The aim of the present study is to characterize novel mechanisms whereby HDL may exert potent vasculoprotective effects independent of reverse cholesterol transport, in particular the effect of HDL on the regulation of the vascular NAD(P)H oxidase enzyme system, a major vascular source of superoxide, known to be important for endothelial dysfunction. In addition, the present study will characterize the effect of HDL on endothelial progenitor cell (EPC) mobilization, nitric oxide production and in vivo regenerative capacity.

Inclusion Criteria:

• Statin treatment for at least 3 weeks
• Reduced HDL: < 40 mg/dL (1.03 mmol/L) in men or < 50 mg/dL (1.29 mmol/L) in women
• Plus TWO of the following (thereby defining the patients to have metabolic syndrome (Grundy et al.; Circulation 2005)):
• Elevated waist circumference: ≥ 102 cm (≥ 40 inches) in men or ≥ 88 cm (≥ 35 inches) in women
• Elevated triglycerides: ≥ 150 mg/dL (1.7 mmol/L
• Elevated blood pressure: ≥ 130 mmHg systolic blood pressure or ≥ 80 mmHg diastolic blood pressure or anti-hypertensive treatment
• Elevated fasting glucose: ≥ 100 mg/dL or on drug treatment for elevated fasting glucose

Exclusion Criteria:

• Hypersensitivity to niacin
• Active liver disease or impaired liver function
• Persistent elevation of transaminases
• Cholestasis
• Gastric ulcer
• Acute coronary syndrome
• Gout
• Pregnancy, lactation
• Active infections
• Cancer
• Untreated concomitant diseases
• Renal insufficiency or renal failure
• Hypothyreosis
• Alcoholism
• Myopathies
• Muscle pain under therapy with fibrates or statins
• Hereditary muscle diseases in family history