Case Presentation: A 62-year-old Caucasian male presented to the hospital with complaints of fever, cough for 1 week. The patient was diaphoretic and also complained of malaise. He was admitted after a failed course of oral antibiotics due to suspected pneumonia. The patient denied any chest pain, dyspnea, or sputum production with the cough. Physical examination was significant for mild expiratory wheezing bilaterally and diaphoretic skin. During his stay on the general medical floor, his oxygen saturation deteriorated despite oxygen by nasal cannula. He was then transferred to the ICU for acute hypoxemic respiratory failure requiring BiPap. Laboratory findings were significant for an unusually elevated high-sensitivity troponin level of 26,000. Blood cultures were positive for Methicillin-Resistant Staphylococcus Aureus (MSSA). EKG had revealed normal sinus rhythm with complete heart block and accelerated junctional rhythm. A 2D Echocardiogram had shown a moderate mitral regurgitation and AV dissociation, with no evidence of wall motion abnormalities or coronary ischemia. A TEE was then performed and showed a large annular abscess involving the AV node, extending down into the base of the mitral annulus with associated vegetations. The patient underwent cardiac catheterization for temporary pacemaker placement and was ultimately transferred to a tertiary care facility for further management.
Discussion: We present this case of a valvular abscess leading to an unusually elevated troponin level. Cardiac troponins are structural proteins of the heart, with high sensitivity and specificity for diagnosing cardiac structural damage, specifically myocardial infarction (1). However, over the years, there have been reports of falsely elevated troponin levels in the absence of coronary disease (2). Several causes of elevated troponin levels include open-heart surgery, acute pulmonary emboli, end-stage renal disease, pericarditis, and myocarditis, none of which were seen in our patient. Infection and sepsis also play a role in elevating troponin levels by increasing oxygen and perfusion demand in the heart, leading to a phenomenon known as demand ischemia (3). The hyperdynamic myocardium, that occurs in the setting of sepsis, may lead to a perfusion defect, thus leading to a pseudo-coronary syndrome. In our case, the patient had an unusually elevated troponin with no classic coronary disease symptomology, specific EKG changes, or echocardiographic findings to suggest coronary ischemia.
Conclusions: This case aims to highlight the importance of maintaining a broad differential when diagnosing a patient who presents with an unusually elevated troponin level. In addition, infective endocarditis is a vast entity that presents with a wide array of clinical symptoms. Therefore, clinical suspicion is a physician’s most potent tool to obtain an appropriate diagnosis.