Does Acute Psychological Stress Predict the Onset of Myocardial Infarction - Essay Example

Does acute psychological stress predict the onset of myocardial infarction? Disclosure to emotionally and physically stressful events normally triggers acute myocardial infarction. A relatively larger percentage of the AMI cases are mainly preceded by underlying prompting event that entail extreme emotional event such as death of a significant individual, anger, fear, work conflicts, anxiety and corresponding legal problems. Moreover, physical effort which entails physical exertion, lifting heavy object, sexual activity and snow shoveling. Even though acute and corresponding chronic stress is the renowned risk factor for the myocardial infarction and abrupt cardiac death, presence of the casual connection has been perceived with skepticism. Nevertheless, an escalating body of evidence confirms a connection though the mechanisms still remain indeterminate (Safren, 2007). Previous observations have resulted to wider field of acute risk in regard to study and have mainly highlighted the prevailing potential role of the psychosocial factors within acute disease onset and corresponding prognosis subsequent to the myocardial infarction. For instance, ST elevation that is the Q-wave myocardial infarction is currently acknowledged to be the preceded by the coronary thrombosis that is correspondingly related to plaque fissuring (Snow, 2004). Moreover, the plaque disruption and corresponding thrombosis often takes place at the site of previously mild stenosis depicting that the transformation from steady to unsteady plaque occurs acutely (Schaie, Leventhal, & Willis, 2002). Chronic psychological disorders such melancholy and corresponding anxiety are renowned to escalate occurrence of the risk of long-term cardiovascular malady. Nevertheless, meta-analysis depict that myocardial infarction incidence is sturdily related to the acute experiences of anger, unhappiness, grief, worry and stress (Topol & Califf, 2007). Underlying evidence depicts that patients who normally experience a myocardial infarction elicited by the acute emotions fare worse psychologically subsequent the myocardial infarction. Potential public health strategies for countering the prevailing risk and the entire physical and emotional triggers are well known (Watson, 2000). Acute emotional triggers result to an IM since it leads to occurrence of neurochormonal activation that possesses both universal and corresponding local haemodynamic impacts. When neurochormonal respond to the underlying emotional trigger it leads to the systemic vasoconstriction and escalation of the arterial blood pressure (Safren, 2007). The response escalates sinus node pumping rates and corresponding atrioventricular transmission velocity thus escalating heart rate. Augmentation of the heart rate and blood pressure results to corresponding increase in the myocardial oxygen consumption and myocardial function that facilitates rupturing of susceptible atherosclerotic plaque (Topol & Califf, 2007). Moreover, systemic neurohormonal impacts of emotional triggers result to decrease in the heart rate inconsistency thus leading to a hazardous factor of the cardiovascular disease and death. Effects of haemodynamic in regard to the emotional triggers normally act in concert with the dual main indigenous neurohormonal impacts of emotional triggers (Snow, 2004). Circadian and corresponding seasonal variations in regard to occurrence of the AMI are the main triggering factor that results to the cardiac events. Underlying circadian rhythm of the circulating catecholamines and other supplementary stress hormones is normally explaining the escalation of the AMI incidence in the morning hours (Safren, 2007). Conversely, seasonal variation within the AMI incidence in regard to the winter peak and summer nadir normally elaborated based on the particular meteorological triggers. Circadian variation in terms of occurrence of myocardial infarction, unsuspected cardiac death and corresponding myocardial ischemia is mainly characterized by the morning peak. According to the Meta analysis of numerous patients suffering from acute myocardial infarction and corresponding patients with abrupt death depicts an extra of myocardial infarctions that is relative risk of the day (Schaie, Leventhal, & Willis, 2002). Moreover, circadian variation in event occurrence depicts that underlying cardiac cases is mainly triggered by external activities especially those emanating from stimulating sympathetic nervous system (Snow, 2004). Research study of patients which are reported an absence of the circadian variation in regard to diabetes especially those who normally experience cardiac automatic neuropathy, lack heart rate variability and those undertaking either beta blockers or aspirin during the admission of a myocardial infarction (Topol & Califf, 2007). Thus, circadian variability in regard to the fibrinolytic capacity is evident as a factor that results to the