The ultimate interest in elevated troponin in a triage center or ED is not to miss a case that fits in the ACS spectrum that is a primary type of MI; and not a differential diagnosis or secondary types of MIs. Thus, an elevated troponin may steer a physician or a physician extender toward ACS and away from the patient’s primary problem on presentation, leading to improper triage, further unwarranted cardiac investigations, and increased hospitalizations. In addition, there are several non-ACS causes that require immediate attention and if overlooked can lead to life-threatening situations.
NON-ACS CAUSES OF TROPONIN REQUIRING IMMEDIATE ATTENTION
There are a few important non-ACS causes of cardiac troponin elevation that require immediate attention and treatment:
Acute aortic dissection
Aortic dissections can present with chest discomfort and dyspnea, mimicking the symptoms of ACS. Although the quality or type of pain is different, most chest pain presentations in the ED are initially evaluated with an ECG, which is required by the standard of care guidelines to meet benchmarks for chest pain evaluation in the ED. Troponins are obtained for triage into possible low- and high-risk patients with chest pains. Those with elevated troponins are usually admitted to chest pain units or for care in coronary care units; the low-risk ones are triaged in the ED to observation units, if one is available, for early discharges. In cases of aortic dissection, the most significant risk is extension of dissection and bleeding, which can cause the blood pressure (BP) to drop and lead to poor perfusion to end organs and major morbidity or mortality. Aortic dissection may cause some coronary compromise, leading to troponin elevation, while increasing morbidity and mortality.4 Chest X-rays done in the ED are often nondiagnostic.5 In such cases, aggressive antiplatelet or antithrombotic therapy, which is the standard therapy in ACS, may be more harmful than beneficial.
Pulmonary embolism (PE)
Patients with a PE can present with chest pain, tachycardia, and diaphoresis. ECG and troponin levels are routinely checked in such cases. PE and other pulmonary-related diseases (eg, pulmonary hypertension, severe COPD exacerbation, pneumonia, etc) can cause strain on the right heart from increased pulmonary artery pressure, leading to a troponin leak.6 Although some of these pulmonary conditions are severe enough to damage myocardial cells, treatment should be focused on the underlying pulmonary cause.
A handful of other medical conditions may present with an isolated elevation of troponin without other common signs associated with ACS.
Troponin leaks from supplydemand mismatch
The most common noncoronary cause of elevated troponin is demand ischemia. Demand ischemia, or increased demand from the cardiac cells, is not classified as an ACS. Common causes include tachycardia, hypovolemia, anemia, and HTN. These conditions are seen in patients with a multitude of systemic disorders, including renal failure, cardiomyopathies, infiltrative disorders, or systemic diseases, such as hypothyroidism, HTN, and diabetes mellitus, which may affect the diastolic properties of the ventricles.
Hypovolemia and anemia. The total blood volume nutrients and oxygen supply are decreased to meet the demand of the organs and circulatory area. This may lead to a decreased systemic BP as well as poor organ perfusion and oxygenation of vital tissues, including myocardial cells.7 The body tries to compensate and keeps up with demand for nutrients and oxygen by increasing the heart rate to maintain cardiac output. By increasing the heart rate, the myocardial contractility increases, using more energy and, hence, requiring more oxygen.8 Thus, the combination of decreased supply and increased demand causes a supply-demand mismatch of oxygen and other nutrients for myocardial tissue, leading to cell injury.
Tachycardia. Persistent tachycardia from numerous etiologies causes strain on the heart, resulting in a measurable troponin leak in the bloodstream. Common causes include pain, sympathetic overactivity, recreational drug use, or even abrupt drug withdrawal especially beta-blocking agents. In addition, patients with atrial fibrillation can present with a detectable troponin in the bloodstream, possibly also due to tachycardia-induced heart failure.8,9 Any cause of tachycardia may lead to a measurable troponin in the bloodstream. Tachycardia is one of the most common causes of a troponin leak in patients who had a normal coronary angiogram.8
HTN. Poorly controlled HTN over time can lead to myocardial strain. This is mainly due to long-term effects of systemic HTN that include hypertrophy of the left ventricle, development of hypertensive cardiomyopathies, and remodeling of the myocardium. Left ventricular hypertrophy happens when the left ventricle works harder to pump blood into the systemic circulation and against the raised systemic resistance.6 Thus, myocardial cells require more nutrients and oxygen and absence of adequate oxygenation and nutrients may lead to cell membrane damage. Hypertrophied myocardium with the same amount of supply of oxygen thus has to support higher demand when heart rate or BP rises. In some cases, this supply-demand mismatch can cause nonocclusive injury and ischemia of the myocardial cells with possibly detectable troponins in the bloodstream.
Detectable troponin due to pulmonary causes
The cardiac and pulmonary circulations are dependent on each other; changes in one can lead to an effect on the other as well. Pulmonary pathology influences the right-sided cardiac chambers, while the left chamber of the heart influences the pulmonary pathophysiology. COPD exacerbation leads to an increased risk of morbidity and mortality from cardiovascular conditions as COPD places increased burden on the right side of the heart secondary to changes in pulmonary artery pressures.6 COPD exacerbations can lead to detectable troponins in the bloodstream. Studies have shown that patients with higher levels of cardiac troponins during a COPD exacerbation have a higher rate of mortality within 3 years.10 Since patients with COPD exacerbations have similar symptoms to those who have ACS, such as chest pain and dyspnea as well as possibly ECG changes, it is, therefore, essential that these be differentiated, as the management strategy is different for each.