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Pathophysiology of Coronary Heart Disease

Pathophysiology of Coronary heart Disease

Abstract

The early development of coronary heart disease (CHD) relates to atherosclerotic narrowing of the coronary arteries, and the growing need of the myocardium for oxygen at the increase of a patient’s activity. The violation of the balance between the need of a cardiac muscle for oxygen and its delivery with blood caused by the disorder of the coronary blood circulation is the cornerstone of the CHD pathogenesis. The need of a myocardium for oxygen depends on the haemodynamic loading of the cardiovascular system, on the sizes of heart, and the intensity of metabolism in the cardiomyocytes. The delivery of oxygen to a myocardium is determined by the condition of a coronary blood-groove, which can decrease in both the organic and the functional disorders in the coronary arteries leading to the myocardium ischemia (Montalescot & Sechtem, 2013, p. 2955). Modern understanding of the pathophysiology of the coronary heart disease consists in the assumption that the majority of episodes have the multiple-factor genesis and are caused by the inadequate delivery of oxygen to a myocardium due to the complex influence of such factors as the increased oxygen inquiry, significant narrowing of coronary arteries, and vasomotor changes. The main clinical manifestations of the CHD include stenocardia of tension and rest, unstable stenocardia, and an acute myocardial infarction.

Keywords: coronary heart disease (CHD), ischemic dystrophy of myocardium, myocardial infarction, atherosclerosis

Pathophysiology of Coronary Heart Disease

Coronary Heart Disease: An Overview

Coronary Heart Disease (CHD) unites the group of the diseases connected with the absolute or relative insufficiency of a coronary blood-groove. It represents the severe form of atherosclerosis and hypertensive disease demonstrating the ischemic dystrophy of a myocardium, myocardial infarction, and atherosclerosis. The Coronary Artery Disease (CAD) is the other name of the CHD (Montalescot & Sechtem, 2013, p. 2955; Warnica, 2013). Approximately two third of death cases are caused by the CHD. Particularly, men at the age of 40-65 years are more vulnerable to the CHD than women (Montalescot & Sechtem, 2013, p. 2956). However, after 70 years, the chances to have the CHD of men and women become equal. The maximum of clinical manifestations (demonstration peak) is between 50 – 60 years for men and 60 – 70 years – for women (fig. 1). (Mozaffarian, D. et al. 2015, p. e48).

Prevalence of Coronary Heart Disease by age and sex

Fig. 1. Prevalence of coronary heart disease by age and sex (Mozaffarian, D. et al. 2015).

The clinical course of the CHD is rather changing, with the episodes of the acute (absolute) coronary heart disease against the chronic (relative) disease of a coronary blood-groove. It is the basis for gradation of the CHD for the acute and chronic forms. From the morphological point of view, the acute CHD presents the ischemic dystrophy of a myocardium or its heart attack; the chronic IBS – a cardiosclerosis (diffused fine focal or postinfarction macrofocal), sometimes complicated by the chronic aneurism of heart (The Center of Excellence for Public Health, 2012).

The ischemic myocardosis is peculiar for rather short-term episodes of CHD with the development of the electrocardiogram changesб but without formation of the necrosis and increase of the activity of cardiac specific enzymes. The risk factors of the early damage of the coronary arteries include the atherosclerotic existence of the CHD cases in a family, especially until the age of 50 years, male gender, hypertension, low level of physical activity, smoking, and diabetes (Montalescot & Sechtem, 2013, p. 2956; Goblirsch et al., 2013, p. 10). The violations of metabolism of lipids is also of high importance, namely due to the ratio of the levels of the LDL and HDL cholesterol. The role of other disorders of lipid metabolism is less significant, but they should be identified at people with the early coronary atherosclerosis. Clinical classification of the CHD includes the sudden coronary death, stenocardia, unstable stenocardia, acute myocardial infarction, and cardiosclerosis (Warnica, 2013).

The Etiology of CHD

Coronary Heart Disease (CHD) arises owing to the lack of oxygen caused by the inadequate perfusion. The etiology of CHD is various. According to the Center of Excellence for Public Health (2012), disorders in the work of the cardiac muscle, because of the discrepancy between the supply of myocardium with oxygen and the need for it, is common for different forms of coronary heart disease. The most frequent reasons of the CHD include atherosclerotic changes of the epicardial coronal arteries, leading to the narrowing of these arteries that causes the reduction of the perfusion of myocardium at rest, or restriction of the possibility of the adequate increase of perfusion of myocardium (The Center of Excellence for Public Health, 2012).

Cardiac ischemia results from imbalance between myocardial oxygen supply and demand. In this review, cardiac ischemia is perceived as myocellular hypoxia or the condition resulting when oxygen supplied to a region of heart muscle is insufficient to meet its needs (Pepine & Nichols, 2007, p. I-4).

Furthermore, a coronary blood-groove decreases in the presence of the blood clots in the coronal arteries, at the emergence of a spasm in them, and sometimes at the embolism of the coronal arteries, narrowed by their syphilitic gummi. The congenital anomalies of the coronal arteries, such as an abnormal development of the left forward descending coronary artery from a pulmonary trunk, can cause the CHD and even a heart attack in children. However, they seldom serve as the reason for the CHD in adults (Pepine & Nichols, 2007, p. I-5).

Moreover, the CHD can arise when there is the increased need of myocardium for oxygen as, for example, at the expressed hypertrophy of the left ventricle owing to the hypertension or the stenosis of the aorta’s mouth. In the latter case, there are the stenocardia attacks that cannot be distinguished from the attacks of stenocardia arising at the atherosclerosis of the coronal arteries (Mandal, 2014). Occasionally, the CHD can occur at the decline in the ability of blood to transfer the oxygen, for instance, at the unusually expressed anemia, or in the presence to the carboxyhemoglobin blood.

