Discuss About The Anatomy And Function Of Coronary Arteries?
Coronary heart disease (CHD), also known as ischaemic heart disease or coronary artery disease is a common form of heart disease characterised by the gradual accumulation of fatty material (plaque) within the walls of the coronary arteries. The build-up of plaque results from a process known as atherosclerosis which is influenced by lifestyle habits such as high cholesterol and smoking, and conditions such as diabetes and hypertension (Nichols, Peterson, Herbert, & Allender, 2015). CHD in its two major clinical forms (angina and myocardial infarction) is the largest contributor to cardiovascular disease (CVD) (Australian Institute of Health and Welfare, 2012)
The condition is responsible for a significant amount of morbidity and mortality globally. In 2015 alone, CHD affected more than a hundred million people and resulted in close to nine million deaths (GBD 2015 Disease and Injury Incidence and Prevalence Collaborators, 2016); accounting for more than fifteen percent of all deaths worldwide. As a result, it ranks at the most common cause of mortality worldwide (GBD 2015 Mortality and Causes of Death Collaborators, 2016). CHD affects approximately 1.2 million Australians. It stands out as the single leading cause of death in Australia, accounting for more than ten percent of all deaths in the country. For instance, in 2015, it accounted for 19, 777 deaths, an equivalent of 12% of all deaths in that year (Australian Bureau of Statistics, 2016).
This paper reviews various aspects of this condition including the anatomy and physiology of the involved systems, its aetiology, clinical presentation, the investigative procedures adopted for the diagnosis, and its management and treatment with more focus on its pharmacology treatment.
Coronary vessels have a different anatomy and physiology compared to the rest of the vessels of the circulatory system. Coronary arteries are much smaller, tortuous vessels which supply the myocardium with blood. The left main coronary artery (LCA) and the right coronary artery (RCA) originate from the aorta as separate vessels and not as a single trunk (Lüdinghausen, 2012). Whereas the LCA rises from the posterior coronary cusp, the RCA arises from the anterior coronary cusp. The course taken by the two large vessels (RCA and LCA) is also different as shown in Figure 1 below.
The RCA supplies blood to the right ventricle and atrium, and the atrioventricular and nodes which serve the role of regulating the heart’s rhythm (Spaan, 2012). The RCA further branches into smaller branches which include the acute marginal artery and the right posterior descending artery. It also teams up with left anterior descending anterior to form the septal perforator (SP) which supplies blood to the septum. The LCA supplies blood to the left ventricle and atrium. It further branches into the left anterior descending artery that supplies blood to the front of the left side of the heart, and the circumflex artery which supplies blood to the back and outer side of the heart. Other smaller branches of the coronary arteries include diagonals, and the obtuse marginal (OM).
Atherosclerosis affects both the structure and function of the coronary arteries. Plaque narrows the arteries (as shown in figure 2 above), and as a result, the blood flow to the myocardium is also reduced. The build-up of plaque also increases the likelihood of blood clots forming in the arteries. The clots can somewhat or totally block the blood flow to the myocardium (ischemia). These processes lead to an imbalance between oxygen supply and oxygen demand. With insufficient oxygen supply to meet the demand, the myocardium becomes hypoxic and this often translates to angina (chest pain) or a heart attack.
A review of literature demonstrates an association between coronary heart disease and certain factors which contribute to atherosclerosis. These factors increase the intrusion of fat into the walls of the arteries. The various risk factors create different risk associations and there is a likelihood that they may be interacting together. The risk factors include both fixed risks (gender, family history, age, ethnicity and lower and middle socioeconomic groups), and modifiable risks (cigarette smoking, hypertension, diabetes mellitus, excessive alcohol intake, central obesity, lipid abnormalities such (high LDL cholesterol and triglycerides, low HDL), physical inactivity, and psychosocial issues (Gupta, Joshi, Mohan, Reddy, & Yusuf, 2013). Research suggests that an individual’s risk is as a risk of the total risk and not just individual risk factors as the existence of the risk factors has a synergistic effect.
