Generally, the clinical manifestation of unstable angina is chest pain, pain or pressure at the back, neck, jaw, shoulder or arm and also abdomen, sweating, dyspnea, nausea and vomiting, dizziness and fatigue. Based on patient’s record, Mr. Zainal Ariffin had a history of abdominal discomfort on the day of admission, 24th October 2018. Besides that, the patient also complains of nausea and vomiting at the early of admission.Based on the patient’s medical history, En. Zainal Arifin suffered from high blood pressure for quite a long period, which might lead to serious health problems.
Blood pressure is determined by the amount of blood pumps through the heart and the amount of resistance to blood flow in the arteries. Hypertension happens when the more blood pumps by the heart and the narrower the arteries. Thus, uncontrolled hypertension increases the risks of serious heart diseases, including stroke and unstable angina.
Unstable Angina is a type of acute coronary syndrome. It is often indistinguishable from NSTEMI and treated with nitroglycerin and aspirin. It occurs when points of high-grade artery stenosis rupture. Thrombi simultaneously forms at these rupture sites resulting in a thromboembolytic occlusion of the vessel. When rupture occurs, ‘sticky’ plaque is exposed to platelets forming a thrombus, bulging and causing vasoconstriction to occlude vessel. As a consequence, the artery is blocked, initiating the heart muscle to become ischemic, resulting in chest pain (angina) to the patient, even at rest.
Plaques are consisting of macrophages, lipids and smooth muscle cells, usually covered by a fibrous cap. Inflammatory factors can cause secretion of MMPs, resulting in cap rupture and activation of the coagulant pathway, forming the thrombus. If the artery vasoconstrics, blood flow is temporarily blocked resulting in complete coronary occlusion which is myocardial infarction or incomplete coronary occlusion, the unstable angina. As the time passes, repeated ruptures result in progressive narrowing of the lumen via a vicious cycle of flow disturbance, endothelial injury and plaque growth. The clinical presentation depends on plaque composition and the degree of injury.
For example, fibrous or calcified plaques, though if stenotic are less likely to rupture compared to soft fatty plaques. This is because even though soft plaques stenosis with less than 50%, they are lipid-rich and extremely vulnerable to rupture. Other than that, diabetes mellitus suffered by the patient may be the cause of unstable angina as a result of high amount of sugar in the blood due to insulin resistance. This condition may cause damage to the inner layer of the coronary arteries. Plaque begins to build up at the damaged arteries. Over time, the plaque hardens and narrows the arteries causing the reduction of oxygen-rich blood flows to the heart muscle.
Sooner or later, the area of plaque may rupture and this condition augments the platelets to clump together with the plaque to form blood clots. The development of coronary atherosclerosis limits the flow of oxygen-rich blood to the heart and may worsen the chest pain (angina).