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Published on: August 8, 2022
Coexistent Diabetes Is Associated With the Presence of Adverse Phenotypic Features in Patients With Hypertrophic
Nicholas Jex1, Amrit Chowdhary1, Sharmaine Thirunavukarasu1
1Multidisciplinary Cardiovascular Research Centre and Biomedical Imaging Science Department, Leeds Institute of Cardiovascular and Metabolic Medicine, University of Leeds, Leeds, U.K.
Insights
Type 2 diabetes mellitus (T2DM) worsens outcomes in hypertrophic cardiomyopathy (HCM). HCM patients with T2DM show reduced heart energy, blood flow, and function, alongside increased scarring, compared to those without diabetes.
Area of Science:
- Cardiology
- Metabolic Diseases
- Cardiovascular Imaging
Background:
- Type 2 diabetes mellitus (T2DM) is linked to poorer outcomes in hypertrophic cardiomyopathy (HCM) patients.
- Understanding the cardiac impact of T2DM in HCM is crucial for patient management.
Purpose of the Study:
- To investigate cardiac alterations in myocardial energetics, function, perfusion, and tissue characteristics in HCM patients with T2DM.
- To compare these parameters between HCM patients with and without T2DM, and healthy volunteers.
Main Methods:
- A study involving 55 participants: 20 with HCM and T2DM (HCM-DM), 20 with isolated HCM, and 15 healthy volunteers (HV).
- Utilized 31P-MRS (phosphorus-31 magnetic resonance spectroscopy) and cardiovascular MRI to assess myocardial energetics, function, and tissue characteristics.
- Groups were matched for HCM phenotype, and HCM groups were compared for risk scores and mutation presence.
Main Results:
- HCM-DM patients exhibited significantly lower phosphocreatine/ATP ratios (myocardial energetics) and stress myocardial blood flow (perfusion) compared to both isolated HCM and HV groups.
- HCM-DM patients showed a greater degree of myocardial fibrosis (scar burden) and lower global longitudinal strain (contractile function).
- Serum NT-proBNP levels were highest in the HCM-DM group, indicating greater cardiac strain, despite similar LV ejection fraction, mass, and wall thickness between HCM groups.
Conclusions:
- HCM patients with T2DM demonstrate significantly impaired myocardial energetics, reduced perfusion, and diminished contractile function compared to those with isolated HCM.
- Increased myocardial scar burden and elevated NT-proBNP levels in HCM-DM patients highlight a more severe cardiac phenotype.
- These findings underscore the detrimental impact of T2DM comorbidity on cardiac health in HCM patients, contributing to adverse clinical manifestations.
Objective:
Type 2 diabetes mellitus (T2DM) is associated with worsened clinical outcomes in hypertrophic cardiomyopathy (HCM) patients. We sought to investigate whether HCM patients with T2DM comorbidity exhibit adverse cardiac alterations in myocardial energetics, function, perfusion, or tissue characteristics.
Research Design And Methods:
A total of 55 participants with concomitant HCM and T2DM (HCM-DM) (n = 20) or isolated HCM (n = 20) and healthy volunteers (HV) (n = 15) underwent 31P-MRS and cardiovascular MRI. The HCM groups were matched for HCM phenotype.
Results:
Mean ± SD European Society of Cardiology sudden cardiac death risk scores were comparable between the HCM groups (HCM 2.2 ± 1.5%, HCM-DM 1.9 ± 1.2%; P = not significant), and sarcomeric mutations were equally common. HCM-DM patients had the highest median NT-proBNP levels (HV 42 ng/L [interquartile range 35-66], HCM 298 ng/L [157-837], HCM-DM 726 ng/L [213-8,695]; P < 0.0001). Left ventricular (LV) ejection fraction, mass, and wall thickness were similar between the HCM groups. HCM-DM patients displayed a greater degree of fibrosis burden with higher scar percentage and lower global longitudinal strain compared with HCM patients. PCr/ATP (the relative concentrations of phosphocreatine and ATP) was significantly lower in the HCM-DM group than in both HCM and HV (HV 2.17 ± 0.49, HCM 1.93 ± 0.38, HCM-DM 1.54 ± 0.27; P = 0.002). In a similar pattern, stress myocardial blood flow was significantly lower in the HCM-DM group than in both HCM and HV (HV 2.06 ± 0.42 mL/min/g, HCM 1.74 ± 0.44 mL/min/g, HCM-DM 1.39 ± 0.42 mL/min/g; P = 0.002).
Conclusions:
We show for the first time that HCM-DM patients display greater reductions in myocardial energetics, perfusion, and contractile function and higher myocardial scar burden and serum NT-proBNP levels compared with 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 T2DM.
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