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. 2017 May 1;18(8):915-921.
doi: 10.1093/ehjci/jex036.

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

Marcelo Dantas Tavares de Melo  1 , Maria Clementina Pinto Giorgi  2 , Antonildes Nascimento Assuncao Jr  3 , Roberto Nery Dantas Jr  3 , Jose de Arimateia Araujo Filho  3 , Jose Rodrigues Parga Filho  3 , Ana Luiza de Souza Bierrenbach  4 , Camila Rocon de Lima  1 , José Soares Jr  2 , José Claudio Meneguetti  2 , Charles Mady  5 , Ludhmila Abrahão Hajjar  4 , Roberto Kalil Filho  4 , Edimar Alcides Bocchi  1 , Vera Maria Cury Salemi  1
Affiliations

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

Marcelo Dantas Tavares de Melo et al. Eur Heart J Cardiovasc Imaging. .

Abstract

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. Patients with LVNC had lower global MGU compared with that in controls (36.9 ± 8.8 vs. 44.6 ± 5.4 μmol/min/100 g, respectively, P = 0.02). Of 17 LV segments, MGU levels were significantly reduced in 8, and also a reduction was observed when compacted segments from LVNC were compared with the segments from control subjects (P < 0.001). Perfusion defects were also found in 15 (50%) patients (45 LV segments: 64.4% match, and 35.6% mismatch perfusion-metabolism pattern). Univariate and multivariate analyses showed that beta-blocker therapy was associated with increased MGU (beta coefficient = 10.1, P = 0.008). Moreover, a gradual increase occurred in MGU across the beta-blocker dose groups (P for trend = 0.01).

Conclusion: The reduction of MGU documented by FDG-PET in LVNC supports the hypothesis that a cellular metabolic pathway may play a role in the pathophysiology of LVNC. The beneficial effect of beta-blocker mediating myocardial metabolism in the clinical course of LVNC requires further investigation.

Keywords: PET; metabolism; pathophysiology; perfusion; non-compaction.

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