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Research Interests: Cardiology, Electrocardiography, Heart Failure, Humans, Female, and 6 moreMale, Exercise, Aged, Middle Aged, Adult, and Exercise Test
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High levels of the triglycerides to high-density lipoprotein cholesterol (TG/HDL-C) ratio are associated with obesity, metabolic syndrome, and insulin resistance. We evaluated variability in the remaining lipid profile, especially remnant... more
High levels of the triglycerides to high-density lipoprotein cholesterol (TG/HDL-C) ratio are associated with obesity, metabolic syndrome, and insulin resistance. We evaluated variability in the remaining lipid profile, especially remnant lipoprotein particle cholesterol (RLP-C) and its components (very low-density lipoprotein cholesterol subfraction 3 and intermediate-density lipoprotein cholesterol), with variability in the TG/HDL-C ratio in a very large study cohort representative of the general U.S. We examined data from 1,350,908 US individuals who were clinically referred for lipoprotein cholesterol ultracentrifugation (Atherotech, Birmingham, AL) from 2009 to 2011. Demographic information other than age and sex was not available. Changes to the remaining lipid profile across percentiles of the TG/HDL-C ratio were quantified, as well as by three TG/HDL-C cut-off points previously proposed in the literature: 2.5 (male) and 2 (female), 3.75 (male) and 3 (female), and 3.5 (male and female). The mean age of our study population was 58.7 years, and 48% were men. The median TG/HDL-C ratio was 2.2. Across increasing TG/HDL-C ratios, we found steadily increasing levels of RLP-C, non-HDL-C and LDL density. Among the lipid parameters studied, RLP-C and LDL density had the highest relative increase when comparing individuals with elevated TG/HDL-C levels to those with lower TG/HDL-C levels using established cut-off points. Approximately 47% of TG/HDL-C ratio variance was attributable to RLP-C. In the present analysis, a higher TG/HDL-C ratio was associated with an increasingly atherogenic lipid phenotype, characterized by higher RLP-C along with higher non-HDL-C and LDL density.
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Many studies have shown that oral supplementation with astaxanthin may be a novel potential treatment for inflammation and oxidative stress in cardiovascular diseases, but evidence of the effects on lipid profile and glucose is still... more
Many studies have shown that oral supplementation with astaxanthin may be a novel potential treatment for inflammation and oxidative stress in cardiovascular diseases, but evidence of the effects on lipid profile and glucose is still inconclusive. Therefore, we performed a meta-analysis to evaluate the efficacy of astaxanthin supplementation on plasma lipid and glucose concentrations. The search included PubMed, Cochrane Library, Scopus, and EMBASE (up to November 27, 2014) to identify randomized controlled trials (RCTs) investigating the effects of astaxanthin supplementation on lipid profile and glucose levels. Two independent reviewers extracted data on study characteristics, methods and outcomes. Seven studies meeting inclusion criteria with 280 participants were selected for this meta-analysis; 163 participants were allocated to the astaxanthin supplementation group and 117 to the control group. A random-effect meta-analysis of data from 7 RCTs (10 treatment arms) did not show ...
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The Kidney Disease Improving Global Outcomes Lipid Work Group recommends statins for adults ≥50 years old with CKD. The American College of Cardiology/American Heart Association endorses statins for adults with atherosclerotic... more
The Kidney Disease Improving Global Outcomes Lipid Work Group recommends statins for adults ≥50 years old with CKD. The American College of Cardiology/American Heart Association endorses statins for adults with atherosclerotic cardiovascular disease, adults with LDL cholesterol≥190 mg/dl, and adults 40-79 years old with LDL cholesterol=70-189 mg/dl and diabetes or a 10-year predicted risk for atherosclerotic cardiovascular disease ≥7.5% estimated using the Pooled Cohort risk equations. Using data from the Reasons for Geographic and Racial Differences in Stroke Study, we calculated the agreement for statin treatment between these two guidelines for adults 50-79 years old with CKD (eGFR<60 ml/min per 1.73 m(2) or albuminuria≥30 mg/g) not on dialysis. We assessed the validity of the Pooled Cohort risk equations in individuals with CKD. Study participants were enrolled between 2003 and 2007, and we report incident cardiovascular disease events (stroke and coronary heart disease) thro...
