Perspective:

This is a contemporary summary of troponin elevation in patients presenting with heart failure (HF) syndromes, including updates on troponin testing, etiologies for troponin elevations, and patient prognosis. The following are 10 points to remember:

1. Troponin elevations can result from spontaneous acute myocardial infarction (MI) (type I MI) and from supply-demand mismatch (type II MI) in absence of acute plaque rupture. Because a large percentage of patients with incident HF present with a type I MI, acute coronary obstruction should be excluded during the initial evaluation.

2. In type II MI, it is believed that subendocardial ischemia may lead to troponin release. This may occur with reduced oxygen delivery in the setting of chronic coronary disease, endothelial dysfunction, anemia, hypotension, high wall stress, or rapid ventricular rates.

3. Cardiomyocyte turnover may result in subtle elevations of troponins measured with high-sensitive troponin assays. Low-level troponins may be released due to wall stress-induced myocyte apoptosis, autophagy, and contractile apparatus proteolysis; cellular toxicity from neurohormones or toxins (alcohol, chemotherapy); infiltrative processes (amyloid); and inflammation (viral myocarditis, SIRS).

4. Extracardiac causes of troponin elevation can be seen in patients without cardiac disease. Causes include the presence of heterophile antibodies, skeletal muscle diseases leading to fetal gene upregulation, or reduced clearance of troponins in renal failure.

5. Patients with renal failure often have elevated troponins. While elevations may be due to reduced troponin renal clearance, patients with renal dysfunction tend to carry risk factors for cardiac disease (coronary disease and/or heart failure), which confounds the interpretation of troponin results.

6. Patients with acute or chronic HF presenting with a troponin elevation above the 99th percentile of the population are more likely to have worse left ventricular function, worse symptomatology, and need for more aggressive support (e.g., inotropes).

7. An elevated troponin is associated with increased mortality risk, independent of B-type natriuretic peptide levels, patient age, and ventricular function.

8. Troponin levels may rise and fall with therapy. The pattern of troponin elevation should not be used to infer coronary versus noncoronary mechanism or be used to exclude the presence of coronary disease.

9. Elevated biomarkers reflective of other pathophysiologic states in HF, such as natriuretic peptides (wall stress), C-reactive protein (inflammation), anemia, etc., afford additive risk when coexistent with elevated troponins.

10. Aside from managing type I MI, data are lacking for therapeutic interventions in patients with troponin elevation in either acute or chronic HF.