Circulation system involves the main human organ, the heart. Cardiovascular disease (CVD) is still regarded as the major problem in Australia in terms of prevalence, death rates, the rate of incidence, burden of disease, and costs. The most widely spread form of CVD, coronary heart disease (CHD), continues to be the major single cause of death and the most common cause of sudden death. However, over the past years, there has been considerable progress in dealing with CVD in Australia. Improvements in the prevention, detection, and clinical management of patients suffering from CVD in combination with laboratory research brought about the decline in CVD (Esselstyn, 2007).
The circulation system is influenced by many negative factors including smoking and alcohol consumption. Stress can be implicated throughout the natural history of coronary heart disease (CHD), in its formation, progression, and in triggering a cardiac event. Risk factors affect CHD mainly through its influences on behavioral factors and activation of the autonomic nervous system. In particular, stress activates the SNS resulting in increases in epinephrine and norepinephrine that lead to increased beta and alpha receptor activity. Briefly, beta activation increases heart rate and heart contractility, therefore increasing cardiac output and blood pressure.
Alpha activation causes vasoconstriction of the arteries and veins and causes increases in total peripheral resistance and venous return, both of which increase blood pressure. All of these physiological events may contribute to CHD. For example, with an increase in blood flow, shear stress on the arteries is increased causing cells in the blood to be damaged and plaque to form and/or rupture. This, along with sharp increases in epinephrine, stimulates platelet activation and the sequelae that follow (Klabunde 2004).
Platelet aggregation, along with coronary vasoconstriction and plaque rupture, can lead to other priming processes such as thrombosis, ischemia, and acute myocardial infarction. As discussed earlier, stress and its related emotional indices (e.g., hostility) increase platelet aggregation through induction of the ANS. Dysfunctions of the circulation system may reduce oxygen delivery to the heart and thereby lower the threshold for myocardial ischemia or may trigger acute arrhythmic events through activation of the ANS, making myocardial infarction more likely. Recent evidence has also suggested that mental stress-induced ischemic episodes are good indicators of 5-year rates of cardiac events. Additionally, silent ischemia occurs much more frequently than is detectable by some clinical measures (Lilly, 2006).
To improve blood circulation, researchers suggest increasing psychical activity and changing the lifestyle. Physical activity could reduce CHD mortality without affecting morbidity by favorably altering the “triggering event” for acute myocardial infarction or cardiac arrest. Recent data indicate that the primary triggering event for many myocardial infarctions is the acute rupture of atherosclerotic lesions and the rapid closure of the artery lumen due to platelet aggregation and cell proliferation.
It could be that physical activity reduces either the risk of lesion rupture, platelet aggregation, or cell proliferation, thus reducing CHD mortality but not the development of atherosclerosis, which may be more related to the development of nonfatal clinical manifestations of myocardial ischemia (Lilly, 2006). Although the epidemiological evidence just reviewed is supportive of the importance of physical activity on CHD, the independent role of physical activity as a cardiovascular disease risk factor currently remains understudied in comparison to other CHD risk factors, such as hypertension or smoking.
References
Esselstyn, C. B. (2007). Prevent and Reverse Heart Disease. Avery.
Lilly, L. S. (2006). Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty. Lippincott Williams & Wilkins; 4th edition.
Klabunde, R. E. (2004). Cardiovascular Physiology Concepts. Lippincott Williams & Wilkins; Pap/Cdr edition.