At a Glance
Acute coronary syndrome (ACS) is a complex group of symptoms associated with acute myocardial ischemia. Many patients with ACS present with chest pain at rest that can radiate to the arms, shoulders, and abdomen. However, many patients are also asymptomatic, and suspicion of ACS is based on the presence of risk factors, such as hypertension and hyperlipidemia (see chapter on Cardiovascular Risk).
The most common cause of ACS is atherosclerotic coronary artery disease (CAD), which progresses from being ayspmtomatic through angina to infarction. Infarction is typically the result of a thrombus that has formed after an arteriosclerotic plaque has ruptured, activating the coagulation cascade. The thrombus partially or transiently occludes coronary vessels in the majority of ACS patients, leading to ischemia without persistent ST-segment elevation (unstable angina or non-ST-elevation myocardial infarction [NSTEMI]). However, approximately 30% of patients will have complete occlusion of a coronary vessel and characteristic ST-elevation myocardial infarction (STEMI).
Patients with symptomology and ST-segment elevation do not require biochemical confirmation of myocardial infarction, but levels may be useful in assessing the size of infarction or reinfarction. Patients without ST-segment elevation (NSTEMI ACS; NSTEACS) include those with unstable angina and NSTEMI. Both conditions are related, but NSTEMI differs in that irreversible damage to myocardium occurs, which is recognized by the measurement of biomarkers of cardiac injury. Patients with unstable angina may have elevated levels of troponin without clinical signs of MI, such as electrocardiogram (ECG). These patients are at high risk for future cardiac events.
In addition to plaque rupture and the accompanying acute thrombosis, ACS is also associated with progressive mechanical obstruction of the vessel as plaque enlarges, inflammation, secondary unstable angina from anemia or hyperthyroidism, and dynamic obstruction of coronary vessels due to vasoconstriction. Typically, more than one of these components are present. Each etiology requires a different therapeutic approach, and several biomarkers are available to assist with targeting interventions according to the underlying causes of the patient’s ACS.
Other less frequent causes of ACS and myocardial injury include coronary artery erosion and vasospasm.
What Tests Should I Request to Confirm My Clinical Dx? In addition, what follow-up tests might be useful?
Biomarkers of myocardial necrosis should be measured in all patients presenting with ACS, and results must be used in conjunction with clinical presentation and electrocardiogram (ECG).
Cardiac troponin (troponin T or troponin I) is the preferred marker of diagnosis of myocardial infarction (MI) in patients with NSTEACS. Troponin I and T can be used interchangeably, and tests performed by your institution will depend on the instrumentation used in the laboratory
If troponin assays are not available, the use of creatine kinase MB (CK-MB) by mass assay is acceptable. CK-MB by mass assay results will be reported in ng/mL. If results are reported as a percentage of total CK, that is an activity assay not suitable for ACS diagnostics. Some clinicians state that CK-MB is the preferred biomarker for detection of reinfarction, infarct sizing, or infarct after percutaneous coronary intervention, but its utility in these settings is controversial.
Serial testing to observe a rise and/or fall of a biomarker is necessary for the diagnosis of acute, evolving, or recent MI. Note that patients with STEMI and positive clinical history should recieve therapy immediately. There is no need to wait for biochemical confirmation.
Are There Any Factors That Might Affect the Lab Results?
Troponins and CK-MB begin to appear in the circulation 3-4 hours after onset of injury, and levels reach maximal sensitivity for detection of necrosis by 6 hours. Levels may be too low to provide useful information when patients present within 6 hours of onset of symptoms, and clinicians should consider adding myoglobin when patients present within 6 hours of onset of symptoms. Myoglobin is released earlier (rises within 1 hour) than troponins and may afford earlier detection of myocardial injury. However, the utility of myoglobin is decreasing as the analytical sensitivity of troponin assays improves.
Given the low to non-detectable circulating levels of troponins or CK-MB in the first few hours after onset, serial sampling is required to observe rises (or falls) of levels.
CK-MB has poor specificity because of its presence in myocardial and skeletal muscle, as well as within the intestine, diaphragm, uterus, and prostate. Use of CK-MB in patients presenting with injury to these organs is impaired.
Non-ischemic conditions that also elevate troponins include acute rheumatic fever, cardiac trauma, congestive heart failure, end-stage renal failure, heart transplantation, myocarditis, pulmonary embolism, sepsis, hypothyroidism, and postoperative non-cardiac surgery. Serial testing is helpful to distinguish ACS from the conditions listed, because, in the listed conditions, the troponin levels do not usually change significantly over time.
Falsely elevated levels of troponin have been reported, resulting from heterophile antibodies, rheumatoid factor, high concentrations of alkaline phosphatase, microparticles or fibrin in the sample, and analyzer malfunction. The different methods available appear to have unique interferences, and clinicians are encouraged to discuss the known issues with the assay in their facility with the laboratory directors.
What Lab Results Are Absolutely Confirmatory?
A positive clinical history and the following are consistent with myocardial infaction:
a concentration of cardiac troponin exceeding the 99th percentile of values for a reference control group at least once during the first 24 hours after presentation, or
a concentration of CK-MB exceeding the 99th percentile of values for a sex-specific reference control group on 2 successive samples.
Obsolete Tests for Acute Coronary Syndrome
Total CK, CK-MB activity, AST, beta-hydroxybutric dehydrogenase, and/or lactate dehydrogenase are no longer recommended as biomarkers for the diagnosis of MI.
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