The Overdiagnosis of Myocardial Infarction

A 72-year-old man with a history of well-controlled hypertension, stage 3a chronic kidney disease, supraventricular tachycardia, and gout went to the emergency department (ED) after nearly fainting while mowing his lawn. After a long wait, the ED staff took blood, started intravenous fluids, and obtained an electrocardiogram (ECG). A few hours later, the ED physician informed the patient that results of the blood test showed a slightly elevated troponin level, which could suggest a heart attack. The patient told the physician that he felt fine other than still being a bit dizzy; he asked why the blood test was done and what was going to be done about his dizziness. The physician explained that the laboratory tests were routine for someone his age after a near-fainting spell. The physician also told the patient that he would need to stay in the hospital for two more troponin tests and an echocardiogram. Several hours later, a cardiologist informed the patient that he may have had a small heart attack based on the troponin levels but that the ECG and echocardiogram results were normal. The patient was admitted to the hospital overnight for further testing. He was relieved that the heart attack was discovered, but when he asked about the cause of his dizziness, he did not receive any answers.

In her book The Danger Within Us, medical journalist Jeanne Lenzer discussed the introduction of highly sensitive blood tests in the late 1970s to detect even very small myocardial infarctions (MIs).¹ Previously, MIs were diagnosed by a combination of symptoms, ECG changes, and elevations in creatine kinase. With the new, more sensitive tests, MIs could be diagnosed in patients without any classic symptoms or ECG abnormalities. The case fatality rate of MIs declined markedly at that time, but the mortality rate remained consistent. This was due to clinicians diagnosing more MIs, thus increasing the denominator (total MIs) without changing the numerator (MI deaths).

Today, many EDs measure troponin levels even in patients without signs or symptoms of MIs, thus increasing the number of patients with an MI diagnosis.² In one study, 27% of patients admitted to the ED received troponin testing, most of whom did not present with symptoms suggesting a cardiac diagnosis.³

Diagnosis of MI

Researchers and cardiologists previously thought that evaluation using only clinical and ECG criteria, followed by confirmatory echocardiography or cardiac catheterization, missed some MIs, leading to increased mortality and morbidity.² Troponin is a highly sensitive laboratory assay that measures myocardial injury. The introduction of troponin testing in the 1990s increased the ability of physicians to identify myocardial damage. Normal troponin values are defined as falling into the 99th percentile for young, healthy patients.⁴ Troponin elevations in conjunction with other abnormal findings (eg, clinical, ECG, echocardiographic) are considered diagnostic of MI. Sequential increases in troponin levels over time can also help diagnose MI in the absence of other parameters.⁵

Although troponin levels are highly sensitive, they are not specific for type 1 MI, in which closure of myocardial vessels results in cardiac damage, and have very low positive predictive value in the absence of other criteria. The positive predictive value is much lower in the United States compared with the United Kingdom (16.4% vs 59.7%) due to the higher rate of troponin testing in the United States and the low pretest probability of MI in patients for whom troponin tests are ordered.⁶ In fact, approximately one-fifth of patients admitted to EDs have elevated troponin levels, and most are not having a type 1 MI.⁷ A type 2 MI is diagnosed in patients who meet troponin criteria for an MI but do not have obstructive coronary artery disease. The prevalence of type 2 MI diagnoses has increased with the use of troponin testing.⁸