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Proprotein convertase subtilisin/kexin 9 (PCSK9) is part of the proteinase K subfamily of subtilases and plays a key role in lipid metabolism. It increases degradation of the low-density lipoprotein receptor (LDL-R), modulates cholesterol... more
Proprotein convertase subtilisin/kexin 9 (PCSK9) is part of the proteinase K subfamily of subtilases and plays a key role in lipid metabolism. It increases degradation of the low-density lipoprotein receptor (LDL-R), modulates cholesterol metabolism and transport, and contributes to the production of apolipoprotein B (apoB) in intestinal cells. Exogenous PCSK9 modifies the activity of 3-hydroxy-3-methylglutaryl-coenzyme A reductase and acyl coenzyme A:cholesterol acyltransferase and enhances secretion of chylomicrons by modulating production of lipids and apoB-48. Statins increase PCSK9 messenger RNA expression and attenuate the capacity to increase LDL-R levels. Therefore, the inhibition of PCSK9 in combination with statins provides a promising approach for lowering low-density lipoprotein cholesterol (LDL-C) concentrations. This review will address new therapeutic strategies targeting PCSK9, including monoclonal antibodies, antisense oligonucleotides, small interfering RNAs, and o...
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The annual meeting of the Heart Failure Association of ESC in Lisbon, in June 2005, was exceptionally successful. There were many very interesting presentations and workshops with the unique title: Statins in heart failure-... more
The annual meeting of the Heart Failure Association of ESC in Lisbon, in June 2005, was exceptionally successful. There were many very interesting presentations and workshops with the unique title: Statins in heart failure- Cholesterol-lowering is not the only goal. Heart failure (HF) is a progressive disease with coronary artery disease (CAD) as the most often underlying etiology. Treatment to prevent progression of heart failure has been targeted to reverse the consequences of HF and to a less extent the cause - the atherosclerotic plaque itself. On the average 50% of patients with heart failure are treated with lipid intervention. Lipid-lowering treatment with statins clearly reduces morbidity and mortality of patients with documented CAD. Since the prevalent etiology of heart failure is CAD, its prevention may reduce heart failure progression. However, recent studies suggest that pleiotropic effects of statins are more important than the influence related to their cholesterol lo...
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The study aimed to identify early echocardiographic and circulating biomarkers of heart failure (HF) in hypertensive patients with normal resting echocardiography. Echocardiography at rest and during exercise, and selected biomarkers were... more
The study aimed to identify early echocardiographic and circulating biomarkers of heart failure (HF) in hypertensive patients with normal resting echocardiography. Echocardiography at rest and during exercise, and selected biomarkers were assessed in control group, dyspnea group, and HF group. On exercise dyspnea patients had lower early diastolic (E') and systolic…
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Research Interests: Kidney diseases, Acute kidney injury, Kidney transplantation, Innate immunity, Toll like receptor signaling, and 16 moreToll Like Receptors, Inflammatory Immune Response, Renal transplantation, Humans, Kidney, Ischemia, Adaptive Immunity, Animals, End Stage Renal Failure, Urinary Tract Infections, Signal Transduction Pathway Models, Transcription Factor, Bacterial infections, Graft Rejection, Bacterial Infection, and Renal disease
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The aim of this cross-sectional study was to examine the relationship between obesity and lipid markers. We divided 66 non-diabetic adult obese patients (mean age: 55.8±11.6 years) into 3 groups according to body mass index (BMI). All... more
The aim of this cross-sectional study was to examine the relationship between obesity and lipid markers. We divided 66 non-diabetic adult obese patients (mean age: 55.8±11.6 years) into 3 groups according to body mass index (BMI). All patients were measured for waist circumference (WC), hip circumference (HC), body mass index (BMI), waist-to-hip ratio (WHR), waist-to-height ratio (WHtR), body adiposity index (BAI), and visceral adiposity index (VAI). Serum levels of total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and triglycerides (TG) were determined, and lipid indices TC/HDL, LDL/HDL, and TG/HDL were also estimated. TC and LDL-C in Group III were lower than in Group I (5.0±1.0 vs. 6.0±1.0 mmol/L, and 2.9±0.9 vs. 3.8±1.2 mmol/L; p<0.05 for both). Negative correlations were found between: BMI and TC, LDL, and HDL (r=-0.291; r=-0.310, r=-0.240, respectively); and WC, WHR, VAI, and HDL (r=-0.371, r=-0.296, r=-0.376,...
