Acute coronary syndrome

Symptoms of the acute coronary syndromes are similar. The cardinal symptom of critically decreased blood flow to the heart is chest pain, experienced as tightness, pressure, or burning. Localization is most commonly around or over the chest and may radiate or be located to the arm, shoulder, neck, back, upper abdomen, or jaw. Though ACS is usually associated with coronary thrombosis, it can also be associated with cocaine use. Chest pain with features characteristic 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. ==Pathophysiology==

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% of the STEMI and vice versa for Non ST elevated myocardial infarction (NSTEMI). In plaque rupture, the content of the plaque is 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. Other, less common, causes of acute coronary syndrome include spontaneous coronary artery dissection, ischemia in the absence of obstructive coronary artery disease (INOCA), and myocardial infarction in the absence of obstructive coronary artery disease (MINOCA). ==Diagnosis==

Electrocardiogram In the setting of acute chest pain, the electrocardiogram (ECG or EKG) 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. ECG changes indicating acute heart damage include: ST elevation, new left bundle branch block and ST depression amongst others. The absence of ECG changes does not immediately distinguish between unstable angina and NSTEMI. ==Prevention==

Acute coronary syndrome often reflects a degree of damage to the coronaries by atherosclerosis. Primary prevention of atherosclerosis is controlling the risk factors: healthy eating, exercise, treatment for hypertension and diabetes, avoiding smoking and controlling cholesterol levels; in patients with significant risk factors, aspirin has been shown to reduce the risk of cardiovascular events. Secondary prevention is discussed in myocardial infarction. After a ban on smoking in all enclosed public places was introduced in Scotland in March 2006, there was a 17% reduction in hospital admissions for acute coronary syndrome. 67% of the decrease occurred in non-smokers. ==Treatment==

People with presumed ACS are typically treated with aspirin, clopidogrel or ticagrelor, nitroglycerin, and, if the chest discomfort persists, morphine. Other analgesics such as nitrous oxide are of unknown benefit. The time frame for door-to-needle thrombolytic administration according to American College of Cardiology (ACC) guidelines should be within 30 minutes, whereas the door-to-balloon percutaneous coronary intervention (PCI) time should be less than 90 minutes. It was found that thrombolysis is more likely to be delivered within the established ACC guidelines among patients with STEMI as compared to PCI according to a 2009 case control study. NSTEMI and NSTE-ACS If the ECG does not show typical changes consistent with STEMI, the term "non-ST segment elevation ACS" (NSTE-ACS) may be used and encompasses "non-ST elevation MI" (NSTEMI) and unstable angina. The accepted management of unstable angina and acute coronary syndrome is therefore empirical treatment with aspirin, a second platelet inhibitor such as clopidogrel, prasugrel or ticagrelor, and heparin (usually a low-molecular weight heparin), with intravenous nitroglycerin and opioids if the pain persists. The heparin-like drug known as fondaparinux appears to be better than enoxaparin. If there is no evidence of ST segment elevation on the electrocardiogram, delaying urgent angioplasty until the next morning is not inferior to doing so immediately. Using statins in the first 14 days after ACS reduces the risk of further ACS. Cocaine-associated ACS should be managed in a manner similar to other patients with acute coronary syndrome except beta blockers should not be used and benzodiazepines should be administered early. ==Prognosis==

Prediction scores The TIMI risk score can identify high risk patients in ST-elevation and non-ST segment elevation MI ACS and has been independently validated. Based on a global registry of 102,341 patients, the GRACE risk scoreestimates in-hospital, 6 months, 1 year, and 3-year mortality risk after a heart attack. Nowadays, GRACE risk score is also used within non-ST elevation ACS patients as a high-risk criteria(GRACE score > 140), which may favor early invasive strategy within 24 hours of the heart attack. Biomarkers 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. This phenomenon is described as weekend effect. == Research ==

A study published in 2024 found that women with acute coronary syndrome in India experience worse outcomes. ==References==