Sameer Nagamia

Effects of Yoga on Inflammation and Exercise Capacity in Patients With Chronic Heart Failure

BACKGROUND Despite recent advances in pharmacologic and device therapy, morbidity and mortality from heart failure (HF) remain high. Yoga combines physical and breathing exercises that may benefit patients with HF. We hypothesized that an 8-week regimen of yoga in addition to standard medical therapy would improve exercise capacity, inflammatory markers, and quality of life (QoL) in patients with HF. METHODS AND RESULTS New York Heart Association Class I-III HF patients were randomized to yoga treatment (YT) or standard medical therapy (MT). Measurements included a graded exercise test (GXT) to V O(2Peak) and the following serum biomarkers: interleukin-6 (IL-6), high-sensitivity C-reactive protein (hsCRP), and extracellular superoxide dismutase (EC-SOD). The Minnesota Living with Heart Failure Questionnaire (MLHFQ) was administered to assess changes in QoL. A total of 19 patients were enrolled after the initial screening. Of the 19 patients, 9 were randomized to YT and 10 to MT. Patients had a mean EF of 25%. GXT time and V O(2Peak) were significantly improved in the YT versus MT groups (+18% in the YT and -7.5% in MT; P = .03 vs. control and +17 in YT and -7.1 in MT; P = .02, respectively). There were statistically significant reductions in serum levels of IL-6 and hsCRP and an increase in EC-SOD in the YT group (all P < .005 vs. MT). MLHFQ scores improved by 25.7% in the YT group and by 2.9% in the MT group. CONCLUSIONS Yoga improved exercise tolerance and positively affected levels of inflammatory markers in patients with HF, and there was also a trend toward improvements in QoL.

The effects of extended-release niacin on carotid intimal media thickness, endothelial function and inflammatory markers in patients with the metabolic syndrome

Background:  Niacin is an agent that significantly increases high‐density lipoprotein cholesterol (HDL‐C), but its effects on surrogate markers of atherosclerosis and inflammatory markers are less clear. We studied the effects of niacin on carotid intimal media thickness (IMT), brachial artery reactivity as well as markers of inflammation and the metabolic profile of patients with metabolic syndrome.

Usefulness of elevations in serum choline and free F2)-isoprostane to predict 30-day cardiovascular outcomes in patients with acute coronary syndrome.

Our objectives were to evaluate the prognostic value of several biomarkers in patients with acute coronary syndrome (ACS) through an evaluation of the 30-day clinical outcomes. Multiple biomarkers have emerged as potentially useful in risk stratification of ACS. Specifically, markers of vascular inflammation and oxidative stress might be helpful in the determination of clinical outcomes. We evaluated patients presenting with chest pain. ACS was defined by symptoms of cardiac ischemia plus electrocardiographic changes or positive troponin I. Levels of serum troponin I, high sensitivity C-reactive protein, serum choline, and free F(2)-isoprostane were obtained. Patients were followed up for 30 days (n = 108) with determination of nonfatal myocardial infarction, congestive heart failure, need for revascularization, and death. Of the 108 patients, 26 had a cardiac event. Free F(2)-isoprostane and choline levels (but not high-sensitivity C-reactive protein levels) predicted 30-day cardiac events. To determine the value of choline and F(2)-isoprostane levels in predicting 30-day cardiac events, receiver operating curves were generated. The optimal cutoff point of these markers was a serum F(2)-isoprostane level of 124.5 pg/ml (r = 0.82) and a serum choline level of 30.5 mumol/L (r = 0.76). F(2)-isoprostane and choline had a positive predictive value of 57% and 44% and a negative predictive value of 90% and 89%, respectively. In conclusion, serum choline and free F(2)-isoprostane are predictors of cardiac events in ACS. A model that includes an array of biomarkers, including troponin, choline, and free F(2)-isoprostane, might be useful in predicting patients at greater risk of future events in ACS.

Revisiting niacin: reviewing the evidence

Atherogenic dyslipidemia, defined by a cluster of lipoprotein abnormalities, including low high-density lipoprotein cholesterol (HDL-C) and elevated serum triglycerides, represents an important potential target for reducing cardiovascular risk. This has paved the way for revisiting niacin as a therapy in preventing progression of atherosclerosis. Niacin remains the safest and most effective agent for raising HDL-C and is a logical choice to target atherogenic dyslipidemia. While the clinical efficacy of niacin has been known for many years, it is only with development of newer formulations, which have lower side-effect profiles and improved compliance, that the potential for this agent been fully realized. In this review, we will examine some of the reasons that niacin can have important implications for reducing progression of atherosclerosis. We will first examine the different formulations and their variability, not only in side-effect profiles, but also in clinical efficacy. We will then consider the theoretical evidence for the benefit of HDL-raising produced by niacin on atherosclerotic progression. Finally, we will review clinical data suggesting the benefit of niacin on cardiovascular outcomes.

Efficacy of controlled-release niacin in treatment of metabolic syndrome: Correlation to surrogate markers of atherosclerosis, vascular reactivity, and inflammation

BACKGROUND The mechanisms that link metabolic syndrome to development of atherosclerosis are largely unknown. There is increasing evidence for the role of adipokines in this process. Niacin would appear to be a logical choice in combating the atherogenic dyslipidemia seen in metabolic syndrome, as it remains the most effective agent in raising high-density lipoprotein cholesterol, and also reduces triglycerides. We hypothesized that statin-intolerant patients with insulin resistance would respond to controlled-release niacin with a rise in plasma adiponectin levels. METHODS Fifty patients with the metabolic syndrome (National Cholesterol Education Program/Adult Treatment Panel III criteria) were randomized to either once-daily controlled-release niacin (1000 mg/day) or placebo. Measurements at baseline and after 52 weeks of treatment were made of the carotid intimal media thickness, flow-mediated dilation of the brachial artery, and blood plasma adiponectin levels. These measures were compared to changes in lipoprotein concentrations in plasma. RESULTS Changes in high-density lipoprotein cholesterol correlated significantly to changes in flow-mediated vasodilation and carotid artery intima-media thickness, and there was a trend toward correlation with plasma adiponectin levels. There was a significant difference in mean serum levels of adiponectin after the treatment period between placebo and niacin groups (16.3 ± 1.7 and 17.7 ± 1.9 mg/dL, respectively) (P = 0.022). CONCLUSIONS Treatment with controlled-release niacin for 52 weeks results in sustained improvements in adiponectin levels compared to placebo in patients with metabolic syndrome. No adverse effects of niacin on glycemic control were found.

Potential role of statin therapy in heart failure, atrial fibrillation and aortic stenosis

3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors, or statins, are widely prescribed throughout the world, and considerable evidence has indicated their powerful effects in ischemic forms of cardiovascular disease. Recently, several trials have demonstrated that statins have pleiotropic effects beyond their lipid-lowering capacities. These findings may play a role in the use of statins to manage forms of cardiovascular disease that may or may not have an ischemic etiology: congestive heart failure, atrial fibrillation and aortic stenosis.