Troponin T is 1 of 3 polypeptide chains that make up the troponin complex. It is a cardiac-specific protein that binds to tropomyosin and is released only from injured heart cells. Cardiac troponins are the most sensitive and specific indicator of myocardial damage. The cause of the damage can range from strenuous exercise to myocardial ischemia. Other causes of increased troponin without myocardial infarction include congestive heart failure, pericarditis, pulmonary embolism, myocarditis, and sepsis. In the absence of other clinical or electrocardiographic evidence of myocardial infarction, increased levels can be of prognostic value. Cardiac troponin T increases after coronary artery bypass grafting are associated with increased mortality at 1 year.1Kathiresan S. Servoss S.J. Newell J.B. Trani D. MacGillivray T.E. Lewandrowski K. et al.Cardiac troponin T elevation after coronary artery bypass grafting is associated with increased one-year mortality.Am J Cardiol. 2004; 94: 879-881Abstract Full Text Full Text PDF PubMed Scopus (66) Google Scholar Asymptomatic troponin increases in patients after vascular surgery have been associated with significantly higher mortality at a median follow-up of 4 years.2Kertai M.D. Boersma E. Klein J. Van Urk H. Bax J.J. Poldermans D. Long-term prognostic value of asymptomatic cardiac troponin T elevations in patients after major vascular surgery.Eur J Endovasc Surg. 2004; 28: 59-66Abstract Full Text Full Text PDF PubMed Scopus (116) Google Scholar This report by Abraham et al documents postoperative asymptomatic troponin T increases that are higher in patients undergoing open abdominal aortic aneurysm repair compared with an endovascular approach. This implies increased myocardial strain during the open procedure. The difference between the 2 groups is more significant given that the incidence of coronary artery disease documented before surgery was higher in the endovascular group. Besides myocardial ischemia, other explanations for this finding include increased blood loss and hypotension during the open procedure. In the absence of these complications, a postoperative troponin T increase is even more significant because it implies myocardial damage under less stress. It is important to note that the authors excluded patients with increased creatinine, in whom troponin T measurement can be less accurate than troponin I. Although increases in troponin T in the absence of other indicators of myocardial ischemia were not associated with an increase in perioperative morbidity or mortality, they identify a group of patients who remain at increased risk of myocardial events during follow-up. These patients should undergo further evaluation to exclude significant coronary artery disease. These findings continue to support the notion that endovascular abdominal aortic aneurysm repair is to be preferred, particularly in higher-risk patients. A prospective study of subclinical myocardial damage in endovascular versus open repair of infrarenal abdominal aortic aneurysmsJournal of Vascular SurgeryVol. 41Issue 3PreviewEndovascular repair of abdominal aortic aneurysms (AAAs) is considered to be less invasive and better tolerated by the cardiovascular system than open repair. Our aim was to assess the true incidence of perioperative myocardial damage associated with endovascular vs open infrarenal AAA repair. Full-Text PDF Open Archive