIC MEDICINE, Issue 9 2007
E.-K. Choi
Abstract Aims, Information on the clinical outcome of patients with diabetes with silent myocardial ischaemia is limited. We compared the clinical and angiographic characteristics, and the clinical outcomes of diabetic patients with asymptomatic or symptomatic coronary artery disease (CAD). Methods, Three hundred and ten consecutive diabetic patients with CAD were divided into two groups according to the presence of angina and followed for a mean of 5 years. Fifty-six asymptomatic patients with a positive stress test and CAD on coronary angiography were compared with 254 symptomatic patients, 167 with unstable angina and 87 with chronic stable angina. Results, Although the severity of coronary atherosclerosis was similar in asymptomatic and symptomatic patients, revascularization therapy was performed less frequently in the asymptomatic than the symptomatic patients (26.8 vs. 62.0%; P < 0.001). Asymptomatic patients experienced a similar number of major adverse cardiac events (MACEs; death, non-fatal myocardial infarction, and revascularization; 32 vs. 28%; P = 0.57), but had higher cardiac mortality than symptomatic patients (26 vs. 9%; P < 0.001). However, patients who underwent revascularization therapy at the time of CAD diagnosis in these two groups showed similar MACE and cardiac mortality (20.0 vs. 22.5%, 6.7 vs. 5.3%, respectively; all P > 0.05). Conclusions, This study suggests that diabetic patients with asymptomatic CAD have a higher cardiac mortality risk than those with symptomatic CAD, and that lack of revascularization therapy may be responsible for the poorer survival. [source]

The Relation between the Color M-Mode Propagation Velocity of the Descending Aorta and Coronary and Carotid Atherosclerosis and Flow-Mediated Dilatation

ECHOCARDIOGRAPHY, Issue 3 2010
Yilmaz Gunes M.D.
Background: To improve clinical outcomes, noninvasive imaging modalities have been proposed to measure and monitor atherosclerosis. Common carotid intima-media thickness (CIMT) and brachial artery flow-mediated dilatation (FMD) have correlated with coronary atherosclerosis. Recently, the color M-mode-derived propagation velocity of descending thoracic aorta (AVP) was shown to be associated with coronary artery disease (CAD). Methods: CIMT, FMD, and AVP were measured in 92 patients with CAD and 70 patients having normal coronary arteries (NCA) detected by coronary angiography. Patients with acute myocardial infarction, renal failure or hepatic failure, aneurysm of aorta, severe valvular heart disease, left ventricular ejection fraction <40%, atrial fibrillation, frequent premature beats, left bundle branch block, and inadequate echocardiographic image quality were excluded. Results: Compared to patients with normal coronary arteries, patients having CAD had significantly lower AVP (29.9 ± 8.1 vs. 47.5 ± 16.8 cm/sec, P < 0.001) and FMD (5.3 ± 1.9 vs. 11.4 ± 5.8%, P < 0.001) and higher CIMT (0.94 ± 0.05 vs. 0.83 ± 0.14 mm, P < 0.001) measurements. There were significant correlations between AVP and CIMT (r =,0.691, P < 0.001), AVP and FMD (r = 0.514, P < 0.001) and FMD and CIMT (r =,0.530, P < 0.001). Conclusions: The transthoracic echocardiographic determination of the color M-mode propagation velocity of the descending aorta is a simple practical method and correlates well with the presence of carotid and coronary atherosclerosis and brachial endothelial function. (Echocardiography 2010;27:300-305) [source]

Fungal rDNA signatures in coronary atherosclerotic plaques

ENVIRONMENTAL MICROBIOLOGY, Issue 12 2007
Stephan J. Ott
Summary Bacterial DNA has been found in coronary plaques and it has therefore been concluded that bacteria may play a role as trigger factors in the chronic inflammatory process underlying coronary atherosclerosis. However, the microbial spectrum is complex and it is not known whether microorganisms other than bacteria are involved in coronary disease. Fungal 18S rDNA signatures were systematically investigated in atherosclerotic tissue obtained through catheter-based atherectomy of 38 patients and controls (unaffected coronary arteries) using clone libraries, denaturating gradient gel analysis (DGGE), in situ hybridization and fluorescence in situ hybridization (FISH). Fungal DNA was found in 35 of 38 (92.11%) coronary heart disease patients by either polymerase chain reaction (PCR) with universal primers or in situ hybridization analysis (n = 5), but not in any control sample. In a clone library with more than 350 sequenced clones from pooled patient DNA, an overall richness of 19 different fungal phylotypes could be observed. Fungal profiles of coronary heart disease patients obtained by DGGE analysis showed a median richness of fungal species of 5 (range from 2 to 9) with a high interindividual variability (mean similarity 18.83%). For the first time, the presence of fungal components in atherosclerotic plaques has been demonstrated. Coronary atheromatous plaques harbour diverse and variable fungal communities suggesting a polymicrobial contribution to the chronic inflammatory aetiology. [source]

