Does pancreatitis affect troponin levels?

From the Guidelines

Pancreatitis can cause elevated troponin levels, as evidenced by various studies, including 1, which highlights that troponin elevations can occur in severe noncardiac conditions such as sepsis, burns, respiratory failure, acute neurological diseases, and critically ill patients.

Mechanisms of Troponin Elevation in Pancreatitis

The mechanisms behind this elevation include:

• Inflammatory mediators released during pancreatitis affecting cardiac function
• Renal impairment from pancreatitis reducing troponin clearance
• Severe pancreatitis causing systemic inflammatory response syndrome (SIRS) that impacts multiple organs, including the heart
• Metabolic disturbances, hypotension, and hypoxemia accompanying severe pancreatitis causing cardiac stress or injury

Clinical Implications

It is crucial to interpret troponin elevations in the context of the patient's overall clinical picture, considering both pancreatic inflammation and potential cardiac issues when managing patients with pancreatitis and elevated troponin levels.

Key Considerations

• Elevated troponin in pancreatitis patients does not always indicate a heart attack but should prompt cardiac evaluation due to increased cardiovascular risk.
• The 2014 AHA/ACC guideline for the management of patients with non-ST-elevation acute coronary syndromes 1 emphasizes the importance of considering serial changes for the diagnosis of myocardial infarction and being aware of the sensitivity of the tests used for troponin evaluation.
• Clinicians should be cautious of chronic elevations of troponin, which can result from structural cardiac abnormalities or renal insufficiency, as noted in 1.

Recommendations for Practice

Given the potential for pancreatitis to cause elevated troponin levels, clinicians should prioritize a comprehensive evaluation, including cardiac assessment, in patients with pancreatitis presenting with elevated troponin levels, to differentiate between cardiac and non-cardiac causes of troponin elevation. This approach is supported by the principles outlined in 1, which defines the universal definition of myocardial infarction and emphasizes the importance of clinical context in interpreting troponin levels.

From the Research

Pancreatitis and Troponin Levels

• Pancreatitis can cause elevated troponin levels, as seen in a case study where a patient presented with epigastric pain, normal electrocardiogram (ECG), elevated high-sensitive troponin-T, and elevated lipase and amylase 2.
• Elevated troponin levels in acute pancreatitis may not always indicate myocardial injury, as shown in a study where patients with acute biliary pancreatitis had high troponin-T levels without evidence of myocardial injury 2.
• Cardiac indicators such as cardiac troponin I (cTNI) and creatine kinase myocardial band (CK-MB) may be elevated in acute pancreatitis, and CK-MB may be a predictive marker for severity and organ failure development 3.

Mechanisms and Clinical Implications

• The pathogenetic factors of cardiac manifestations in acute pancreatitis include hypovolemia and metabolic disturbances, such as hyperkalemia, hypomagnesemia, and hypophosphatemia 4.
• Approximately 50% of patients with acute pancreatitis have electrocardiographic changes, most commonly T-wave flattening and ST-segment depression 4.
• Cardiovascular dysfunction is common in severe acute pancreatitis, with diastolic dysfunction being the most common type, and is associated with poor outcome 5.

Diagnosis and Management

• The presentation of retrosternal chest pain with normal ECG during chest pain followed by initial presentation of acute pancreatitis can lead to a dilemma in managing such a patient, and whether to thrombolyse such a patient is a real controversy 6.
• Echocardiography can be used to characterize cardiac dysfunction in early severe acute pancreatitis, and may help determine the frequency, nature, and prognostic significance of cardiac dysfunction 5.