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How to minimise risks of a surprise heart attack and young deaths

I had a major heart attack when I was 39. It was completely unexpected because I had never noticed any symptoms and all the prior annual blood tests and physicals had not alerted me to any immediate risks. This is still an unsolved problem – the heart attack is the first shocking revelation of the underlying disease for many young and seemingly fit individuals. (The deaths of young public figures in the past few years serve as a jarring reminder.) Asymptomatic and otherwise fit individuals, as they approach middle age, worry about the risk of such a sudden event. Surprisingly, the commonly available information on heart attack risk reduction for this population is still mostly limited to major lifestyle changes such as diet, exercise, and smoking cessation. Sometimes counter-productive unnecessary testing is also recommended.

Going beyond the cliched recommendations requires understanding the mechanism of these unexpected heart attacks. My research suggests that in addition to the big-picture lifestyle changes, daily decisions to avoid overlap of stressors such as lack of sleep, physical and mental stress are vital in reducing this risk. Furthermore, frequent tests (other than basic blood tests) are not helpful.

There are three contributing reasons. One is the presence of plaque – commonly termed as blockages – in the coronary arteries. Coronary arteries are blood vessels that supply blood to the heart and enable it to pump properly. Blockages restrict this blood supply and cause the heart to malfunction.

If these blockages are large then people feel symptoms such as chest pain and breathlessness, especially during any exertion, and can seek attention before an attack ensues.

A common misconception is that a blockage results from deposits of fat (lipids, cholesterol) and cells on the artery wall – similar to blocks in household plumbing. This is incorrect. The figure below depicts this incorrect view.

The blockages are a result of cells and cholesterol particles breaking through the barrier of endothelial cells and infiltrating the lining of the artery. As a result, there is a bump in the artery wall – like a pimple. This is known as plaque or stenosis. The per cent (%) stenosis is typically measured as the per cent of artery diameter that is blocked. The plaque need not bulge into the artery but could protrude outwards as well (known as positive remodelling). See figure below.

The sudden attacks are caused by smaller blockages. These are “clinically silent” and do not restrict blood flow (and, therefore, cause no symptoms) but cause problems if they break apart. This is the second factor. Break-up and disruption of such blockages inside the coronary artery, as shown in the figure below, initiates blood clotting mechanisms to “repair” the injury from the plaque disruption.

The third factor is the intensity of clotting. Severe clotting results in a large blockage in the artery and causes a heart attack. Thus, the clot – and not the plaque – stops the blood flow. If clotting is less severe, smaller clots form. These are enough for injury repair and don’t affect blood flow. Shockingly, this type of plaque break-up – with small clot formation – is quite common. According to a 2015 article in the Journal of the American College of Cardiology (JACC), many millions undergo such events without suffering any symptoms. These individuals dodge a sudden attack due to the lower clotting intensity.

Can testing help?

So, three things need to be detected: Presence of small plaque, likelihood of plaque disruption (known as vulnerability), and the clotting intensity of blood. Reliable non-invasive diagnostic tests are available only for the first – detection of small plaque. Nevertheless, testing (even if it were to be available) for each of these will not offer a guaranteed window into the future because all the three factors change depending on lifestyle and environmental conditions.

New plaques can develop and existing ones can change in size. A vulnerable plaque can become stable and vice-versa. And, the clotting intensity of blood changes depending upon factors such as time of day, content of past meal, emotional state of the individual and many others. Whether the changes happen in seconds or over many months is not understood. This dynamic aspect makes it impossible to predict these sudden attacks because the problem is not limited to identifying individuals at risk from the three contributory factors. In addition to marking the at-risk person, a “blockage flash point” for that person has to be identified as well – a time when these three elements coalesce and lead to a sudden attack.

A logical inference is that presence of only one or two elements is not an immediate threat. The data above – indicating that many individuals undergo plaque disruption without symptoms – supports the inference. Additional support comes from population statistics. A 2021 article in Circulation reported a study in Sweden of around 30,000 individuals between 50 and 64 without a diagnosis of coronary disease. It showed that around 42 per cent carried some plaque! All these individuals seem to be living without awareness of the disease. Furthermore, about 0.3 per cent of the population suffers a heart attack annually (2019 statistics).

The implication for testing is that the benefit of detecting plaque (only one of the three elements) in the asymptomatic population is questioned. Especially so, because the risk of heart attack over 10 years can also be estimated through a review of lifestyle factors and blood tests. Risky tests such as the Computed Tomography (CT) tests that use X-rays have to show evidence that testing ultimately results in heart attack prevention — an endeavour that is still in-progress. The current American Heart Association (AHA) guidelines advocate only a limited role for testing (only the CT calcium score test is recommended for a specific population) in asymptomatic patients.

Is daily life a suspense then?

Does the knowledge that a sudden attack is an event requiring three factors to coincide provide some relief? Or, should individuals worry about being in the population subset that suffers the attack? In addition to following the AHA guidance, insights based on the flash point concept can help reduce the risk further. As this quote from a research article from Falk and others [1995, Circulation: 92-657] explains: “Onset of acute coronary syndromes [heart attacks] does not occur at random; a large fraction appear to be triggered by external factors or conditions.” Examples are mornings, Mondays, vigorous exercise, cold weather and emotional stress.

Triggers can be thought of as events that create optimal conditions for flash point development. Typically, triggers are stressors that cause inflammation. Inflammation “activates” different systems of the body and is one of the causes for plaque build-up, plaque disruption, and clotting. The conceptual graphic below shows some triggers affecting the “activation” state of the body over a 24-hour duration. Beyond a certain threshold, plaque disruption and extensive clotting are triggered causing a sudden attack.

The visual shows the cumulative activation state as a sum of a baseline and stressors such as lack of sleep, the daily (circadian) body cycle. The variable daily events and triggers are added on top. An important note is that although some of the triggers are known to increase inflammation, there is no data to indicate the magnitude and shape of these trendlines and the threshold level. Nevertheless, the visual helps to inform and impress that overlapping of stressors leads to a higher activation state and takes the individual closer to the flash point.

A heart attack could be triggered by “the-straw-that-broke-the camel’s-back” type of situation wherein a seemingly routine activity such as morning exercise, or an emotionally difficult conversation, if coincident with an already elevated activation level, leads to a sudden attack. My heart attack happened around noon during my routine, moderate intensity gym workout. This was “on top” of a hectic travel schedule and many nights of poor sleep during the prior ten days.

Action is possible on two fronts based on the graphic. The baseline can be thought of as contributed by genetics, age, risk factors such as diabetes, hypertension, lipid levels, obesity, smoking, and, now, possibly COVID. This risk can be reduced through major lifestyle changes and medications. Techniques such as meditation and yoga can also help.

The second risk is from the daily stressors and this is managed by ensuring stressors do not overlap. Some practical tips are avoiding succession of late nights, avoiding strenuous exercise the morning subsequent to a late night or to an intense travel schedule, and understanding one’s emotional stressors. Also, remember that baseline risk increases with age. Therefore, any exercise regimen should be adjusted as one becomes older (with medical input). Unexpected heart attacks are a reality that are not completely understood and, therefore, not yet eliminated. Frequent testing does not eliminate this risk. A lifestyle with some thumb rules to stay away from the flash point, however, can minimise daily concerns and worry.

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