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Epidemiological studies and clinical trials report the beneficial effects of fish or fish oil consumption on cardiovascular disease outcomes including sudden death. We performed a systematic review of the literature on controlled animal... more
Epidemiological studies and clinical trials report the beneficial effects of fish or fish oil consumption on cardiovascular disease outcomes including sudden death. We performed a systematic review of the literature on controlled animal studies that assessed the effects of omega-3 fatty acids on selected arrhythmia outcomes. On the basis of predetermined criteria, 27 relevant animal studies were identified; 23 of
Research Interests: Animal Studies, Metabolism, Clinical Trial, Cardiovascular disease, Sudden Death, and 14 moreFish Oil, Animal Model, Meta Analysis, Systematic review, Clinical Sciences, Rat Model, Arrhythmia, Infarct Size, Epidemiologic Studies, Ventricular Tachycardia, Eicosapentaenoic Acid, Docosahexaenoic Acid, Normal Sinus Rhythm, and Alpha-linolenic acid
Atorvastatin is a potent hydroxy-methyl-glutaryl-coenzyme A (HMG-CoA) reductase inhibitor that decreases low-density lipoprotein (LDL) cholesterol and triglyceride concentrations, but little is known about its effects on LDL subtype... more
Atorvastatin is a potent hydroxy-methyl-glutaryl-coenzyme A (HMG-CoA) reductase inhibitor that decreases low-density lipoprotein (LDL) cholesterol and triglyceride concentrations, but little is known about its effects on LDL subtype distribution in different types of hyperlipoproteinemia. Thus, we evaluated the influence of atorvastatin (10 mg/d, 4 weeks) on lipid concentrations and LDL subtype distribution in patients with hypercholesterolemia (n = 9; LDL cholesterol, 227 +/- 30 mg/dL; triglycerides, 137 +/- 56 mg/dL), patients with type 2 diabetes and dyslipoproteinemia (n = 11; LDL cholesterol, 163 +/- 34 mg/dL; triglycerides, 260 +/- 147 mg/dL), and controls (n = 10; LDL cholesterol, 116 +/- 20 mg/dL; triglycerides, 130 +/- 47 mg/dL). Cholesterol concentration was determined in 7 LDL subfractions isolated by density gradient ultracentrifugation before and during atorvastatin treatment. Atorvastatin decreased LDL cholesterol (-36%, -28%, and -41%, all P &lt;.01) and triglyceride (-4%, NS; -2%, NS; -24%, P &lt;.05) concentrations but had little effect on high-density lipoprotein (HDL) cholesterol (-1%, NS; +10%, P &lt;.05; +6%, NS) in hypercholesterolemic, diabetic, and control subjects, respectively. In all 3 groups, a significant reduction in cholesterol in each LDL subfraction was observed. Large-buoyant (LDL-1, LDL-2) and intermediate-dense (LDL-3, LDL-4) LDL were reduced more than small-dense (LDL-5 through LDL-7) LDL in hypercholesterolemic (-45%, -35%, and -32%, P &lt;.05) and control subjects (-48%, -44%, and -25%, P &lt;.05), but in diabetic patients cholesterol reduction was uniform in all LDL subtypes (-32%, -27%, and -29%, P =.45). Thus, atorvastatin decreases cholesterol concentration in all LDL subfractions in hypercholesterolemic, diabetic, and control subjects. However, the relative reduction of individual LDL subtypes differed between these groups. This finding suggests that the effect of atorvastatin on LDL subtype distribution depends on the type of underlying hyperlipoproteinemia.
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Research Interests: Echocardiography, Heart Failure, Prospective studies, Humans, Congestive Heart Failure, and 19 moreFemale, Male, Atrial Fibrillation, Body Mass Index, Dilated cardiomyopathy, Aged, Middle Aged, Pilot study, Body mass index (BMI), Adult, Tumor necrosis factor-alpha, Left Ventricular Function, Pilot Projects, Tumor Necrosis Factor–α (TNF), Condition Factor, Laboratory Tests, Brain Natriuretic Peptide, Interleukin, and Blood Plasma
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Biomarkers should have high sensitivity, specificity, reproducibility, be cost-effective, and provide incremental predictive or diagnostic utility over standard risk factors or tests. Despite numerous studies investigating biomarkers in... more
Biomarkers should have high sensitivity, specificity, reproducibility, be cost-effective, and provide incremental predictive or diagnostic utility over standard risk factors or tests. Despite numerous studies investigating biomarkers in heart failure (HF), there are only a few that predict HF in hypertensive patients. This article summarizes data from numerous studies concerning possible biomarkers of HF in hypertensive patients such as: serum uric acid (SUA), interleukins, monocyte chemoattractant protein one (MCP-1), cardiotrophin-1 (CT-1), carboxy-terminal propeptide of procollagen type I (PICP), type I collagen telopeptide (CITP) and N-terminal propeptide of type III procollagen (PIIINP), metalloproteinases (MMPs), B-type natriuretic peptide (BNP) and its derivatives, glycoprotein CA125 and cystatin C. Early detection of patients of increased risk of hypertensive heart disease may result in early implementation of effective preventive strategies. Therefore, there is need to identify newer biomarkers, if they can improve risk prediction, identifying patients, in which earlier or more aggressive intervention will improve clinical outcomes.