Smoking leads to the exposure of heart and blood vessels to nicotine and carbon monoxide which in turn causes constriction of blood vessels, increase in blood pressure and a rise in cholesterol levels. It also deprives the body’s tissues of oxygen and this allows the growing of plaques.
Hypertension can lead to the damage of blood vessels hence increasing the chances of plaques forming. High blood pressure also causes arterial walls to thicken and stiffen, and less able to undergo expansion and contraction in line with body activity and other physical demands.
Diabetes is characterised by high levels of glucose in blood that can cause harm to blood vessels, and this increases the risk of developing atherosclerotic plaques. Evidence from research studies actually shows that one out of every three persons with diabetes also has CHD (Mohammed, Narayan, & Tandon, 2013).
Excessive alcohol intake – Individuals who drink moderately (3 units/day for males and 1 unit/day for females) have a lower mortality from CHD compared to non-drinkers (Mukamal & Rimm, 2016), whereas binge drinking above these levels increases the risk for CHD due to the increased risk for the development of high blood cholesterol and hypertension.
Hyperlipidaemia – The risk of CHD is increased with the level of cholesterol in the blood. Cholesterol levels, on the other hand, are dependent on factors such as diet, exercise, genetics, and some diseases.
Obesity puts more strain on the heart, and also makes it difficult in controlling blood pressure, diabetes and high cholesterol levels. According to Khosravi, et al., (2012), obesity increases the risk for cardiovascular disease by 46% in males and 645 in females.
Physical inactivity weakens the muscles and makes it harder to control other risk factors for cardiovascular disease which include obesity, diabetes, blood pressure and cholesterol levels.
Psychosocial issues such as stress, anxiety, depression and social isolation are also claimed to be risk factors for CHD (Khayyam-Nekouei, Neshatdoost, Yousefy, Sadeghi, & Manshaee, 2013). Symptomatic CHD can be triggered by acute events such as the loss of a loved one, and catastrophic events such as a terrorist attack.
Gender – Males are at increased risk of developing cardiovascular disease than females, but the difference seems to disappear after the onset of menopause (National Institutes of Health, 2016).
Family history – An individual’s risk for CHD is doubled if a parent or sibling developed cardiovascular disease early in life (before age 55 for males, and 65 for females) (National Institutes of Health, 2016).
Age – The risk of CHD increases with the increase in age (National Institutes of Health, 2016). For males, the risk is heightened from about 45 years and above and is doubled at 55 upwards. For females, the risk is heightened as from age 55 upwards.
Ethnicity – The risk for CHD has shown to be increased among persons of African Caribbean heritage, followed by Hispanics and South Asians (Leigh, Alvarez, & Rodriguez, 2016)
Socioeconomic status – It is an established fact that socioeconomically disadvantaged groups have a higher prevalence of CHD and CVD mortality (Psaltopoulou, et al., 2017). The gradient incidence of this morbidity and mortality is attributed to differences in income, occupation, and educational status.
The most prevalent CHD symptom is angina pectoris/chest pain. Approximately thirty percent of adults who present o the emergency department with an unclear cause of pain, the pain is often attributed to CHD (Kontos, Diercks, & Kirk, 2013). Angina is also described as “chest discomfort, heaviness, tightness, pressure, aching, burning, numbness, fullness, or squeezing” (WebMD, 2017). It is often felt in the chest but may radiate to other parts including the shoulder, arms, neck or jaw. Angina results from the partial blockage of coronary arteries. This symptom is usually triggered by physical activity or emotional distress.
Angina may present in any of its variants. Stable angina is characterised by a short-term discomfort resembling indigestion. A stable angina occurs when the heart is working harder than usual such as in an event of physical activity. It has a regular pattern. Unstable angina, on the other hand, occurs during rest, it is severe, last longer, and often worsens with time. It is referred to as unstable owing to the changes in intensity, character, and frequency.
Shortness of breath may also result from the heart’s incapacity to pump adequate blood to meet the body’s demands. This symptom may also be accompanied with extreme fatigue with exertion.
Heart attacks result if the arteries become completely blocked. Myocardial infarctions can cause permanent damage to the heart muscles if they are not treated immediately, and can also be fatal. Signs and symptoms of an MI include chest discomfort, dyspnoea, light-headedness, sweating, nausea.
