Concentric vs. eccentric remodelling in heart failure with reduced ejection fraction: clinical characteristics, pathophysiology and response to treatment

Nauta, Joske; Hummel, Yoran M.; Tromp, Jasper; Ouwerkerk, Wouter; Meer, Peter van der; Jin, Xuanyi; Lam, Carolyn S.P.; Bax, Jeroen J.; Metra, Marco; Samani, Nilesh J.; Ponikowski, Piotr; Dickstein, Kenneth; Anker, Stefan D.; Lang, Chim C.; Ng, Leong Loke; Zannad, Faı̈ez; Filippatos, Gerasimos; Veldhuisen, Dirk J. van; Melle, Joost P. van; Voors, Adriaan A.

doi:10.1002/ejhf.1632

Cited by 58 publications

(59 citation statements)

References 19 publications

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“…Thus, considering this accumulation of data and the fact that obese people with signs and symptoms of HF but with low levels of NP have been generally excluded from many trials [7,81], a new obesity-related HFpEF phenotype has been proposed [6,74]. These low levels of NPs could be explained by the limited cardiomyocyte stretch, specific to HFpEF with diastolic dysfunction [83] overlapped with the excess adipose tissue, responsible for both overexpression of natriuretic peptide clearance receptors (NPRC) and increased neprilysin secretion [11,82]. Neprilysin is also secreted by proximal renal tubular epithelial cells, in response to sympathetic nerve stimulation [11,84], that can occur in the presence of abdominal aortic stenosis.…”

Section: Discussionmentioning

confidence: 99%

Protective Effects of a Discontinuous Treatment with Alpha-Lipoic Acid in Obesity-Related Heart Failure with Preserved Ejection Fraction, in Rats

et al. 2020

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Obesity induces hemodynamic and humoral changes that are associated with functional and structural cardiac remodeling, which ultimately result in the development of heart failure (HF) with preserved ejection fraction (HFpEF). In recent years, pharmacological studies in patients with HFpEF were mostly unsatisfactory. In these conditions, alternative new therapeutic approaches are necessary. The aim of our study was (1) to assess the effects of obesity on heart function in an experimental model and (2) to evaluate the efficacy of an alpha-lipoic acid (ALA) antioxidant treatment. Sprague-Dawley rats (7 weeks old) were either included in the control group (n = 6) or subjected to abdominal aortic banding (AAB) and divided into three subgroups, depending on their diet: standard (AAB + SD, n = 8), hypecaloric (AAB + HD, n = 8) and hypercaloric with discontinuous ALA treatment (AAB + HD + ALA, n = 9). Body weight (BW), glycemia, echocardiography parameters and plasma hydroperoxides were monitored throughout the study. After 36 weeks, plasma adiposity (leptin and adiponectin) and inflammation (IL-6 and TNF-alpha) markers, together with B-type natriuretic peptide and oxidative stress markers (end-products of lipid peroxidation and endogenous antioxidant systems) were assessed. Moreover, cardiac fiber diameters were measured. In our experiment, diet-induced obesity generated cardiometabolic disturbances, and in association with pressure-overload induced by AAB, it precipitated the onset of heart failure, cardiac hypertrophy and diastolic dysfunction, while producing a pro-oxidant and pro-inflammatory plasmatic status. In relationship with its antioxidant effects, the chronic ALA-discontinuous treatment prevented BW gain and decreased metabolic and cardiac perturbations, confirming its protective effects on the cardiovascular system.

