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Changes brought on by anger or other strong emotions are linked to future arrhythmias and sudden cardiac arrests, says a new study, says study researcher Rachel Lampert, M.D., F.A.C.C., associate professor, Yale University School of Medicine. There is a spate of recent studies that correlate stress to sudden cardiac arrests, which are blamed for 400,000 deaths annually. Chronic work stress and coronary heart disease As per a study published in the European Heart Journal, the stressed had less time to exercise and eat well and also showed signs of biochemical changes. The study conducted on more than 10,000 British civil servants found out that those under 50 who said their work was stressful were nearly 70 per more likely to develop heart disease than the stress-free. The study documented how workers felt about their job, and also monitored heart rate variability, blood pressure, and the amount of the stress hormone cortisol in the blood, diet, exercise, smoking and drinking patterns. Researchers then conducted studies to find out how many people had developed coronary heart disease or suffered a heart attack and how many had died of it. It was found that chronic work stress was directly associated with coronary heart disease. Stress upsets the neuroendocrine system and the part of the nervous system which controls the heart, telling it how to work and control the heart rate. Anger and arrhythmia Anger is even more detrimental says another study at Yale University which links changes brought on by anger or other strong emotions to future arrhythmias. Published in the March 3, 2009, issue of the Journal of the American College of Cardiology the paper explains how anger-induced electrical changes in the heart can predict future arrhythmias in patients with implantable cardioverter-defibrillators (ICDs). While previous studies have demonstrated an increased incidence of sudden cardiac death during times of population stress such as earthquake and war, this study provides the first evidence that changes brought on by anger and other strong emotions can predict arrhythmias. "It's an important study because we are beginning to understand how anger and other types of mental stress can trigger potentially lethal ventricular arrhythmias, especially among patients with structural heart abnormalities," says Rachel Lampert, M.D., F.A.C.C., associate professor, Yale University School of Medicine. 62 patients with ICDs who underwent monitoring during a mental stress test were studied. Patients who had coronary artery disease or dilated cardiomyopathy (a condition in which the heart muscle is enlarged) and a standard indication for ICD were recruited from the Yale Electrophysiology practice. The mental stress test, conducted in a laboratory setting shortly after ICD implantation (about 3 months), asked patients to recall a recent situation in which they were angry or aggravated. T-wave alternans (TWA), a measure of the heart's electrical instability, was analysed. Follow-up averaging three years was conducted to determine who had arrhythmias requiring termination by the ICD. "We know strong emotion increases sympathetic arousal," says Dr. Lampert. "In this study, we found patients with higher levels of anger-induced TWA were more likely to experience arrhythmias requiring ICD termination." Even when other clinical factors that predispose patients to higher TWA levels and/or higher risk of ventricular tachycardia/ventricular fibrillation were controlled for (e.g., heart failure or history of arrhythmia), anger-induced TWA remained a significant predictor of arrhythmias, which led to a heightened risk of up to ten times that of other patients. The development of accurate, non-invasive risk stratification tests to identify those individuals at greatest risk of life-threatening arrhythmia is critical. The present study suggests that mental stress, namely anger, may be yet another pathway provoking arrhythmias. In contrast to exercise, mental stress doesn't elevate one's heart rate much, suggesting that changes seen with mental stress may be due to a direct effect of adrenaline on the heart cells. Therefore, mental stress testing could provide an alternative to atrial pacing for patients unable to exercise, according to Dr Lampert. 'More research is needed, but these data suggest that therapies focused on helping patients deal with anger and other negative emotions may help reduce arrhythmias and, therefore, sudden cardiac death in certain patients.' Short periods of stress protect the heart muscle Instances of the response plateauing off and aiding your heart to tackle a lethal attack are seen in another study by researchers at the University of Cincinnati. The study suggests that experiencing brief periods of blocked blood flow may condition a person to survive a full-blown heart attack later. The five-year laboratory study showed that short periods of stress, either from reduced blood flow or high blood pressure, activates a protective molecular pathway in the heart called JAK-STAT, which protects the heart muscle. Dr. Karyn Butler, a surgeon-scientist at the university, says that the JAK-STAT pathway can help precondition and protect the heart from damage caused when blood flow is restored after a period of decreased flow, as occurs after a heart attack. ''These mini stressors appear to push the heart muscle into an adaptive state where it gets used to how long-term stress feels. This preconditioning helps the heart muscle better tolerate longer episodes of compromised blood flow,'' she said. ''The concept is similar to how we approach a new physical fitness regimen with incremental steps. You wouldn't try to condition yourself for a marathon by running 10 miles on your first day of training. You'd prepare yourself incrementally,'' said Butler. ''The body appears to be doing the same thing for the heart. Patients often endure short periods of reduced blood flow before the blockage causes irreversible cardiac damage. When the JAK-STAT pathway is activated, however, it appears to have a protective effect and may help the heart recover,'' she added.
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