Approach

Optimal care for patients presenting with chest pain suggestive of unstable angina (UA) includes accurate and timely diagnosis utilizing a combination of clinical, ECG, and laboratory markers, to minimize time to appropriate therapy.

History

Acute coronary syndrome (ACS) should be suspected in any patient with acute chest pain, which includes pain in other areas (e.g., the arms, back, or jaw), that lasts longer than 15 minutes, is associated with nausea and vomiting, marked sweating, breathlessness, or particularly a combination of these, and/or is either new in onset or occurs as sudden worsening of known stable angina (i.e., recurrent episodes of chest pain lasting longer than 15 minutes that occur frequently and with little or no exertion, or decreasing efficacy of antianginal drugs).[1]

Typical features include age >45 years, smoker, with long-standing hypertension, diabetes, or hypercholesterolemia. A history of peripheral vascular disease or preexisting heart disease should be determined.

Most patients present with chest pain, although women, people with diabetes, and older people may present with noncharacteristic symptoms of ischemia.

Cardiac chest pain is often described as a retrosternal pressure or heaviness that radiates to the jaw, arm, or neck, and may be intermittent or persistent. Patients may perceive anginal symptoms as pain, discomfort, heaviness, tightness, pressure, constriction, or squeezing.[78] Specific clinical findings in UA include prolonged (>20 minutes) angina at rest, new onset of severe angina; angina increasing in frequency, longer in duration or lower in threshold; or angina that occurs after a recent episode of myocardial infarction (MI).[1]​ Pain may be accompanied by other symptoms such as diaphoresis, nausea, dyspnea, and syncope.[1][79]

Patients may present with a range of noncharacteristic classic symptoms, any of which may be the sole presenting symptom. These include weakness, nausea, vomiting, abdominal pain, and syncope. These are more common in women, older people, and those with diabetes or chronic kidney disease.[1]​ Symptoms usually considered noncardiac may still be ischemic in origin.[78] In appropriate clinical situations, a diagnosis of UA should be considered when patients present with epigastric pain, recent-onset heartburn/indigestion (particularly if unrelated to meals), shoulder pain (with or without neck, jaw, or arm pain), back pain, or isolated dyspnea. Rarely the presenting symptom may be sharp/stabbing or pleuritic chest pain. However, pain described as sharp, fleeting (few seconds duration), related to inspiration (pleuritic) or position, or which is shifting in location, suggests a lower likelihood of ischemia.

Examination

Physical exam is generally normal in patients with UA. However, the patient may have significant sweating due to high sympathetic drive.[1][79]​​​ If the patient is hemodynamically unstable (low blood pressure [BP] or shock), has evidence of left ventricular failure, or has a life-threatening arrhythmia (ventricular tachycardia or ventricular fibrillation) an acute MI should be suspected; these are unlikely to be features of UA.[80][81]​​​ See Shock, Acute heart failure, Sustained ventricular tachycardias, ST-elevation myocardial infarction, and Non-ST-elevation myocardial infarction.

Rarely, murmur of ischemic mitral regurgitation, concomitant valvular disease (e.g., aortic stenosis), or signs of heart failure may be present.

Presence of bruits and peripheral arterial disease suggests extracardiac vascular disease and identifies patients with higher likelihood of significant coronary artery disease (CAD).

Physical exam is critical in making important alternative diagnoses in patients with chest pain. For example, aortic dissection is suggested by pain radiating to the interscapular region and the back with unequal pulses, or murmur of aortic regurgitation. Fever may be suggestive of endocarditis or pneumonia. Acute pericarditis is suggested by pericardial friction rub, and cardiac tamponade may be evidenced by pulsus paradoxus. A large pneumothorax may lead to tracheal deviation, hyper-resonance, and unilaterally decreased air entry. A large pulmonary embolism may result in hypotension with elevated jugular venous pressure with clear lung fields. Exam also helps in identifying possible precipitating and contributing factors such as malignant hypertension, thyrotoxicosis, or anemia.

