A Systemic Review of Drug Pravastatin Sodium for The Treatment of Atherosclerosis

Background: Pravastatin sodium, one of the 3-hydroxy-3methylglutaryl-coenzyme A HMG-CoA reductase inhibitors (statins) commonly used in the treatment of hypercholesterolemia, possesses pharmacokinetic properties that are unique among statins. Pravastatin sodium is a BCS class iii medication with low permeability and high water solubility (about 300 mg/ml). Due to reduced permeability and high first-pass metabolism, it has a poor absolute oral bioavailability (about 17%). The medication is rapidly absorbed from the upper small intestine, most likely through proton-coupled carriermediated transport. As a result, pravastatin sodium (an HMG-CoA reductase inhibitor) reduces both the level of lowdensity lipoprotein cholesterol and the risk of cardiovascular disease in a dose-dependent manner. Objective: The primary goal of this study is to describe pravastatin sodium's pharmacology, pharmacokinetic characteristics, clinical safety, and tolerability, as well as its role in the treatment of atherosclerosis. Method: A thorough literature search of review articles and research publications from multiple sources was conducted using the terms pravastatin sodium for atherosclerosis, hypercholesterolemia, hypertriglyceridemia, and HMG-CoA reductase inhibitors. PubMed(20002021) scholar on Google (2001-2020) Science Direct (2000-2020) and Web of Science (20002021) are both English-language publications. In addition, drug banks and pub chem, FDA websites are being combed for additional information. Rani Kumari*, Girish Chandra Soni, Ravi Kumar Institute Of Pharmacy Bundelkhand University Jhansi, Uttar Pradesh (India). Submitted: 20 September 2021 Accepted: 26 September 2021 Published: 30 October 2021 www.ijppr. humanjournals.com Citation: Rani Kumari et al. Ijppr.Human, 2021; Vol. 22 (3): 177-193. 178 INTRODUCTION: Hypercholesterolemia is a major factor in the progression of atherosclerotic illnesses in general, and coronary heart disease in particular. At both the individual and social levels, the risk of development of the atherosclerotic process to coronary heart disease increases with increasing levels of total serum cholesterol or low-density lipoprotein (LDL) cholesterol. The diseases of high-income countries are not limited to coronary heart disease. Over the last few decades, the burden of coronary artery disease has disproportionately increased in lowand middle-income nations, which now account for over 80% of all cardiovascular disease deaths. According to the Global Burden of Diseases, Injuries, and Risk Factors Study, coronary artery disease affected an estimated 422 million people and caused an estimated 179 million deaths worldwide in 2015, accounting for 31% of all global deaths; by 2020, the global prevalence of increased coronary artery disease is expected to be 276% or 106670 million people. The prevalence of increasing coronary artery disease grew continuously with age and was higher in males than in women, a percentage change of 5746 percent since 2000. Approximately 236 million people are expected to die each year from coronary heart disease by 2030. Along with their demonstrated efficacy and safety profile, statins are the treatment of choice for hypercholesterolemia control. They are also playing an increasingly important role in the management of cardiovascular risk in patients with relatively normal plasma cholesterol levels. Although all statins have the same mechanism of action, their chemical structures, pharmacokinetic profiles, and lipid-modifying potency differ. Lipid-lowering medication was unsatisfactory in the 1970s due to its side effects, toxicity, and lack of efficacy. Statins became commercially marketed in the United States in 1987, with lovastatin being the first. Pravastatin was found as a bioactive metabolite of mevastatin in dog urine and was later synthesized by microbial transformation of mevastatin using Streptomyces acidophilus. Pravastatin sodium received FDA approval for the first time in 1991 to treat hypercholesterolemia. Pravastatin, unlike other statins, is relatively hydrophilic and does not appear to be appreciably metabolized by cytochrome P450 enzymes. Because of excellent first-pass uptake, all statins have a selective impact on the liver; lipophilic statins are taken up by passive diffusion through hepatocyte cell membranes, whereas hydrophilic statins are taken up by active diffusion via hepatocyte cell membranes. Pravastatin and rosuvastatin have a higher hepatoselectivity and a lower capacity for peripheral cell absorption than www.ijppr. humanjournals.com Citation: Rani Kumari et al. Ijppr.Human, 2021; Vol. 22 (3): 177-193. 179 lipophilic agents. The clinical pharmacokinetics of pravastatin are reviewed in this article, with an emphasis on the mechanisms that influence particular pharmacokinetic events. The microscopic variables such absorption rate, bioavailability, and clearance. Based on the mechanisms presented, the impact of various conditions (such as diseases and other medicines) on pravastatin pharmacokinetics is also explored. Finally, the importance of mechanistic research in the development of pravastatin's pharmacokinetic-pharmacodynamic correlations is emphasized.