PET myocardial perfusion imaging in the diagnosis of apical hypertrophic cardiomyopathy
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Department of Cardiology, Rush University Medical Center, Chicago
Received Jul 24, 2020; accepted Jul 27, 2020 doi:10.1007/s12350-020-02344-5
INTRODUCTION Hypertrophic cardiomyopathy is underdiagnosed in the clinical setting. In patients that present with chest pain or other non-specific findings such as troponin elevation, oftentimes nuclear stress testing is obtained as a first test. Findings in cardiac positron emission tomography (PET) myocardial perfusion imaging (MPI) should trigger additional imaging for diagnosis and risk stratification. Case Summary A 50-year-old man with no known past medical history presented to the ED complaining of fevers and diarrhea. Blood pressure was 115/66 mmHg, heart rate was 117 bpm, temperature of 103.1 F, and oxygen saturation was 99%. Physical exam was unremarkable. Labs were notable for troponin of 0.30 ngmL-1. EKG showed left ventricular hypertrophy and T-wave inversions (Figure 1) and PCR was positive for influenza A. PET MPI showed a small, mild completely reversible defect in the apex, apical thickening, normal left ventricular function, and no evidence of coronary artery
Reprint requests: Claudia Lama von Buchwald, MD, Department of Cardiology, Rush University Medical Center, Chicago; [email protected] J Nucl Cardiol 1071-3581/$34.00 Copyright Ó 2020 American Society of Nuclear Cardiology.
calcium (Figure 2). Global myocardial flow reserve was normal at 2.89, but with a clear gradient of diminishing flow reserve from the basal to the apical segments (Figure 3B). Echocardiogram demonstrated a normal ejection fraction with apical thickening on contrast images (Figure 4). Cardiac magnetic resonance (CMR) confirmed the diagnosis of apical hypertrophic cardiomyopathy (HCM) (Figure 5).1 The patient was treated with oseltamivir with improvement of his symptoms. An increased number of apical counts on rest volume-weighted polar maps, as well as relative apical ischemia in the absence of coronary artery disease, have previously been described in single-positron emission computer tomography (SPECT), as a ‘‘Solar Polar’’ map pattern.2 These findings can be evidenced on PET, with the normal apical thinning of PET now ‘‘normalized.’’ In addition, flow quantification demonstrates a relative reduction in flow from the basal to the apical segments with stress. The reduction in flow reserve is likely caused by microvascular ischemia in the setting of supply-demand mismatch from apical hypertrophy.
von Buchwald and Sanghani PET myocardial perfusion imaging
Journal of Nuclear CardiologyÒ
Figure 1. EKG showing marked left ventricular hypertrophy (LVH) and prominent T-wave inversions, predominantly in the lateral leads.
Journal of Nuclear CardiologyÒ
von Buchwald and Sanghani PET myocardial perfusion imaging
Figure 2. PET myocardial perfusion imaging showed a small sized, mild severity, completely reversible defect in the apex (solid arrows). Normal rest PET would show mildly decreased apical counts of the thinner apical wall. In this case, the apex is ‘‘normal
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