Clinical diabetic cardiomyopathy: a two-faced disease with restrictive and dilated phenotypes
Open accessAbstract
Diabetes mellitus-related cardiomyopathy (DMCMP) was originally described as a dilated phenotype with eccentric left ventricular (LV) remodelling and systolic LV dysfunction. Recently however, clinical studies on DMCMP mainly describe a restrictive phenotype with concentric LV remodelling and diastolic LV dysfunction. Both phenotypes are not successive stages of DMCMP but evolve independently to respectively heart failure with preserved left ventricular ejection fraction (HFPEF) or reduced left ventricular ejection fraction (HFREF). Phenotype-specific pathophysiological mechanisms were recently proposed for LV remodelling and dysfunction in HFPEF and HFREF consisting of coronary microvascular endothelial dysfunction in HFPEF and cardiomyocyte cell death in HFREF. A similar preferential involvement of endothelial or cardiomyocyte cell compartments explains DMCMP development into distinct restrictive/HFPEF or dilated/HFREF phenotypes. Diabetes mellitus (DM)-related metabolic derangements such as hyperglycaemia, lipotoxicity, and hyperinsulinaemia favour development of DMCMP with restrictive/HFPEF phenotype, which is more prevalent in obese type 2 DM patients. In contrast, autoimmunity predisposes to a dilated/HFREF phenotype, which manifests itself more in autoimmune-prone type 1 DM patients. Finally, coronary microvascular rarefaction and advanced glycation end-products deposition are relevant to both phenotypes. Diagnosis of DMCMP requires impaired glucose metabolism and exclusion of coronary, valvular, hypertensive, or congenital heart disease and of viral, toxic, familial, or infiltrative cardiomyopathy. In addition, diagnosis of DMCMP with restrictive/HFPEF phenotype requires normal systolic LV function and diastolic LV dysfunction, whereas diagnosis of DMCMP with dilated/HFREF phenotype requires systolic LV dysfunction. Treatment of DMCMP with restrictive/HFPEF phenotype is limited to diuretics and lifestyle modification, whereas DMCMP with dilated/HFREF phenotype is treated in accordance to HF guidelines.
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Lower-extremity artery disease, longer diabetes duration, ageing, increased BMI, and chronic kidney disease are associated with heart failure in patients with diabetes.
“Observational data have also identified that lower-extremity artery disease (LEAD), longer diabetes duration, ageing, increased BMI, and CKD (Section 9) are associated with HF in patients with diabetes (Table 10). [449]][450][451][452]”
From 2023 ESC guidelines for the management of cardiovascular disease in patients with diabetes. (2023) · cites this paper as [449]
Ischaemic heart disease is often accelerated, severe, diffuse, and silent, and increases the risk of myocardial infarction and ischaemic myocardial dysfunction.
“IHD is often accelerated, severe, diffuse, and silent, and increases the risk of MI and ischaemic myocardial dysfunction.[449][450][451][452]”
From 2023 ESC guidelines for the management of cardiovascular disease in patients with diabetes. (2023) · cites this paper as [449]
Diabetic cardiomyopathy may clinically manifest as eccentric LV dilatation impairing systolic function or as restrictive concentric LV remodeling determining diastolic dysfunction.
“Diabetic cardiomyopathy may clinically manifest as a condition of eccentric left ventricle (LV) dilatation impairing systolic function, as classically described, or as a restrictive concentric LV remodeling determining diastolic dysfunction.”
From Dysregulated epicardial adipose tissue as a risk factor and potential therapeutic target of heart failure with preserved ejection fraction in diabetes (2022) · cites this paper as [65]
Hyperglycemia can directly determine mitochondrial network fragmentation and oxidative stress, with consequent contractile dysfunction.
“Directly, hyperglycemia can determine mitochondrial network fragmentation and oxidative stress, with a consequent contractile dysfunction [65].”
From Dysregulated epicardial adipose tissue as a risk factor and potential therapeutic target of heart failure with preserved ejection fraction in diabetes (2022) · cites this paper as [65]
Impaired bioavailability of nitric oxide impairs its downstream cGMP protein kinase G (PKG) pathway in cardiomyocytes, which become hypertrophied and stiffened.
