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148 Coexistent diabetes is associated with the presence of adverse phenotypic features in patients with hypertrophic cardiomyopathy
  1. Nicholas Jex1,
  2. Sharmaine Thirunavukarasu2,
  3. Amrit Chowdhary3,
  4. Henry Procter4,
  5. Anshuman Sengupta4,
  6. Pavithra Natarajan5,
  7. Sindhoora Kotha5,
  8. Ana-Maria Poenar4,
  9. Peter Swoboda2,
  10. Hui Xue6,
  11. Richard Cubbon5,
  12. Peter Kellman6,
  13. John P Greenwood2,
  14. Sven Plein2,
  15. Stephen Page4,
  16. Eylem Levelt2
  1. 1University of Leeds, Leeds Institute of Cardiovascular and Metabolic Medicine, Leeds General Infirmary, Great George Street, Leeds, WYK LS1 3EX, United Kingdom
  2. 2Leeds Institute of Cardiovascular and Metabolic Medicine
  3. 3University of Leeds, Leeds Institute of Cardiovascular and Metabolic Medicine
  4. 4Leeds Teaching Hospitals
  5. 5University of Leeds
  6. 6National Institutes of Health


Background Type 2 diabetes mellitus (DM) is associated with worsened clinical outcomes in hypertrophic cardiomyopathy (HCM) patients. The reasons for this adverse prognostic association are incompletely understood. Although distinct entities both HCM and DM share common features of impaired myocardial energetics and coronary microvascular function.

Purpose We sought to test the hypothesis that co-existent diabetes is associated with greater reductions in myocardial energetics and perfusion, and higher scar burden in HCM.Research design and methods- Seventy-five age- and sex-matched participants with concomitant HCM and DM (HCM-DM, n=20), isolated HCM (n=20), isolated DM (n=20) and healthy volunteers (HV, n=15) underwent 31phosphorus magnetic resonance spectroscopy and cardiovascular magnetic resonance imaging. The HCM groups were matched for HCM phenotype. The DM groups were matched for diabetes treatment, duration, HbA1c, body mass index and hypertension comorbidity.

Results ESC sudden cardiac death risk scores were comparable between the HCM groups (HCM:2.2±1.5%, HCM-DM:1.9±1.2%; p=NS) and sarcomeric mutations were equally common. HCM-DM had the highest NT-proBNP levels (HV:42ng/L[IQR:35–66], DM:118ng/L[IQR:53–187], HCM:298ng/L[IQR:157–837], HCM-DM:726ng/L[IQR:213–8695];p<0.0001). Left-ventricular ejection fraction, mass and wall thickness were similar between the HCM groups. HCM-DM displayed a greater degree of fibrosis burden with higher scar percentage, and lower global longitudinal strain compared to the isolated HCM. PCr/ATP was similarly decreased in the HCM-DM and DM (HV:2.17±0.49, DM:1.61±0.23, HCM:1.93±0.38, HCM-DM:1.54±0.27; p=0.0003). HCM-DM had the lowest stress myocardial blood flow (HV:2.06±0.42 ml/min/g, DM:1.78±0.45 ml/min/g, HCM:1.74±0.44 ml/min/g, HCM-DM:1.39±0.42 ml/min/g; p=0.004).

Abstract 148 Table 1

CMR and 31P-MRS findings

Abstract 148 Figure 1

Representative examples of mid-left ventricular stress perfusion maps from a healthy volunteer (first column), a patient with DM (second column), a patient with HCM (third column) and a patient with HCM-DM (fourth column)

Conclusions We show for the first time that HCM patients with DM comorbidity display greater reductions in myocardial energetics, perfusion, contractile function and higher myocardial scar burden and serum NT-proBNP levels compared to patients with isolated HCM despite similar LV mass and wall thickness and presence of sarcomeric mutations. These adverse phenotypic features may be important components of the adverse clinical manifestation attributable to a combined presence of HCM and DM.

Conflict of Interest None

  • Diabetes
  • Cardiac Magnetic Resonance
  • Hypertrophic Cardiomyopathy

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