Providing independent clinical excellence since 2005
Posted on Friday November 22, 2024 in Naked Heart
An article written by Dr Edward Leatham, Consultant Cardiologist
Tags: Aspirin, Coronary heart disease, Medication, NH1 search website using Tags to find related stories.
Aspirin, or acetylsalicylic acid, is one of the oldest and most widely used medications in the world. Well known for its analgesic effects, it was later discovered to be effective in much smaller doses in preventing platelet aggregation that had a pivotal role in arterial thrombosis. Its role in inhibiting platelet activity has made it a cornerstone in the prevention and treatment of arterial thrombosis. In this article, we will explore the fascinating role of platelets in acute coronary thrombosis, the mechanisms by which aspirin exerts its protective effects, and the clinical considerations for its use.
Platelets are small, disc-shaped cell fragments in the blood that play a pivotal role in haemostasis—the process of blood clot formation to prevent excessive bleeding. However, in pathological conditions such as acute coronary thrombosis, platelets can become overactive and initiate harmful clotting processes.
In the setting of atherosclerosis, the rupture of a plaque within the arterial wall exposes subendothelial structures, such as collagen, to circulating platelets. This triggers platelet adhesion to the site of injury, followed by activation and the release of pro-thrombotic substances. Activated platelets recruit additional platelets to the site, forming a platelet plug that serves as the nidus for further clot formation.
While platelets initiate the clotting process, the coagulation cascade amplifies it, ultimately leading to the formation of a stable, fibrin-rich “red clot.” This cascade involves a series of enzymatic reactions where inactive coagulation proteins are sequentially activated, culminating in the conversion of fibrinogen to fibrin by thrombin. Fibrin strands stabilise the platelet plug, forming a robust clot that can occlude an artery, causing myocardial infarction (heart attack) or stroke.
Aspirin exerts its anti-thrombotic effects by irreversibly inhibiting cyclooxygenase-1 (COX-1) in platelets. This inhibition prevents the production of thromboxane A2, a molecule that makes platelets sticky and promotes aggregation. By reducing platelet stickiness, aspirin significantly lowers the risk of arterial thrombosis while having only a modest impact on venous thrombosis. This selective benefit stems from the fact that arterial clots are platelet-rich, whereas venous clots are primarily fibrin-rich.t)
A daily dose of between 50 and 100 mg of aspirin (in the UK 75 mg is often used as it is equivalent to a quarter of a 300 mg tablet) is sufficient to achieve significant platelet inhibition. This “junior aspirin” dosage has been shown to markedly reduce platelet activity. Patients taking this dose may notice prolonged bleeding times, such as when shaving or after minor cuts. The bleeding time test, a standardised assessment using a template or sharp blade, has confirmed that aspirin prolongs bleeding time. More advanced platelet function tests have corroborated its efficacy.
The landmark Physicians’ Health Study provided early proof of aspirin’s effectiveness in reducing coronary events. Since then, numerous trials have established its role in secondary prevention, particularly for patients who have experienced a heart attack or acute coronary syndrome. Aspirin remains a foundational therapy for individuals with coronary artery disease.
However, aspirin’s efficacy does not extend to all thrombotic conditions. For example, while there was initial hope that aspirin might prevent stroke related to atrial fibrillation (AF), meta-analyses revealed that it is no more effective than anticoagulants in this setting and carries similar bleeding risks. As a result, aspirin is not recommended for stroke prevention in AF.
Although aspirin is a simple and affordable medication, it is not without risks. In a small subset of individuals, it can cause significant bleeding, particularly gastrointestinal bleeding. This underscores the importance of selecting patients carefully for aspirin therapy. It is generally reserved for those at high risk of acute coronary events, such as:
In these groups, aspirin helps prevent the catastrophic consequences of plaque rupture and subsequent thrombus formation.
Aspirin, even in low doses, can cause gastric irritation and, in some cases, ulcers. To minimise this risk, it is advisable to take aspirin with food rather than on an empty stomach. Soluble aspirin may reduce gastric discomfort, although there is no conclusive evidence that enteric-coated formulations offer superior protection against gastrointestinal bleeding.
It is also worth noting that aspirin does not typically need to be discontinued before surgical procedures. Unlike anticoagulants such as warfarin or direct oral anticoagulants (DOACs), aspirin’s impact on bleeding is primarily through its effect on platelets rather than the coagulation cascade.
Aspirin’s ability to prevent arterial thrombosis has undoubtedly saved countless lives worldwide. Its discovery, originally derived from willow bark, represents one of medicine’s most significant achievements. While its impact on venous thrombosis is minimal, there may be a role for aspirin in preventing venous thromboembolism in specific scenarios, such as long-haul flights or periods of prolonged immobility.
Aspirin’s effects on platelets last for the lifespan of the platelet, which is approximately 7–10 days. This means that it takes several days for aspirin to achieve full antiplatelet efficacy and an equal duration for its effects to dissipate after discontinuation. This extended duration of action is both a benefit and a limitation, as it ensures prolonged protection but also requires careful management in patients undergoing surgical procedures.
Aspirin remains a cornerstone of cardiovascular medicine, particularly in the prevention of arterial thrombosis. Its mechanism of action, centred on platelet inhibition, explains its effectiveness in conditions such as acute coronary syndrome. However, its use must be balanced against the risk of bleeding, and it should be reserved for patients who will derive the most benefit. When used appropriately, this inexpensive and time-tested medication continues to save lives and improve outcomes for millions of people globally.
For other stories related to cholesterol, coronary heart disease, and LDL, explore the archives by entering a tag under the search function above.
The Naked Heart is an educational project owned and operated by Dr Edward Leatham. It comprises a series of blog articles, videos and reels distributed on Tiktok, Youtube and Instagram aimed to help educate both patients and healthcare professionals about cardiology related issues.
If you would like to receive email notification each week from the Naked Heart, follow me on social media or please feel free to subscribe to the Naked Heart email notifications here
The CaRi Heart Score leverages artificial intelligence and advanced imaging techniques to provide a more comprehensive assessment of coronary inflammation, even before non calcified and calcified plaque becomes detectable on CT.
Written by Dr Edward Leatham, Consultant Cardiologist: Groundbreaking research from Oxford University reveals it is possible to detect and quantify ‘coronary inflammation’ – invisible to the human eye on conventional CT images, but detectable using artificial intelligence techniques.
While aiming for the lowest possible blood pressure without experiencing adverse effects, individuals can explore a range of non-pharmacological strategies to maintain or improve their cardiovascular health. Personalised experiments, supported by accurate home monitoring, can lead to significant insights and potentially delay or reduce the need for medication, contributing to a healthier, longer life.