Decreased glycolytic metabolism in non-compaction cardiomyopathy by 18F-fluoro-2-deoxyglucose positron emission tomography: new insights into pathophysiological mechanisms and clinical implications.

Aims: The pathophysiological mechanisms of left ventricular non-compaction cardiomyopathy (LVNC) remain controversial. This study performed combined 18F-fluoro-2-deoxyglucose dynamic positron emission tomography (FDG-PET) and 99mTc-sestamibi single-photon emission computed tomography (SPECT) studies to evaluate myocardial glucose metabolism and perfusion in patients with LVNC and their clinical implications.

Methods And Results: Thirty patients (41 ± 12 years, 53% male) with LVNC, diagnosed by cardiovascular magnetic resonance (CMR) criteria, and eight age-matched healthy controls (42 ± 12 years, 50% male) were prospectively recruited to undergo FDG-PET with measurement of the myocardial glucose uptake rate (MGU) and SPECT to investigate perfusion-metabolism patterns.

Noncompaction cardiomyopathy: a substrate for a thromboembolic event.

Background: Noncompaction cardiomyopathy (NCC) is a rare genetic cardiomyopathy characterized by a thin, compacted epicardial layer and an extensive noncompacted endocardial layer. The clinical manifestations of this disease include ventricular arrhythmia, heart failure, and systemic thromboembolism.

Case Presentation: A 43-year-old male was anticoagulated by pulmonary thromboembolism for 1 year when he developed progressive dyspnea.