Purpose of this paper is to analyze a given case-study, considering patient’s clinical picture. Furthermore, this paper stands for diagnosis of possible pathology, mechanisms of experienced symptoms and ultimately, possible outcomes and complications including individual’s prognosis.
At the first site, the age of a patient must be taking into account as one of the possible risk factors for a pathology. Ageing has a great impact on the human body. The decline in cardiovascular function is one of the factors suggested by Houghton D. et al (2016). Patient’s medical history relates increased cholesterol levels and mild hypertension. Increased cholesterol levels consequently, increase the risk for developing heart disease. High blood pressure and hypercholesterolemia are linked, as hypertension may be a result of deposits of LDL cholesterol in the arteries. This process is known as atherosclerosis and will be discussed later on in this paper. If the deposits of LDL cholesterol are located on the endothelium of coronary arteries an individual may experience chest pain or anginal pain. This pain is usually associated with hypoxic heart muscle due to blockage, narrowing or obstruction of the arteries that supply blood to the myocardium. Chest pain may also be a result of other conditions. Sigurdsson A.(2017) suggested that pulmonary embolism is accompanied by cough, shortness of breath and chest pain that gets worse when breathing; pneumothorax presents its symptoms as shortness of breath and sudden onset of chest pain that also is worsening by breathing; patients with pneumonia experience chest tightness with fever and productive cough; pleuritis is a condition resulting in sharp and stabbing chest pain associated with worsening when moving, sneezing or coughing; pulmonary hypertension is associated with prominent chest pain on exertion including shortness of breath; individuals with aortic dissection usually present with abrupt and severe onset of chest and back pain; pericarditis is also a cardiac condition that is accompained by sharp, stabbing and sudden pain behind the sternum which tipically worsens when lying down or breathing in. Chest pain may also arise from musculoskeletal, gastrointestinal and psychiatric causes, however, these conditions are accompanied by other symptoms which are not present in the case-study.
After analyzes of clinical features of the individual, it is most likely to be a cardiac condition. As there is not enough evidence to conclude about different pathology, the individual is possibly suffering from angina pectoris.
Angina pectoris can be defined as a chest pain or discomfort due to coronary heart disease. In the majority of the cases, the underlying cause of angina is atherosclerosis of one or more coronary arteries which supply oxygenated blood to the heart muscle. Other conditions include hypertrophic cardiomyopathy (enlargement and thickening of myocardium), aortic stenosis (narrowing of the aortic valve) and hypertension.
During rest, when a demand for the oxygen is lower, extremely narrowed arteries may permit enough amount of blood to reach the heart muscle – although, it does not occur with physical exertion (American Heart Association, 2015). Risk factors for developing angina pectoris include lack of exercise, obesity, tobacco use, high blood pressure, high blood cholesterol, history of heart disease and stress (Mayo Clinic, 2016).
Mattson P.C. (2015, pp.446-456) suggested that coronary artery disease is divided into two major groups: 1. Stable Angina which is associated with a fixed atherosclerotic obstruction and pain that is induced by exercise and relieved by rest; 2. Acute coronary syndromes that include unstable angina (occurs at rest), Non-ST-segment elevation myocardial infarction (MI) and ST-segment elevation MI. Mattson P.C (2015, pp.446-456) also mentioned that Chronic ischaemic heart disease is divided into 3 groups: chronic stable angina, silent myocardial ischemia which occurs with an absence of symptoms and variant or vasospastic angina occurs at rest and usually during nighttime.
· MECHANISMS OF SYMPTOMS
According to Morris P. and Warriner D. (2015), Ischaemic heart disease arises from the development of atherosclerotic plaques in the coronary arterial lumen. Thus, Lilly (2011, pp.144-147) said that the pattern of symptoms is usually related to the degree of stenosis. When the oxygen demand exceeds available supply, myocardial ischemia results and it is commonly accompanied by the chest discomfort of angina pectoris (Lilly,pp.144-147, 2011).
