Acute coronary syndromes
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Unstable Angina
Non ST Elevation Myocardial Infarction
ST Elevation Myocardial Infarction
Overview of Acute Coronary Syndromes
An acute coronary syndrome (ACS) is a set of signs and symptoms, usually a combination of chest pain and other features, interpreted as being the result of abruptly decreased blood flow to the heart (cardiac ischemia); the most common cause for this is the disruption of atherosclerotic plaque in an epicardial coronary artery. The subtypes of acute coronary syndrome include unstable angina (UA, not associated with heart muscle damage), and two forms of myocardial infarction (heart attack), in which heart muscle is damaged. These types are named according to the appearance of the electrocardiogram (ECG/EKG) as non-ST segment elevation myocardial infarction (NSTEMI) and ST segment elevation myocardial infarction (STEMI).
ACS should be distinguished from stable angina, which develops during exertion 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.
Signs and symptoms
The cardinal sign of decreased blood flow to the heart is chest pain experienced as tightness around the chest and 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 and a feeling of being acutely ill.
Diagnosis
Electrocardiogram
In the setting of acute chest pain, the electrocardiogram is the investigation that most reliably distinguishes between various causes.[1] 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.
Imaging and bloods
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 a D-dimer if a pulmonary embolism is suspected), and telemetry (monitoring of the heart rhythm).
Prediction scores
The ACI-TIPI score can be used to aid diagnosis; using 7 variables from the admission record, this score predicts crudely which patients are likely to have myocardial ischemia.[1]
Prognosis
TIMI score
The TIMI risk score can identify high risk patients[1] and has been independently validated.[1][1]
Biomarkers for diagnosis
The aim of diagnostic markers is to identify patients with ACS even when there is no evidence of myocyte necrosis.
- Ischemia-Modified Albumin (IMA) - In cases of Ischemia - Albumin undergoes a conformational change and loses its ability to bind transitional metals (copper or cobalt). IMA can be used to assess the proportion of modified albumin in ischemia. Its use is limited to ruling out ischemia rather than a diagnostic test for the occurrence of ischemia.
- Myeloperoxidase (MPO) - The levels of circulating MPO, a leukocyte enzyme, elevate early after ACS and can be used as an early marker for the condition.
- Glycogen Phosphorylase Isoenzyme BB-(GPBB) is an early marker of cardiac ischemia and is one of three isoenzymeof Glycogen Phosphorylase.
Biomarkers for Risk Stratification
The aim of prognostic markers is to reflect different components of pathophysiology of ACS. For example:
- Natriuretic peptide - Both B-type natriuretic peptide (BNP) and N-terminal Pro BNP can be applied to predict the risk of death and heart failure following ACS.
- Monocyte chemo attractive protein (MCP)-1 - has been shown in a number of studies to identify patients with a higher risk of adverse outcomes after ACS.
Treatment
STEMI
If the ECG confirms changes suggestive of myocardial infarction (ST elevations in specific leads, a new left bundle branch block or a true posterior MI pattern), thrombolytics may be administered or primary coronary angioplasty may be performed. In the former, medication is injected that stimulates fibrinolysis, destroying blood clots obstructing the coronary arteries. In the latter, a flexible catheter is passed via the femoral or radial arteries and advanced to the heart to identify blockages in the coronaries. When occlusions are found, they can be intervened upon mechanically with angioplasty and perhaps stent deployment if a lesion, termed the culprit lesion, is thought to be causing myocardial damage.
NSTEMI and NSTE-ACS
If the ECG does not show typical changes, the term "non-ST segment elevation ACS" is applied. The patient may still have suffered a "non-ST elevation MI" (NSTEMI). The accepted management of unstable angina and acute coronary syndrome is therefore empirical treatment with aspirin, heparin (usually a low-molecular weight heparin such as enoxaparin) and clopidogrel, with intravenous glyceryl trinitrate and opioids if the pain persists.
A blood test is generally performed for cardiac troponins twelve hours after onset of the pain. If this is positive, coronary angiography is typically performed on an urgent basis, as this is highly predictive of a heart attack in the near-future. If the troponin is negative, a treadmill exercise test or a thallium scintigram may be requested.
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.
References
Acknowledgement and Attribution Regarding Sources of Content
Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .
