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It is well known that stress causes ill health. Stress can lead to cardiovascular diseases, especially heart attack. Several mechanisms leading to this effect are at work. Acute stress episodes are proven to be particularly dangerous for some people.

The sympathetic pathway, when activated by stress, releases stress hormones - adrenaline and cortisol. These hormones respond to stress by increasing heart rate, narrowing the blood vessels, increasing blood pressure and activating and aggregating platelets that contribute to the formation of thrombus (blood clot). All these factors ultimately lead to heart attack if they affect the coronary arteries that supply blood to heart. The HPA axis responds to stress by stimulating the release of the stress hormone cortisol (through a cascade of reactions) from the adrenal glands.

Elevated cortisol levels can lead to various negative effects, such as increased blood sugar levels and suppression of the immune system. Over time, this can contribute to inflammation and damage to the artery walls.

Persistent stress can reduce blood supply to heart

Stress is also found to play a role in the development of atherosclerosis which on the long run can lead to cardiovascular diseases including heart attack.

Atherosclerosis is characterized by the inflammation of the walls of arteries along with the deposition of cholesterol particles, cellular waste products, white blood cells and smooth muscle cells in the inner layer of arterial walls to form plaques. A plaque grows over a long period of time and when it disrupts from the wall of an artery, it attracts platelets and forms a blood clot subsequently leading to the occlusion of the artery. When the arteries nourishing the heart are occluded, the result is more commonly a heart attack.

But what is the role of stress in this long process?

Stress-induced activation of the HPA axis impairs the lipid and glucose metabolism. A series of metabolic events result in the cholesterol accumulation in various parts of the body, including arterial walls, thus contributing to the plaque formation.

Chronic stress can lead to conditions like obesity and diabetes, which are significant risk factors for heart disease. Stress can alter metabolic functions, leading to fat accumulation, especially around the belly area, and can increase insulin resistance.

Studies suggest that chronic stress can affect the functions of the endothelial cells that are found along the inner wall of blood vessels. The endothelial cells produce nitric oxide (NO) which normally inhibits accumulation of white blood cells and platelets. This ensures smooth blood flow through the arteries. 

Chronic stress causes endothelial cell damage and reduces the nitric oxide production thus triggering atherosclerosis.

Psychological stress is also found to increase the circulating levels of certain proteins called inflammatory cytokines IL-6 and TNF-α. These are produced by the white blood cells that constitute the body’s immune system. IL-6 plays a major role in causing platelet activation, aggregation and plaque formation.

Frequent acute stress episodes can lead to heart attack

While chronic stress takes time and contributes to formation of atherosclerotic plaques in the long run, the acute triggers are found to affect mostly the last step of the process.

If a person already has atherosclerotic plaques, an acute stress outburst can result in narrowing of blood vessels, plaque disruption, clot formation and blockage of blood vessels supplying the heart. Even in the absence of a plaque or clot, an acute trigger stimulates the sympathetic pathway and may result in ventricular fibrillation, a condition where the heart beats abnormally leading to sudden death.

Studies suggest that acute mental stress can also impair the functions of endothelial cells. Though the endothelial dysfunction is transient in this case, lasting up to 1.5  hours, researchers say that frequent encounter of such short-lived episodes of acute stress are likely to initiate or accelerate atherosclerosis in early life.

Hot-tempered people are at higher risk of heart attack

A recent study that focused on the effect of acute triggers on heart was published in the European Heart Journal.

The researchers found that the outbursts of anger are associated with a transiently higher risk of cardiovascular events especially heart attack.

See Also: Best Tips for Stress Management

According to this study, the risk of heart attack is higher in the first two hours following an outburst of anger. The effects of anger outbursts on heart are usually transient with infrequent episodes, but with increased frequency of episodes, the impact may be larger. The effects are also found to be more in people who already have other risk factors.

Stress, either directly or indirectly, is found to be a cause of serious cardiovascular events, especially heart attack. But it is a modifiable risk factor. Researchers are realizing the need for further studies to develop stress management programs that would have a favorable impact on cardiac health of people.

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  • Photo courtesy of 080780 by FreeImages : www.freeimages.com/photo/761892/?forcedownload=1
  • Photo courtesy of William Brawley by Flickr : www.flickr.com/photos/williambrawley/4045524560

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