“As a result, the impaired bioavailability in nitric oxide impairs its downstream cGMP protein kinase G (PKG) pathway in cardiomyocytes which become hypertrophied and stiffened [65,67].”
From Dysregulated epicardial adipose tissue as a risk factor and potential therapeutic target of heart failure with preserved ejection fraction in diabetes (2022) · cites this paper as [65]
These two phenotypes are not successive stages of diabetic cardiomyopathy, but two pictures that independently may evolve to HFrEF or HFpEF.
“These two phenotypes are not successive stages of diabetic cardiomyopathy, but two pictures that independently may evolve to HFrEF or HFpEF, respectively [65].”
From Dysregulated epicardial adipose tissue as a risk factor and potential therapeutic target of heart failure with preserved ejection fraction in diabetes (2022) · cites this paper as [65]
Hyperglycemia indirectly, through paracrine endothelial signaling, causes mitochondrial hyper-production of superoxide, with impaired activation of endothelial nitric oxide synthase.
“Indirectly, through a paracrine endothelial signaling, hyperglycemia causes a mitochondrial hyper-production of superoxide, with impaired activation of endothelial nitric oxide synthase.”
From Dysregulated epicardial adipose tissue as a risk factor and potential therapeutic target of heart failure with preserved ejection fraction in diabetes (2022) · cites this paper as [65]
The most important causes of HF in T2DM are coronary artery disease, arterial hypertension, and a direct detrimental effect of T2DM on the myocardium.
“The most important causes of HF in T2DM are coronary artery disease, arterial hypertension and a direct detrimental effect of T2DM on the myocardium.”
From Type 2 diabetes mellitus and heart failure: A position statement from the Heart Failure Association of the European Society of Cardiology (2018) · cites this paper as [4]
The major causes of HF in T2DM include coronary artery disease and hypertension, but also a possible direct detrimental effect of T2DM on the myocardium.
“The major causes of HF in T2DM include coronary artery disease (CAD) and hypertension, but also, a possible direct detrimental effect of T2DM on the myocardium.4”
From Type 2 diabetes mellitus and heart failure: A position statement from the Heart Failure Association of the European Society of Cardiology (2018) · cites this paper as [4]
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- Authors
- Seferović, P. M., & Paulus, W. J.
- Affiliations
- Amsterdam Cardiovascular Sciences (NL)
- ORCID
- Paulus, Walter J.
- Venue
- European Heart Journal
- Publisher
- Oxford University Press (OUP)
- Published
- 2015-04-17
- Volume
- 36
- Issue
- 27
- Pages
- 1718-1727
- ISSN
- 0195-668X (ISSN-L)
- 1522-9645
- OpenAlex
- W2066000449
- Cited by
- 552
- References
- 126
- Citations by year
- 2026: 32 · 2025: 40 · 2024: 62 · 2023: 41 · 2022: 52 · 2021: 66 · 2020: 66 · 2019: 61 · 2018: 43 · 2017: 46 · 2016: 34 · 2015: 8
- FWCI
- 7.53
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- European Heart Journal (publishedVersion)
- PubMed (publishedVersion)
- Pure Amsterdam UMC (publishedVersion, other-oa)
- Amsterdam UMC (VU Amsterdam) - Institutional Repository (publishedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- Funders
- European Commission (FP7-Health- 2010, 261409)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Function and Risk Factors
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiomyopathy and Myosin Studies
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Keywords
- diabetic cardiomyopathy, restrictive cardiomyopathy, dilated cardiomyopathy, heart failure with preserved ejection fraction, heart failure with reduced ejection fraction, left ventricular remodeling, diastolic dysfunction, systolic dysfunction, coronary microvascular dysfunction, cardiomyocyte death, advanced glycation end products, type 1 diabetes, type 2 diabetes, autoimmunity, hyperinsulinemia, lipotoxicity, hyperglycemia, obesity, diagnosis, treatment
- MeSH terms
- Cardiomyopathy, Dilated, Cardiomyopathy, Restrictive, Heart Failure, Humans, Hyperglycemia, Hypoglycemic Agents, Insulin Resistance, Phenotype, Autoimmunity, Glycation End Products, Advanced, Ventricular Dysfunction, Risk Reduction Behavior, Diabetic Cardiomyopathies
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