Statin Wars: The Heavyweight Match-Atorvastatin versus Rosuvastatin for the Treatment of Atherosclerosis, Heart Failure, and Chronic Kidney Disease

Abstract

Statins are a standard of care in many clinical settings, especially for dyslipidemia management, and are used for the primary and secondary prevention of cardiovascular disease. Importantly, not all statins are born equal. The statin class consists of a number of heterogenous drugs, which vary in properties such as potency in lowering low-density lipoprotein cholesterol levels, lipophilicity, renoprotection, increasing high-density lipoprotein cholesterol levels, lowering triglyceride levels, and effects on glucose metabolism and myocardial function. It remains unclear whether these differences significantly impact clinical outcomes or if 1 statin should be preferred over another. This review summarizes the properties of the 2 most potent statins available (atorvastatin and rosuvastatin), as well as assesses the comparative experimental and clinical trials that have been conducted on these 2 agents. We believe that the available body of evidence indicates that atorvastatin may have several advantages over rosuvastatin, despite the latter's greater potency, suggesting that atorvastatin should be the potent statin of choice, especially in treating patients with renal impairment or heart failure with concomitant coronary artery disease. The recent availability of atorvastatin as a generic option gives this drug another practical and compelling advantage over rosuvastatin.

A comparative study on the cardioprotective potential of atorvastatin and simvastatin in hyperhomocysteinemic rat hearts

“…Statins, the HMGCoA reductase inhibitors, have been extensively used for the treatment of hyperlipidemia (Law et al, 2003). Atorvastatin and Simvastatin, the potent inhibitors of HMG-CoA reductase, have been well reported to possess various beneficial effects in the treatment of various cardiovascular diseases such as myocardial infarction, stroke, unstable angina and revascularization due to their potent antioxidant properties (Law et al, 2003;DiNicolantonio et al, 2013;Owens et al, 2014). Atorvastatin treatment reduced the infarct size in isolated Langendorff-perfused heart model by activating pro-survival kinases and NO levels (Bell and Yellon, 2003;Efthymiou and Yellon, 2005).…”

Rosuvastatin suppresses platelet-derived growth factor-BB-induced vascular smooth muscle cell proliferation and migration via the MAPK signaling pathway

“…As a result, HMG-CoA reductase inhibitors, such as statins, may be utilized for lowering cholesterol. Among all statins, rosuvastatin is a selective HMG-CoA reductase inhibitor, the main action site of which is the liver, the target organ for lowering cholesterol (11). Rosuvastatin increases the number of hepatic cell surface receptors for low-density lipoprotein-cholesterol (LDL-C), promotes the absorption and catabolism of LDL-C and inhibits the synthesis of very low-density lipoprotein-cholesterol (VLDL-C), thereby reducing total VLDL-C and LDL-C levels.…”

“…Moreover, rosuvastatin is also able to reduce plasma triglycerides and increase high-density lipoprotein-cholesterol (HDL-C) levels (12). It has been shown that rosuvastatin is able to slow atherosclerosis progression and improve coronary heart disease outcomes (11); however, the molecular mechanism behind the action of rosuvastatin on vascular cell dynamics has not been fully elucidated.…”

Inhibition of inflammation mediates the protective effect of atorvastatin reload in patients with coronary artery disease undergoing noncardiac emergency surgery

“…These properties of statins result in cardiac function improvement [26] and coronary plaque stabilization. A variety of physiologic disturbances induced by certain aspects of the perioperative status, particularly plaque instability and thrombosis, may precipitate AHF during emergency surgical procedures.…”