Subendocardial Late Gadolinium Enhancement Without Troponin Elevation: A Case of Apical Hypertrophic Cardiomyopathy...

Apical hypertrophic cardiomyopathy (AHCM), also known as Yamaguchi syndrome, is a rare variant of hypertrophic cardiomyopathy (HCM) characterized by localized thickening of the left ventricular apex. Clinically, it may mimic acute coronary syndrome (ACS), myocarditis, or pericarditis. Cardiac magnetic resonance (CMR) allows the identification of myocardial involvement even in the absence of elevated serum biomarkers. A 39-year-old Hispanic man presented with a four-day history of oppressive chest pain radiating to the left arm, associated with dyspnea, fever, and dysuria. On admission, ECG demonstrated deep T-wave inversions; initial risk stratification (a thrombolysis in myocardial infarction (TIMI) score of 3 and a history, ECG, age, risk factors, and troponin (HEART) score of 4) indicated intermediate probability of ACS. hs-cTn remained negative; however, laboratory tests showed leukocytosis with neutrophilia, elevated inflammatory markers, and a positive urine culture for Escherichia coli. The transthoracic echocardiogram (TTE) showed apical hypokinesia and hypertrophy, and coronary CT angiography (CCTA) excluded obstructive disease, while CMR confirmed apical hypertrophy with evidence of myocardial involvement. The patient improved with targeted antibiotic and medical therapy and was discharged with outpatient cardiology follow-up for risk stratification and consideration of implantable cardioverter-defibrillators (ICD); however, it was deferred as no advanced atrioventricular (AV) block, syncope, or ventricular arrhythmias were documented.  AHCM is infrequent in the Hispanic population and may present with chest pain and intermediate risk scores for ACS despite negative troponins. Myocardial involvement, characterized by CMR, helps identify the etiology of chest pain and differentiate ischemic from nonischemic injury, even when serum biomarkers are normal or inconclusive, which in our case was due to the intrinsic microvascular dysfunction of AHCM, likely aggravated by the systemic inflammatory response syndrome (SIRS) triggered by a urinary tract infection.