Efficacy and safety of simvastatin for high-risk hypercholesterolemia

• Published in: The American journal of cardiology 1999-04, Vol.83 (7), p.1043-1048
• Main Authors: Mölgaard, Jörgen, Wärjerstam-Elf, Susanne, Olsson, Anders G
• Format: Article
• Language: English
• Subjects: Alanine Transaminase - blood; Anticholesteremic Agents - adverse effects; Anticholesteremic Agents - therapeutic use; Aspartate Aminotransferases - blood; Biological and medical sciences; Cholesterol; Cholesterol - blood; Cholesterol, HDL - blood; Creatine Kinase - blood; Drug therapy; Female; General and cellular metabolism. Vitamins; Health risk assessment; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors - adverse effects; Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use; Hypercholesterolemia - blood; Hypercholesterolemia - drug therapy; Male; Medical sciences; Middle Aged; Pharmacology; Pharmacology. Drug treatments; Risk Factors; Simvastatin - adverse effects; Simvastatin - therapeutic use; Treatment Outcome; Triglycerides - blood
• ISSN: 0002-9149; 1879-1913
• DOI: 10.1016/S0002-9149(99)00012-0

Ten years′ experience of treatment with the 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor simvastatin in 45 hypercholesterolemic high-risk patients is reported. All patients started with 20 mg simvastatin/day. The simvastatin dose was increased to 40 mg in 22 patients. Fourteen patients needed further addition of cholestyramine. Simvastatin reduced plasma cholesterol by 33% after 1 month and was further reduced after adjustment of the lipid-lowering treatment. The mean reduction in plasma cholesterol varied between 30% and 35% in 2 to 10 years. Low-density lipoprotein cholesterol demonstrated mean reductions of 34% to 42%. Mean plasma triglycerides were reduced by 26% after 1 month and by 1% to 19% the following years. High-density lipoprotein (HDL) cholesterol increased initially by 8% and remained elevated at 7% to 11% during the first 6 years, but then dropped slightly below baseline. HDL 2 cholesterol increased by 9% to 25% the first 6 years and then decreased. HDL 3 cholesterol showed a persistent elevation during simvastatin treatment. About half of the subjects had minor transient but clinical insignificant increases in creatine kinase. No cases of myopathy were seen. Mean serum aspartate aminotransferase and alanine aminotransferase increased significantly but within the normal ranges during the 10 years. The tolerability and compliance of simvastatin treatment was excellent as judged from patients’ reports and from analyses of low-density lipoprotein cholesterol. This 10-year study demonstrates that simvastatin is an effective and safe drug with excellent tolerability with only few minor side effects, and causes a pronounced and persistent cholesterol-lowering effect during long-term treatment of hypercholesterolemic patients at risk.