Mechanisms underlying the pathophysiology of heart failure with preserved ejection fraction: the tip of the iceberg

Miranda-Silva, Daniela; Lima, Tânia; Rodrigues, Patrícia; Leite‐Moreira, Adelino; Falcão-Pires, Inês

doi:10.1007/s10741-020-10042-0

Cited by 29 publications

(24 citation statements)

References 217 publications

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“…Ca 2+ released from the sarcoplasmic reticulum ( 50 ) acts as a direct activator of myofilaments and will cause cardiac contraction ( 51 ). Cardiac relaxation, as a key player in the pathophysiology of HFpEF ( 52 ), depends on the reduction of intracellular calcium (Ca 2+ ) levels ( 24 ), which can be reduced by (1) SERCA, (2) sarcolemmal Na+/Ca 2+ exchange, (3) sarcolemmal Ca 2+ -ATPase, and (4) mitochondrial Ca 2+ UniProt ( 51 , 52 ). Myocardial Ca 2+ levels are increased in patients with HFpEF, but elevated calcium levels ( 53 ) are not associated with an impaired Na+ gradient, in contrast to the case in HFrEF patients who have elevated myocardial [Na+]I ( 54 ).…”

Section: Underlying Mechanisms Of Hfpef and Hfmrefmentioning

confidence: 99%

Similarities and Differences Between HFmrEF and HFpEF

Zhao

Zhang

et al. 2021

Front. Cardiovasc. Med.

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The new guidelines classify heart failure (HF) into three subgroups based on the ejection fraction (EF): HF with reduced EF (HFrEF), HF with mid-range EF (HFmrEF), and HF with preserved EF (HFpEF). The new guidelines regarding the declaration of HFmrEF as a unique phenotype have achieved the goal of stimulating research on the basic characteristics, pathophysiology, and treatment of HF patients with a left ventricular EF of 40–49%. Patients with HFmrEF have more often been described as an intermediate population between HFrEF and HFpEF patients; however, with regard to etiology and clinical indicators, they are more similar to the HFrEF population. Concerning clinical prognosis, they are closer to HFpEF because both populations have a good prognosis and quality of life. Meanwhile, growing evidence indicates that HFmrEF and HFpEF show heterogeneity in presentation and pathophysiology, and the emergence of this heterogeneity often plays a crucial role in the prognosis and treatment of the disease. To date, the exact mechanisms and effective treatment strategies of HFmrEF and HFpEF are still poorly understood, but some of the current evidence, from observational studies and post-hoc analyses of randomized controlled trials, have shown that patients with HFmrEF may benefit more from HFrEF treatment strategies, such as beta-blockers, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, mineralocorticoid receptor antagonists, and sacubitril/valsartan. This review summarizes available data from current clinical practice and mechanistic studies in terms of epidemiology, etiology, clinical indicators, mechanisms, and treatments to discuss the potential association between HFmrEF and HFpEF patients.

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Section: Underlying Mechanisms Of Hfpef and Hfmrefmentioning

confidence: 99%

Similarities and Differences Between HFmrEF and HFpEF

Zhao

Zhang

et al. 2021

Front. Cardiovasc. Med.

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“…However, the detection of HFpEF imposes more difficulties, in T2D as well as in people without diabetes. In principle, one can postulate that HFpEF diagnosis can be based on the presence of sign and symptoms of HF (although with preserved systolic LV function and LVEF > 50%), together with the evidence of left ventricle diastolic dysfunction (LVDD), based either on criteria from echocardiography or a set of biomarkers [12]. However, the presence of the signs and symptoms might not be abundant, and echocardiography findings might also be frequently insufficient [12].…”

Section: Heart Failure In Diabetes: Hfrrf Vs Hfpef From Diabetologist Standpointmentioning

confidence: 99%

“…In principle, one can postulate that HFpEF diagnosis can be based on the presence of sign and symptoms of HF (although with preserved systolic LV function and LVEF > 50%), together with the evidence of left ventricle diastolic dysfunction (LVDD), based either on criteria from echocardiography or a set of biomarkers [12]. However, the presence of the signs and symptoms might not be abundant, and echocardiography findings might also be frequently insufficient [12]. Despite the initial beliefs that HFpEF is a less threatening form of HF compared to HFrEF, it has been demonstrated in a prospective population study that the survival rate has been similar, reconfirming the need for early detection of HFpEF [12,13].…”

Section: Heart Failure In Diabetes: Hfrrf Vs Hfpef From Diabetologist Standpointmentioning

confidence: 99%

“…However, the presence of the signs and symptoms might not be abundant, and echocardiography findings might also be frequently insufficient [12]. Despite the initial beliefs that HFpEF is a less threatening form of HF compared to HFrEF, it has been demonstrated in a prospective population study that the survival rate has been similar, reconfirming the need for early detection of HFpEF [12,13].…”

Section: Heart Failure In Diabetes: Hfrrf Vs Hfpef From Diabetologist Standpointmentioning

confidence: 99%

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Interdisciplinary assessment and diagnostic algorithm: The role of the diabetologist

Lalić

2021

Diabetes Research and Clinical Practice

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“…Cristae are studded with many proteins (i.e., ATP synthase, complexes I-IV) that are involved in electron transport, ATP synthesis, and transport of metabolites in and out of the mitochondrial matrix. (18) There are also other mitochondrial components such as granules, ribosomes, and mitochondrial deoxyribonucleic acid (mtDNA). The mtDNA play an important role in the regulation of apoptosis, free radical generation, and cellular metabolism (19).…”

Section: Mitochondria and Bioenergeticsmentioning

confidence: 99%

Mitochondrial bioenergetics and D-ribose in HFpEF: a brief narrative review

Krueger¹,

Rahman²,

Shen³

et al. 2021

Ann Transl Med

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In this review article, we briefly describe the status of treatment options for HFpEF and the role of mitochondrial dysfunction in the pathogenesis of HFpEF as an alternative therapeutic target. We also examine the mechanisms of D-ribose in cellular energy production and discuss the potential disadvantages and benefits of supplemental use of D-ribose in patients with HFpEF.Background: Heart failure is a major cardiovascular disease that impacts over 6 million Americans and is one of the leading causes for morbidity and mortality. Patients with heart failure often experience shortness of breath and fatigue along with impaired physical capacity, all leading to poor quality of life. As a subtype of heart failure, heart failure with preserved ejection fraction (HFpEF) is characterized with impaired diastolic function. Currently, there are no effective treatments specifically for HFpEF, thus clinicians and researchers are searching for therapies to improve cardiac function. Emerging evidence indicate that mitochondrial dysfunction and impaired cardiac bioenergetics are among the underlying mechanisms for HFpEF. There is increased interest in investigating the use of supplements such as D-ribose to enhance mitochondrial function and improve production of adenosine triphosphate (ATP).

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Mechanisms underlying the pathophysiology of heart failure with preserved ejection fraction: the tip of the iceberg

Cited by 29 publications

References 217 publications

Similarities and Differences Between HFmrEF and HFpEF

Similarities and Differences Between HFmrEF and HFpEF

Interdisciplinary assessment and diagnostic algorithm: The role of the diabetologist

Mitochondrial bioenergetics and D-ribose in HFpEF: a brief narrative review

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