Association Between Smoking and Serum GlycA and High-Sensitivity C-Reactive Protein Levels: The Multi-Ethnic Study of Atherosclerosis (MESA) and Brazilian Longitudinal Study of Adult Health (ELSA-Brasil).

Background: Inflammation is suggested to be a central feature of atherosclerosis, particularly among smokers. We studied whether inflammatory biomarkers GlycA and high-sensitivity C-reactive protein are associated with cigarette smoking.

Methods And Results: A total of 11 509 participants, 6774 from the MESA (Multi-Ethnic Study of Atherosclerosis) and 4735 from ELSA-Brasil (The Brazilian Longitudinal Study of Adult Health) were included.

CETP Inhibition: does the future look promising?

Based on epidemiologic studies conducted throughout the world, it is established that there is an inverse relationship between high-density lipoprotein cholesterol (HDL-C) and risk for coronary artery disease (CAD). The incidence of low HDL-C is high and increasing throughout the world. A variety of pharmacologic approaches are being developed to therapeutically modulate serum levels of HDL-C.

Linagliptin: a new DPP-4 inhibitor for the treatment of type 2 diabetes mellitus.

Incretin-based therapies constitute a relatively new pharmacological approach to the treatment of type 2 diabetes mellitus. As reflected in the rapidly growing body of literature and the number of glucagon-like peptide-1 and dipeptidyl peptidase-4 inhibitor (DPP-4) compounds that are either approved or in development, there is considerable interest in treatments that target the incretin axis. Linagliptin is a recently approved DPP-4 inhibitor with unique pharmacological properties, including very high affinity for the DPP-4 enzyme, postdose DPP-4 inhibition>80% after 24 hours, and a primarily fecal route of elimination.

Familial hypercholesterolemia: screening, diagnosis and management of pediatric and adult patients: clinical guidance from the National Lipid Association Expert Panel on Familial Hypercholesterolemia.

The familial hypercholesterolemias (FH) are a group of genetic defects resulting in severe elevations of blood cholesterol levels and increased risk of premature coronary heart disease. FH is among the most commonly occurring congenital metabolic disorders. FH is a treatable disease.

Pleiotropic effects of angiotensin receptor blockers: addressing comorbidities by optimizing hypertension therapy.

The efficacy of angiotensin receptor blockers (ARBs) in the management of hypertension is well established. Whether these agents induce pleiotropic effects that promote the amelioration of vascular disorders independent of blood pressure reduction remains controversial. This review examines preclinical and clinical data that highlight a potentially important role for ARBs in several common vascular disorders, including cardiovascular, cerebrovascular, renal, and metabolic disorders.

Activation of intracellular signaling systems by high-density lipoproteins.

The proteosome of high-density lipoprotein particles is quite complex and consists of up to 75 different proteins and enzymes. The specific protein cargo of HDL particles regulates their functionality. In addition to their documented capacity to engage in reverse cholesterol transport, reduce oxidized lipid, and function as apoprotein donors, HDL particles can activate a variety of signaling systems in endothelial cells, smooth muscle cells, and platelets.

High-density lipoproteins: marker of cardiovascular risk and therapeutic target.

The high-density lipoproteins (HDLs) are complex, polymolecular assemblies produced by the jejunum, liver, in serum, and on the surface of macrophages. HDL cholesterol (HDL-C) levels are an independent predictor of risk for cardiovascular events in both men and women. High serum levels of this lipoprotein are associated with reduced risk for atherosclerosis and its clinical sequelae, such as myocardial infarction, ischemic stroke, and death.

Pharmacomodulation of high-density lipoprotein metabolism as a therapeutic intervention for atherosclerotic disease.

The high-density lipoproteins (HDLs) are produced by the liver and small intestine as well as on the surface of lipid-enriched macrophages in the subendothelial space of arterial walls. Unlike the apo B100-containing lipoproteins, the HDLs are uniquely antiatherogenic. Based on prospective observational studies performed throughout the world, there is a consistent inverse relationship between serum levels of HDLs and risk for cardiovascular events: low levels of high-density lipoprotein-cholesterol (HDL-C) are associated with increased risk, whereas high levels are usually associated with reduced risk for myocardial infarction, ischemic stroke, and cardiovascular mortality.

Fibrate therapy in the management of diabetic dyslipidemia: there is no ACCORD to be found.

Mixed dyslipidemia is a complex clinical entity that contributes significantly to the increased risk for cardiovascular morbidity and mortality that is observed in patients with type 2 diabetes mellitus. Insulin resistance is associated with reduced serum lipoprotein lipase activity, increased serum levels of very low-density lipoproteins and triglyceride, low serum high-density lipoproteins, and increased concentrations of small, dense low-density lipoproteins. Combinations of medications are frequently required in order to achieve guideline-specified goals for the various lipid fractions of diabetic patients.

Drug treatment of hyperlipidaemia: a guide to the rational use of lipid-lowering drugs.

Mammalian sterol and lipid metabolism depends on a large number of highly evolved biochemical and histological processes responsible for the absorption, distribution and steady-state anabolic/catabolic handling of these substances. Lipoproteins are complex polymolecular assemblies comprising phospholipids, cholesterol and cholesterol esters, triglycerides and a variety of apolipoproteins. The primary function of lipoproteins is to facilitate the systemic distribution of sterols and lipids.

The role of statins in managing diabetic dyslipidemia.

