Anatomy and Physiology of Coronary Artery Anomalies - Essay Example

The group of cardiovascular diseases is the permanent leader amongst the causes of deaths. By the assessment of CDC (Center of Disease Control) coronary heart disease and stroke make nearly 40% of all deaths in the United States. In other words more than 900,000 Americans die of coronary artery disease or stroke while more than 25% of US population suffering the cardiovascular disease (CDC, 2005). Furthermore, in our country there are more than 23 millions of non-institutionalized adults suffering heart disease and nearly 4 millions of people treated in hospitals due to coronary artery disease. 696,947 deaths in 2004 were registered as the direct consequence of coronary artery disease. This is an evidence of the highest pertinence of this disease for modern civilization. But what is anatomical and physiological background for coronary heart disease developing How knowledge of anatomy and physiology could be used for management this serious health condition Coronary heart disease can be determined as "an imbalance between myocardial functional requirements and the capacity of the coronary vessels to supply sufficient blood flow" (MESH, 2005). Decreased capacity of the coronary vessels to supply sufficient blood flow leads to myocardial ischemia, i.e. the shortage of blood flow in cardiac muscle. The requirements of myocardium in blood (and correspondingly in oxygen and nutritive substances) is the highest among other organs and tissues of human body. There is known that normal myocardial perfusion (blood flow) is equal to 0.80.06 ml/min per gram of myocardial tissue (Porenta et al., 1999) at rest and can rise in several times during vigorous physical efforts or stress. Thus obstruction or spasm of coronary vessels significantly restrict functional capabilities of heart muscle and can be resulted in the medical emergencies. The coronary circulation consists of the coronary arteries and veins together with the lymphatics of the heart. The coronary arteries are the first branches of the ascending portion of the aorta arising from the aorta root immediately above its attachment to the heart. Normally, there are three aortal sinuses but only two coronary arteries (left and right) arising from the aortic sinuses (Fuster et al., 2004). The left coronary artery divides into two branches (the left anterior descending artery and the circumflex branch) supplying blood to both heart ventricles and left atrium. In 37% of the general population so called ramus intermedius occurs which is an anastomosis between left anterior descending artery and the circumflex branch of left coronary arteria. The right coronary artery with its branches (the right posterior descending artery and a large marginal branch) supplies blood to the ventricles, right atrium and sinoatrial node (Braunwald et al., 2004). If work out in the details which regions of supplying are characteristic for the different coronary arteries and their branches we can see that the circumflex artery supplies blood to the posterior side of the heart and left anterior descending artery supplies blood to the anterior part of the heart including heart apex, and interventricular septum. There is known that left anterior descending artery is dividing into the septal and diagonal branches (Fuster et al., 2004). The septals derive from the left anterior descending artery at 90 to the surface of the heart. These branches also perforate and supply blood to the intraventricular septum. Diagonal branches run along the heart surface. They supply blood to the lateral wall of the left ventricle and to the papillary muscles. Another branch of the left coronary artery, the circumflex artery participates in supplying blood to the papillary muscles and to the back of lateral parts of the left ventricle. In 38% of the general population this branch is responsible also for supplying blood to the sinoatrial node. Contrarily to the branches of left coronary artery, the right coronary artery plays role in supplying blood to the right ventricle mainly, but nevertheless 25-35% of blood required by the left ventricle is supplied by the branches of right coronary artery (Fuster et al., 2004). Other important anatomical vascular structure is the posterior descending artery, which is originated from the right coronary artery in 85% of cases and relatively infrequently (other 15% of cases) can be originated from the left circumflex artery. This artery participates in blood supply to the inferior wall of the heart, ventricular septum, the papillary muscle and to the sinoatrial node (in 60% of cases). The RCA also supplies the SA nodal artery in 60% of patients (Fuster et al., 2004). Dependently on the role of the branches of left and coronary arteries in supplying blood to the heart structures the general population can be classified as the "right-dominant" or "left-dominant". The dominance is estimated as the relationship to the source of posterior descending artery (Fuster et al., Braunwald et al., 2004). If pathological process injures the "dominant" artery the consequences are more threatening. By the statistics there are 70% of right dominant persons, 20% - co-dominant and only 10% - left dominant ( ). There is an interesting issue of the character of supplying blood to the papillary muscles. These muscles tie to the