As suggested by Cross, Gallagher and van der Wal (2013), coronary artery disease affects large and medium-sized arteries. The formation of lesions starts in young kids and therefore the earliest significant lesion is termed a fatty streak. Response to injury hypothesis suggests that atherosclerosis arises from seven pathogenic events. These include: ”1-Endothelial cell (EC) injury, which allows entry and modification of lipids in the vessel subintima; these lipids then serve as pro-inflammatory mediators that initiate leukocyte recruitment and foam cell formation (Yelle, Chaudhry and Wong, 2012). EC loss due to different types of injury leads to intimal thickening, however, early human coronary-artery disease lesions begin at sites of intact, however dysfunctional, endothelium. These dysfunctional ECs exhibit enhanced permeability, increased white blood cell adhesion, and altered gene expression, all of which can contribute to the development of atherosclerosis. Nevertheless, the two most significant causes of endothelial dysfunction are hemodynamic disturbances and hypercholesterolemia. In vitro studies demonstrate that nonturbulent laminar flow ends up in the induction of endothelial genes whose products shield against atherosclerosis; 2-Accumulation of lipoproteins(mainly oxidized LDL and cholesterol crystals) within the vessel wall; 3-Platelet adhesion to damaged blood vessels, as an important part of homeostasis; 4-Monocyte adhesion to the endothelium, migration into the intima, and differentiation into macrophages and foam cells. Upon getting into the intima, monocytes differentiate within phagocytic macrophages then upregulate their manifestation of scavenger receptors in response to local macrophage colony-stimulating factor (Yelle et al, 2012). Scavenger receptors mediate the uptake of modified LDL into macrophages. Macrophages develop into foam cells which produce extra cytokines that perpetuate the process of atherosclerotic plaque formation(Yelle, Chaudhry and Wong, 2012); 5-Lipid accumulation inside macrophages, which respond by releasing inflammatory cytokines; 6- Smooth muscle cell recruitment due to growth factors (TNF-?, IL-1, FGF, TGF-?) and cytokines discharged from activated platelets, macrophages and vascular wall cells; 7-Smooth muscle cell proliferation and extracellular matrix production” (Kumar, Abbas and Aster, 2018). As mentioned by Yelle, Chaudhry and Wong (2012), SMC activation and cytokine release reinforces and keeps inflammation in the lesion, therefore, fatty streak evolves into a fibrofatty lesion. Yelle et al., (2012) also add that calcification may appear at later stages and fibrosis continues. Late plaque increase may considerably restrict the vessel lumen and obstruct perfusion. Thus, flow-limiting plaques can lead to tissue ischemia, producing symptoms such as angina pectoris or claudication (cramping or pain in the lower leg resulting from improper blood flow).
As mentioned above, atherosclerosis has the similar pattern of chronic inflammation.
It may develop as a result of a recurrent yet progressive acute inflammatory process. Instead of vascular permeability changes, edema, and predominantly neutrophilic infiltration seen in acute inflammation, chronic inflammation is characterized by infiltration including mononuclear cells (macrophages, lymphocytes, and plasma cells) and attempted connective tissue repair involving angiogenesis and fibrosis (Mattson C., 2015). Although it may additionally follow acute inflammation, chronic inflammation generally begins insidiously as an assymptomatic low-grade process. National Cancer Institute (2015), adds that over time, chronic inflammation can cause DNA damage and lead to cancer.
Classic signs of inflammation include redness (vasodilation and increased blood flow to the site where inflammation takes place), swelling ( accumulation of leukocytes), heat ( increased temperature), loss of function and pain. Studies have shown that the cause of anginal pain may be adenosine as the main chemical mediator. Alaeddini (2016), mentioned that during ischemia, ATP is degraded to adenosine, which, after diffusion to the extracellular space, causes arteriolar dilation and anginal pain. Adenosine induces angina mainly by stimulating the A1 receptors in cardiac afferent nerve endings (Mitchel and Sidawy, 1998). Symptoms usually occur when superior lesions are complicated by way of plaque rupture, hemorrhage into the plaque, emboli ( the unattached mass that travels through the bloodstream), and thrombosis(blood clot which obstructs the blood flow) (Mitchel and Sidawy,1998).