Significance of white blood cell count and its subtypes in patients with acute coronary syndrome

EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 5 2009
G. Huang
Abstract Background, Inflammation plays a role in the pathogenesis of coronary atherosclerosis. Materials and methods, Six hundred twenty-three patients with acute coronary syndrome (ACS) referred for coronary angiography for the first time in our hospital were enrolled in this study. White blood cell and its subtypes were measured on admission. The study population was divided into three groups based on total white blood cell count and followed up. Clinical end points were major adverse cardiac events (MACEs), including cardiogenic death, stroke, heart failure, non-fatal myocardial infarction, rehospitalization for angina pectoris. Results, The median age was 68 years (range 31,92) and 64·2% of the patients were men. The median white blood cell count was 6·48 × 109 L,1 (range 2·34,27·10 × 109 L,1). The median follow-up duration was 21 months (range 1,116) and MACEs occurred in 167 patients. The multivariable Cox proportional hazards regression model revealed that neutrophil count [Relative risk = 1·098, 95% Confidence interval (CI): 1·010,1·193, P = 0·029) was a risk factor for MACEs. The logistic regression model revealed that lymphocyte count [Odds ratio (OR) = 1·075, 95% CI: 1·012,1·142, P = 0·018] and monocyte count (OR = 8·578, 95% CI: 2·687,27·381, P < 0·001) were predictive of stenosis , 75%; Neutrophil proportion (OR = 1·060, 95% CI: 1·007,1·115, P = 0·026), monocyte count (OR = 12·370, 95% CI: 1·298,118·761, P = 0·029) were predictive of the presence of multivessel disease. Kaplan,Meier analysis of short-term and long-term cumulative survival showed no significant statistical differences among three groups. Conclusions, Neutrophil count adds prognostic information to MACEs in ACS. Monocyte count and lymphocyte count are predictive of severity of coronary atherosclerosis. [source]

Impact of postprandial lipaemia on low-density lipoprotein (LDL) size and oxidized LDL in patients with coronary artery disease

EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 11 2006
M. Granér
Abstract Background, Remnant lipoprotein particles (RLPs) and oxidative stress are components of postprandial state. We investigated the concentrations of triglyceride-rich lipoproteins (TRLs), RLPs, low-density lipoprotein (LDL) size, and oxidized LDL (oxLDL) during alimentary lipaemia, and evaluated whether changes among these variables could be associated with the severity and extent of coronary artery disease (CAD). Materials and methods, Eighty men and 27 women with clinically suspected CAD underwent quantitative coronary angiography (QCA). TRLs were isolated by density gradient ultracentrifugation before and 6 h after an oral fat load. RLPs were measured by an immunoseparation method, oxLDL by ELISA, and LDL size by gradient gel electrophoresis. Results, Triglycerides, apolipoprotein (apo) B-48, and apoB-100 concentration in Swedberg flotation units (Sf) > 400 and in Sf 12,400 fractions were markedly increased at 6 h. Postprandial cholesterol content of RLPs (RLP-C) correlated with respective triglycerides in Sf > 400 (r = 0·737) and Sf 12,400 (r = 0·857), apoB-48 in Sf > 400 (r = 0·710) and Sf 12,400 (r = 0·664), apoB-100 in Sf > 400 (r = 0·812) and Sf 12,400 (r = 0·533). RLP-C correlated with oxLDL both in fasting and in fed state (r = 0·482 and r = 0·543, respectively) and inversely with LDL size (r = ,0·459 and r = ,0·442, respectively). (P < 0·001 for all). OxLDL was elevated postprandially (P < 0·001). In multivariate analysis, oxLDL was a determinant of severity and extent of CAD. Conclusion, Postprandial state is associated with oxidative stress. The magnitude of oxLDL increases during alimentary lipaemia and is associated with coronary atherosclerosis. [source]

