Stress results when something causes your body to behave as if it were under siege triggering physiologic and behavioral responses that is aimed at reestablishing the predefined steady state (homeostasis) essential for life and well-being. Sources of stress can be physical, like injury or illness. Or they can be emotional, like marital unhappiness, job and financial loses and the death of a loved one. Stress can also come from occupational pressures and obligations that are not rewarding and perceived to be out of control.
When stress occurs, the body prepares to take action through a fight-or-flight response. In this response, levels of many hormones mostly   cortisol and catecholamines (adrenaline and noradrenaline) shoot up. The net effect is mobilization of stored energy-glucose and fat-which ultimately cause elevated blood glucose and cholesterol levels.
High blood cholesterol, triglycerides, and blood pressure (partly due to increased vascular tone) increases  the risk for cardiovascular diseases. The narrowing of blood vessels by deposits of fatty plagues may cause poor blood and oxygen supply to the heart muscle thereby enabling heart attacks.
Emotional stress as well causes activation of the sympathetic nervous system, which is associated with enhanced norepinephrine release in the heart and blood vessels, that then caused increased cardiac output and vascular resistance.  Furthermore, the adrenal medulla secretes more adrenaline and noradrenaline that augments cardiovascular effects.  Activation of the sympathetic nervous system also increases circulating  angiotensin II, aldosterone, and vasopressin which are known to elevates systemic vascular resistance in addition to fluid retention.  The net effect of the increased cardiac output, vascular resistance and fluid retention is high blood pressure.
Many sources of stress such as chronic diseases and occupational pressures are long-term. As a result  hormones that are designed to deal with short-term stress stay elevated for a long time. Prolonged elevation of angiotensin II and catecholamines can contribute to development of coronary artery diseases (angina, ischemia,myocardial infarction, arrhythmias) through coronary artery vasospasm,  sustained increase in blood pressure as well as vascular occlusion by artherosclerotic fat deposits.
Long-term stress also affect blood clotting through increased fibrinogen, platelet aggregation and adhesiveness, polycythemia, which   promotes blood clotting. The increased coagulabiliry makes blood stickier and increases the risk of ischemia and stroke.
Scientific studies strongly suggest that stress-related sympathetic nervous system drive is the major factor in coronary heart disease. Behavioral modification is aimed at turning off the epinephrine-norepinephrine rush. And propanolol and other beta-blockers may be recommended for all heart-attack patients provided there are no contraindications.

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