Since my research on ‘coronary thrombosis’ in 1996 and 25 years as an interventional cardiologist, I’ve pondered why heart attacks occur unpredictably across individuals with varying levels of coronary plaque and risk factors. The answer seems to lie in the role of chance in heart disease, akin to accidents that result from a series of underlying causes, not just isolated incidents.
This concept is well illustrated by the Swiss Cheese Model of system accidents. The model describes a stack of spinning disks, each representing a layer of defence with holes. An accident, like a heart attack, occurs when these holes align, allowing hazards to reach victims. In heart disease, the ‘layers’ are biological processes affecting the coronary arteries. A heart attack happens when the ‘holes’ in at least four layers align by chance. Understanding this model helps us realise that heart attack prevention involves more than dealing with just one factor, such as by taking a statin.
Fig 1. Four identifiable ‘risk’ layers contribute to a heart attack in an individual patient, where the risk of a heart attack can be linked to the number and size of the holes in each layer. Whereas the holes in the first layer can change over many years those in the latter layers vary day by day and even hour by hour. The four layers are spinning and the holes in three of the four distinct layers constantly vary in size as they open and shut thus only align infrequently by chance, explaining the random timing of a heart attack as well as why one patient, even left untreated can have their second event decades after their first.
I Coronary Plaque
High LDL cholesterol is a principle risk factor for heart disease. Coronary artery disease (CAD) builds up layer by layer, starting in our 20s with fatty streaks in the arteries. Over years, LDL cholesterol accumulated, leading to plaque accumulation and calcification. The first layer in the Swiss cheese model is therefore the accumulation of LDL laden plaque in and around the coronary arteries, creating the potential for a future heart attack.
II The Thin Line between Stability and Disaster
As coronary plaque builds up, it becomes vulnerable to plaque rupture. Plaque vulnerability can lead to temporary thinning of its fibrous cap, increasing the risk of rupture. Inflammatory processes, driven by factors such as raised blood glucose cause plaque instability. Sudden changes in blood pressure can exert shear stress on a weakened fibrous cap, causing it to rupture. This concept helps explain why cardiac events are associated with factors such as inflammatory conditions, glucose dysregulation and unaccustomed physical exertion.
III Thrombosis and Platelets: The Silent Guardians
When plaque ruptures, platelets form a plug to seal off the area, protecting against larger thrombotic proteins. However, the effectiveness of this response varies. During periods of high platelet activation, even minor plaque ruptures can trigger a more aggressive platelet response, leading to clot formation. Antiplatelet drugs like aspirin reduce this risk.
IV Body’s Fibrinolytic Defence: Our Natural Clot Busters
Our arteries have a clot-busting pathway, the fibrinolytic pathway, which is finely balanced to deal with arterial thrombosis. Factors like statin therapy and exercise improve our ability to handle arterial thrombosis, whereas a sedentary lifestyle and diabetes increase the risk.
Preventive Measures
Understanding heart attacks through the Swiss Cheese Model emphasises the need for a multifaceted approach to prevention. This includes focusing on cholesterol-lowering, good glucose regulation, inhibiting platelets, encouraging exercise, and considering beta-blockers in high-risk patients.
Conclusion
The Swiss Cheese Model provides insight into how multiple factors, when aligned, can lead to catastrophic events like heart attacks. By identifying and reducing these risks through education, intervention, and awareness, we can work towards preventing such tragedies.
Bibliography
Reason J. Human error: models and management. BMJ. 2000;320:768–70. doi: 10.1136/bmj.320.7237.768. [PubMed]
Cardiovascular computed tomography imaging for coronary artery disease risk: plaque, flow and fat: Keith M Channon, David E Newby, Edward D Nicol, John Deanfield http://dx.doi.org/10.1136/heartjnl-2021-320265
Fig 1. Four identifiable ‘risk’ layers contribute to a heart attack in an individual patient, where the risk of a heart attack can be linked to the number and size of the holes in each layer. Whereas the holes in the first layer can change over many years those in the latter layers vary day by day and even hour by hour. The four layers are spinning and the holes in three of the four distinct layers constantly vary in size as they open and shut thus only align infrequently by chance, explaining the random timing of a heart attack as well as why one patient, even left untreated can have their second event decades after their first.