Impact of genetic defects on coronary atherosclerosis in patients suspected of having familial hypercholesterolaemia

PON1 L55M polymorphism is not a predictor of coronary atherosclerosis either alone or in combination with Q192R polymorphism in an Italian population

EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 1 2002
M. Arca
Abstract Background, The present study evaluated the role of the PON1 L55M polymorphism independently and in conjunction with the Q192R polymorphism on the risk of coronary atherosclerosis in an Italian population. Materials and methods, Three hundred and ninety-one subjects with significant coronary stenosis (> 50%) (coronary artery disease-positive; CAD+), 196 subjects with normal coronary arteries (< 10% stenosis) (CAD,) and 178 healthy controls were screened using a combination of polymerase chain reaction and restriction enzyme digestion. Results, In the pooled population, the frequencies of L and M alleles were 0·63 and 0·37, respectively; the most common haplotypes were QQ/LM (24·2%) and QR/LL (21·8%) and a strong linkage disequilibrium between L/55 and R/192 alleles was observed (D, = ,0·91; P < 0·0001). CAD+ subjects did not show any significant differences in the distribution of PON1,55 genotypes as compared to CAD, subjects and population controls (,2 = 1·5, P = 0·8). After controlling for other risk factors, the low-concentration M allele was not associated with a significant change of CAD risk (OR 1·02; 95% CI 0·80,1·29; P = 0·87). Moreover, the L55M polymorphism did not show any interaction with other risk factors such as smoking, diabetes, hypertension, low levels of high-density lipoprotein (HDL) or high ratios of low-density to high-density lipoproteins. The combination of L55M with the Q192R polymorphism did not show any effect on CAD risk. However, a marginal decrease in myocardial infarction risk was detected when QQ/MM carriers (OR 0·51; 95% CI 0·26,0·99; P = 0·048), but not LL/RR carriers, were compared with subjects not homozygous for an L or R allele. Conclusions, These findings did not indicate a major effect of the PON1 L55M polymorphism, either alone or in combination with the Q192R polymorphism, on CAD risk. Additional studies are needed for a better evaluation of the role of the 55/192 PON1 genotypes in combination on myocardial infarction risk. [source]

Plaque cholesterol and calcium: the value of EBCT in the detection of coronary atherosclerosis

EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 6 2001
B. E. Cham
[source]

Inflammatory Cytokine Imbalance after Coronary Angioplasty: Links with Coronary Atherosclerosis

Anti-beta 2 glycoprotein I antibodies and the risk of myocardial infarction in young premenopausal women

JOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 12 2007
P. L. MERONI
Summary Background:,Contrasting data have been reported on the association between the presence of anti-phospholipid antibodies (aPL) and arterial thrombotic events, particularly those in coronary arteries. This discrepancy is perhaps related to the confounding effect of traditional risk factors. Among them, coronary atherosclerosis appears to be the most important in studies conducted in middle-aged and elderly patients.Objective:,To minimize such confounding effects, a multicenter case,control study on the association between aPL and myocardial infarction (MI) was carried out in a rare cohort of young premenopausal women.Methods:,We evaluated 172 cases hospitalized for a first MI before the age of 45 years and 172 controls individually matched with cases for age, sex and geographical origin. Clinical and laboratory data were collected and levels of anti-cardiolipin (aCL), anti-beta2 glycoprotein I (anti-,2GPI) and anti-nuclear antibodies (ANA) were measured.Results:,A significant association between MI and IgG/IgM anti-,2GPI antibodies was observed; the results were confirmed after adjusting for smoking and hypertension (anti-,2GPI IgG OR = 2.47, 95% CI 1.81,3.38; anti-,2GPI IgM 4th quartile OR 3.68, 95% CI 1.69,8.02). The association between anti-,2GPI antibodies and MI was detected in both subgroups with and without coronary artery stenosis. Whereas the association of aCL IgG with MI was modest, ANA showed no significant association with MI. No aPL were found in unselected patients (mainly males) who recently developed acute MI.Conclusions:,Anti-,2GPI antibodies are a significant risk factor for MI in young premenopausal women independently of other risk factors, including the degree of coronary artery stenosis. [source]

The association between effort,reward imbalance and coronary atherosclerosis in a Chinese sample

