Key result
Type 2 diabetes linked to ~8-point higher risk of adverse cardiovascular events in HCM.
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Why the study?
Does coexisting type 2 diabetes mellitus worsen clinical outcomes and myocardial mechanics in patients with hypertrophic cardiomyopathy?
Cohort (n=582)
Does coexisting type 2 diabetes mellitus worsen clinical outcomes and myocardial mechanics in patients with hypertrophic cardiomyopathy?
In patients with hypertrophic cardiomyopathy, coexisting type 2 diabetes is associated with increased myocardial fibrosis, worse left ventricular mechanics, and a significantly higher risk of adverse clinical events.
Type 2 diabetes was associated with higher event rates in hypertrophic cardiomyopathy; leaves open whether glycemic control modifies prognosis.
BACKGROUND The impact of coexisting type 2 diabetes mellitus (T2DM) on the phenotype and prognosis of hypertrophic cardiomyopathy (HCM) remains insufficiently studied. We aimed to evaluate the structural, functional, and prognostic effects of T2DM in HCM using cardiac magnetic resonance (CMR). METHODS This retrospective cohort included 582 HCM patients (mean age 55.1 ± 11.4 years, 69% male), stratified into T2DM (n = 127) and non-T2DM (n = 455) groups. The primary endpoint was a composite of sudden cardiac death (SCD), aborted SCD, heart transplantation, heart failure hospitalization, and stroke. Mediation analysis evaluated CMR parameters' mediating effects on the HbA1c-outcome association. RESULTS Despite comparable left ventricular (LV) mass and ejection fraction, T2DM patients exhibited worse LV global longitudinal strain (LVGLS absolute value: 11.0% vs 11.9%; p = 0.002) and greater late gadolinium enhancement (LGE) extent (6.1% vs 2.3%; p < 0.001) than non-T2DM patients. Over a median 35-month follow-up, T2DM increased the risk of endpoint events (24% vs 16%; log-rank p = 0.015). Multivariable analysis identified HbA1c, NT-proBNP, LVGLS, LGE extent, and maximal wall thickness as independent predictors. Mediation analysis revealed the prognostic effect of HbA1c was largely mediated by LGE extent (71% mediation; p < 0.001) and partially by LVGLS (26%; p = 0.010), but not by macroscopic hypertrophy. CONCLUSIONS T2DM exacerbates replacement fibrosis, impairs LV mechanics, and worsens clinical outcomes in HCM. The prognostic impact of glycemic burden appears closely tracked with fibrotic remodeling and systolic dysfunction rather than structural hypertrophy. These associative, hypothesis-generating findings warrant future prospective validation.
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Cao et al. (2026) conducted a cohort in Hypertrophic cardiomyopathy (HCM) (n=582). Type 2 diabetes mellitus (T2DM) vs. Non-T2DM was evaluated on Composite of sudden cardiac death (SCD), aborted SCD, heart transplantation, heart failure hospitalization, and stroke (p=0.015). Type 2 diabetes increased the risk of adverse cardiovascular events in patients with hypertrophic cardiomyopathy compared to those without diabetes (24% vs 16%; P=0.015).
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