Associations and prognostic significance of diffuse myocardial fibrosis by cardiovascular magnetic resonance in heart failure with preserved ejection fraction

Roy, Clotilde; Slimani, Alisson; Meester, Christophe de; Amzulescu, Mihaela Silvia; Pasquet, Agnès; Vancraeynest, David; Beauloye, Christophe; Vanoverschelde, Jean–Louis; Gerber, Bernhard; Pouleur, Anne‐Catherine

doi:10.1186/s12968-018-0477-4

Cited by 88 publications

(70 citation statements)

References 32 publications

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“…Thus, the cardiac fibroblast response to "diabetic" conditions is to produce excess ECM, which aligns with the fibrosis observed in the diabetic heart in experimental models including the Lepr db/db mouse [28]. Underscoring the clinical significance of this relationship, diabetes was associated with cardiac fibrosis in humans [29,30].…”

Section: Extracellular Matrix Productionmentioning

confidence: 80%

The Diabetic Cardiac Fibroblast: Mechanisms Underlying Phenotype and Function

Levick

Widiapradja

2020

IJMS

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Diabetic cardiomyopathy involves remodeling of the heart in response to diabetes that includes microvascular damage, cardiomyocyte hypertrophy, and cardiac fibrosis. Cardiac fibrosis is a major contributor to diastolic dysfunction that can ultimately result in heart failure with preserved ejection fraction. Cardiac fibroblasts are the final effector cell in the process of cardiac fibrosis. This review article aims to describe the cardiac fibroblast phenotype in response to high-glucose conditions that mimic the diabetic state, as well as to explain the pathways underlying this phenotype. As such, this review focuses on studies conducted on isolated cardiac fibroblasts. We also describe molecules that appear to oppose the pro-fibrotic actions of high glucose on cardiac fibroblasts. This represents a major gap in knowledge in the field that needs to be addressed.

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Section: Extracellular Matrix Productionmentioning

confidence: 80%

The Diabetic Cardiac Fibroblast: Mechanisms Underlying Phenotype and Function

Levick

Widiapradja

2020

IJMS

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“…This fibrosis is the consequence of a systemic and cardiac inflammation in both HFpEF and HFrEF, but is significantly greater in HFpEF [38]. Interstitial fibrosis is characterized by the expansion of the ECM surrounding the cardiomyocytes, occurring in HF without cardiomyocyte loss [163], including non-ischemic HFrEF and HFpEF [39][40][41]. Unlike other organs, the heart has a very limited regenerative capacity, therefore repair processes involving the removal of necrotic cardiomyocytes followed by replacement fibrosis aim to preserve myocardial structural and functional integrity [164].…”

Section: Different Types Of Cardiac Fibrosis In Hfref and Hfpefmentioning

confidence: 99%

Cellular and Molecular Differences between HFpEF and HFrEF: A Step Ahead in an Improved Pathological Understanding

Simmonds

Cuijpers

Heymans

et al. 2020

Cells

236

219

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Heart failure (HF) is the most rapidly growing cardiovascular health burden worldwide. HF can be classified into three groups based on the percentage of the ejection fraction (EF): heart failure with reduced EF (HFrEF), heart failure with mid-range—also called mildly reduced EF— (HFmrEF), and heart failure with preserved ejection fraction (HFpEF). HFmrEF can progress into either HFrEF or HFpEF, but its phenotype is dominated by coronary artery disease, as in HFrEF. HFrEF and HFpEF present with differences in both the development and progression of the disease secondary to changes at the cellular and molecular level. While recent medical advances have resulted in efficient and specific treatments for HFrEF, these treatments lack efficacy for HFpEF management. These differential response rates, coupled to increasing rates of HF, highlight the significant need to understand the unique pathogenesis of HFrEF and HFpEF. In this review, we summarize the differences in pathological development of HFrEF and HFpEF, focussing on disease-specific aspects of inflammation and endothelial function, cardiomyocyte hypertrophy and death, alterations in the giant spring titin, and fibrosis. We highlight the areas of difference between the two diseases with the aim of guiding research efforts for novel therapeutics in HFrEF and HFpEF.

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“…Coronary microvascular dysfunction is exceptionally common in HFpEF and, when present, is associated with a two‐fold increase in the prevalence of AF . Cardiac magnetic resonance imaging (MRI) reveals meaningful myocardial fibrosis (in the LA and LV) in both patients with HFpEF and those with AF . Fibrosis is indicative of an underlying atrial and ventricular myopathy and may precede the clinical identification of AF or HFpEF …”

Section: Pathophysiological Mechanisms Leading To Hfpefmentioning

confidence: 99%

Do most patients with obesity or type 2 diabetes, and atrial fibrillation, also have undiagnosed heart failure? A critical conceptual framework for understanding mechanisms and improving diagnosis and treatment

Packer

2019

European J of Heart Fail

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Obesity and diabetes can lead to heart failure with preserved ejection fraction (HFpEF), potentially because they both cause expansion and inflammation of epicardial adipose tissue and thus lead to microvascular dysfunction and fibrosis of the underlying left ventricle. The same process also causes an atrial myopathy, which is clinically evident as atrial fibrillation (AF); thus, AF may be the first manifestation of HFpEF. Many patients with apparently isolated AF have latent HFpEF or subsequently develop HFpEF. Most patients with obesity or diabetes who have AF and exercise intolerance have increased left atrial pressures at rest or during exercise, even in the absence of diagnosed HFpEF. Among patients with AF, those who also have latent HFpEF have increased risk for systemic thromboembolism and death. The identification of HFpEF in patients with obesity or diabetes alters the risk‐to‐benefit relationship of commonly prescribed treatments. Bariatric surgery and statins can ameliorate AF and reduce the risk for HFpEF. Conversely, antihyperglycaemic drugs that promote adipogenesis or cause sodium retention (insulin and thiazolidinediones) may increase the risk for heart failure in patients with an underlying ventricular myopathy. Patients with obesity and diabetes who undergo catheter ablation for AF are at increased risk for AF recurrence and for post‐ablation increases in pulmonary venous pressures and worsening heart failure, especially if HFpEF coexists. Therefore, AF may be the earliest indicator of HFpEF in patients with obesity or type 2 diabetes, and recognition of HFpEF alters the management of these patients.

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Associations and prognostic significance of diffuse myocardial fibrosis by cardiovascular magnetic resonance in heart failure with preserved ejection fraction

Cited by 88 publications

References 32 publications

The Diabetic Cardiac Fibroblast: Mechanisms Underlying Phenotype and Function

The Diabetic Cardiac Fibroblast: Mechanisms Underlying Phenotype and Function

Cellular and Molecular Differences between HFpEF and HFrEF: A Step Ahead in an Improved Pathological Understanding

Do most patients with obesity or type 2 diabetes, and atrial fibrillation, also have undiagnosed heart failure? A critical conceptual framework for understanding mechanisms and improving diagnosis and treatment

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