atrioventricular valves - mitral and tricuspid, and their weakness can lead to blood regurgitation during the systole (the contraction of the ventricles). Because posteromedial papillary muscle is supplied with blood only from one source (posterior descendent artery) whereas anteromedial papillary muscle receives blood supply from two sources (left lateral descending artery and circumflex branch) than the posteromedial papillary muscle is more susceptible to ischemia (Angelini, 2002). Correspondingly, if this muscle will be injured the mitral regurgitation signs can occur (Fuster et al., 2004). Further discussion of pathophysiologic peculiarities of coronary artery disease require understanding the fact that the shortage of blood flow in particular artery will cause degenerative changes in the appropriate zone of heart muscle. This can lead to anginal chest pains and in the severest cases could result in death. Blood circulation in the system of coronary arteries depends on a plenty of factors. During systole the subendocardial coronary vessels entering to the inner layer of the myocardium are compressed. This compression is caused by the high intraventricular pressures. In other words, there is no blood flow in the subendocardial part of the myocardium during the systole. Consequently the perfusion of subendocardial myocardium is possible only during the diastole, when heart muscle is relaxed. Any changes in the conditions of coronary vessels can manifest in the ischemia, e.g. an absolute or relative shortage of the blood supply. There are several scenarios of the occurrence of myocardial ischemia. The first one can be described by the reduction of coronary blood flow due to the stenosis of coronary artery/arteries. This variant is the most frequent. Rarely the myocardial ischemia results the abnormal constriction of coronary vessels or related to the deficient relaxation of coronary microcirculation. Finally, severe anemia or other conditions characterized with the reduced oxygen-carrying capacity of the blood could cause myocardial ischemia also. In severe cases prolonged ischemia leads to necrosis (death of cells). Thus ischemia is associated with the risk of irreversible lesion of heart muscle. By the definition using in the MESH database, the myocardial infarction is a "gross necrosis of the myocardium, as a result of interruption of the blood supply to the area" (MESH, 2005). The interruption of blood supply often is caused by the thrombus appearing in the vessels damaged by the atherosclerotic process. The occlusion by the blood clot can be total or subtotal. An atheroma, the atherosclerotic plaque on the artery walls, changes mechanical resistance and elasticity of the vessel. This narrow spot will make the blockage of blood supply more likely. Thrombus resorption may be followed by collagen accumulation and smooth muscle cell growth. Thus the blood clot will form on the atheroma easier. Sometimes a clot forms in the cavity of the heart and goes in a coronary artery with the flow of blood. Rarely myocardial ischemia can be caused by the spasm of the coronary arteries. Slowly accruing stenosis of epicardial coronary arteries may proceed to complete occlusion but do not usually lead to the myocardial infarction because of the development over time of a rich collateral network. With time the resultant thrombus can completely occlude the epicardial infarct artery. If there is an insufficient collateral supply, a wave front of myocardial necrosis begins within 15 minutes and spreads from the endocardium toward the epicardium. This may be modulated by the extent of collateral flow and determinants of myocardial oxygen consumption, affording opportunity for significant myocardial salvage. The main determinants of acute myocardial infarctions are an acute parietal vascular lesion; local coronary vasoconstriction and a platelet and fibrin thrombus. The coronary spasm and the thrombotic cascade can be triggered by the parietal fissuration i.e. lesion of vessel wall (Golino et al., 2002). A key concept in the pathophysiology of acute myocardial infarction is ventricular remodeling - changing size, shape, and thickness of the ventricle walls involving both the damaged and intact segments of the ventricle (Tardif, 2005). Acute dilatation and thinning of the area of infarction that is not due to additional myocardial necrosis is referred to as infarct expansion. An extraload is placed on the residual functioning myocardium, which results in compensatory hypertrophy. Thus inhibition of the renin-angiotensin-aldosterone system is a key therapeutic maneuver in patients with infarction (Fuster et al., Kasper et al., Braunwald et al., 2004). Additional important pathophysiological concepts in patients with infarct include cardiac arrhythmias such as those that result from electrical instability, pump failure/excessive sympathetic stimulation, and conduction disturbances. Mechanical problems that result from dysfunction or disruption of critical myocardial structures (e.g. mitral regurgitation, rupture of the interventricular septum, formation of ventricular aneurysm i.e. dilatation of ventricle wall, and free wall rupture) may require a combination of pharmacological, catheter-based, and surgical treatments (Fuster et al., 2004). Fortunately myocardial infarction is not so common condition; the most of people suffering