morning escalation within the myocardial infarction. Patients with steady coronary heart malady, plasminogen activator inhibitor-1 action peaks in the early morning whilst tissue plasminogen activator activity is at its underlying nadir, whose treatment as a beta blocker ameliorate is relatively prothrombotic rate. Coronary atherosclerotic plaque rupture and corresponding occlusive thrombus development is a rampant mechanism of acute STEMI (Safren, 2007). Moreover, coronary plaque occurs due to rupture of a negligibly angiographically noticeable lesion that occurs devoid of showing any symptom prior to it ruptures. The rupture is normally spontaneous and can also occur due to exposure of an underlying emotional and physical trigger. Probable mechanisms that are normally responsible to plaque rupture entail catecholamine surge resulting to escalation of the heart rate, myocardial oxygen requirement and blood pressure. It also results from hypercoagulability state, depressed fibrinolysis, escalated platelet adhesiveness and corresponding aggregability, angiotensin II motivation, escalated vascular tone and baroreceptor reflexes reticence (Safren, 2007). Meta-analysis of the prevailing onset of the AMI depicts that STEMI is mainly attributed by triggering events, and is mainly examined within the AMI located within the emotional stress preceded, substantial physical exertion and sexual activity (Topol & Califf, 2007). Anger is preceded and twenty hour instantaneously precedes the underlying onset of the symptoms. Taking into consideration the trigger of the prevailing patient in duration of two days normally depict preceding onset of the chest pain. Hazard duration according to the researchers is considerably shorter in regard to anger and sexual activity and physical activity (Schaie, Leventhal, & Willis, 2002). Nevertheless, temporal period of the prevailing pathophysical alteration mainly induced by the trigger can considerably extend to limited days to a single week subsequent to the exposure (Safren, 2007). Numerous cultural, economic and social factors account for the regional and geographical locations in regard to the prevalence and types of the triggers. Diverse ethnic populaces within similar geographic location depict difference in the prevailing circadian variation within the onset of the AMI. Exposure to the corresponding triggers does not unavoidably result to the AMI (Snow, 2004). Even though there exits presence of a susceptible coronary plaque is normally one of the fundamental prerequisite, there are some evidence that regular exercise, stress management, controlling risk factors, quitting smoking and utilization of aspirin, calcium and beta blockers act as a safeguarding impacts against the underlying trigger mainly induced by the coronary occurrence. Early morning duration and corresponding few hours subsequent to waking up, individuals do experience relatively higher instances of AMI than corresponding remaining period of the day (Topol & Califf, 2007). Moreover, higher number of patients normally experience cases on onset of chest pain after waking up. Such cases of circadian rhythm are normally recognized to the early morning hypercoagulability and corresponding catecholamine surge. Seasonal variation in regard to the incidence of the AMI is mainly explained by particular meteorological factors, infections and corresponding variability of the cholesterol blood levels that escalate during winter (Safren, 2007). It is common in the coldest months of winter and hot month. Absence of the seasonal variation within the AMI is common in locations where there exists no life-threatening temperature. Moreover, non-equivalent seasonal variation within the AMI in diverse subgroups of similar population depicts the incidence of particular biological variations that occur because of racial, cultural and genetic differences (Topol & Califf, 2007). In sum, acute psychological stress can be utilized to predict the underlying myocardial infarction. This is because myocardial infarction normally results from emotional and physical stressful events that precede events. The main extreme emotional event that can results to myocardial infarction include death of a significant individual, anger, fear, work conflicts, anxiety and corresponding legal problems. Whilst physical effort which entails physical exertion, lifting heavy object, sexual activity and snow shoveling. References Topol, E. J., & Califf, R. M. (2007). Textbook of cardiovascular medicine. Philadelphia: Lippincott Williams & Wilkins. Safren, S. (2007). Cbt for depression and adherence in individuals with chronic illness. therapists guide. Oxford: Oxford University Press. Snow, V. (2004). Screening for diseases: Prevention in primary care. Philadelphia: American College of Physicians. Schaie, K. W., Leventhal, H., & Willis, S. L. (2002). Effective health behavior in older adults. New York, NY: Springer Pub. Co. Watson, D. (2000). Mood and temperament. New York, NY [u.a.: Guilford Press Read More