For many decades, aspirin has been recommended for heart attack prevention, both for those with pre-existing cardiovascular disease (CVD) and for coronary heart disease (CHD). Pediatric aspirin (low-dose aspirin – usually 75-81 mg tablets) has become a fiduciary material for heart protection in American adults. Therefore, for many Americans, it has come as a surprise that recent guidelines from the American Heart Association and the American College of Cardiology have changed their recommendations for prescribing aspirin for primary prevention of cardiovascular disease and coronary heart disease. Although the UK and Europe had earlier changed their positions on the use of aspirin to prevent heart attacks, US guidelines affect medical practice in many other parts of the world. Therefore, the reasons for the change of position in these guidelines should be understood even in India.
How does aspirin reduce the risk?
Coronary artery disease is caused by two main pathological processes that affect the arteries that supply blood to the heart. Atherosclerosis involves the deposition of fat in parts of the arterial wall with fibrosis. Sometimes, these “plaques” become calcified. If the plaques reduce the luminal diameter of the coronary artery, by growing to 70% or higher than the width of that passage (50% in the case of the left main coronary artery), blood flow is significantly impeded. Especially during periods of high physical activity or stress, when high blood pressure and an elevated heart rate increase the oxygen requirements of the heart muscle. A mismatch between supply and demand leads to angina or chest discomfort. settles to rest.
However, soft plaques are prone to rupture even if they are small and not usually obstructive. When it ruptures, its exposed fatty nuclei come into contact with the blood flowing through the artery. Activates the “platelets” that are part of the blood cells. The platelet aggregation forms a clot. If the clot is large, it can completely block (block) the passage of blood. While an “obstruction” causes angina, an “obstruction” leads to a heart attack. At some point, a ruptured plaque can lead to angina even at rest or minimal exertion (unstable angina) before the initiation of a heart attack or myocardial infarction (MI). These acute conditions are often grouped together as “acute coronary syndromes” (ACS).
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Aspirin is an anti-platelet drug that irreversibly inactivates platelet cyclooxygenase and inhibits the production of thromboxane A2. This makes the platelets unable to clump together. Since the effect of each dose is limited only to the platelets that then circulate, and a new generation of platelets continues to be produced to replace those that naturally die within a few days, a daily dose of aspirin is prescribed to prevent young and sticky platelets from clumping together.
Aspirin pathways from secondary to primary prevention
The initial clinical trials were aimed at evaluating the protective effect of aspirin in those who had already had a heart attack. Numerous trials, in different parts of the world, have unequivocally shown a significant benefit in reducing mortality and recurrent heart attacks in people who have survived a heart attack or myocardial infarction. Therefore, aspirin has become an indispensable part of secondary prophylaxis after MI for all persons who can tolerate the drug without gastrointestinal side effects. It has also been used after coronary stent insertion.
Given this success, attention has turned to primary prevention. “Why not prevent a heart attack in the first place, by preventing a clot from forming on any plate?” , was the question asked. In 2003 Wald & Law of the United Kingdom suggested a combination of six “Poly Peel” medicines for the prevention of heart attacks, for use in all people over 55 years of age. Besides aspirin, the others selected were a beta-blocker, diuretic, angiotensin-converting enzyme (ACE-I) inhibitor, statin, and folic acid.
The editor of the British Medical Journal (BMJ) went abroad, calling this untested hypothesis the most important scientific publication in the BMJ in 50 years. This was followed by several multi-pill trials and separate aspirin trials for primary prevention of CHD. The folic acid disappeared quickly because it was ineffective. Of the three blood pressure-lowering drugs, beta-blockers and ACE-I initially remained for CHD treatment, while diuretics proved powerful in preventing stroke. As the undesirable metabolic effects of prolonged beta-blocker therapy on glycemia, triglycerides and HDL cholesterol became known, this class of drugs gave way to calcium channel blockers such as amlodipine for blood pressure control in primary prevention. Stats continued to be steady. ACE-1 and related angiotensin-receptor blockers (ARBs) have gained a reputation for controlling blood pressure and protecting blood vessels.
