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The Six Ways Stress Triggers Death From Heart Fatalities

Arterial Blockage

Stress causes the body's cholesterol levels to skyrocket (increased serum cholesterol) as means of supplying emergency fuel to the body.  Elevated cholesterol and triglyceride levels can cause clogged arteries and massive heart attacks.

Coronary Thrombosis

Hormones, triggered by stress, elevate the body's blood-clotting factor, making blood platelets become "stickier." This change in blood chemistry greatly increases the risk of a blood clot forming, triggering fatal coronary-thrombosis heart attack.

Cardiac Dysfunctions / Sudden Cardiac Death

Prolonged stress causes excess electrical stimulation of the heart, disrupting its natural rhythms, causing cardiac dysfunctions like palpitations, fibrillation (most common is atrial fibrillation) and arrhythmia (most common is premature ventricular beat). The American Heart Association found that each year, over 1/4 million Americans -- people who have had no pain symptoms at all -- die from sudden cardiac death.

Congestive Heart Failure

Continual stress, overtime, can wear out your heart, causing Congestive Heart Failure (CHF), a condition where the heart becomes too weak to supply enough blood and oxygen.  Five million Americans suffer from this right now (with over a half-million new cases each year), and experts predict 1-in-5 adults over 40 will be struck by congestive heart failure.

Ischemic Attacks

Stress from mental agitation reduces blood flow to the heart, called ischemia. Ischemic attacks are painless, so people don't feel the reduced-blood-flow doing damage to their heart, which over time, leads to fatal heart attacks. There is a wealth of anecdotal evidence that links stress from mental agitation to heart attacks and sudden cardiac death, including reports of dramatic increases in these deaths after Hurricane Katrina, 9/11, and the bombing of Israel during the first Gulf War. According to Louis Cataldie, MD, acting state medical examiner for Louisiana, a disproportionate number of the roughly 1,300 confirmed Katrina deaths occurred among older people, and most victims did not drown. Almost 200 victims were evacuees who died outside the state within a month of the hurricane. Although the precise causes of deaths for Katrina victims will never be known, Dr. Cataldie says stress from mental agitation probably played a key role in many deaths. Also during Iraqi missile attacks in the first Gulf War, researchers in Israel reported an immediate rise in heart attacks and sudden deaths in Tel Aviv. The increase lasted a few days, after which the occurrence of heart attacks and deaths returned to normal.

Inflammation of Arteries

Many of the neurotransmitters involved in depression, anger and fear have effects throughout the body. Feeling negative, "toxic emotions" releases excessive amounts of cortisol steroids, contributing to a low-level inflammation of the coronary arteries all around the heart. (It is well established that cortisol and other stress-related substances damage the endothelium, a single layer of flat cells lining the entire circulatory system through the heart.) This low-level inflammation bombards arterial plaque with damaging chemicals that make the plaque squishy and fragile. Even a small amount of plaque can burst, prompting the formation of a clot that chokes off blood flow, triggering a fatal heart attack. Five years research by Dr. Paul Ridker of Brigham Hospital has shown this inflammation is a central factor in cardiovascular disease (the world’s biggest killer) and is twice as likely as high cholesterol to trigger heart attacks.

© 2009 Five-Minute Stress Relief - All Rights Reserved

Sources: Stress and the Heart: Biobehavioral Aspects of Sudden Cardiac Death Psychosomatics 1990; 31:255-264Psychological Stress and Disease Journal of the American Medical Association  2007;298:1685-1687 Protective and Damaging Effects of Stress Mediators New England Journal of Medicine Volume 338:171-179 Jan 15, 1998 Chronic Stress and the Heart Journal of the American Medical Association October 10, 2007 Vol. 298 No. 14

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