International journal of cardiology · 2026
Impact of type 2 diabetes on myocardial mechanics, fibrosis, and prognosis in hypertrophic cardiomyopathy: A cardiac magnetic resonance study.
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Cao Yukun, Li Yumin, Ming Zhenglin, Huang Mengting, Zhang Kailu, Zhao Jie, Xu Cihao, Liu Xiaoqing, Wang Hua, Shi Heshui
Аннотация
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.
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.