From the Guidelines
Yes, troponins can be elevated during congestive heart failure (CHF) exacerbations, even in the absence of acute coronary syndrome or myocardial infarction. During CHF exacerbations, cardiac troponins (both troponin T and troponin I) may rise due to several mechanisms including myocardial strain, volume overload, subendocardial ischemia from increased wall tension, inflammatory cytokines, and oxidative stress 1. These factors can cause cardiomyocyte injury and subsequent troponin release. The elevation is typically mild to moderate compared to the more dramatic increases seen in acute myocardial infarction.
Some key points to consider:
- Elevated troponins in CHF are associated with worse outcomes and higher mortality 1.
- Abnormal troponin levels can occur from myocardial ischemia, myocardial stress, cardiomyocyte apoptosis and autophagy, and exosomal release of cytosolic troponin 1.
- Serial testing of high-sensitivity cardiac troponin (hs-cTn) concentrations can help differentiate myocardial infarction from chronic hs-cTn elevations due to heart failure 1.
- Clinicians should interpret elevated troponins in the context of the patient's overall clinical presentation, and consider other potential causes of troponin elevation while managing the underlying heart failure with appropriate therapies 1.
When evaluating a patient with CHF exacerbation and elevated troponins, it's essential to consider the patient's overall clinical presentation and manage the underlying heart failure with appropriate diuretics, ACE inhibitors/ARBs, beta-blockers, and other heart failure therapies as indicated. The presence of elevated troponins should prompt a thorough evaluation and management of the patient's heart failure, rather than solely focusing on the troponin elevation.
From the Research
Troponin Elevation in CHF Exacerbation
- Troponin levels can be elevated in patients with congestive heart failure (CHF) exacerbation, as shown in studies 2, 3, 4, 5.
- The mechanism of troponin elevation in CHF is thought to be related to ventricular remodeling, ongoing myocyte degeneration, and reduced coronary reserve 2, 3.
- Troponin elevation in CHF is associated with decreased left ventricular ejection fraction and poor prognosis 2, 3.
- The release of cardiac troponins in CHF may also be related to supply-demand inequity, cellular necrosis, apoptosis, or autophagy in the context of wall stress, as well as toxic effects of circulating neurohormones, toxins, inflammation, and infiltrative processes 4.
- Elevated levels of troponin I have been regarded as biochemical markers of myocyte necrosis in CHF, and are correlated with disease severity 5.
- Clinicians should be aware of the high frequency of troponin elevation in patients with CHF, and recognize the considerable ramifications of troponin elevation in this setting, independent of a diagnosis of 'acute MI' 4.
Clinical Importance of Troponin Elevation
- Elevated troponin levels are strongly predictive of an adverse outcome in patients with CHF 4.
- The measurement of troponin levels, along with B-type natriuretic peptide (BNP), can help risk-stratify patients and manage them effectively 2.
- Troponin elevation is more common in severely symptomatic patients with CHF, particularly those with New York Heart Association (NYHA) class III-IV 5.
Mechanisms of Troponin Elevation
- Possible mechanisms for the release of cardiac troponins in CHF include ventricular remodeling, presence of coronary artery disease, abnormalities of coronary microcirculation, and reduced coronary reserve 3.
- Non-coronary triggers, such as cellular necrosis, apoptosis, or autophagy in the context of wall stress, may also explain the troponin release in CHF 4.