· COMPLICATIONS AND PROGNOSIS
Cross, Gallagher and van der Wal (2013) said that over a lifetime, atherosclerotic plaques are inclined to modifications in a given patient. Progressive lumen narrowing due to high-grade stenosis may additionally appear and can conduct to ischaemic pain also at rest. Acute atherothrombotic occlusion may lead to irreversible ischemia, causing necrosis of the tissues supplied by the obstructed artery. Atheroembolism might also develop which causes plaque to discharge particles into the bloodstream. Aneurysm formation is also one of the clinical modifications considered. Loss of elastic tissue causes structural weakening that may lead to aneurysmal dilation and rupture (Kumar, Abbas and Aster, 2018). Cross et al. (2013), additionally mentioned that vulnerable plaques have a high chance of developing thrombotic complications. Proteolytic enzymes, cytokines and reactive oxygen species produced by the plaque inflammatory cells cause weakening and rupture of the fibrous cap and consequent thrombosis. Plaques that progressively progress to highly stenotic lesions, as in stable angina pectoris, frequently have an extensive fibrocalcific component with little inflammatory activity (Cross, Gallagher and van der Wal, 2013). Major clinical complications as per Kumar et al. (2018), are myocardial infarction, cerebral infarction, aortic aneurysm and peripheral vascular disease.
The treatment goals for stable angina in the given case-study, are directed towards symptom reduction and prevention of myocardial infarction via nonpharmacologic strategies, pharmacologic therapy, and coronary interventions. Nonpharmacologic techniques are aimed at symptom monitoring and lifestyle adjustments to minimize risk factors for coronary disease. They include stress reduction, regular exercise and lowering the intake of meals high in cholesterol and saturated fats (Mattson P.C., 2001 ).
According to Morris P. and Warriner D. (2015), pharmacologic/medication therapy is divided into symptomatic therapies, which minimize symptoms, and prognostic therapies, which enhance outcome. Symptomatic therapies decrease cardiac preload and afterload, and encourage coronary dilation, through vasodilating systemic (and coronary) arteries and veins. These treatment options include nitrates such as glyceryl trinitrate (short-acting) or isosorbide mononitrate (long-acting); calcium channel antagonists such as amlodipine; and, potassium channel blockers such as nicorandil. Prognostic therapies include cardioselective beta-blockers (e.g. atenolol), which reduce sympathetic stimulation of the myocardium and decrease myocardial work; aspirin, which reduces platelet function and the development of atherosclerotic plaques; and stains (e.g. simvastatin), which stabilize present plaques via decreasing blood cholesterol. However, in order to choose correct treatment method, further analysis must be performed such as blood test, ECG, and Echocardiogram. In cases of severe uncontrolled anginal pain despite medical therapy, surgery is the ultimate method to adopt. Percutaneous Coronary Intervention (PCA) also known as Angioplasty is a procedure where a balloon is used to force the narrowed coronary lumen open and squeeze the fatty plaque to either side. A scaffold known as a stent is then inserted into the arterial lumen to keep the plaque in position and the lumen open.
Thus, the patient must be referred for further analyses for a better understanding of the location of the atherosclerotic artery.
Symptoms experienced by the individual in the given case study, as well as clinical features, suggest Stable Angina Pectoris as a diagnosis. However, future investigations should be made in order to better visualize patients’ clinical picture for clearer management and treatment. The most common cause of angina pectoris is atherosclerosis which if left untreated may lead to superior lesions by way of plaque rupture, hemorrhage into the plaque, and thrombosis – resulting in myocardial infarction, stroke, aortic aneurysm and peripheral vascular disease. Management of angina pectoris comprises three stages of treatment: nonpharmacological – symptom monitoring and lifestyle adjustments to minimize risk factors; medication therapy to minimize symptoms and enhance the outcome, and PCA if the patient develops uncontrolled anginal pain and does not respond to medication therapy.