Electrocardiogram (ECG or EKG) detects and records the heart’s electrical activity. An ECG shows the heart beat rate, its rhythm, and also the strength and timing of electrical signals passing through the heart (Saint Thomas Health, 2015).
Echo is a procedure that uses sound waves for the evaluation o he heart’s structure and function. Echo provides information on the systolic and diastolic function, condition and function of valves, contractility, can also measure the pressure of pulmonary vessels (Heart Foundation, 2014).
Stress testing is done with heart stimulation, using either exercise on a treadmill, with a connection to an ECG. Stress testing helps identify possible signs and symptoms of CHD including myocardial ischaemia, electrical instability or any other signs and symptoms related to exertion (dyspnoea, abnormal changes in blood pressure and heart rate) (Garber, Hlatky, Chareonthaitawee, & Askew, 2017). Stress testing can also be induced using medications in cases where the patient cannot endure exercise tests.
It is the most accurate way of defining the presence and severity of CHD. The process investigates the integrity of the coronary arteries by inserting a catheter into the coronary vasculature and the use of a contrast medium to produce images. Coronary angiography yields information on the extent of the vessel narrowing an also the culprit lesions (Gorenoi, SchönermarK, & Hagen, 2012). This information is vital for the treatment and management of the presentation.
A chest x-ray aid in the investigation of the cause of dyspnoea (cardiac or respiratory) (Heart Foundation, 2014). A CXR can help reveal causes of symptoms of CHD, alongside lung disorders.
Blood tests may also be carried out to check the levels of cholesterol, glucose, proteins, and fats in the body. Abnormal levels are indicative of increased risk for CHD. Recommended basic screening involves testing for fasting blood glucose, a full blood count, serum lipids including high-density lipoproteins (HDL) and triglycerides, serum urates and blood urea and electrolytes (Ministry of Health and Quality of Life; Mauritius Institute of Health; World Health Organisation, 2015).
This procedure is used for the detection of abnormal electrical conduction, abnormal cardiac rhythm, and ischaemic changes even in asymptomatic cases (Galli, Ambrosini, & Lombardi, 2016).
Thallium is a radioactive substance which is injected into a vein and then taken up by cardiac muscles. In the case of narrowed coronary arteries, less thallium reaches the muscles (Saint Thomas Health, 2015). This procedure helps detect significant coronary artery narrowing, and also damage to cardiac muscles due to a heart attack.
Cardiac MR involves the use of magnetic and radiofrequency fields to produce high-resolution images of the heart and its vasculature. The procedure provides information on the structure, function, perfusion, and viability of cardiac muscles, and also on the coronary arteries and peripheral vessels (Saint Thomas Health, 2015).
There are two key goals in the treatment and management of CHD. First, it is to prevent myocardial infarction and death, as a result, improve life expectancy, and secondly is to reduce the symptoms of angina and the occurrence of ischaemia, for improved life quality (Ministry of Health and Quality of Life; Mauritius Institute of Health; World Health Organisation, 2015). The cornerstone therapy for CHD includes both medical therapy accompanied with aggressive cardiovascular risk modification. As such, the treatment strategies can be divided into medical treatment, coronary interventions (angioplasty, coronary stent), coronary artery bypass grafting (CABG), and education and risk factor modification (Kasper, et al., 2015). These interventions are aimed at lowering the risk of formation of blood clots, prevention of CHD complications, reducing risk factors so as to prevent stop, slow or reverse plaque build-up, symptoms relieve, and widening or bypassing of the clogged vessels.
Under cardiovascular risk modification, the doctor may recommend heart-healthy lifestyle changes. These changes include a heart-healthy eating (consumption of low-fat dairy products, fruits, legumes, vegetables, whole grains and omega-3-rich fish), limiting alcohol, maintaining healthy weight, quitting smoking, managing stress and any other form of psychosocial factors, and routine physical activity (Mannu, Zaman, A Gupta Rehman, & Myint, 2013). These lifestyle changes can help reduce the risk of further angina or MI episodes.