AMERICAN JOURNAL OF INDUSTRIAL MEDICINE, Issue 7 2010
Weixian Xu MD
Abstract Background Previous studies of job strain and coronary heart disease (CHD) have produced mixed findings. We aimed to examine the association between job stress evaluated by the effort,reward imbalance (ERI) model and coronary atherosclerosis assessed by coronary angiography in a Chinese sample. Methods Three-hundred twenty participants accepting coronary angiography for the first time were enrolled in series. Job stressors were evaluated by the ERI model. The presence and severity of CHD were assessed by measuring the coronary artery stenosis (the presence of >50% luminal stenosis in one or more major coronary arteries). The association between job stressors and CHD was examined by multivariate analysis. Results Compared with the low-level group, high-level effort, overcommitment, and ERI increased CHD risk with odds ratio (OR) 2.5 (95% confidence interval (CI): 1.2,5.0), 2.5 (95% CI: 1.2,5.0), 2.4 (95% CI: 1.2,4.9), respectively, after adjustment for confounders. They were also significantly positively correlated with the complexity of coronary artery lesions, respectively. Dose,response relationships were observed. Conclusions ERI was associated with coronary artery lesions in a sample of Chinese workers. Longitudinal research and interventional designs are needed to confirm the mechanism and to provide evidence for the prevention of CHD. Am. J. Ind. Med. 53:655,661, 2010. © 2010 Wiley-Liss, Inc. [source]

Electron Beam Computed Tomographic Scanning in Preventive Medicine

PREVENTIVE CARDIOLOGY, Issue 2 2002
David G. King BSc
Undetected coronary atherosclerosis is present in the majority of patients suffering myocardial infarction or sudden death. Electron beam computed tomography affords noninvasive scanning of the heart to detect and measure coronary calcification. These data permit dramatically improved assessment of both short term and future risk for cardiac and other events. Knowledge of this risk gives the physician an opportunity for timely and cost-effective interventions. [source]

Adipocytokines, insulin resistance, and coronary atherosclerosis in rheumatoid arthritis

ARTHRITIS & RHEUMATISM, Issue 5 2010
Young Hee Rho
Objective The prevalence of subclinical coronary atherosclerosis is increased in patients with rheumatoid arthritis (RA), and the increased risk is associated with insulin resistance. Adipocytokines have been linked to obesity, insulin resistance, inflammation, and coronary heart disease in the general population. This study was undertaken to examine the hypothesis that adipocytokines affect insulin resistance and coronary atherosclerosis among patients with RA. Methods The coronary calcium score, homeostatic model assessment for insulin resistance (HOMA-IR) index, and serum adipocytokine (leptin, adiponectin, resistin, and visfatin) concentrations were determined in 169 patients with RA. The independent effect of each adipocytokine on insulin resistance according to the HOMA-IR index and on coronary artery calcification determined by electron beam computed tomography was assessed in models adjusted for age, race, sex, body mass index (BMI), traditional cardiovascular risk factors, and inflammation mediators. In addition, an interaction analysis was performed to evaluate whether the effect of the HOMA-IR index on the coronary calcium score is moderated by adipocytokines. Results Increased concentrations of leptin were associated with a higher HOMA-IR index, even after adjustment for age, race, sex, BMI, traditional cardiovascular risk factors, and inflammation mediators (P < 0.001), but concentrations of visfatin (P = 0.06), adiponectin (P = 0.55), and resistin (P = 0.98) showed no association with the HOMA-IR index. None of the adipocytokines was independently associated with the coronary calcium score (all P > 0.05). Serum leptin concentrations showed a significant interaction with the HOMA-IR index (P for multivariate interaction = 0.02). Increasing leptin concentrations attenuated the increased risk of coronary calcification related to insulin resistance. Serum concentrations of the other adipocytokines showed no significant interactions with the HOMA-IR index (each P > 0.05). Conclusion Leptin is associated with insulin resistance in patients with RA but, paradoxically, attenuates the effects of insulin resistance on coronary calcification. [source]

