Statin treatment and the risk of recurrent pulmonary embolism
| Autor: | Barbara A. Hutten, Alessandro Squizzato, Patrick C. Souverein, S. Biere-Rafi, Walter Ageno, Anton de Boer, Victor E. A. Gerdes, Pieter Willem Kamphuisen, Harry R. Büller |
|---|---|
| Přispěvatelé: | ACS - Amsterdam Cardiovascular Sciences, Epidemiology and Data Science, Vascular Medicine, Other departments, Faculteit Medische Wetenschappen/UMCG, Cardiovascular Centre (CVC), Vascular Ageing Programme (VAP) |
| Jazyk: | angličtina |
| Rok vydání: | 2013 |
| Předmět: |
Male
Vitamin K Farnesyl pyrophosphate THERAPY law.invention chemistry.chemical_compound Randomized controlled trial Risk Factors law Secondary Prevention Medicine Registries Myocardial infarction Stroke First episode Recurrent pulmonary embolism Statins Vitamin K antagonists biology Incidence (epidemiology) Geranyl pyrophosphate CHOLESTEROL Hazard ratio Vitamin K antagonist Middle Aged Thrombosis Pulmonary embolism Treatment Outcome Cohort HMG-CoA reductase Cardiology Regression Analysis lipids (amino acids peptides and proteins) Female Cardiology and Cardiovascular Medicine medicine.medical_specialty medicine.drug_class COA REDUCTASE INHIBITORS Internal medicine Humans COHORT cardiovascular diseases METAANALYSIS Aged VENOUS THROMBOEMBOLISM Proportional hazards model business.industry Cholesterol MORTALITY Anticoagulants medicine.disease Surgery THROMBOSIS ARTERIAL CARDIOVASCULAR EVENTS chemistry ATHEROSCLEROSIS Heart failure biology.protein Hydroxymethylglutaryl-CoA Reductase Inhibitors business Pulmonary Embolism |
| Zdroj: | European heart journal, 34(24), 1800-1806. Oxford University Press European Heart Journal, 34(24), 1800-1806. Oxford University Press |
| ISSN: | 1522-9645 0195-668X |
| Popis: | This editorial refers to ‘Statin treatment and the risk of recurrent pulmonary embolism’[†][1], by S. Biere-Rafi et al. , on page 1800 Statin treatment is well established for the primary and secondary prevention of atherothrombotic disease in the coronary and cerebral arterial circulation.1 Cholesterol and in particular LDL-cholesterol (LDL-C) is log linearly associated with risk of fatal and non-fatal myocardial infarction; therefore, not unsurprisingly, the benefit of statins on coronary heart disease (CHD) risk appears to be log-linear, with about a one-fifth to one-quarter lowering of CHD risk per 1 mmol/L lowering of LDL-C.1 Whilst the relationship between the effect of cholesterol and LDL-C on incident stroke is less clear, there is clear evidence that statins reduce stroke by about one-fifth, raising the possibility that the clinical benefit may be unrelated to lowering of LDL-C. Statins block hydroxymethylglutaryl (HMG)-CoA reductase, which is a rate-limiting enzyme not only for the production of cholesterol via the squalene pathway but also for the generation of several isoprenoids such as geranyl geranyl pyrophosphate and farnesyl pyrophosphate which prenylate small molecules such as Rho and Ras involved in particular with inflammatory cell signalling, thus leading to activation of various transcription factors.2 These non-LDL- C-dependent but HMG-CoA-related effects have often been referred to as pleiotropic effects and, whilst readily demonstrated in vitro , the clinical relevance of these effects have never been conclusive. Several observational studies and post-hoc data from randomized controlled trials have suggested a range of benefits on cardiovascular disease and the vascular system, from favourable effects on renal function, to favourable effects on heart failure among those with CHD,3 which appear unrelated to effects on LDL-C. It is not surprising, therefore, that interest has focused on venous thrombo-embolic disease⇓ … [1]: #fn-2 |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|