CAD is also known as atherosclerotic heart disease, coronary atherosclerosis, coronary arteriosclerosis, coronary heart disease, Hyperlipidaemia, Deposition of cholesterol and lipids, Statins. Coronary artery disease (CAD) is a common type of heart disease. It affects the main blood vessels that supply blood to the heart, called the coronary arteries.

Coronary artery disease is caused by the buildup of fats, cholesterol and other substances in and on the walls of the heart arteries. This condition is called atherosclerosis. The buildup is called plaque. Plaque can cause the arteries to narrow, blocking blood flow. The plaque also can burst, causing a blood clot. Abnormal accumulation of lipids or fatty substances and fibrous tissues in the vessels or walls of vessels. These substances block’s or narrows the blood vessels there by reducing the blood flow to the myocardium and resulting in coronary artery disease. The formation of plaque is generally called as atherosclerosis. The main cause for myocardial infraction is coronary artery disease.  A narrowing of the coronary arteries that prevents adequate blood supply to the heart muscle is called coronary artery disease. Usually caused by atherosclerosis, it may progress to the point where the heart muscle is damaged due to lack of blood supply. Such damage may result in infarction, arrhythmias, and heart failure.

HMG-CoA reductase inhibitors (statins) are lipid-lowering medications used in the primary and secondary prevention of coronary heart disease. This activity reviews the indications, contraindications, and mechanism of action of statins for the management of coronary heart disease and familial dyslipidaemias. This activity will cover the indications, contraindications, activity, adverse events, and other critical elements of statin therapy, and highlight the crucial role of the interprofessional team in the management of patients with clinically significant atherosclerotic cardiovascular disease or individuals with risk factors for heart disease who can benefit from statin therapy.

Hydroxymethylglutaryl-CoA (HMG-CoA) reductase inhibitors, also known as "statins," are used adjunctively to diet and exercise to treat hypercholesterolemia by lowering total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and triglycerides (TG) concentrations while increasing high-density lipoprotein cholesterol (HDL-C) concentrations. The approved FDA indications vary slightly between each statin but generally are indicated for the treatment and/or prevention of primary and secondary prevention clinical atherosclerotic cardiovascular disease (ASCVD) (e.g., myocardial infarction or stroke). Conversion of 3-hydroxy-3-methyl glutaryl-CoA (HMG-CoA) to mevalonate by HMG-CoA reductase in the hepatocytes is the first and rate-limiting step in cholesterol biosynthesis.

 Statins competitively inhibit HMG-CoA reductase enzyme. Statins bind to the active site of the enzyme and induce a conformational change in its structure, thus reducing its activity. Also, the binding affinity of statins for HMG-CoA reductase is 10,000 times higher than the substrate (HMG-CoA), thus preventing the action of the enzyme and reducing the intracellular synthesis of cholesterol. Statins have a significant impact on lowering cholesterol since most of the circulating plasma cholesterol comes from the internal synthesis in hepatocytes rather than the diet. The reduced intracellular concentrations of cholesterol in hepatocytes secondary to statin use activate the proteases that cleave membrane-bound sterol regulatory element-binding proteins (SREBP), which further migrate to the nucleus and bind to sterol response elements. This binding results in increased transcription of the LDL receptor, which translocate to the liver cell membrane. The LDL and VLDL particles in plasma bind to the LDL receptors and endocytose in hepatocytes, where their cholesterol component gets processed into bile salts, which are then excreted or recycled. This process increases the catabolism of LDL and VLDL cholesterol and results in further reduction of plasma cholesterol concentrations.

Statins reduce the plasma concentrations of total cholesterol, LDL-C, VLDL-C, triglycerides, apo-B, and increase the plasma concentrations of HDL-C. Apart from lowering lipid concentrations, statins also have cardiovascular protective effects (pleiotropic effects), which are primarily because of the inhibition of the production of prenylated proteins (mainly farnesyl pyrophosphate and geranylgeranyl pyrophosphate) in the cholesterol biosynthetic pathway. Statins prevent cardiovascular disease progression via the following mechanisms.Plaque stabilization: Coronary artery plaque rupture predisposes to acute coronary syndrome. Statins maintain the integrity of the fibrous cap of atherosclerotic plaque, inhibit the proliferation of macrophages, and decrease the expression of matrix metalloproteinases (MMP).Reduces inflammation: Inflammation plays an essential role in atherosclerotic plaque rupture. Statins reduce the level of pro-inflammatory cytokines (TNF-a, IL-6, IL-8) and decrease the concentration of CRP.Improve endothelial function: Statins increase eNOS activity within the endothelial cells resulting in vasodilation and thus improving myocardial blood flow.Decreased thrombogenicity: Statins decrease the activity of platelets and reduce thromboxane A2 synthesis.

The study was conducted at Apollo Hospital, Kakinada, over a six-month period, from August 2024 to February 2025, with a sample size of 100 cases. It was a prospective observational study involving both male and female patients, including geriatrics, aged 20-80 years, who are receiving hypolipidemic drugs (statins) data were collected on patient demographics, lab parameters (LDL, HDL, total cholesterol levels were monitored during a 1 month follow up. The Descriptive statistics were used for data analysis and findings were represented through bar graphs.