Papel del colágeno miocárdico en la estenosis aórtica grave con fracción de eyección conservada y síntomas de insuficiencia cardiaca

Echegaray, Kattalin; Andreu, Ion; Lazkano, Ane; Villanueva, Iñaki; Sáenz, Alberto; Elizalde, M.R.; Echeverría, Tomás; López, Begoña; Garro, M. Asier; González, Arantxa; Zubillaga, Elena; Solla, Itziar; Sanz, Iñaki; González, J.; Elosegui‐Artola, Alberto; Roca‐Cusachs, Pere; Dı́ez, Javier; Ravassa, Susana; Querejeta, Ramón

doi:10.1016/j.recesp.2016.12.018

Cited by 28 publications

(2 citation statements)

References 27 publications

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“…There were also pathological changes in LV morphology (LV weight/ body weight and EDV), myocardial collagen deposition, and reduction in vascular tone (Table 2). These abnormalities were similar to those observed in other animal studies (2-4, 12, 42, 45, 53) and in patients with HF with dilated cardiomyopathy from aortic valve insufficiency (6,7,11,13,15,18,21,43,54). These data justified the use of the rat HF model induced by aortic valve insufficiency to investigate the pharmacology of sacubitril/valsartan.…”

Section: Validation Of the Rodent Model Of Hf Induced By Aortic Valve Disruption Leading To LV Volume Overloadsupporting

confidence: 90%

Synergy between sacubitril and valsartan leads to hemodynamic, antifibrotic, and exercise tolerance benefits in rats with preexisting heart failure

Maslov

Foianini

Mayer

et al. 2019

American Journal of Physiology-Heart and Circulatory Physiology

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Simultaneous neprilysin inhibition (NEPi) and angiotensin receptor blockade (ARB) with sacubitril/valsartan improves cardiac function and exercise tolerance in patients with heart failure. However, it is not known whether these therapeutic benefits are primarily due to NEPi with sacubitril or ARB with valsartan or their combination. Therefore, the aim of the present study was to investigate the potential contribution of sacubitril and valsartan to the benefits of the combination therapy on left ventricular (LV) function and exercise tolerance. Heart failure was induced by volume overload via partial disruption of the aortic valve in rats. Therapy began 4 wk after valve disruption and lasted through 8 wk. Drugs were administered daily via oral gavage [sacubitril/valsartan (68 mg/kg), valsartan (31 mg/kg), and sacubitril (31 mg/kg)]. Hemodynamic assessments were conducted using Millar technology, and an exercise tolerance test was conducted using a rodent treadmill. Therapy with sacubitril/valsartan improved load-dependent indexes of LV contractility (dP/d tmax) and relaxation (dP/d tmin), exercise tolerance, and mitigated myocardial fibrosis, whereas monotherapies with valsartan, or sacubitril did not. Both sacubitril/valsartan and valsartan similarly improved a load-independent index of contractility [slope of the end-systolic pressure-volume relationship ( Ees)]. Sacubitril did not improve Ees. First, synergy of NEPi with sacubitril and ARB with valsartan leads to the improvement of load-dependent LV contractility and relaxation, exercise tolerance, and reduction of myocardial collagen content. Second, the improvement in load-independent LV contractility with sacubitril/valsartan appears to be solely due to ARB with valsartan constituent. NEW & NOTEWORTHY Our data suggest the following explanation for the effects of sacubitril/valsartan: 1) synergy of sacubitril and valsartan leads to the improvement of load-dependent left ventricular contractility and relaxation, exercise tolerance, and reduction of myocardial fibrosis and 2) improvement in load-independent left ventricular contractility is solely due to the valsartan constituent. The findings offer a better understanding of the outcomes observed in clinical studies and might facilitate the continuing development of the next generations of angiotensin receptor neprilysin inhibitors.

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Section: Validation Of the Rodent Model Of Hf Induced By Aortic Valve Disruption Leading To LV Volume Overloadsupporting

confidence: 90%

Synergy between sacubitril and valsartan leads to hemodynamic, antifibrotic, and exercise tolerance benefits in rats with preexisting heart failure

Maslov

Foianini

Mayer

et al. 2019

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

show abstract

“…Second, cardiac fibrosis impairs interactions between endomysial components such as laminin, which connect adjacent cardiomyocytes and capillaries, and their receptors, thereby disrupting the cardiomyocyte mass and systolic reserve [148]. This contrasts with HFpEF, where excessive collagen deposition and a reduction of the more flexible collagen III results in increased cardiac stiffness [40,149].…”

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

239

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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Cardiac Microvascular Endothelial Cells and Pressure Overload-Induced Cardiac Fibrosis

Al-Hasani

Hecker

2023

Cardiac and Vascular Biology

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Papel del colágeno miocárdico en la estenosis aórtica grave con fracción de eyección conservada y síntomas de insuficiencia cardiaca

Cited by 28 publications

References 27 publications

Synergy between sacubitril and valsartan leads to hemodynamic, antifibrotic, and exercise tolerance benefits in rats with preexisting heart failure

Synergy between sacubitril and valsartan leads to hemodynamic, antifibrotic, and exercise tolerance benefits in rats with preexisting heart failure

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

Cardiac Microvascular Endothelial Cells and Pressure Overload-Induced Cardiac Fibrosis

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