Besides, the CHD can be caused by two or more reasons simultaneously, for example, the increase in the need for oxygen owing to the hypertrophy of the left ventricle and the reduction of the supply of myocardium with oxygen because of atherosclerosis of coronal arteries. According to Singh, et al. (2012), normal coronary blood circulation is regulated and controlled by the need of myocardium for oxygen, which is the result of the changing coronary resistance and, consequently, a blood-groove. At the same time, the amount of the oxygen extracted by a myocardium from blood is rather constant and high. Normal intra myocardial resistive arteries possess a considerable ability to expand. The change of the need for oxygen arising at physical and emotional pressure influences the coronary resistance and, thus, regulates the supply of blood and oxygen (metabolic regulation). The same vessels adapt to the physiological changes of the arterial pressure, thus maintaining the coronary blood-groove at the level corresponding to the requirement of myocardium (autoregulation). The big epicardial coronal arteries, capable of narrowing and expansion, serve as the tank, and are considered only as the carrying-out vessels. At the same time, the intramiocardial arteries can change the tone substantially, and therefore, are recognized as the resistive vessels (Singh, et al, 2012, p. 252).

Pathogenesis and Pathophysiology of CHD Symptoms

Disorders in the metabolism of lipids, or the increased level of the cholesterol and consumption of the saturated fats, especially imposed on genetic predisposition, trigger artherogenesis. The lipid stripes representing the subendothelial congestions of lipids, and the macrophages/monocytes loaded with the lipids constitute the first stage of the development of atherosclerosis (Mandal, 2014). The LDL are exposed to the oxidation that complicates their metabolism and mobilization as well as enables to have the local cytotoxic effects. The macrophages migrate to the subendothelial layer and absorb the lipids, being transformed to the so-called “foam cells.” The smooth muscle cells migrate to the area of the defeat in the development process of an atherosclerotic plaque. At this stage of the pathological process, the haemo dynamic disorders can be insignificant (Leon & Bronas, 2009, p. 381).

When the atherosclerotic formation becomes strong and stable, the fibrous tire is formed, the plaque is qualified, and the gleam of a vessel is progressively narrowed. Some of the atherosclerotic plaques remain permanent or progressively increase with a small speed. The integrity of others can suddenly be broken, initiating the cascade of reactions, the culmination point of which is represented by the intra vascular thrombosis with the partial or full occlusion of arterial branch. It is followed by the symptoms of arisen stenocardia, unstable stenocardia, the development of myocardial infarction, or even sudden death. In other cases, the plaque can be stabilized after the damage of a tire, which will correspond, as a rule, to the more severe haemodynamic disorders with a smaller diameter of the struck vessel (Pepine & Nichols, 2007, p. I-7).

Owning to the effective hypolipidemic therapy, the clinical cases of the regression of the CHD symptoms are explained, first of all, by the regression of the non-fibrous atherosclerotic formations. There is a need to dedicate specific attention to the pathogenetic concept, according to which the development of the atherosclerosis represents the inflammatory reply of a vascular wall initiated or provoked at an aggravation by the infectious agents. The presence of the high plasma levels of the S-jet protein as well as other markers of the nonspecific inflammatory reaction correspond to the increase of the “ischemic” episodes. The pathogenic role of such infectious agents as Chlamydia pneumoniae, Helicobacter pylory, and a cytomegalovirus are rather powerful (Leon & Bronas, 2009, p. 383). Thus, there is the regularity of the decline of the CHD symptoms caused by the decrease of the atherosclerotic formations.

At the expressed coronary atherosclerosis and even full occlusion of the coronary arteria, the clinical symptoms can be not obvious, as there is no accurate communication between the prevalence of the anatomic changes and the expressiveness of the clinical symptomatology. The assessment of the prevalence and localization of atherosclerotic formations is possible to perform only by means of a coronary angiography. However, it is possible to prove the existence of the HCD with the help of other, less invasive methods (Goblirsch et al., 2013, p. 12).

The increase of the need of the myocardium for oxygen is the prevailing ischemia mechanism. On the other hand, the acute coronary syndromes of the unstable stenocardia and myocardial infarction are caused by the rupture of the atherosclerotic formations, aggregation of platelets, and the intravascular thrombosis (Singh, et al, 2012, p. 252). There is the tendency of emergence of similar episodes in early morning hours or directly after awakening. The outcomes of any of these coronary events are predetermined by the development of a full occlusion of a vessel, or, on the contrary, thrombolysis – both spontaneous or as a consequence of the therapy with the subsequent gradual stabilization of the earlier “vulnerable” atherosclerotic plaque (Warnica, 2013).

Some episodes of the HCD may be painless; the others can be accompanied with the classical stenocardia course – the Baumes’s symptom; the majority of the CHD cases are induced by the physical or mental activity (Singh, et al, 2012, p. 253). As for the patients with HCD, demonstrating the myocardial infarction or stenocardia, the episodes of the painless ischemia have the same predictive value as well as the classical anginous attacks.

To conclude, it is evident that the CHD can be the result of either the increase of the myocardium for oxygen (a physical or mental overwork), or spontaneous changes of the heart rhythm frequency, or the decrease in the delivery of the oxygen, caused by the coronary spasm, blockage by thrombocytes, or partial thrombosis. The malfunction of the endothelia affects the change of a threshold of ischemia development. The main factor of the relaxation of endothelia – the violations of the nitrogen oxide release – can promote the development of vasoconstriction and facilitate the adhesion of platelets.

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