Key result
Type 2 diabetes with apical HCM is linked to a ~34-point increase in myocardial scar over 9 years.
Why the study?
To review the natural history of comorbid type two diabetes and apical hypertrophic cardiomyopathy using serial imaging, assessing their combined impact on myocardial structure and perfusion.
Case Report (n=1)
No
Co-morbid Type 2 diabetes and apical HCM can lead to severe progressive coronary microvascular dysfunction, refractory angina, and a dramatic increase in myocardial scar burden (from 6% to 40%) with NSVT even when the ESC 5-year SCD risk score remains below the 5% threshold.
May warrant serial microvascular assessment in diabetes with apical HCM; leaves open effects on arrhythmia risk stratification.
Background: Using serial imaging over time, this case reviews the natural history of co-morbid Type two diabetes (T2D) and apical hypertrophic cardiomyopathy (HCM) and assesses the potential combined impact on myocardial structure and perfusion. Case summary: A 59-year-old patient with concomitant T2D and an apical phenotype of HCM was seen over a 11-year period with a significant burden of anginal chest pain. Chest pain was refractory to anti-anginal medical therapy and persisted at on-going follow-up. Multi-modality imaging demonstrated significant deterioration in coronary microvascular function and increased myocardial scar burden despite unobstructed epicardial coronary arteries. Discussion: Comorbidity with T2D and apical HCM resulted in a significant increase in myocardial fibrosis and deterioration in coronary microvascular function.
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Jex et al. (2022) conducted a case report in Apical hypertrophic cardiomyopathy and Type 2 diabetes with refractory angina (n=1). Concomitant Type 2 diabetes and apical hypertrophic cardiomyopathy managed with serial cardiac magnetic resonance imaging and anti-anginal therapy was evaluated on Progression of myocardial scar burden on late gadolinium enhancement (LGE) and coronary microvascular dysfunction (MPR and stress MBF). Co-morbid Type 2 diabetes and apical HCM resulted in LGE myocardial scar burden increasing from 6% to 40% and MPR declining from 2.9 to 1.3 over 9 years.
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