Cerivastatin for lowering lipids

Abstract

BackgroundCerivastatin was the most potent statin until it was withdrawn from the market due to a number of fatalities due to rhabdomyolysis, however, the dose-related magnitude of e ect of cerivastatin on blood lipids is not known. Objectives Primary objectiveTo quantify the e ects of various doses of cerivastatin on the surrogate markers: LDL cholesterol, total cholesterol, HDL cholesterol and triglycerides in children and adults with and without cardiovascular disease.The aim of this review is to examine the pharmacology of cerivastatin by characterizing the dose-related e ect and variability of the e ect of cerivastatin on surrogate markers. Secondary objectivesTo quantify the e ect of various doses of cerivastatin compared to placebo on withdrawals due to adverse e ects. To compare the relative potency of cerivastatin with respect to fluvastatin, atorvastatin and rosuvastatin for LDL cholesterol, total cholesterol, HDL cholesterol and triglycerides. Search methodsThe Cochrane Hypertension Information Specialist searched the following databases for RCTs up to March 2019: CENTRAL (2019, Issue 3), Ovid MEDLINE, Ovid Embase, the WHO International Clinical Trials Registry Platform, and ClinicalTrials.gov.We also searched the European Patent O ice, FDA.gov, and ProQuest Dissertations & Theses, and contacted authors of relevant papers regarding further published and unpublished work. The searches had no language restrictions. Selection criteriaRCTs and controlled before-and-a er studies evaluating the dose response of di erent fixed doses of cerivastatin on blood lipids over a duration of three to 12 weeks in participants of any age with and without cardiovascular disease.

Effect of Patient Financial Incentives on Statin Adherence and Lipid Control

“…This is especially possible because the effect of statins on LDL-C reduction at the start of medication regimens is substantial and well-documented. [23][24][25] Second, our data present the possibility that financial incentives improved adherence, but that this better statin adherence did not lead to greater improvements in LDL-C levels vs control. To explore this idea, we used values from the first 6 months of adherence data when the interventions were in effect.…”

Role of Traditional Cardiovascular Risk Factors after Initiation of Statin Therapy: A PharmLines Inception Cohort Study

“…The statin adherence was categorized into two classes: (1) high adherence, more than 80%, and (2) low adherence, 0-80%. We further developed an equivalent doses (EQD) scheme of different statins such that the dose lowers the LDL-C in percentage points about the same [ 6 , 29 – 31 ]. We categorized these EQD's into three classes: less than 30%, 30-45%, and more than 45% (see Table 1 ).…”

The Immunomodulatory Effects of Statins on Macrophages

“…Plaques can become unstable and rupture unexpectedly, exposing the lipid core to the blood and triggering thrombosis, which can result in partial or complete vessel occlusion and culminate in myocardial infarction, stroke, and other ischemic events. [20] 37-55 [21,22] Lipophilic [15] Acid [15] 14 [15,20] CYP3A4 [15] Cerivastatin a Baycol 0.02-0.8 [23] 12-42 [24] Lipophilic [15] Acid [15] 2-4 [23] CYP3A4, 2C8 [15,23] Fluvastatin Lescol 20-80 [25] 21-33 [21,22] Lipophilic [15] Acid [15] 3 [25] CYP2C9 [15,25] Lovastatin Mevacor 10-80 [26] 21-45 [21] Lipophilic [15] Lactone [15] 3 [15] CYP3A4 [15,26] Metavastatin b Lipophilic [27] Pitavastatin Livalo 1-4 [28] 33-44 [29] Lipophilic [15] Acid [15] 12 [28] CYP2C8, 2C9 [15,28] Pravastatin Pravachol 10-80 [30] 20-33 [21] Hydrophilic [15] Acid [15] 1.8 [15,30] Non-CYP [...…”