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Section: Discussionmentioning

confidence: 99%

Protective Effects of a Discontinuous Treatment with Alpha-Lipoic Acid in Obesity-Related Heart Failure with Preserved Ejection Fraction, in Rats

et al. 2020

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“…Absolute LV contractile reserve by dobutamine stress CMR and female gender predicted LVEF increase over 12 months. Nauta et al 12 . retrospectively evaluated the association between LV geometry, clinical and biomarker phenotypes, and therapeutic response in patients with chronic HF.…”

Section: Cardiac Imagingmentioning

confidence: 99%

July 2020 at a glance: focus on imaging and cardiomyopathies

Tomasoni

Adamo

Metra

2020

European J of Heart Fail

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“…The current concept of heart failure (HF) pathogenesis includes a broad spectrum of structural, functional, electrophysiological, cellular, and molecular abnormalities [1]. Pathological molecular mechanisms, including myocyte loss, cardiac hypertrophy, the alteration of extracellular matrix homeostasis, fibrosis, defective autophagy, metabolic abnormalities, and mitochondrial dysfunction eventually lead to left ventricular remodeling and cardiac dysfunction [2,3]. Patients with advanced HF develop various additional derangements, including changes in adipokine levels, long-term systemic inflammation, and progressive catabolism [4,5].…”

Section: Introductionmentioning

confidence: 99%

The Role of Cardiac T-Cadherin in the Indicating Heart Failure Severity of Patients with Non-Ischemic Dilated Cardiomyopathy

et al. 2020

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Background and objectives: T-cadherin (T-cad) is one of the adiponectin receptors abundantly expressed in the heart and blood vessels. Experimental studies show that T-cad sequesters adiponectin in cardiovascular tissues and is critical for adiponectin-mediated cardio-protection. However, there are no data connecting cardiac T-cad levels with human chronic heart failure (HF). The aim of this study was to assess whether myocardial T-cad concentration is associated with chronic HF severity and whether the T-cad levels in human heart tissue might predict outcomes in patients with non-ischemic dilated cardiomyopathy (NI-DCM). Materials and Methods: 29 patients with chronic NI-DCM and advanced HF were enrolled. Patients underwent regular laboratory investigations, echocardiography, coronary angiography, and right heart catheterization. TNF-α and IL6 in serum were detected by enzyme-linked immunosorbent assay (ELISA). Additionally, endomyocardial biopsies were obtained, and the levels of T-cad were assessed by ELISA and CD3, CD45Ro, CD68, and CD4- immunohistochemically. Mean pulmonary capillary wedge pressure (PCWP) was used as a marker of HF severity, subdividing patients into two groups: mean PCWP > 19 mmHg vs. mean PCWP < 19 mmHg. Patients were followed-up for 5 years. The study outcome was composite: left ventricular assist device implantation, heart transplantation, or death from cardiovascular causes. Results: T-cad shows an inverse correlation with the mean PCWP (rho = −0.397, p = 0.037). There is a tendency towards a lower T-cad concentration in patients with more severe HF, as indicated by the mean PCWP > 19 mmHg compared to those with mean PCWP ≤ 19 mmHg (p = 0.058). Cardiac T-cad levels correlate negatively with myocardial CD3 cell count (rho = −0.423, p = 0.028). Conclusions: Univariate Cox regression analysis did not prove T-cad to be an outcome predictor (HR = 1, p = 0.349). However, decreased T-cad levels in human myocardium can be an additional indicator of HF severity. T-cad in human myocardium has an anti-inflammatory role. More studies are needed to extend the role of T-cad in the outcome prediction of patients with NI-DCM.

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Concentric vs. eccentric remodelling in heart failure with reduced ejection fraction: clinical characteristics, pathophysiology and response to treatment

Cited by 58 publications

References 19 publications

Protective Effects of a Discontinuous Treatment with Alpha-Lipoic Acid in Obesity-Related Heart Failure with Preserved Ejection Fraction, in Rats

Protective Effects of a Discontinuous Treatment with Alpha-Lipoic Acid in Obesity-Related Heart Failure with Preserved Ejection Fraction, in Rats

July 2020 at a glance: focus on imaging and cardiomyopathies

The Role of Cardiac T-Cadherin in the Indicating Heart Failure Severity of Patients with Non-Ischemic Dilated Cardiomyopathy

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