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How do HMG-CoA reductase inhibitors prevent stroke?
Am J Cardiovasc Drugs. 2002; 2(1):7-14.AJ

Abstract

Stroke is a heterogeneous disorder with significantly high morbidity and mortality. The relationship between serum cholesterol level and the incidence of stroke remains controversial. Recent evidence from primary and secondary prevention trials suggests that treatment with hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitors may reduce the incidence of stroke in patients with coronary artery disease (CAD). In this review, we attempt to outline and describe the potential mechanisms of HMG-CoA reductase inhibitors in the prevention of stroke. In addition to their lipid-lowering action HMG-CoA reductase inhibitors appear to exert their beneficial effects by various nonlipid-lowering mechanisms including anti-inflammatory effects, effect on endothelial function and coagulation cascade. Treatment with HMG-CoA reductase inhibitors is associated with decreased progression, plaque stablization and even regression of atheromatous plaque in the carotid arteries. HMG-CoA reductase inhibitors also inhibit the coagulation cascade at various levels such as activation of prothrombin, factor V, factor X and liberation of tissue factor in response to vascular injury. Inhibition of fibrinolysis occurs secondary to inhibition of plasmin generation. Pravastatin therapy is associated with a reduction in the size of aortic atheroma which is an independent risk factor for stroke. Lastly, left ventricular dysfunction after acute myocardial infarction is associated with an increased risk of stroke and HMG-CoA reductase inhibitors may indirectly decrease the incidence of stroke by reducing coronary events. Most of these effects are independent of the cholesterol-lowering effects of HMG-CoA reductase inhibitors. In conclusion, HMG-CoA reductase inhibitors may have a role in primary prevention of stroke in patients with CAD.

Authors+Show Affiliations

Division of Cardiology, Department of Internal Medicine, University of Missouri, Columbia 65212, USA.No affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

14727994

Citation

Bedi, Ashwani, and Gregory C. Flaker. "How Do HMG-CoA Reductase Inhibitors Prevent Stroke?" American Journal of Cardiovascular Drugs : Drugs, Devices, and Other Interventions, vol. 2, no. 1, 2002, pp. 7-14.
Bedi A, Flaker GC. How do HMG-CoA reductase inhibitors prevent stroke? Am J Cardiovasc Drugs. 2002;2(1):7-14.
Bedi, A., & Flaker, G. C. (2002). How do HMG-CoA reductase inhibitors prevent stroke? American Journal of Cardiovascular Drugs : Drugs, Devices, and Other Interventions, 2(1), 7-14.
Bedi A, Flaker GC. How Do HMG-CoA Reductase Inhibitors Prevent Stroke. Am J Cardiovasc Drugs. 2002;2(1):7-14. PubMed PMID: 14727994.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - How do HMG-CoA reductase inhibitors prevent stroke? AU - Bedi,Ashwani, AU - Flaker,Gregory C, PY - 2004/1/20/pubmed PY - 2004/4/15/medline PY - 2004/1/20/entrez SP - 7 EP - 14 JF - American journal of cardiovascular drugs : drugs, devices, and other interventions JO - Am J Cardiovasc Drugs VL - 2 IS - 1 N2 - Stroke is a heterogeneous disorder with significantly high morbidity and mortality. The relationship between serum cholesterol level and the incidence of stroke remains controversial. Recent evidence from primary and secondary prevention trials suggests that treatment with hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitors may reduce the incidence of stroke in patients with coronary artery disease (CAD). In this review, we attempt to outline and describe the potential mechanisms of HMG-CoA reductase inhibitors in the prevention of stroke. In addition to their lipid-lowering action HMG-CoA reductase inhibitors appear to exert their beneficial effects by various nonlipid-lowering mechanisms including anti-inflammatory effects, effect on endothelial function and coagulation cascade. Treatment with HMG-CoA reductase inhibitors is associated with decreased progression, plaque stablization and even regression of atheromatous plaque in the carotid arteries. HMG-CoA reductase inhibitors also inhibit the coagulation cascade at various levels such as activation of prothrombin, factor V, factor X and liberation of tissue factor in response to vascular injury. Inhibition of fibrinolysis occurs secondary to inhibition of plasmin generation. Pravastatin therapy is associated with a reduction in the size of aortic atheroma which is an independent risk factor for stroke. Lastly, left ventricular dysfunction after acute myocardial infarction is associated with an increased risk of stroke and HMG-CoA reductase inhibitors may indirectly decrease the incidence of stroke by reducing coronary events. Most of these effects are independent of the cholesterol-lowering effects of HMG-CoA reductase inhibitors. In conclusion, HMG-CoA reductase inhibitors may have a role in primary prevention of stroke in patients with CAD. SN - 1175-3277 UR - https://www.unboundmedicine.com/medline/citation/14727994/How_do_HMG_CoA_reductase_inhibitors_prevent_stroke L2 - https://dx.doi.org/10.2165/00129784-200202010-00002 DB - PRIME DP - Unbound Medicine ER -