Elevated cardiac troponin, a diagnostic marker of damage to the heart, may occur even if a patient has not had a heart attack, according to a study published in JACC: Basic to Translational Science.
In a porcine model of brief ischemia leading to reversible stunning in the absence of myocardial tissue necrosis, Brian R. Weil, PhD, and colleagues demonstrated delayed release of cardiac troponin I that exceeded the 99th percentile for normal animals 60 minutes after reperfusion and rose to readily detectable levels 24 hours later. Although tissue analysis at 60 minutes showed no evidence of necrotic myocyte cell death seen with a myocardial infarction, TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling) staining demonstrated isolated myocytes undergoing apoptosis, which was absent after 24 hours. These results demonstrate that cardiac troponin I elevations occur after cardiac injury that is not severe enough to produce classic myocyte necrosis that is observed following heart attack and that elevated troponin levels may reflect myocyte injury in the absence of pathological evidence of infarction.
"This study by Weil and colleagues, although performed in a large animal model, may have important implications for health care systems, which are currently overwhelmed with trying to understand how to choose the appropriate diagnostic codes for hospitalized patients who have elevated troponin levels, which are being detected with alarming regularity following the FDA approval of new 'high sensitivity' troponin assays," said Douglas L. Mann, MD, FACC, editor-in-chief of JACC: Basic to Translational Science. "A rise in troponin has traditionally been associated with an acute myocardial infarction. Accordingly, when a patient has an elevated troponin level, they are often subjected to a battery of expensive non-invasive and invasive testing in order to be certain that the patient is not at risk of dying from a 'heart attack.'
"This study by Weil and colleagues clearly shows that troponin elevations can occur in the absence of a classic myocardial infarction, but can occur from a different form of cell death, called apoptosis. Although the study may not immediately stop the unnecessary testing that follows the incidental detection of an elevated troponin level, it should focus future research efforts on understanding how and why troponin is released from the heart, so that we have a better understanding of what to say to patients when they have an elevated troponin level detected on a routine laboratory test."
The American College of Cardiology is the professional home for the entire cardiovascular care team. The mission of the College and its more than 52,000 members is to transform cardiovascular care and to improve heart health. The ACC leads in the formation of health policy, standards and guidelines. The College operates national registries to measure and improve care, offers cardiovascular accreditation to hospitals and institutions, provides professional medical education, disseminates cardiovascular research and bestows credentials upon cardiovascular specialists who meet stringent qualifications. For more, visit acc.org.
The Journal of the American College of Cardiology is the most widely read cardiovascular journal in the world and is the top ranked cardiovascular journal for its scientific impact. JACC is the flagship for a family of journals that publish peer-reviewed research on all aspects of cardiovascular disease. JACC: Cardiovascular Interventions, JACC: Cardiovascular Imaging and JACC: Heart Failure also rank among the top ten cardiovascular journals for impact. JACC: Clinical Electrophysiology and JACC: Basic to Translational Science are the newest journals in the JACC family. Learn more at JACC.org.