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Review
. 2021 Nov 6;20(1):218.
doi: 10.1186/s12933-021-01408-1.

Heart failure in type 2 diabetes: current perspectives on screening, diagnosis and management

Antonio Ceriello  1 , Doina Catrinoiu  2 , Chanchal Chandramouli  3   4 , Francesco Cosentino  5 , Annique Cornelia Dombrowsky  6 , Baruch Itzhak  7 , Nebojsa Malić Lalic  8 , Francesco Prattichizzo  9 , Oliver Schnell  10 , Petar M Seferović  11 , Paul Valensi  12 , Eberhard Standl  10 ; D&CVD EASD Study Group
Affiliations
Review

Heart failure in type 2 diabetes: current perspectives on screening, diagnosis and management

Antonio Ceriello et al. Cardiovasc Diabetol. .

Abstract

Type 2 diabetes is one of the most relevant risk factors for heart failure, the prevalence of which is increasing worldwide. The aim of the review is to highlight the current perspectives of the pathophysiology of heart failure as it pertains to type 2 diabetes. This review summarizes the proposed mechanistic bases, explaining the myocardial damage induced by diabetes-related stressors and other risk factors, i.e., cardiomyopathy in type 2 diabetes. We highlight the complex pathology of individuals with type 2 diabetes, including the relationship with chronic kidney disease, metabolic alterations, and heart failure. We also discuss the current criteria used for heart failure diagnosis and the gold standard screening tools for individuals with type 2 diabetes. Currently approved pharmacological therapies with primary use in type 2 diabetes and heart failure, and the treatment-guiding role of NT-proBNP are also presented. Finally, the influence of the presence of type 2 diabetes as well as heart failure on COVID-19 severity is briefly discussed.

Keywords: Guidelines; Heart failure; NT-proBNP; Type 2 diabetes.

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Conflict of interest statement

AC: Advisory Board, Consultancy, Lectures: Berlin Chemie, Eli Lilly, Novo Nordisk, Mitsubishi, Roche Diagnostics, Theras.

DC: Advisory Board, Lectures, Consultancy: Novo Nordisk, Eli Lilly, Sanofi, Servier, MSD, Merck, Alfa Wasserman, Bayer, Astra Zeneca, Boehringer-Ingelheim.

CC: The authors declare that they have no competing interests.

FC: research grants from Swedish Research Council, Swedish Heart & Lung Foundation, and King Gustav V and Queen Victoria Foundation, as well as advisory board, consultancy fees from Abbott, AstraZeneca, Bayer, Bristol-Myers Squibb, Boehringer Ingelheim Merck Sharp & Dohme, Lilly, Novo Nordisk, and Pfizer.

ACD: The authors declare that they have no competing interests.

BI: Advisory Board, Consultancy, Lectures: Novo Nordisk, Sanofi, Eli Lilly, Bayer, AstraZeneca, Boehringer Ingelheim, Pfizer, MSD, Roche.

NML: Advisory Board and Lectures for NovoNordisk, Sanofi, Boehringer Ingelheim, Astra Zeneca, Medtronic, Roche, Eli Lilly, Berlin Chemie.

FP: lectures for Berlin Chemie.

OS: AstraZeneca, Bayer, Boehringer Ingelheim, Grünethal, Lilly, MSD, Mundipharma, Novo Nordisk, Roche, Sanofi, Wörwag.

PMS: Lectures for Servier, Astra Zeneca, Respicardia, Menarini; Consultancy agreement for Boehringer Ingelhein, Vifor Pharma, Novartis, Roche diagnostic.

PV: Lectures for Abbott, AstraZeneca, Bayer, Eli Lilly, Hikma Pharmaceuticals, Merck Sharp & Dohme, Novo Nordisk, Novartis, Pfizer, Sanofi; research grants from Abbott, Bristol-Myers-Squibb–AstraZeneca, Novo Nordisk; participation in expert committees for AstraZeneca, Boehringer Ingelheim, Novo Nordisk, Daiichi Sankyo, Sanofi, Servier, Stendo.

ES: Personal fees from Oxford Diabetes Trials Unit, Bayer, Berlin Chemie, Boehringer Ingelheim, Menarini, Merck Serono, EXCEMED, Novartis, Novo Nordisk, and Sanofi.

Figures

Fig. 1
Fig. 1
Pathophysiological mechanisms of cardiomyopathy in type 2 diabetes (CMiPD). Fatty acids (FAs) are preferentially metabolized to ATP, sustaining muscle contraction. During progression to severe stages of cardiomyopathy, both the increased FA metabolism and accumulated ceramide contribute to inflammation and fibrosis, leading to cardiac stiffness and reduced contractility
Fig. 2
Fig. 2
Mechanism for interaction between the metabolism disturbances and the heart. Insulin interferes with the free fatty acids (FFAs) metabolism. Consequently, a high amount of FFAs is present in the bloodstream, which impairs the insulin-mediated glucose uptake leading to hyperglycemia and insulin resistance, and promotes hypertension via increased sodium reabsorption and chronic sympathetic activity. In addition, insulin itself promotes hypertension. Metabolic disturbances impart a high risk for type 2 diabetes and heart failure progression, apart from FFA-rich epicardial fat tissue (EFT) that also facilitates heart failure
Fig. 3
Fig. 3
Heart-kidney interaction is mediated by the natriuretic peptide system counterbalanced by the RAAS and the SNS. In early heart failure, the natriuretic peptide action dominates, leading to suppression of the SNS manifested as vasorelaxation and to natriuresis and diuresis in the kidney, which all translate into a lowered blood pressure. In chronic heart failure, the effectiveness of natriuretic peptides is lost, and actions of the overactivated RAAS and SNS dominate leading to vasoconstriction and expression of renin and angiotensin, which both mediate an increased blood pressure
See this image and copyright information in PMC

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