Table 1

 Causes of elevated troponins, prevalence, and underlying mechanism

Troponin elevation (disease)Prevalence of troponins (cut-offs)Key referencesMechanism of troponin release
ACS, acute coronary syndrome; AMI; acute myocardial infarction, ESRD; end stage renal disease; HF; heart failure; NSTEMI, non-ST elevation myocardial infarction; PCI; percutaneous coronary intervention; STEMI, ST elevation myocardial infarction.
ACS related
AMI100% per definitionAlpert JS. J Am Coll Cardiol 2000;36:959–69.Thrombotic occlusion of coronary artery (STEMI), microembolisation (NSTEMI)
Post-PCI31% (cTnI) – 40% (cTnI); 24% (cTnT)Nageh T. Heart 2005; 91:1181–5. Okmen E. J Invasive Cardiol 2005;17:63–7.Side branch occlusion, coronary dissection, bulky devices causing transient ischaemia and microembolisms
Open heart surgery100% (cTnT)Lehrke S. Clin Chem 2004;50:1560–7.Myocardial infarction, incomplete cardioprotection, reperfusion injury, direct surgical trauma
Non-ACS related
Acute pulmonary embolismVariable, depending on cut-off; 32% at cTnT >0.1 ng/ml – 50% at cTnT >0.01 ng/mlGiannitsis E. Circulation 2000;102:211–7. Pruszczyk P. Chest 2003;123:1947–52.Right ventricular strain
Asymptomatic patients with ESRDVariable, depending on cut-off; 99th centile/10% CV/ROC: 82%/53%/20% for cTnT and 6%/1%/0.4% for cTnIApple FS. Circulation 2002;106:2941–5.Several possible reasons including coronary and non-coronary cardiac origin; prolonged renal elimination; non-dialysable, intact cTnT; differences to cTnI may be related to higher affinity to dialysis membrane, unstable molecule (fragments), smaller protein
Pericarditis/myocarditis32–49% (cTnI)Smith SC. Circulation 1997;95:163–8. Imazio M. J Am Coll Cardiol 2003;42:2144–8. Bonnefoy E. Eur Heart J 2000;21:832–6.Direct damage of myocytes
Aortic dissection Stanford A24% (cTnI >1.5 ng/ml)Bonnefoy E. Acta Cardiol 2005;60:165–70.Dissection of coronary artery
Chronic HF15% (cTnT >0.1 ng/ml) –23% (stable and unstable) (cTnI >0.3 ng/ml)Missov E. Am Heart J 1999;138:95–9. La Vecchia L. Am J Cardiol 1997;80:88–90.Global wall stretch, degradation of contractile protein and cellular injury due to oxidative stress and neurohumoral factors
Acute HF52% (cTnT ⩾0.02 ng/ml) –55% (cTnT ⩾0.1 ng/ml)Setsuda K. Am J Cardiol 1999; 84: 608–11. Perna ER. Am Heart J 2002;143:814–20.Global wall stretch, hypoxaemia, systemic hypoperfusion, coronary malperfusion
Strenuous exercise/ultra-endurance athletes26% (cTnT), 9% (cTnI); 23% (cTnT), 32% (cTnI)Rifai N. Am J Cardiol 1999;83:1085–9. Urhausen A. Am J Cardiol 2004;94:696–8.Ventricular stretch, release of soluble troponin, underlying cardiac disease
Cardiotoxic chemotherapyUnknownYeh ET. Circulation 2004;109:3122–31.Direct toxic effect on myocytes
High frequency ablation/ current cardioversion-defibrillator shocks90% (cTnI)Madrid AH. Am Heart J 1998;136:948–55.Direct myocardial damage
Cardiac infiltrative disorders (amyloidosis)UnknownDispenzieri A. Lancet 2003;361:1787–9.Myocyte compression
Heart transplant100% (up to 3 months) variable after 3 monthsZimmermann R. Br Heart J 1993;69:395–8. Labarrere CA. JAMA 2000;284:457–64.Inflammatory/immune mediated
Cardiac contusion after blunt chest wall trauma12% (cTnI) – 15% (cTnT)Edouard AR. Anesthesiology 2004;101:1262–8. Collins JN. Am J Surg 2001;67:821–5.Direct myocardial damage
Sepsis/critical ill patients36% (cTnT ⩾0.1 ng/ml) – 85% (cTnT >0.1 ng/ml)ver Elst KM. Clin Chem 2000;46:650–7. Ammann P. Intensive Care Med 2001;27:965–9Oxygen supply/demand mismatch, cytokine/endotoxin mediated toxicity, heterophilic antibodies (false positive)
RhabdomyolysisUnknownLavoinne A. Clinical Chemistry 1998;44:667–8.Cross-reactivity between skeletal and cardiac muscle isoforms of troponins in first and second generation troponin assays