Hydroxymethylglutaryl-coenzyme A reductase inhibitor
Hydroxymethylglutaryl-coenzyme A reductase inhibitors, also called statins, are antilipemic agents "that inhibit HMG-CoA reductases, which reduce the chemical 3-hydroxy-3-methyl-glutaryl CoA. They have been shown to directly lower cholesterol synthesis.[1]
Classification
The following classification has been proposed based on molecular structure:[2][3]
Type 1
Type 1 statins (e.g., mevastatin, lovastatin, pravastatin, simvastatin) bind to HMG-CoA reductase using a decalin ring.
Type 2
Type 2 statins (e.g., fluvastatin, cerivastatin, atorvastatin, and rosuvastatin) bind to HMG-CoA reductase using a fluorophenyl group.
Effectiveness
Statins can help in the primary prevention of coronary heart disease among patients at risk.[4]
Diabetic patients
Statin therapy benefited about 1 of every 24 diabetic patients who used the treatment for 5 years if they are similar to the patients in the meta-analysis by Kearney et al (number needed to treat is 24).[5]
Patients with average LDL cholesterol levels
Statin therapy benefited about 1 of every 24 patients with LDL cholesterol that averaged 150 mg per deciliter who took lovastatin 20-40 mg daily for 5 years if they are similar to the patients in the AFCAPS/TexCAPS randomized controlled trial (number needed to treat is 24).[6]
Patients with normal LDL cholesterol levels
Statin therapy benefited about 1 of every 170 patients with LDL cholesterol less than 130 mg per deciliter (3.4 mmol per liter) and high-sensitivity C-reactive protein levels of 2.0 mg per liter or higher who took rosuvastatin 20 mg daily for 2 years if they are similar to the patients in the JUPITER randomized controlled trial (number needed to treat for two years is 170).[7][8] The frequency of death from any cause fell from 2.8% to 2.2% (number needed to treat for two years is 180). However, this trial was stopped early afer an interim analysis so it is likely that the result is exaggerated.
References
- ↑ Anonymous. Hydroxymethylglutaryl-coenzyme A reductase inhibitors. National Library of Medicine. Retrieved on 2008-01-18.
- ↑ Istvan ES, Deisenhofer J (2001). "Structural mechanism for statin inhibition of HMG-CoA reductase". Science 292 (5519): 1160–4. DOI:10.1126/science.1059344. PMID 11349148. Research Blogging.
- ↑ Istvan E (2003). "Statin inhibition of HMG-CoA reductase: a 3-dimensional view". Atheroscler Suppl 4 (1): 3–8. PMID 12714031. [e]
- ↑ Brugts JJ, Yetgin T, Hoeks SE, et al. (2009). "The benefits of statins in people without established cardiovascular disease but with cardiovascular risk factors: meta-analysis of randomised controlled trials". BMJ 338: b2376. PMID 19567909. [e]
- ↑ Kearney PM, Blackwell L, Collins R, et al (2008). "Efficacy of cholesterol-lowering therapy in 18,686 people with diabetes in 14 randomised trials of statins: a meta-analysis". Lancet 371 (9607): 117–25. DOI:10.1016/S0140-6736(08)60104-X. PMID 18191683. Research Blogging.
- ↑ Downs JR, Clearfield M, Weis S, et al (May 1998). "Primary prevention of acute coronary events with lovastatin in men and women with average cholesterol levels: results of AFCAPS/TexCAPS. Air Force/Texas Coronary Atherosclerosis Prevention Study". JAMA 279 (20): 1615–22. PMID 9613910. [e]
- ↑ Ridker PM, Danielson E, Fonseca FA, et al (November 2008). "Rosuvastatin to Prevent Vascular Events in Men and Women with Elevated C-Reactive Protein". N. Engl. J. Med.. DOI:10.1056/NEJMoa0807646. PMID 18997196. Research Blogging.
- ↑ Ridker PM (November 2003). "Rosuvastatin in the primary prevention of cardiovascular disease among patients with low levels of low-density lipoprotein cholesterol and elevated high-sensitivity C-reactive protein: rationale and design of the JUPITER trial". Circulation 108 (19): 2292–7. DOI:10.1161/01.CIR.0000100688.17280.E6. PMID 14609996. Research Blogging.