chronic coronary artery diseases has symptoms of angina pectoris. This disease is characterized with chest pain irradiating (spreading) into the left arm, jaw and other organs. Sometimes the patients characterize their sensations as not pain but discomfort. Nevertheless the retrosternal localization of chest pain or discomfort, its relationship to the physical efforts or stress, the effectiveness of anti-anginal medications (e.g. nitroglycerin) is very suspicious for angina pectoris (Braunwald et al., 2004). Stable form of angina has predictable character - heart attacks occur after vigorous physical activity, awakening or stress while unstable angina is characterized with the changeability of character, frequency and/or intensity of heart attacks. Other forms of angina pectoris are presented by the Prinzmetal type and so called X syndrome. Prinzmetal's type of angina is characterized with specific changes of the electrocardiogram due to the spasm of coronary vessels. This type of angina can occur in those have focal deficiency of nitric oxide production, patients suffering with hyperinsulinemia (high level of insulin in the blood) or/and low intracellular magnesium levels; smoking tobacco, and using cocaine (Lip et al., 1998). The term syndrome X is used for episodes of myocardial ischemia in the absence of organic disease of coronary diseases (Fuster et al., 2004). Nevertheless the absolute majority of angina cases are related to the atherosclerotic lesions of the coronary vessels. There is known that arteriosclerosis results the disorders of lipid metabolism. High intake of cholesterol with food ad well as increased endogenous synthesis of cholesterol can lead to the lesions of vessels (Fuster et al.; Kasper et al.; Braunwald et al., 2004). Nowadays there are determined several risk factors for arteriosclerosis development. They include a family history of coronary artery disease (especially if the cases occurred in relatively young age), tobacco addiction, systemic hypertension, diabetes mellitus and idiopathic hypercholesterolemia (high level of serum cholesterol). Obesity, congenital disorders of lipid metabolism, metabolic syndrome also associated with increased risk of atherosclerosis (Fuster et al., 2004; Richter et al., 2005). Correspondingly for preventing coronary artery disease we can effectively use health promotion, smoking cessation, weight control and other simple interventions (Fuster et al., 2004; ). In the cases when treatment and rehabilitation is required the character and localization of pathological processes caused symptoms of angina pectoris should be taken into the account. Currently, the most effective approach in the treatment of coronary artery disease is surgery. There are two main variants of surgical procedures using widely for coronary revascularization (renewing blood supply) - percutaneous transluminal coronary angioplasty (PTCA), with or without coronary stenting, and coronary artery bypass grafting (Fuster et al., 2004). Both methods are considered in patients with the stenosis of the left coronary artery greater than 50% of its diameter, in patients having occlusion/stenosis of 2 or more coronary vessels and in those having the signs of left ventricular insufficiency and other severe symptoms regardless of intensive medical therapy. Pharmacotherapy (use of medications for treatment) based on several approaches. The newest is risk modification for complications of atherosclerosis by the use especial medications inhibiting synthesis of endogenous cholesterol. Nevertheless classical use of anti-anginal drugs e.g. organic nitrates, beta-adrenoblockers and blockers of Ca-channels (Braunwald et al., 2004). But the discussion of mechanisms of their action is out of the objectives of this short review. References: 1. 13Angelini P. Coronary artery anomalies--current clinical issues: definitions,classification, incidence, clinical relevance, and treatment guidelines. Tex Heart Inst J. 29(4): pp. 271-278. 2002; 2. Braunwald et al. Heart disease: a textbook of cardiovascular medicine. W.B. Saunders Company, 7 ed., 2004 2288 p. 3. 13CDC (2005) Heart Disease Statistics Available at the web-site http://www.cdc.gov/nchs/fastats/heart.htm Accessed on 12/07/2005 4. Fuster et al. Hurst's The Heart. McGrwa-Hill Professional 11 ed. 2004 2400 p. 5. Golino, Grea & Willerson How to study the effects of platelet aggregation and thrombosis on coronary vasomotion and their clinical relevance Italian Heart Journal 3 :pp. 220-225; 2002; 6. Harrisons' Principles of Internatl Medicine McGrwa-Hill Professional. 16th ed. 2004 2607 p. 7. 13Lip GY, Ray KK, Shiu MF. Coronary spasm in acute myocardial infarction. Heart. 80(2):197-199. 1998 Aug; 8. 13MESH (2005) Available at the web-site http://www.ncbi.nlm.nih.gov/entrez/query.fcgicmd=Retrieve&db=mesh&list_uids=68003327&dopt=Full Accessed on 12/07/2005 9. 13Porenta et al. Noninvasive determination of myocardial blood flow, oxygen consumption and efficiency in normal humans by carbon-11 acetate positron emission tomography imaging European Journal of Nuclear Medicine and Molecular Imaging Volume 26, Number 11 P:1465 - 1574 October 1999 10. 13Richter S et al. Prevention of sudden cardiac death: lessons from recent controlled trials. Circ J. 69(6): 625-629. 2005 Jun; 11. 13Tardif JC. Atherosclerosis imaging. Can J Cardiol.; 21(12): 1035-1039 2005 Oct Read More