The disease burden due to major noncommunicable diseases (NCDs) including cardiovascular disease (CVD), cancer, diabetes, chronic respiratory diseases, and mental disorders are higher with an estimated death rate of 71% whereas, globally CVD is classed as a major NCD causing nearly one-third of deaths across the world. In 2021, more than 15 million deaths between the age of 30 and 69 were due to noncommunicable diseases, 85% are in low and middle-income countries.1 Most NCDs deaths account for CVD, where 17.9 million people die every year due to cancers (9.3 million), respiratory diseases (4.1 million), and diabetes (1.5 million).1 Over recent years’ morbidity and mortality associated with cardiovascular diseases (CVDs) have grown exponentially in many low- and middle-income countries (LMICs).

CVD is a collective term used for a broad range of conditions that affect the heart and blood vessels. The World Health Organization (WHO)1 categorizes CVD into broad conditions. Atherosclerosis refers to the narrowing of the lumen of blood vessels secondary to the deposition of atherosclerotic plaque on the walls of blood vessels.2 Rheumatic heart disease is an acquired, chronic, heart condition secondary to rheumatic fever (a streptococcal group A infection).3 Congenital heart disease is a defect in the structure of the heart. It is a birth defect affecting mostly the walls of the heart, the valves of the heart, and the arteries and veins near the heart.4 Deep Vein Thrombosis and Pulmonary Embolism refer to a condition in which blood clots in the leg veins, can dislodge and move to the heart and lungs.

There are certain risk factors associated with CVD that increase the risk of developing the disease. The more risk factors for CVD, the greater the chance of getting the disease. Risk factors for cardiovascular disease are classified into modifiable and nonmodifiable risk factors.5 Modifiable risk factors can be changed by taking certain measures although, all have 2 things in common: (1) they occur on a spectrum of risk, that is, the risk increases as the exposure to that risk increases – the more salt you eat, the greater the risk, the less exercise the greater the risk, and (2) by modifying (and not necessarily removing) the exposure the risk will change. Nonmodifiable risk factors include age, family history, and gender.6

Globally CVD is the most common cause of death. According to the 2019 Global Burden of Disease study, worldwide about 30% of deaths were due to CVD.7 In England, the overall survival rate from myocardial infarction has improved over the last decade. From 2012 to 2021 in England, the acute myocardial infarction event, case fatality, and total mortality rates declined at an average annual rate of 4.8% (95% confidence interval 3.0%-6.5%), 3.6% (3.4%-3.7%), and 8.6% (5.4%-11.6%) in men respectively. In women the corresponding values were 4.5% (1.7%-7.1%), 4.2% (4.0-4.3%), and 9.1% (4.5%-13.6%).8 Moreover, nearly 30% of all deaths in low and middle-income countries are attributable to CVD, and more than 80% of CVD-associated deaths fall in low and middle-income countries.9

Different inflammatory biomarkers have been used to forecast cardiovascular risks. Various circulating biomarkers have been suggested in the last few years as adding to inflammation in atherosclerosis and may suggest cardiovascular events.10 The risk for CVD may be identified by biomarkers of inflammation and oxidative stress. It is used to monitor the efficacy of treatments and to develop new pharmacological tools.11 Biomarkers of cardiovascular events can be classified as primary and secondary markers. Markers for primary cardiovascular events include, from high to low results: C-reactive protein, fibrinogen, cholesterol, Apo lipoprotein B, the Apo lipoprotein A/Apo lipoprotein B ratio, high-density lipoprotein, and vitamin D. Markers for secondary cardiovascular events include, from high to low result: cardiac troponins I and T, C-reactive protein, serum creatinine, and cystatin C. For primary stroke, fibrinogen and serum uric acid are strong risk markers.12,13

The lethal complications of cardiovascular diseases (CVD) most commonly occur in the middle-aged or elderly. The principal pathological processes that lead to coronary artery disease, cerebrovascular diseases, and peripheral arterial disease are thought to start early in life and slowly progress through adolescence and early adulthood.14 The results of the Bogalusa Heart Study and other epidemiological studies of children indicate the need to begin the prevention of adult heart disease in early life.15 Cardiovascular disease risk factors influenced the rate of progression of atherosclerosis: tobacco use, an unhealthy diet, physical inactivity (both associated with obesity), high blood pressure (hypertension), abnormal blood lipids (dyslipidemia), and high blood glucose (diabetes). Atherosclerosis mainly results due to continuous exposure to these risk factors leading to unstable angina, atherosclerotic plaques, narrowing of blood vessels, and obstruction of blood flow to vital organs, such as the heart and brain. The consequences of these diseases include angina, myocardial infarction, transient cerebral ischemic attacks, and strokes.16

