Acute coronary syndrome

Acute coronary syndrome (ACS) is a syndrome (set of signs and symptoms) due to decreased blood flow in the coronary arteries such that part of the heart muscle is unable to function properly or dies. The most common symptom is chest pain, often radiating to the left shoulder or angle of the jaw, crushing, central and associated with nausea and sweating. Many people with acute coronary syndromes present with symptoms other than chest pain, particularly, women, older patients, and patients with diabetes mellitus. Acute coronary syndrome (ACS) is a syndrome (set of signs and symptoms) due to decreased blood flow in the coronary arteries such that part of the heart muscle is unable to function properly or dies. The most common symptom is chest pain, often radiating to the left shoulder or angle of the jaw, crushing, central and associated with nausea and sweating. Many people with acute coronary syndromes present with symptoms other than chest pain, particularly, women, older patients, and patients with diabetes mellitus. Acute coronary syndrome is commonly associated with three clinical manifestations, named according to the appearance of the electrocardiogram (ECG): ST elevation myocardial infarction (STEMI, 30%), non-ST elevation myocardial infarction (NSTEMI, 25%), or unstable angina (38%). There can be some variation as to which forms of myocardial infarction (MI) are classified under acute coronary syndrome. ACS should be distinguished from stable angina, which develops during physical activity or stress and resolves at rest. In contrast with stable angina, unstable angina occurs suddenly, often at rest or with minimal exertion, or at lesser degrees of exertion than the individual's previous angina ('crescendo angina'). New-onset angina is also considered unstable angina, since it suggests a new problem in a coronary artery. The cardinal symptom of critically decreased blood flow to the heart is chest pain, experienced as tightness around or over the chest and (often, but not always) radiating to the left arm and the left angle of the jaw. This may be associated with diaphoresis (sweating), nausea and vomiting, as well as shortness of breath. In many cases, the sensation is 'atypical', with pain experienced in different ways or even being completely absent (which is more likely in female patients and those with diabetes). Some may report palpitations, anxiety or a sense of impending doom (angor animi) and a feeling of being acutely ill. The description of the chest discomfort as a pressure has little utility in aiding a diagnosis as it is not specific for ACS. Though ACS is usually associated with coronary thrombosis, it can also be associated with cocaine use. Chest pain with features characteric of cardiac origin (angina) can also be precipitated by profound anemia, brady- or tachycardia (excessively slow or rapid heart rate), low or high blood pressure, severe aortic valve stenosis (narrowing of the valve at the beginning of the aorta), pulmonary artery hypertension and a number of other conditions. In those who have ACS, atheroma rupture is most commonly found 60% when compared to atheroma erosion (30%), thus causes the formation of thrombus which block the coronary arteries. Plaque rupture is responsible for 60% in ST elevated myocardial infarction (STEMI) while plaque erosion is responsible for 30% if the STEMI and vice versa for Non ST elevated myocardial infarction (NSTEMI). In plaque rupture, the content of the plaque are lipid rich, collagen poor, with abundant inflammation which is macrophage predominant, and covered with a thin fibrous cap. Meanwhile, in plaque erosion, the plaque is rich with extracellular matrix, proteoglycan, glycoaminoglycan, but without fibrous caps, no inflammatory cells, and no large lipid core. After the coronary arteries are unblocked, there is a risk of reperfusion injury due spreading inflammatory mediators throughout the body. Investigations is still underway on the role of Cyclophilin D in reducing the reperfusion injury. In the setting of acute chest pain, the electrocardiogram is the investigation that most reliably distinguishes between various causes. The ECG should be done as early as practicable, including in the ambulance if possible. If this indicates acute heart damage (elevation in the ST segment, new left bundle branch block), treatment for a heart attack in the form of angioplasty or thrombolysis is indicated immediately (see below). In the absence of such changes, it is not possible to immediately distinguish between unstable angina and NSTEMI. As it is only one of the many potential causes of chest pain, the patient usually has a number of tests in the emergency department, such as a chest X-ray, blood tests (including myocardial markers such as troponin I or T, and H-FABP and/or a D-dimer if a pulmonary embolism is suspected), and telemetry (monitoring of the heart rhythm). Combination of troponin levels (less than 5 ng/l) with low TIMI scores can help to predict those with low possibility of myocardial infarction and discharge them safely from the emergency department. Coronary CT angiography combined with Troponin levels is also helpful to triage those who are susceptible to ACS. F-fluoride positron emission tomography is also helpful in identifying those with high risk, lipid-rich coronary plaques.