ECG

Guidelines recommend that an ECG be obtained and interpreted by a qualified physician within the first 10 minutes after a patient presents with chest pain.[1][78]​​[82]

ST-segment depression and T-wave changes may be seen in patients with UA. Alternatively, the initial ECG may show transient ST elevation, or may be normal.[1] 

Transient ST-segment depression (>0.05 mV) or T-wave inversion (>0.2 mV) during the symptomatic period that resolve when the patient becomes asymptomatic strongly suggest acute ischemia and severe underlying coronary artery disease.[2] The extent of ST-segment depression, as well as the magnitude in millimeters from baseline, are important prognostic indicators.[83][84] Additional ECG leads (V3R, V4R, V7-V9) are recommended if ongoing ischemia is suspected when standard leads are inconclusive.[1]

In patients with recurrent symptoms or in case of diagnostic uncertainty, additional 12-lead ECG should be obtained.[1]

If the initial ECG is not diagnostic but the patient remains symptomatic and there is a high clinical suspicion for acute coronary syndrome, serial ECGs should be performed to detect ischemic changes.[2][78]

The timing for repeat ECGs should be guided by symptoms, especially if chest pain recurs or a change in clinical condition develops.[78] In clinical practice a repeat ECG is usually performed at 6 and 24 hours (more frequently if clinical status changes). If possible, previous ECGs should be obtained for comparison.

Cardiac biomarkers

Cardiac biomarkers (troponin I or T) should be measured on presentation.

High-sensitivity cardiac troponin (hs-cTn) assays allow rapid exclusion of myocardial necrosis and are recommended by guidelines in the US and Europe.[1][78][82]​​​ The 0 hour/1 hour algorithm (where a high-sensitive cardiac troponin measurement is made at presentation [0 hours] and at 1 hour after presentation) is recommended to rule out non-ST-elevation acute coronary syndromes, or the 0 hour/2 hour algorithm may be used as a second-best option. Additional testing after 3 hours is recommended if the first two cardiac troponin measurements of the 0 hour/1 hour algorithm are not conclusive and the clinical condition is still suggestive of acute coronary syndrome.[1]​ A diagnosis of UA can usually be made if subsequent dynamic troponin testing shows cardiac troponin remaining below the 99th percentile. Diagnostic imaging including invasive coronary angiography, functional (stress) testing, or coronary computed tomography angiography may be useful for patients in whom cardiac troponin and ECG results remain inconclusive.[1]

​In clinical practice, diagnostic algorithms for non-ST-elevation acute coronary syndromes should be used in conjunction with all available clinical information and ECG. Additional serial cardiac troponin testing should be pursued if clinical suspicion remains high, or whenever the patient develops recurrent chest pain.[1][78]

When a previous-generation troponin assay is used, cardiac-specific troponin (troponin I or T) levels should be measured at presentation and 3 to 6 hours after symptom onset in all patients who present with symptoms consistent with acute coronary syndromes.[2] Additional troponin levels should be obtained beyond 6 hours after symptom onset in patients with normal troponins on serial examination when, based on clinical presentation and/or ECG changes, there is an intermediate or high index of suspicion for acute coronary syndrome.[2] In low-to-intermediate risk patients with suspected acute coronary syndrome, undetectable high-sensitivity troponin T values at admission are associated with very low risk of death or MI within 90 days.[85]

Troponin remains elevated up to 10 to 14 days after release. Thus, in a patient who had an acute MI several days earlier presenting with chest discomfort, a single, slightly elevated troponin level may represent old ischemia. In patients in whom a re-infarction is suspected, a troponin re-elevation of 20% or more has been advocated as a marker.[86]

Among patients presenting to the emergency department with chest pain, even slightly elevated blood levels of high-sensitivity cardiac troponin T are associated with adverse clinical outcomes, with a strong and graded association between all detectable levels of high-sensitivity cardiac troponin T and risk for myocardial infarction, heart failure, and cardiovascular and noncardiovascular mortality. The yearly rate of death was 0.5% among patients with high-sensitivity cardiac troponin T levels <0.005 micrograms/L, and this rate increased in a graded manner with increasing levels to 33% among patients with high-sensitivity cardiac troponin T levels ≥0.05 micrograms/L.[87]

Cardiac troponins are more sensitive and specific markers of cardiomyocyte damage than creatine kinase (CK), its myocardial band isoenzyme (CK-MB), and myoglobin. In patients with MI, troponin levels rise rapidly (usually within 1 hour from symptom onset if using high-sensitivity assays) and remain elevated for several days. Hence, with the advent of hs-cTn, other biomarkers such as CK, CK-MB, and myoglobin should not be used in diagnosis.[1][2][78][88]

If there is no evidence of myocardial injury or necrosis, the patient with history and ECG changes suggestive of non-ST-elevation MI (non-STEMI) is considered to have UA.[2]

Other blood tests

Baseline bloods for complete blood count, electrolytes, renal function, liver function, blood sugar, C-reactive protein, lipid/cholesterol profile and coagulation profile should be taken at presentation. Serum cholesterol falls significantly after a few hours of admission following an MI, so it should be measured at the time of initial presentation.[89]