Coronary Artery Bypass Grafting for Hemodialysis- Dependent Patients

ARTIFICIAL ORGANS, Issue 4 2001
Hitoshi Hirose
Abstract: Patients with end-stage renal disease carry a risk of coronary atherosclerosis. This study was performed to evaluate the perioperative and remote data of coronary artery bypass grafting (CABG) in hemodialysis dependent patients. We retrospectively analyzed the results of isolated CABG performed at Shin-Tokyo Hospital between June 1, 1993 and May 31, 2000. Preoperative, perioperative, and follow-up data of the patients on hemodialysis (Group HD, n = 37) were collected and compared with those of control patients (Group C, n = 1,639). Group HD consisted of 26 males and 11 females with a mean age of 59.9 ± 8.1 years, and the mean number of bypasses was 2.5 ± 1.1. Group HD had a longer postoperative intubation time, ICU stay, and hospital stay than Group C. The postoperative major complication rate in Group HD (18.9%) was not significantly different from that in Group C (11.3%). However, the inhospital mortality rate in Group HD (5.4%) was higher than Group C (0.6%). At the mean follow-up of 2.4 years, the actuarial 3-year survival of Groups HD and C were 90.6% and 97.6%, respectively (p < 0.001), excluding hospital mortality. The actuarial 3-year cardiac event-free rates were 84.3% in Group HD and 88.8% in Group C, showing no difference. Patients on chronic hemodialysis carry a significant risk of prolonged inhospital care and hospital death. Once successful surgical revascularization was completed, their long-term cardiac events could be controlled as effectively. The increased distant death rates was probably associated with the nature of renal disease. [source]

Long-term mortality among young ischemic stroke patients in western Norway

ACTA NEUROLOGICA SCANDINAVICA, Issue 3 2007
U. Waje-Andreassen
Objectives,,, To obtain data on long-term mortality among young ischemic stroke patients compared with controls in this population-based study. Material and methods ,, We used Kaplan,Meier survival analysis to compare 232 patients aged 15,49 years with first-ever cerebral infarction in 1988,1997 and 453 controls followed from inclusion to death or 1 August 2005 for 2515 and 5558 person-years respectively. In a subanalysis of 192 patients, we compared risk factor variables using the Kaplan,Meier method and log-rank testing. We applied a Cox proportional hazards model to adjust for multiple risk factors. Results ,, Forty-five patients and nine controls died during follow-up (P < 0.0005). Independent risk factors for mortality were active tumor disease (P < 0.0005), high consumption of alcohol (P < 0.0005), coronary atherosclerosis (P < 0.001), living alone (P < 0.02), seizures (P < 0.04) and smoking (P = 0.08). Conclusions ,, Long-term mortality was significantly increased among young stroke patients, mainly due to such lifestyle factors as high consumption of alcohol and tobacco. [source]

Annual Scientific Meeting of ASCEPT, 1999 Careful Screening To Target Interventions To Prevent Sudden Cardiac Death

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 3 2001
Allan D Struthers
SUMMARY 1. Cardiac death is due not only to coronary artery disease, but also to left ventricular (LV) abnormalities (fibrosis, dysfunction) and arrhythmogenic triggers, such as autonomic imbalance. 2. Nitric oxide deficiency could be a key mediator leading not only to coronary atherosclerosis, but also to LV abnormalities and autonomic imbalance. 3. It may be possible to screen for the above abnormalities (e.g. echocardiography and brain natriuretic peptide levels for LV abnormalities, 24 h tapes for autonomic imbalance and QT interval analysis). 4. Once individuals are identified as being at high risk, a range of interventions is possible (e.g. intensive statin therapy or angiotensin-converting enzyme inhibitors if LV abnormalities or autonomic imbalance are found). [source]

Aortic sclerosis,a marker of coronary atherosclerosis

CLINICAL CARDIOLOGY, Issue 12 2004
Yogendra Prasad M.D.
Abstract Aortic valve sclerosis is defined as calcification and thickening of a trileaflet aortic valve in the absence of obstruction of ventricular outflow. Its frequency increases with age, making it a major geriatric problem. Of adults aged> 65 years, 21,29% exhibit aortic valve sclerosis. Incidence of aortic sclerosis increases with age, male gender, smoking, hypertension, high lipoprotein (Lp) (a), high low-density lipoprotein (LDL), and diabetes mellitus. Aortic valves affected by aortic sclerosis contain a higher amount of oxidized LDL cholesterol and show increased expression of metalloproteinases. Clinically, it can be suspected in the presence of soft ejection systolic murmur at the aortic area, normal split of the second heart sound, and normal volume carotid pulse, but it can be best detected by echocardiography. Aortic sclerosis may be accompanied by mitral annulus calcification up to 50% of cases. It is associated with an increase of approximately 50% in the risk of death from cardiovascular causes and the risk of myocardial infarction. The mechanism by which aortic sclerosis contributes to or is associated with increased cardiovascular risk is not known. Aortic sclerosis is associated with systemic endothelial dysfunction, and a small percentage of cases may progress to aortic stenosis. Lowering of LDL cholesterol by 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors have been shown to decrease progression of aortic valve calcification. Aortic sclerosis is not a mere benign finding. Once diagnosis of aortic sclerosis has been made, it should be considered a potential marker of coexisting coronary disease. Aggressive management of modifiable risk factors, especially LDL cholesterol lowering, may slow progression of the disease. [source]