Lifestyle changes alone are not sufficient to control factors precipitating atherosclerosis. Therefore, medicines are indicated to either reduce the blood pressure or widen the coronary arteries. Different classes of medicines are used. They include
Medical and surgical interventions may also be sought if the symptoms cannot be controlled using pharmacological means. Blocked arteries can be opened up or bypassed using coronary angioplasty (also known as percutaneous coronary intervention (PCI), or coronary artery bypass grafting (CABG) (Ministry of Health and Quality of Life; Mauritius Institute of Health; World Health Organisation, 2015). CABG involves the use of autologous arteries or veins as grafts to bypass coronary arteries partially or completely obstructed by plaques (Alexander & Smith, 2016). The procedure is quite effective for the durable relief of angina, and it significantly improves the survivability in patients with CHD (Go, et al., 2013). PCI, on the other hand, is used to open up coronary arteries narrowed or blocked by plaques using catheterization.
Beta-blockers e.g. Acebutolol
They are also known as beta-adrenoceptor antagonists. They offer competitive antagonistic action on beta-adrenoreceptors (B1, B2, and B3) (Frishman, Cheng-Lai, & Chen, 2013).
They are used in the treat cardiac arrhythmias, management of angina, prevention of myocardial infarction, and also the treatment of hypertension (Gorre & Vandekerckhove, 2012).
Beta-blockers function by antagonising the effects of sympathetic nerve stimulation of circulation of catecholamines at beta-adrenoceptors throughout the body (Kaplan, 2015; Frishman, Cheng-Lai, & Chen, 2013). B1 receptors are predominantly found in the heart and kidney whereas [email protected] receptors are found in the lungs, skeletal muscles and peripheral vasculature. With relevance to CHD, beta-blockers block B1 receptors of the heart, at the Sino-atrial node and this reduces heart rate, and also blocking the B1 receptors in the myocardium to reduce contractility (Frishman, Cheng-Lai, & Chen, 2013). The mode of action of beta-blockers as an antihypertensive agent is still debated. However, it is postulated that the effects of decreased heart rate and cardiac output affect blood pressure.
All beta-blockers are contraindicated in persons presenting with asthma and chronic obstructive pulmonary disease (COPD) (Kaplan, 2015).
According to Frishman, Cheng-Lai, and Chen, (2013), beta-blockers may produce the following side effects.
Revascularization techniques such as the CABG procedure may produce cardiac complications. These may include perioperative myocardial infarction, arterial infarction is a common complication of CABG and it can lead to the development of blood clots in the heart that may travel to the rest of the body, the “Post-pericardiotomy syndrome” (fever and chest pain) may also occur, and kidney failure (Aranki, Cutlip, & Aroesty, 2016). Possible complications in coronary angiography include Heparin-Induced Thrombocytopenia (HIT) which is an immune-mediated complication of administering heparin from heparinised saline (Tavakol, Ashraf, & Brener, 2012). Another complication may be contrast-induced nephropathy which is defined as a rise in serum creatinine due to the effects of contrast media on vasoactive substances such as endothelin (Tavakol, Ashraf, & Brener, 2012). The distal embolization of cholesterol crystals following PCI may also cause a systemic syndrome. There is also the risk of hematoma and retroperitoneal haemorrhage resulting from poorly controlled haemostasis after femoral sheath removal (Tavakol, Ashraf, & Brener, 2012).
The pharmacological treatment process may also produce some complications. These may include a bleeding risk in individuals with an underlying haemostatic defect and gastrointestinal toxicity due to the administration of antiplatelet agents such as aspirin (Casado-Arroyo, Sostres, & Lanas, 2013).
Conclusion
CHD is a common disease in the western countries with a significant burden of morbidity and mortality. It results from atherosclerotic plaque deposition which is facilitated by a number of risk factors; both modifiable and non-modifiable. The goals in the management of the condition are to prevent the occurrence of angina, myocardial infarctions, and slowing down, stopping or preventing the development of plaques. Management of the condition requires both pharmacological, medical and surgical interventions and lifestyle changes.
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