Author
BOSTOM A G - RHODE ISLAND HOSP | |
HUME A L - UNIV OF RHODE ISLAND | |
EATON C B - BROWN UNIVERSITY | |
LAURINO J P - BROWN | |
YANEK L R - BROWN | |
REGAN M S - BROWN | |
MCQUADE W H - BROWN | |
CRAIG W Y - FOUNDATION FOR BLOOD RES | |
PERRONE G A - TUFTS-HNRCA | |
JACQUES P F - TUFTS-HNRCA |
Submitted to: Pharmacotherapy
Publication Type: Peer Reviewed Journal Publication Acceptance Date: 5/1/1995 Publication Date: N/A Citation: N/A Interpretive Summary: Lipoprotein(a) [Lp(a)] is a particle similar to LDL or "bad" cholesterol. Studies have established Lp(a) as an independent risk factor for premature coronary heart disease (CHD). It has been hypothesized that Lp(a) was a biological surrogate for vitamin C. One study reported a marked reduction in blood Lp(a) levels in 11 CHD patients treated with high doses of vitamin nC. The present study attempted to replicate these observations in a larger randomized, double-blinded, placebo-controlled trial. Forty-four patients with documented premature CHD were randomized on the basis of age, gender, and screening Lp(a) concentrations to receive 4.5 grams of vitamin C or a placebo daily for 12 weeks. High dose vitamin C treatment was well tolerated and produced a marked elevation in vitamin C levels in the blood, but there was no significant effect on Lp(a) levels. Our findings do not support a clinically important lowering effect of high-dose vitamin C on Lp(a) blood levels in patients with premature CHD. Technical Abstract: STUDY OBJECTIVE. To determine the efficacy of a high dose ascorbate supplement in lowering lipoprotein(a) [Lp(a)] levels in patients with premature coronary heart disease (CHD). DESIGN. Randomized, double-blinded, placebo-controlled trial. SETTING. Outpatient clinic. PATIENTS. Forty-four patients with documented premature CHD (confirmed myocardial infarction and/or angiographically-determined stenosis >/=50% in at least one major coronary artery before age 60). INTERVENTIONS. Patients were block randomized on the basis of age, gender, and screening Lp(a) concentrations to receive ascorbate 4.5 grams daily or placebo for 12 weeks. MEASUREMENT AND MAIN RESULTS. High dose ascorbate treatment was well tolerated and produced a marked elevation in mean plasma ascorbate levels (+1.2 mg/dL; p<0.001). Multiple linear regression analysis revealed that there was no significant effect of high dose ascorbate supplementation on post-intervention Lp(a) levels (p=0.39) in a model that included treatment group assignment, and baseline Lp(a) level. CONCLUSIONS. Our findings do not support a clinically important lowering effect of high dose ascorbate on plasma Lp(a) in patients with premature CHD. |