CENTER ON BEHAVIORAL MEDICINE
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Acute Stress as a Trigger for Myocardial Infarction
Stress is a normal part of everyday life. Stress can be caused by any situation that makes a person feel frustrated, anxious or angry. In small quantities, stress is usually manageable and rarely harmful. Conversely, large amounts of stress or a strong response to stress can be very harmful and can cause a number of health problems. Acute and chronic stress have been associated with a number of diseases and conditions. One of the more serious of these conditions is cardiovascular disease and the resulting cardiac events (Ballas, 2005). Acute stress has been specifically indicated as a trigger of myocardial infarction in a number of research studies (Mittleman et. al., 1995, Suzuki et. al., 1995, Trichopoulos et. al., 1981, Kloner, 1996). The research supporting the theory that acute stress can trigger myocardial infarction will be discussed as well as the likely mechanism of action.
A myocardial infarction, which is often called a heart attack, is an extremely serious cardiovascular event that is usually the result of coronary artery disease. Coronary artery disease is when arteries becoming narrowed or hardened due to cholesterol plaque build-up. This process is known as atherosclerosis. Additional narrowing or blockage can arise from blood clots that develop on the surface of a plaque disruption. A myocardial infarction happens when an artery becomes blocked to the point that there is an insufficient amount of blood flow to an area of the heart. The lack of blood causes damage to the affected area and the heart muscle begins to die. This event can often result in the death of a patient (Imaginis, 2005). In fact, “myocardial infarction is the leading cause of death in the United States as well as in most industrialized nations throughout the world” (Bajzer, 2002, p. 1).
Research Supporting Acute Stress as a Trigger
The underlying cause for myocardial infarction is nearly always coronary artery disease, but the onset of a cardiac event usually indicates a shift in homeostasis. Triggers are events that cause homeostatic shifts that lead to the onset of myocardial infarction (Mittleman et. al., 1995). Nearly half of all patients that survive a myocardial infarction have reported some type of triggering activity. The most common of these reported activities is emotional stress (Tofler et. al., 1990).
A number of studies have been conducted indicating acute stress as a trigger of myocardial infarction. Retrospective studies following the occurrence of earthquakes have yielded significant evidence demonstrating the rise in myocardial infarction following these extremely stressful events (Suzuki et. al., 1995, Trichopoulos et. al., 1981, Kloner, 1996). Following the 1995 Hanshin-Awaji earthquake, which was the most destructive earthquake ever recorded in Japan, the number of myocardial infarctions increased 3.5 times the normal rate (Suzuki et. al., 1995) Similar increases were reported in the studies on the 1981 Athens earthquake and the 1994 Northridge earthquake. Both of these studies showed that following the earthquake there was a substantial increase in death related to cardiovascular events. The research also showed that during the same time there was no significant increase in mortality related to any other disease conditions (Trichopoulos et. al., 1981, Kloner, 1996).
Research has shown that
even stress caused by watching sporting events can trigger myocardial
infarction. The results of a Dutch
study designed to examine spectator stress and myocardial infarction
significant increase in cardiovascular events on the day of important
football games. Additionally, the study determined that the number of
cardiovascular deaths increased by 50% in the Dutch population the 4
following the elimination of the Dutch football team from the
et. al., 2000). A similar study was conducted in
Acute stress in the form of anger has been demonstrated to be a significant trigger in myocardial infarction. A study was conducted to examine episodes of anger in the period just preceding the onset of myocardial infarction. The results of the analysis found that the relative risk of a myocardial infarction occurring was over twice as likely in the 2 hours preceding an episode of anger (Mittleman et. al., 1995).
Acute Stress Response
The acute stress response, often called the fight or flight response, is the body’s physiological response to negative emotions. The acute stress response is viewed as an adaptive response designed to prepare an individual to deal with a threatening situation in which they may need to either fight or run. This response is facilitated by a reaction of the autonomic nervous system, specifically the sympathetic branch, and the endocrine system (Carlson, 2004).
The acute stress response is initiated by inducing the cell bodies of the sympathetic motor neurons in the thoracic and lumbar regions of the spinal cord. The fibers of the sympathetic motor neurons signal the organs of the body through the neurological pathways of spinal nerves and sympathetic ganglia. The sympathetic neurons also signal the adrenal medulla to cause epinephrine and norepinephrine to be released. Additionally, the adrenal cortex is activated through hormone signals in the hypothalamus and anterior pituitary gland, which allows for glucocorticoids to be released for rapid conversion of protein and fat into glucose for available energy (Carlson, 2004).
The sympathetic response is facilitated by the direct neural interaction with the organs and the release of epinephrine and norepinephrine throughout the body. The sympathetic response causes the pupils to dilate, salvia production to decrease, heartbeat, breathing and sweating to increase, blood vessels to constrict, digestion to slow down and the bladder to relax. The most important reactions relating to myocardial infarction are the increased heart beat and breathing and the vasoconstriction. These reactions in concert usually cause a rapid increase in both systolic and diastolic blood pressure (Carlson, 2004).
Nearly all cases of myocardial infarction are the result of plaque disruption. Arteriolosclerosis results in plaque build up on endothelium of the arterial wall. Atherosclerotic plaques are formed through a complex interaction between blood elements, flow pattern and vessel abnormalities, which can cause plaque to be inherently unstable and prone to disruption (Falk, Shah & Fuster, 1995). The disruption of a plaque initiates a sequence of reactions starting with the adhesion of platelets to the newly exposed endothelium surface. This is followed by the activation of the platelet glycoprotein IIb-IIIa receptor which causes platelet aggregation and forms a blood clot known as a thrombus. The size of the thrombus is determined by the relative size of the plaque disruption and the degree of platelet aggregation (Davies, 1997).
The cause of plaque disruption is widely debated, but the leading theory is that blood pressure plays a critical role in the process. Research has shown that a sudden onset of high blood pressure can trigger plaque disruption through hemodynamic stress (Falk, Shah & Fuster, 1995). The likely mechanism is attributed to turbulent pressure fluctuation created by the rapid change in pressure through stenotic vessels (Loree, Kamm, Atkinson & Lee, 1991).
Research has demonstrated through retrospective studies that there is a significant association between acute stress and the onset of myocardial infarction (Mittleman et. al., 1995, Suzuki et. al., 1995, Trichopoulos et. al., 1981, Kloner, 1996). The acute stress response has been shown to cause a rapid increase in blood pressure due to an increase in heart rate, breathing and vasodilatation (Carlson, 2004). A sudden increase in blood pressure has been shown to cause turbulent pressure fluctuations that lead to plaque disruptions (Falk, Shah & Fuster, 1995, Loree, Kamm, Atkinson & Lee, 1991). The exposed endothelium activates platelet adhesion and aggregation which results in a thrombus. If the size of the thrombus is large enough it will block blood flow to the heart and cause myocardial infarction (Davies, 1997).
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