Cardiac amyloidosis presenting with elevations of cardiac troponin I and angina pectoris

Abstract

Summary:We present the case of a 43-year-old male who was initially evaluated for angina pectoris and dyspnea. His CK, CK-MB, and cTnI were all elevated following a blood transfusion and he underwent coronary arteriography, which demonstrated no luminal obstructions. After several months, he was transferred to Mayo Clinic where diagnoses of fulminant cardiac amyloidosis and systemic multiple myeloma were established. The cTnI remained elevated despite normalization of the CK and CK-MB. Despite aggressive treatment, the patient died. Postmortem analysis demonstrated amyloid cardiac deposition including involvement of the coronary microvasculature. Electron microscopy revealed myocyte compression injury from amyloid infiltration. We believe this is the first report of elevated troponin I in a patient with cardiac amyloidosis. The electron microscopy in our case confirms cardiac damage as the mechanism for cTnI elevation. This observation strengthens our knowledge about the specificity of cTnI for the detection of cardiac injury.

Elevated troponin level is not synonymous with myocardial infarction

“…Infiltrative conditions like amyloidosis are associated with myocyte compression injury that precipitates the cTnI release [19,41]. Elevated cTnI is frequently seen in end stage renal failure patients, even in the absence of uremic perimyocarditis (pericardial effusion) or pulmonary congestion [42].…”

Narrative Review: Alternative Causes for Elevated Cardiac Troponin Levels when Acute Coronary Syndromes Are Excluded

“…The positive and negative predictive values of an elevated troponin level were 21% and 94%, making troponin testing a valuable tool in excluding significant myocardial injury after trauma. Other reasons for traumatic troponin elevation include implantable cardioverter defibrillator shocks (28) and infiltrative disorders such as amyloidosis (29). It has been postulated that extracellular amyloid deposition may lead to myocyte compression injury, leading to myocardial damage and troponin release.…”

It’s Time for a Change to a Troponin Standard

“…28 Unfortunately, only 2 case reports have been published in humans that pathologically confirm cardiac injury in association with subtle increases in troponin. 29,30 Additional pathological studies are needed.…”