Key result
Type 2 diabetes mellitus had an additive deleterious effect on left ventricular deformation in patients with non-ischemic dilated cardiomyopathy, independently reducing global circumferential and longitudinal peak strain.
Why the study?
Although type 2 diabetes mellitus increases the risk of worse long-term outcomes in non-ischemic dilated cardiomyopathy, its additive effects on left ventricular function remain unclear.
Does comorbid Type 2 Diabetes Mellitus worsen left ventricular deformation assessed by CMR in patients with non-ischemic dilated cardiomyopathy?
Observational (n=515)
No
Does comorbid Type 2 Diabetes Mellitus worsen left ventricular deformation assessed by CMR in patients with non-ischemic dilated cardiomyopathy?
Absolute Event Rate: -4.54% vs -5.59%
p-value: p=<0.017
Comorbid T2DM and poor glycemic control have an additive deleterious effect on left ventricular myocardial strain in patients with non-ischemic dilated cardiomyopathy.
May warrant glycemic assessment in non-ischemic dilated cardiomyopathy; leaves open whether T2DM treatment improves strain or outcomes.
BACKGROUND: Type 2 diabetes mellitus (T2DM) increases the risk of worse long-term outcomes in patients with non-ischemic dilated cardiomyopathy (NIDCM). However, the additive effects of T2DM on left ventricular (LV) function in NIDCM remain unclear. Accordingly, we aimed to investigate the impact of comorbid T2DM on LV deformation in NIDCM individuals. MATERIALS AND METHODS: Three hundred forty-two NIDCM patients without T2DM [NIDCM (T2DM-)], 93 with T2DM [NIDCM (T2DM+)] and 80 age- and sex-matched normal controls who underwent cardiac magnetic resonance scanning were included. LV geometry, function, and LV global strains, including peak strain (PS), peak systolic strain rate (PSSR) and peak diastolic strain rate (PDSR) in the radial, circumferential and longitudinal directions, were measured. NIDCM (T2DM+) patients were divided into two subgroups based on the HbA1c level (< 7.0% and ≥ 7.0%). The determinants of reduced LV myocardial strain for all NIDCM individuals and NIDCM (T2DM+) patients were assessed using multivariable linear regression analyses. RESULTS: Compared with normal controls, both NIDCM (T2DM -) and NIDCM (T2DM+) patients exhibited increased LV end-diastolic and end-systolic volume index and decreased LV ejection fraction. LV global strains progressively declined from the normal controls to the NIDCM (T2DM-) group to the NIDCM (T2DM+) group (all p < 0.017), except for radial PDSR and PSSR. Subgroup analysis showed that LV global radial PS and longitudinal PS, PSSR-L and PDSR-L were worse in NIDCM patients with poor glycemic control than in those with good glycemic control (p < 0.017). T2DM was an independent determinant of reduced LV global circumferential PS and longitudinal PS in patients with NIDCM (both p < 0.05). An increased HbA1c level was independently associated with a decreased global radial PS (β = - 0.285, p < 0.01) and longitudinal PS (β = 0.320, p < 0.01) in NIDCM (T2DM+) patients. CONCLUSIONS: T2DM has an additive deleterious effect on LV systolic and diastolic function in NIDCM patients. Among NIDCM patients with T2DM, HbA1c was found to be associated with reduced LV myocardial strain.
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Shen et al. (2022) conducted an observational in Non-ischemic dilated cardiomyopathy (n=515). Type 2 diabetes mellitus vs. Non-ischemic dilated cardiomyopathy without Type 2 diabetes mellitus was evaluated on Left ventricular global longitudinal peak strain (GLPS) (p=<0.017). Type 2 diabetes mellitus had an additive deleterious effect on left ventricular deformation in patients with non-ischemic dilated cardiomyopathy, independently reducing global circumferential and longitudinal peak strain.
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