The prediction of coronary atherosclerosis employing artificial neural networks

CLINICAL CARDIOLOGY, Issue 6 2000
Jacob George M.D.
Abstract Background: Atherosclerosis is a complex histopathologic process that is analogous to chronic inflammatory conditions. Several factors have been shown to correlate with the extent of atherosclerosis. Whereas hypertension, obesity, hyperlipidemia, diabetes, smoking, and family history are all well documented, recent literature points to additional associated factors. Thus, antibodies to oxidized low-density lipoprotein (oxLDL), cytomegalovirus (CMV), Chlamydia pneumonia, Helicobacter pylori, as well as homocysteine and C-reactive protein (CRP) levels have all been implicated as independent markers of accelerated atherosclerosis. Hypothesis: In the current study we attempted to formulate a system by which to predict the extent of coronary atherosclerosis as assessed by angiographic vessel occlusion. Methods: The 81 patients were categorized as having single-, double-, triple-, or no vessel involvement. The clinical data concerning the "classic" risk factors were obtained from clinical records, and sera were drawn from the patients for determination of the various parameters that are thought to be associated with atherosclerosis. Results: Using four artificial neural networks, we have found the most effective parameters predictive of coronary vessel involvement were (in decreasing order of importance) antibodies to oxLDL, to cardiolipin, to CMV, to Chlamydia pneumonia, and to ,2-glycoprotein I (,2GPI). Although important in the prediction of vessel occlusion, hyperlipidemia, hypertension, CRP levels, and diabetes were less accurate. Conclusion: The results of the current study, if reproduced in a larger population, may establish an integrated system based on the creation of artificial neural networks by which to predict the extent of atherosclerosis in a given subject fairly and noninvasively. [source]

Increased epicardial adipose tissue (EAT) volume in type 2 diabetes mellitus and association with metabolic syndrome and severity of coronary atherosclerosis

CLINICAL ENDOCRINOLOGY, Issue 6 2009
Chao-Ping Wang
Summary Objective, Epicardial adipose tissue (EAT) is a part of visceral fat deposited around the heart between the pericardium and myocardium along the distribution of coronary arteries. EAT thickness is reported to be associated with coronary atherosclerosis; however, no study has measured EAT volume in patients with type 2 diabetes or investigate its association with coronary artery disease. Design, A hospital-based case control study. Patients, A total of 49 patients with type 2 diabetes mellitus (T2DM) and 78 nondiabetic controls were studied. Measurements, Cardiac multislice computed tomography was used to measure EAT volume, Gensini score, coronary artery calcium score and, coronary lesions. The relationships between EAT volume, markers of coronary atherosclerosis and anthropometric and biochemical parameters of metabolic syndrome (MetS) were investigated. Results, EAT volume was significantly higher in patients with T2DM than in nondiabetic subjects (166·1 ± 60·6 cm3 vs. 123·4 ± 41·8 cm3, P < 0·0001). Logistic regression analysis revealed independent and significant associations between EAT and diabetic status. EAT volume was significantly associated with components of MetS (BMI, waist circumference, fasting serum glucose, total cholesterol, HDL-cholesterol, and triglycerides levels), Gensini score, coronary lesions, coronary disease and coronary calcium scores. Univariate, multivariate and trend analyses confirmed that EAT volume was associated with MetS component clustering and the coronary atherosclerosis index. Conclusions, The analytical results indicate that EAT volume is increased in T2DM patients and is associated with unfavourable components of MetS and coronary atherosclerosis. The close anatomical relationship between EAT and the coronary arteries, combined with other evidence indicating that EAT is a biologically active adipokine-secreting tissue, suggest that EAT participates in the pathogenesis of diabetic coronary atherosclerosis. [source]