The common lipid abnormalities associated with T2DM confer substantial CV risk. Statins are a safe and well-established treatment option for lowering this atherogenic burden and improving outcomes in this patient population. Nonetheless, many patients with T2DM are not receiving a statin, and even those who receive treatment may not be achieving recommended lipid targets.

Lipoprotein-associated phospholipase A2: role in atherosclerosis and utility as a cardiovascular biomarker.

Atherosclerosis and its clinical manifestations are widely prevalent throughout the world. Atherogenesis is highly complex and is modulated by numerous genetic and environmental risk factors. A large body of basic scientific and clinical research supports the conclusion that inflammation plays a significant role in atherogenesis along the entire continuum of its progression.

Should we target HDL cholesterol level in lowering cardiovascular risk?

In prospective observational studies and retrospective case control studies performed throughout the world, low serum levels of high-density lipoprotein cholesterol (HDL-C) are consistently associated with increased risk for all forms of atherosclerotic disease and its clinical sequelae, including myocardial infarction, stroke, and sudden death. In contrast, high serum levels of this lipoprotein are associated with reduced risk for these outcomes. The metabolism of high-density lipoproteins (HDLs) is complex, and a very large number of genetic polymorphisms influence the serum level of HDL particles in any given individual.

Thienopyridine therapy and risk for cardiovascular events in secondary prevention.

Platelets are critical modulators of atherothrombotic events. In the acute setting, platelets are activated and aggregate on the surface of atherosclerotic plaque that has ruptured, fissured, or developed erosions. The overlying thrombus leads to sudden development of arterial luminal obstruction, inducing ischemia and cellular necrosis.

Clinical insights from the Fenofibrate Intervention and Event Lowering in Diabetes study: a community practice perspective.

Achieving adequate control of cardiovascular risk in type 2 diabetes mellitus (DM) is crucially important; however, the atherogenic dyslipidaemia (including low high-density lipoprotein cholesterol and hypertriglyceridaemia) typically encountered in type 2 DM is often managed inadequately. Evidence from the Fenofibrate Intervention and Event Lowering in Diabetes study suggests that fenofibrate reduces the risk of long-term macrovascular and microvascular type 2 diabetic complications, especially in patients demonstrating features of the metabolic syndrome. Fenofibrate represents a useful treatment option for controlling cardiovascular risk in type 2 diabetes patients in the community setting.

Niacin and fibrate use among patients with high triglycerides and low high-density lipoprotein cholesterol.

Background: National guidelines recommend treating low HDL and/or high triglycerides (TG) with adjunctive therapy that supplements statin monotherapy in patients with multiple cardiovascular disease (CVD) risk factors. Niacin and fibrates have been shown in clinical trials to be effective as adjunctive therapy for these lipid abnormalities.

Objective: To evaluate the pharmacologic treatment of low HDL and high TG in real-world practice by assessing a large managed-care population with CVD risk factors enrolled in a commercial health plan.

Novel therapies for increasing serum levels of HDL.

The protectiveness of elevated HDL-C against CHD and its long-term sequelae is a subject of intense investigation throughout the world. HDL has the capacity to modulate a large number of atherogenic mechanisms, such as inflammation, oxidation, thrombosis, and cell proliferation. Among lipoproteins, HDL is also unique, in that it promotes the mobilization and clearance of excess lipid via the series of reactions collectively termed "reverse cholesterol transport.

Drug therapy for hypertriglyceridemia: fibrates and omega-3 fatty acids.

The reduction of low-density lipoprotein cholesterol in patients at risk for acute cardiovascular events is the cornerstone of lipid management in both the primary and secondary prevention settings. Serum triglyceride levels exceeding 150 mg/dL are abnormal and confer increased risk for developing coronary artery disease in both men and women. Serum triglycerides are derived from both dietary and endogenous biosynthetic pathways.

When high is low: raising low levels of high-density lipoprotein cholesterol.

Low serum levels of high-density lipoprotein cholesterol (HDL-C) are highly prevalent and are recognized as an independent risk factor for cardiovascular morbidity (myocardial infarction, stroke, peripheral arterial disease, and restenosis after coronary stenting) and mortality. HDL plays an important role in modulating atherogenesis, although its functions are varied and complex and the mechanisms for its antiatherogenic effects have not been completely elucidated. The inverse relationship between HDL-C and cardiovascular risk is well established, and epidemiologic studies and clinical trials have provided ample evidence that higher levels of HDL-C are vasculoprotective.

Lipid therapy utilization rates in a managed-care mixed dyslipidemia population.

Background: National clinical treatment guidelines recommend pharmacologic treatment in addition to therapeutic lifestyle modifications in patients with mixed dyslipidemia and multiple risk factors for coronary heart disease (CHD).

Objectives: To evaluate real-world pharmacologic treatment of mixed dyslipidemia patients with cardiovascular disease (CVD) risk factors.

Methods: Commercial health plan members in a large, United States managed-care database with complete lipid panel results (ie, high-density lipoprotein cholesterol [HDL-C], low-density lipoprotein cholesterol [LDL-C], total cholesterol [TC], triglycerides [TG]) between January 1, 2006 and December 31, 2006 were included.

Clinical characterization and molecular mechanisms of statin myopathy.

Myopathy has been reported in a small percentage of statin-treated patients for the past 30 years, but the etiologic mechanisms for inducing muscle injury have not yet been fully characterized. Statin-induced myopathy is now understood to be a heterogeneous condition that may be due to: mechanisms of the drug itself; interactions with other drugs; or genetic, metabolic and immunological vulnerabilities in individual patients. In some cases, statins may unmask latent conditions (e.