Statins belong to a class of lipid-lowering drugs. It is also called HMG-CoA reductase inhibitors that inhibit the enzyme HMG-CoA reductase which plays a key role in the production of cholesterol.17 Statins are used to lower the level of low-density lipoprotein cholesterol (LDL) in plasma. Patients who are at high risk of cardiovascular disease and mortality statins have been found to reduce the patients at higher risk. Studies show strong evidence that statins are efficacious in both secondary and primary prevention of CVD.18 Patients at high risk of developing CVD shortly are usually recommended lifestyle measures to reduce the risk before starting therapy with statins by clinicians.19 Lifestyle modifications that can reduce cholesterol levels and CVD risk include a healthy and balanced diet, regular exercise, maintaining a healthy weight, smoking cessation, and limiting alcohol consumption. Statins are recommended if these measures don't work.20 Statins have the same effect in both men and women.21

Studies show that statins are effective in primary prevention (in preventing heart disease in those with high cholesterol, but no history of heart disease). Primary prevention with statins is likely to be cost-effective and may improve patient quality of life according to the evidence available to date.22 Statins are found in reducing death rates in patients with pre-existing CVD. Recent studies proposed the use of statins at high risk of developing heart disease. Statins decrease LDL cholesterol by 1.8 mmol/L (70 mg/dL) on average. It estimates a 60% reduction in the number of cardiac events (heart attack, sudden cardiac death) and a 17% reduced risk of stroke after long-term treatment.23 In people with familial hypercholesterolemia, statins are the first line of treatment in reducing LDL cholesterol, especially in people with homozygous deficiencies. People having familial hypercholesterolemia have defects in either LDL receptor or Apo lipoprotein genes. Both are responsible for LDL clearance from the blood.24

Due to inhibition of specific prenylated proteins, statins are associated with potentially serious side effects. About 10% of statins users get aches and pains. The higher the dose, the more likely it is to experience aches and pains. Pain is usually in the thighs, shoulder, upper arms, and lower back.25 Much less common but more serious is Rhabdomyolysis, in which muscle cells break down and release proteins such as myoglobin that damage kidneys.26 This is due to a decrease in coenzyme Q10 level with statin use, therefore Co-Q10 supplements are given to patients for treating statin-associated myopathy.27 Occasionally statins could cause the increased synthesis of liver enzymes that digest food, drinks, and medications. If the increase is mild, statin can be continued but in case of a severe increase, statin therapy should be stopped. Since there are no symptoms to indicate an increase, therefore an enzyme blood test within 6 days of statin therapy should be performed.28 Blood sugar levels may rise with statin therapy, which may lead to developing type 2 diabetes. FDA has issued a warning on statin labels regarding blood glucose levels and diabetes.29 There are unscientific reports of cognitive decline with statins. A meta-analysis report suggests that there is an average quality report of no increase in dementia, mild cognitive impairment, or cognitive performance. But the evidence is very limited. According to some unscientific reports statins are associated with memory loss, forgetfulness, and confusion, so the FDA added to the labeling of statins drugs, a warning about possible cognitive impacts.30

The objective of study was that the “goalposts” for the management of cardiovascular diseases and especially primary prevention have moved markedly in the past several years. This is exemplified with the controversial changes to the national guidance relating to cardiovascular disease prevention.

The reduction in the threshold for drug intervention to 10% over 10 years from 20% is a move that potentially “medicalizes” a huge number of people within the population. The use of a drug therapy (ie, low intensity statins) effectively makes risk of cardiovascular disease a “disease” in its own right. The psychological consequences of being diagnosed as being at “high” risk and then treated is hardly mentioned, but those put on medication often adopt what is known as the “sick role,” that is the medical profession has effectively said you are unwell (prescription of a medicine) and therefore psychologically this status is adopted even (and this is very important in this context) if there's nothing actually “wrong.”

The magnitude of the response of the intervention must be such that it overcomes the potential adverse effects of treatment (and that includes the point above), so when we are treating (potentially) hundreds of thousands (if not millions) of people with these drugs, the magnitude of the effect as to be substantial because there is a definite risk to each individual. This is especially the case for myositis (although in most it is an inconvenience) where some may go on to suffer an extreme version (Rhabdomyolysis) which can cause kidney damage and even death if the heart tissue is affected. Therefore, it was to investigate whether or not there exists the evidence to substantiate that change.