Imaging

Chest x-ray should be performed on presentation to identify other causes of chest pain.[82]

An emergent echocardiogram should always be performed in patients with cardiogenic shock or hemodynamic instability.[1][90]​​​ Point-of-care transthoracic echocardiogram can also be used to look for regional wall motion abnormalities of the left ventricle in patients with an atypical presentation or equivocal ECG, look for mechanical complications of acute MI (such as left ventricular function, right ventricular function, ventricular septal rupture, left ventricular free wall rupture, acute mitral regurgitation, pericardial effusion, cardiac tamponade) and for evidence to suggest alternative etiologies associated with chest pain (e.g., acute aortic disease, pulmonary embolism).[1][2][90]​​​​[91][92]

A predischarge echocardiogram is indicated for all patients postacute MI to assess left ventricular function after coronary reperfusion therapy and to guide prognostication.​[2][93]

Invasive coronary angiography (with or without revascularization) should be considered for a patient with suspected UA (with a negative troponin testing result) based on the risk assessment and clinical presentation, and is the investigation of choice for assessing the presence and severity of CAD, and allows concurrent treatment with angioplasty and stenting.[94]​ Patients with UA have a significantly lower risk of death compared with those with non-STEMI and get less benefit from an immediate invasive approach.[95]​ An inpatient invasive strategy (coronary angiography within 72 hours of admission, with follow-on percutaneous coronary intervention if indicated) is generally recommended for patients with a high index of suspicion for UA, particularly for those who have an intermediate or higher risk of adverse cardiovascular events.[1]

Functional (stress) testing with stress echocardiography, perfusion/stress cardiac magnetic resonance (CMR) imaging, myocardial perfusion scan, may be considered by the cardiology team as part of the initial workup in patients with suspected ACS but nonelevated (or inconclusive) hs-cTn, no ECG changes, and no recurrence of pain.[1]​ They can also be performed after stabilization, to identify the extent of myocardial ischemia and direct patients for possible invasive management.[78]​ However, do not perform stress CMR in patients with acute chest pain and high probability of CAD.​[96]

In patients with normal ECG and normal cardiac troponins, computed tomographic (CT) angiography to assess coronary artery anatomy, or rest myocardial perfusion imaging to exclude myocardial ischemia, may reasonably be performed.[2][78]​ Coronary CT angiography has been accepted in the acute setting to identify significant proximal coronary artery stenosis when ECG is not helpful and an intermediate clinical suspicion of acute coronary syndrome exists, as indicated by mild angina, prior MI, compensated or prior heart failure, diabetes, or renal insufficiency.[97][98]​ However, do not use coronary CT angiography in high-risk emergency department patients presenting with acute chest pain as it is not indicated for patients with high-risk features, for example, ischemic ECG changes or positive cardiac markers.[1][96]​​

Venepuncture and phlebotomy: animated demonstration
Venepuncture and phlebotomy: animated demonstration

How to take a venous blood sample from the antecubital fossa using a vacuum needle.

How to perform an ECG: animated demonstration
How to perform an ECG: animated demonstration

How to record an ECG. Demonstrates placement of chest and limb electrodes.

Risk stratification

The American College of Cardiology (ACC)/American Heart Association (AHA) recommend the use of validated chest pain risk scores as part of standardized clinical decision pathways to determine which patients require further investigation, particularly in settings where high-sensitivity cardiac troponin assays are not available.[78][82]

Risk scoring systems provide a summative assessment of the risk of a patient experiencing a major adverse cardiovascular event, or death, within the next 30 days from presentation with a possible ACS.[78] They combine troponin levels with other clinical information, such as age, ST segment changes on ECG, symptoms, and CAD risk factors. Emergent diagnostic testing for suspected CAD is not needed for patients deemed low risk.[78]

Example validated risk scores recommended by the ACC/AHA include the Thrombolysis in Myocardial Infarction (TIMI) risk score and the Global Registry of Acute Coronary Events (GRACE) risk model.[2] [ Thrombolysis in Myocardial Infarction (TIMI) Score for Unstable Angina Non ST Elevation Myocardial Infarction Opens in new window ] [ GRACE Score for Acute Coronary Syndrome Prognosis Opens in new window ]

Do not order a coronary artery calcium (CAC) test in patients with known atherosclerotic disease, including those with stents and bypass grafts, as this offers limited incremental prognostic value for these individuals.[96][100][101]

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