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Review
. 2024 Sep 28:23:200338.
doi: 10.1016/j.ijcrp.2024.200338. eCollection 2024 Dec.

Diabetic cardiomyopathy: pathophysiology, imaging assessment and therapeutical strategies

Vincenzo Rizza  1 , Lara Tondi  2   3 , Angelo Maria Patti  4 , Damiano Cecchi  1 , Massimo Lombardi  2 , Francesco Perone  5 , Marco Ambrosetti  6 , Manfredi Rizzo  4 , Domenico Cianflone  1   7 , Francesco Maranta  1   7
Affiliations
Review

Diabetic cardiomyopathy: pathophysiology, imaging assessment and therapeutical strategies

Vincenzo Rizza et al. Int J Cardiol Cardiovasc Risk Prev. .

Abstract

Diabetes mellitus (DM) is one of the most prevalent cardiovascular risk factors in the general population, being associated with high morbidity and socioeconomic burden. Diabetic cardiomyopathy (DCM) is a non-negligible complication of DM, whose pathophysiological fundaments are the altered cardiac metabolism, the hyperglycemia-triggered formation of advanced glycation end-products (AGEs) and the inflammatory milieu which are typical in diabetic patients. These metabolic abnormalities lead to cardiomyocytes apoptosis, interstitial fibrosis and mechanical cardiac dysfunction, which can be identified with non-invasive imaging techniques, like echocardiography and cardiac magnetic resonance. This review aims to: 1) describe the major imaging features of DCM; 2) highlight how early identification of DCM-related anatomical and functional remodeling might allow patients' therapy optimization and prognosis improvement.

Keywords: Diabetic cardiomyopathy; Heart failure; cardiac imaging; diabetes mellitus.

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Conflict of interest statement

The authors report no relationships that could be construed as a conflict of interest.

Figures

Fig. 1
Fig. 1
Left ventricle concentric hypertrophy assessed with the parasternal long-axis (Panel A) and short-axis (Panel B) B-mode echocardiographic views.
Fig. 2
Fig. 2
Grade II diastolic dysfunction assessed using mitral inflow E and A velocities (with the PWD, Panel A), lateral e’ and septal e’ velocities (with TDI, Panels B and C). LN0 = Line number 0 corresponding to the interventricular septum thickness; LN1 = Line number 1 corresponding to the posterior wall thickness; LN2 = Line number 2 corresponding to the left ventricular end-diastolic diameter.
Fig. 3
Fig. 3
Diabetic cardiomyopathy associated with biatrial enlargement (Panel A), left ventricular hypertrophy and large amount of epicardial fat (Panel B), intramyocardial LGE in the interventricular septum (Panels D and E), pre- and post-contrast MOLLI sequences showing elevated myocardial native T1 (Panel C) and increased ECV (Panel F). MOLLI - Modified Look-Locker inversion recovery.
Fig. 4
Fig. 4
Diabetic cardiomyopathy associated with left atrial enlargement (Panel A) and interstitial fibrosis as illustrated by elevated native T1 (Panel B) and increased ECV (Panel D) in pre and post-contrast ShMOLLI sequences, in the absence of LGE (Panel C). ShMOLLI - shortened Modified Look-Locker inversion recovery.
See this image and copyright information in PMC

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