An 85-year-old female with a history of coronary artery disease (CAD) presented to the Emergency Department (ED) with altered mental status. While she was admitted for sepsis and had positive blood cultures for methicillin-resistant Staphylococcus aureus (MRSA), the patient was also noted to have an elevated troponin level of 1.32 (higher than the local laboratory normal values). Given the history of CAD with altered mental status, she was placed on an acute coronary syndrome (ACS) protocol with serial electrocardiograms (ECGs) and enzymes. However, her ECG remained normal, and her cardiac troponin levels trended downward in the Intensive Care Unit (ICU) as she recovered from sepsis. Since her transthoracic echocardiogram performed at that time was normal and did not show any regional wall motion abnormality, her troponin enzyme elevations were considered to be secondary to sepsis; however, initial emphasis at admission was on ACS.
DISCUSSION
Cardiovascular disease is a leading cause of morbidity and mortality in the United States. It can be a silent killer or may present as a lifethreatening event, such as ventricular fibrillation, sudden death, or acute myocardial infarction (MI) with or without classic signs and symptoms of ACS. Not uncommonly ACS symptoms may be vague. When missed, ACS can lead to a devastating event, such as cardiovascular collapse, death, loss of cardiac muscle, ventricular irritability, and to significant changes in a person’s quality of life. Thus, there is a heightened awareness for ACS. These lifethreatening events are important, and as such ACS should not be missed when it is presented in the ED or when a person is found unresponsive. The ACS spectrum includes unstable angina, non-ST elevation MI (NSTEMI), and ST elevation MI (STEMI). Since ECG changes may be transient, and patients may have atypical symptoms, sensitive blood tests such as cardiac troponins help identify ACS and have revolutionized cardiology, leading to identification of the smallest amount of myocardial damage in a setting of ACS.
The cardiac troponin biomarkers have revolutionized the diagnostic abilities of physicians in the ambulatory and hospitalized patient settings, including the ED, in recognizing myocardial cell death. Physicians determine the presence of cardiac injury by measuring serum levels of cardiac troponins in order to diagnose and treat true MIs. However, these sensitive biomarkers have also led to increased recognition of myocardial cell injury from causes other than ACS. Thus, these markers may be elevated in a setting associated with occlusion of the coronary vasculature, which is the typical presentation of an ACS, but also can be due to a supply and demand mismatch for the myocardial cells.
The true diagnosis of MI, however, requires the typical rise and fall of the cardiac enzymes with either ischemic symptoms or electrocardiogram (ECG) changes suggestive of ischemia, development of pathological Q waves, or imaging evidence of recent loss of viable myocardium or wall motion abnormalities along with presenting symptoms either typical or atypical. Without this evidence supporting the elevation of troponin as an ACS, the diagnosis of ACS needs to be made with caution.
This case is a reminder to physicians and physician extenders not to exclude non-ACS causes of troponin elevation and to use clinical context and judgment along with diagnostic tests in a case of troponin elevation, especially now when more triaging to fast-track pathways of medical management occurs, such as 23-hour observation and chest pain center units.
Cardiac Biomarkers
Today, cardiac biomarkers, such as troponin (cTnT and cTnI) levels, are commonly used to determinewhether a patient is presenting with an ACS. ACS is defined by reduced coronary blood flow to the cardiac muscles, which leads to an MI. The spectrum of ACS has a range from unstable angina to a transmural MI or STEMI and includes NSTEMI in the spectrum. Unstable angina is diagnosed by clinical history with possible ST segment, T-wave changes on ECG, or wall motion abnormalities on imaging, but without cardiac troponin elevation. Troponin elevation then changes the diagnosis of unstable angina to NSTEMI or STEMI based on ECG findings. Thus, the clinical presentation, electrocardiographic changes, and biochemical cardiac markers make up the triad of characteristics that determine the diagnosis of ACS and type of ACS.
No doubt, ACS requires prompt recognition, since the beneficial effects of therapies are time sensitive. The diagnosis of an acute MI is confirmed by ECG changes and serum cardiac biomarker elevation. In STEMI, the ECG shows classic ST elevation of at least 1 mm in 2 contiguous leads. NSTEMI does not have ST elevation on EKG but has ST-T abnormalities with positive cardiac biomarkers, including troponins. Diagnosis of STEMI results in prompt activation of cardiac catheterization laboratory for procedure or a consideration of giving intravenous thrombolytics to all patients, without consideration to initial cardiac biomarkers that may be negative. In other words, in case of STEMI, the cardiac biomarkers are drawn, but the results are not acted on or waited for, as the biomarkers, in spite of all their sensitivity, tend to be negative in the first few hours. In cases of NSTEMI, the troponins are negative initially when drawn on early arrival with classic history of unstable angina with or without ECG changes in the form of ST depression or T-wave changes from baseline. In unstable angina, the ECG changes may be transient and troponins are negative. The biomarkers are, therefore, relied on and become positive after 4 to 6 hours of initial presentation of symptoms in cases of ACS, as more cases of unstable angina are now diagnosed with NSTEMI due to increased sensitivity of these troponin biomarkers.