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From pathophysiology to targeted therapy for atherothrombosis: a role for the combination of statin and aspirin in secondary prevention.
Pharmacol Ther. 2007 Jan; 113(1):184-96.P&T

Abstract

Atherothrombosis results from direct interaction between the atherosclerotic plaque and arterial thrombosis, and underlies most forms of cardiovascular disease (CVD). The pathophysiology of atherosclerosis is now recognised to involve endothelial dysfunction and dyslipidemia with cholesterol accumulation, as well as critical immuno-inflammatory and apoptotic dimensions. Erosion or rupture of a vulnerable, lipid-rich, inflammatory atherosclerotic plaque triggers the formation of a platelet-rich thrombus that may partially or completely occlude the artery, with resultant clinical scenarios including stable and unstable angina, acute myocardial infarction (MI) and ischaemic stroke. Insight into the pathophysiology of atherothrombosis indicates that an integrated risk factor approach, focusing particularly on management of dyslipidaemia (with a statin) and thrombosis (with aspirin), may constitute an optimal therapeutic approach. Both agents have established roles in secondary prevention. Statin action on atherogenic lipoproteins mediates plaque stabilisation, modification of plaque morphology and attenuation of inflammation, and may lead to plaque regression, while aspirin reduces platelet activation and aggregation, decreases release of inflammatory cytokines at sites of vascular injury and attenuates vasoconstriction. Given these complementary modes of action, this combination would be a logical choice for reducing atherothrombotic risk in patients with CVD. Meta-analysis of 5 major clinical studies has demonstrated that the combination of pravastatin plus aspirin was significantly more effective than either agent alone in reducing the relative risk of key cardiovascular endpoints including MI and ischaemic stroke. This combination may therefore represent an important, cost-efficient therapeutic approach to reduction of cardiovascular risk and prevention of recurrent events in stable CVD.

Authors+Show Affiliations

National Institute for Health and Medical Research (INSERM), Unité 551, Dyslipoprotéinemies et Athérosclérose: Génétique, Métabolisme et Thérapeutique, Hôpital de la Pitié, 75651-Paris Cedex 13, France. chapman@chups.jussieu.fr

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

17070923

Citation

Chapman, M John. "From Pathophysiology to Targeted Therapy for Atherothrombosis: a Role for the Combination of Statin and Aspirin in Secondary Prevention." Pharmacology & Therapeutics, vol. 113, no. 1, 2007, pp. 184-96.
Chapman MJ. From pathophysiology to targeted therapy for atherothrombosis: a role for the combination of statin and aspirin in secondary prevention. Pharmacol Ther. 2007;113(1):184-96.
Chapman, M. J. (2007). From pathophysiology to targeted therapy for atherothrombosis: a role for the combination of statin and aspirin in secondary prevention. Pharmacology & Therapeutics, 113(1), 184-96.
Chapman MJ. From Pathophysiology to Targeted Therapy for Atherothrombosis: a Role for the Combination of Statin and Aspirin in Secondary Prevention. Pharmacol Ther. 2007;113(1):184-96. PubMed PMID: 17070923.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - From pathophysiology to targeted therapy for atherothrombosis: a role for the combination of statin and aspirin in secondary prevention. A1 - Chapman,M John, Y1 - 2006/09/15/ PY - 2006/08/14/received PY - 2006/08/15/accepted PY - 2006/10/31/pubmed PY - 2007/3/16/medline PY - 2006/10/31/entrez SP - 184 EP - 96 JF - Pharmacology & therapeutics JO - Pharmacol. Ther. VL - 113 IS - 1 N2 - Atherothrombosis results from direct interaction between the atherosclerotic plaque and arterial thrombosis, and underlies most forms of cardiovascular disease (CVD). The pathophysiology of atherosclerosis is now recognised to involve endothelial dysfunction and dyslipidemia with cholesterol accumulation, as well as critical immuno-inflammatory and apoptotic dimensions. Erosion or rupture of a vulnerable, lipid-rich, inflammatory atherosclerotic plaque triggers the formation of a platelet-rich thrombus that may partially or completely occlude the artery, with resultant clinical scenarios including stable and unstable angina, acute myocardial infarction (MI) and ischaemic stroke. Insight into the pathophysiology of atherothrombosis indicates that an integrated risk factor approach, focusing particularly on management of dyslipidaemia (with a statin) and thrombosis (with aspirin), may constitute an optimal therapeutic approach. Both agents have established roles in secondary prevention. Statin action on atherogenic lipoproteins mediates plaque stabilisation, modification of plaque morphology and attenuation of inflammation, and may lead to plaque regression, while aspirin reduces platelet activation and aggregation, decreases release of inflammatory cytokines at sites of vascular injury and attenuates vasoconstriction. Given these complementary modes of action, this combination would be a logical choice for reducing atherothrombotic risk in patients with CVD. Meta-analysis of 5 major clinical studies has demonstrated that the combination of pravastatin plus aspirin was significantly more effective than either agent alone in reducing the relative risk of key cardiovascular endpoints including MI and ischaemic stroke. This combination may therefore represent an important, cost-efficient therapeutic approach to reduction of cardiovascular risk and prevention of recurrent events in stable CVD. SN - 0163-7258 UR - https://www.unboundmedicine.com/medline/citation/17070923/From_pathophysiology_to_targeted_therapy_for_atherothrombosis:_a_role_for_the_combination_of_statin_and_aspirin_in_secondary_prevention_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0163-7258(06)00153-7 DB - PRIME DP - Unbound Medicine ER -