Change your attitude to aspirin
Aspirin has gone through phases of universal acceptance, skepticism, discussion, and revised recommendations in the field of primary prevention. While it remains undisputed for secondary prevention, the question has been raised as to whether the benefits of aspirin use in the primary prevention of CHD unequivocally exceed the risks of severe bleeding in the brain or stomach. Over time, evidence has accumulated, through clinical trials, meta-analyses, and post-marketing surveillance. As the evidence has grown, the recommendations have changed.
In May 2009, the Anti-Thrombotic Experts Collaboration (ATT) published a study in The Lancet, saying: “In primary prevention without pre-existing disease, aspirin is of an uncertain net value as the decrease in embolistic events must be weighed against any increase in the incidence of bleeding severe.” British clinical practice is becoming more cautious about the routine use of aspirin for the primary prevention of CHD. Clinical trials have continued to evaluate the role of aspirin, alone or in combination. Because statins effectively lowered blood lipids such as LDL cholesterol, blood pressure lowering drugs brought this risk factor under control, smoking rates were reduced in Western populations, healthy eating habits were adopted and physical activity promoted, and questions about benefits were raised. extra aspirin.
In 2017, a review by Paltrano and colleagues in the Journal of the American College of Cardiology (JACC) stated that the role of anti-platelet drugs in primary prevention of arterial thrombosis “remains controversial due to the uncertain balance of potential benefits and risks when combined with other preventive strategies.” The risk of coronary artery disease increases with age. The risk of severe bleeding from aspirin also increases with age. Therefore, it is particularly necessary to weigh the benefits and risks in that age group and to ask whether these benefits cannot be achieved by other means, including non-pharmacological measures.
The remarkable benefits of a Mediterranean diet and other wise diets for primary prevention of CHD have been well demonstrated in clinical trials and long-term cohort studies. Blood pressure and cholesterol-lowering medications have also shown a significant benefit for primary prevention. So why would aspirin risk primary prevention, even if it could go on for secondary prevention? This line of thinking has emerged in recent years.
Furthermore, there has been criticism that most risk calculators overestimate the 10-year risk of a cardiovascular event, because they do not take into account other treatment benefits that would potentially reduce this risk over that long period.
Recent US Guidelines
The US Preventive Services Task Force (USPSTF) published its latest guidance in the April 26, 2022 issue of the Journal of the American Society (JAMA). It is recommended that low-dose aspirin should not be used to prevent cardiovascular disease in people 60 years of age or older. The decision on the use of aspirin, for people aged 40-59 years who have a projected 10% or higher risk of cardiovascular disease in the next 10 years, is left to the treating physician. It concluded that the net benefit of aspirin use in this group was small. The decision should be individualized, based on the nature of risk factors and associated conditions such as diabetes.
It doesn’t make sense, for example, to put a heavy smoker on aspirin because of its high risk for 10 years, without making that person stop smoking. Especially since smoking increases the risk of SAH, the use of aspirin can increase the risk.
One of the arguments used to advance the routine use of aspirin for primary prevention of CHD was that the drug was also protective against colorectal cancer. This was initially based on flimsy evidence. The USPSTF, in a detailed review of the available evidence, found it insufficient to support a protective effect. Hence, the overall benefits do not outweigh the risks in the overall age group 40-59 years. It further concluded with “moderate certainty that initiation of aspirin for primary prevention of CVD events in adults 60 years of age or older has no net benefit.”
Guidelines for the primary prevention of CHD and CVD are subject to periodic reviews, based on an objective assessment of the best evidence available to date. A recent change in the guidelines, not in favor of routine use of aspirin for this purpose, takes into account the reduced expected benefit of aspirin due to the increased protection offered by other drugs and non-pharmacological measures with the risk of serious bleeding complications of aspirin use remaining undiminished. There will be subgroups of individuals where the drug can be used with caution, if the expected benefits are high due to the associated risk factors and the drug is well tolerated. It can still be used selectively, even if the “magic medicine” cap has slipped and routine use is best avoided.
K. Srinath Reddy is the Chairperson of the Public Health Corporation of India and previously headed the Department of Cardiology, AIIMS, Delhi. He was the first Indian president of the World Heart Federation.