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Research Interests: Chronic kidney disease, Treatment Outcome, Vascular Surgery, California, Prospective studies, and 15 moreHumans, United States, Female, Hemodialysis, Male, Clinical Sciences, Aged, Middle Aged, Adult, Time Factors, Biological markers, Chi Square Distribution, Enzyme Linked Immunosorbent Assay, Renal Dialysis, and Matrix Metalloproteinase
Diabetes mellitus (DM) alters arterial wall compliance and causes aortic stiffness, which is a predictor of vascular mortality. Heat shock proteins (HSPs) are involved in the protection of cells under stress. We evaluated aortic stiffness... more
Diabetes mellitus (DM) alters arterial wall compliance and causes aortic stiffness, which is a predictor of vascular mortality. Heat shock proteins (HSPs) are involved in the protection of cells under stress. We evaluated aortic stiffness in DM and the effects of glutamine (which induces HSP 70) on HSP 70 levels in experimental DM. Male Sprague-Dawley rats (n = 30) were divided into three groups: Control (Group 1), DM (Group 2) and glutamine-treated DM (Group 3). DM was induced using streptozocin injection. Group 3 rats received two doses of glutamine during the fourth week. Blood and infrarenal aortic tissue samples were obtained for analysis at the end of the fourth week. Compared with Group 1, serum HSP 70 levels were significantly increased in Groups 2 and 3. Aortic HSP 70 was increased in DM. There was a significant difference in aortic HSP 70 with glutamine injection (Group 1 versus Group 3). DM also interfered with the elastin content of the aorta. There was a significant correlation between the serum glucose and serum and aortic HSP 70 levels and between serum and aortic HSP 70 levels; as well as between severity of DM and aortic elastin levels. DM causes aortic stiffness and this may contribute to the increase in mortality and morbidity associated with DM. The expression of HSP 70 may become a therapeutic target.
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Atherosclerosis and its complications represent the leading cause of morbidity and mortality. Heat shock protein 70 (HSP70) protects cellular elements from injury by reducing oxidation, inflammation and apoptosis and by refolding damaged... more
Atherosclerosis and its complications represent the leading cause of morbidity and mortality. Heat shock protein 70 (HSP70) protects cellular elements from injury by reducing oxidation, inflammation and apoptosis and by refolding damaged proteins. HSP70 improves viability of stressed vascular smooth muscle cells, possibly via its chaperone functions. It has been proposed that the response mounted against bacterial HSPs results in an autoimmune reaction, which has the potential to cause complement-mediated endothelial injury, and hence accelerate atherogenesis. to examine the roles of HSPs in atherosclerosis. A literature review. The role of HSPs in atherosclerosis is controversial. HSP60 probably acts as an autoantigen, and may trigger both cell- and antibody-mediated immune responses, while HSP70 is likely to be involved in cytoprotection. The significance of this inverse relation between HSP70 and atherosclerosis has not yet been elucidated. Whether HSPs will become therapeutic targets remains to be established.
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Atrial fibrillation (AF) is the most common arrhythmia encountered in clinical practice. Rhythm control strategy for AF is limited by drug toxicity and side effects, and recent trials have shown that this strategy is not superior to a... more
Atrial fibrillation (AF) is the most common arrhythmia encountered in clinical practice. Rhythm control strategy for AF is limited by drug toxicity and side effects, and recent trials have shown that this strategy is not superior to a rate control one. New antiarrhythmic drugs, free of undesired effects, would enhance rhythm control, with the possibility of sinus rhythm restoration and maintenance. A promising find in the search for new antiarrhythmic therapies is atrial-tissue specific ion channels. The findings that the ultrarapid delayed rectifier (I(Kur)) and the inwardly rectifying, acetylcholine-regulated current (I(K-Ach)) exist in atrial but not ventricular tissue increase the probability that atrioselective drugs without ventricular proarrhythmic toxicity can be developed for treatment of patients with AF. There are also other potential targets for atrial-selective therapy: transient outward current (I(to)), rapidly and slowly activating delayed rectifier currents (I(Kr) and I(Ks)), atrial sodium current (I(Na)) and atrially expressed connexins. New drugs under development with promising atrial-selectivity include: tertiapin, NIP-142, NIP-141, JTV-519, AVE0118, AVE1231, DPO-1, AZD7009 and many others. Among such new agents, vernakalant hydrochloride is currently in an advanced phase of development and has already been evaluated in clinical trials. In this overview, we describe the history and current state of developmental process of the drug, as well as its mechanism of action and influence on electrophysiological parameters. Vernakalant seems to be effective in terminating recent-onset AF, but is not efficacious in long-lasting AF and atrial flutter. The drug may be relatively free of proarrhythmic effects, and exerts a protective effect on ventricular tissue and ventricular repolarization. It is expected that the intravenous formulation will soon be approved for the pharmacological termination of recent-onset AF.