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M A Aldridge

Publications and source records attributed to M A Aldridge.

4 recordsLinked to original sources
PubMed2001

The relationship between low-density lipoprotein cholesterol goal attainment and prevention of coronary heart disease--related events.

BACKGROUND: According to the National Cholesterol Education Program (NCEP) treatment guidelines, patients with preexisting coronary heart disease (CHD) or other atherosclerotic vascular disease should lower low-density lipoprotein (LDL) cholesterol to < or = 100 mg/dL. Recent statin trials document the benefit of cholesterol lowering on CHD events but do not address the optimal goal of LDL cholesterol. METHODS: The pravastatin to simvastatin conversion-lipid optimization program (PSCOP) at the VA San Diego Healthcare System (VASDHS) was a formulary-conversion program designed to increase the percentage of patients who meet their recommended NCEP LDL cholesterol goal. We compared the incidence of clinical outcome and mortality between CHD patients from the original PSCOP cohort with postconversion LDL cholesterol greater than and < or = 100 mg/dL. A total of 524 patients were stratified by postconversion LDL cholesterol levels (greater than [N=183]) or < or = 100 mg/dL [N=341]) and observed for a mean duration of 27.7 months. Patients' VASDHS records were reviewed for postconversion mortality from any cause and CHD-related events. Patients were mailed a questionnaire to capture similar events that may have occurred outside of VASDHS, which might not be present in the patient's VASDHS record. RESULTS: Lipid-lowering therapy < or = 100 mg/dL was associated with a significantly lower percentage of total deaths and CHD-related events (40% vs 61%, P=0.008). In patients with LDL cholesterol >100 mg/dL, the relative risk of unstable angina (relative risk, 2.2; 95% confidence interval, 1.3 to 3.8; P=0.004) and stroke (relative risk, 3.0; 95% confidence interval, 1.04 to 8.6; P=0.04) were significantly greater compared to patients meeting their LDL cholesterol goal. CONCLUSIONS: Our study results support reducing LDL cholesterol to at least 100 mg/dL in the patient with CHD.

Aged↗
PubMed2001

Fenofibrate and warfarin interaction.

A 79-year-old man with atrial fibrillation and coronary heart disease who was taking warfarin (Coumadin) was converted to fenofibrate from gemfibrozil therapy for persistently elevated triglyceride levels. The patient took fenofibrate for 1 month and subsequently experienced rectal bleeding that required a visit to the emergency room. Before starting fenofibrate therapy, his coagulation values were within therapeutic range, but when measured in the emergency room the international normalized ratio (INR) was grossly elevated. The patient denied any changes in diet, alcohol ingestion, compliance with therapy, or use of other new drugs except for fenofibrate. His drug therapy profile consisted of digoxin, fosinopril, and furosemide for chronic heart failure, allopurinol for gout, and potassium supplementation. To minimize the risk of supratherapeutic INR values and/or hemorrhagic events, clinicians should perform serial monitoring of INR when initiating fenofibrate therapy in a patient previously stabilized on a coumarin anticoagulant.

Aged↗
PubMedDate not supplied

Colesevelam hydrochloride: a novel bile acid-binding resin.

OBJECTIVE: To review the pharmacology, pharmacokinetics, efficacy, and adverse effects of colesevelam hydrochloride, a bile acid-binding resin. METHODS: MEDLINE searches (1966-June 2000) and manufacturer prescribing literature were employed to find articles on colesevelam. Additional studies and abstracts were identified from the bibliographies of reviewed literature. STUDY SELECTION AND DATA EXTRACTION: All articles identified from data sources were evaluated, and all information deemed relevant was included in this review. Priority was given to randomized, double-blind, placebo-controlled studies. FINDINGS: Colesevelam HCl is a nonabsorbed hydrogel with bile acid sequestrant properties. Monotherapy using colesevelam in once-daily or two divided daily doses of 1.5-4.5 g has produced significant reductions in total cholesterol and low-density lipoprotein (LDL) cholesterol. Mean LDL cholesterol decreases to 20% have been noted when the patient is on 3.75-4.5 g/d. Increases in high-density lipoprotein (HDL) cholesterol have been observed (up to 9%), whereas triglycerides (TG) have increased significantly to 25% in some studies. In unpublished studies, combined use of colesevelam plus hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitor have produced greater reductions in LDL cholesterol than either the statin or colesevelam administered alone. The efficacy of colesevelam monotherapy is slightly less than or similar to cholestyramine or colestipol in decreasing LDL cholesterol, although colesevelam is more potent on a gram-to-gram basis. Adverse effects have been minimal with colesevelam in published studies; this suggests an advantage over cholestyramine or colestipol therapy. Colesevelam appears to be more cost-effective than the packet dosage form of the brand formulation of the older bile acid resins. Care in selection of an appropriate agent should be exercised when considering the issues of adverse effects and palatability. CONCLUSIONS: Colesevelam alone or combined with an HMG-CoA reductase inhibitor is effective in the reduction of total and LDL cholesterol. Since colesevelam is formulated as a tablet, problems with palatability such as with the powder formulation of the bile acid-binding resins are likely to be eliminated.

Adult↗