The Sympathetic Nervous System in Hypertensive Heart Failure with Preserved LVEF

Triposkiadis, Filippos; Briasoulis, Alexandros; Sarafidis, Pantelis; Magouliotis, Dimitrios; Athanasiou, Thanos; Paraskevaidis, Ioannis; Skoularigis, John; Xanthopoulos, Andrew

doi:10.3390/jcm12206486

Cited by 3 publications

(2 citation statements)

References 115 publications

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“…The chronotropic action of aldosterone was averted by spironolactone, indicating the role of MRA in this response ( 12 , 13 ). HF is also associated with increased activity of the sympathetic nervous system ( 14 ). This chronic elevated plasma catecholamines lead to desensitization of the β-adrenergic signaling pathway.…”

Section: Clinical Presentationmentioning

confidence: 99%

Ion channel trafficking implications in heart failure

Reisqs,

Qu,

Boutjdir

2024

Front. Cardiovasc. Med.

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Heart failure (HF) is recognized as an epidemic in the contemporary world, impacting around 1%–2% of the adult population and affecting around 6 million Americans. HF remains a major cause of mortality, morbidity, and poor quality of life. Several therapies are used to treat HF and improve the survival of patients; however, despite these substantial improvements in treating HF, the incidence of HF is increasing rapidly, posing a significant burden to human health. The total cost of care for HF is USD 69.8 billion in 2023, warranting a better understanding of the mechanisms involved in HF. Among the most serious manifestations associated with HF is arrhythmia due to the electrophysiological changes within the cardiomyocyte. Among these electrophysiological changes, disruptions in sodium and potassium currents’ function and trafficking, as well as calcium handling, all of which impact arrhythmia in HF. The mechanisms responsible for the trafficking, anchoring, organization, and recycling of ion channels at the plasma membrane seem to be significant contributors to ion channels dysfunction in HF. Variants, microtubule alterations, or disturbances of anchoring proteins lead to ion channel trafficking defects and the alteration of the cardiomyocyte's electrophysiology. Understanding the mechanisms of ion channels trafficking could provide new therapeutic approaches for the treatment of HF. This review provides an overview of the recent advances in ion channel trafficking in HF.

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Section: Clinical Presentationmentioning

confidence: 99%

Ion channel trafficking implications in heart failure

Reisqs,

Qu,

Boutjdir

2024

Front. Cardiovasc. Med.

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“…The sympathetic nervous system plays a pivotal role in modulating Ca 2+ sensitivity in both HFpEF and HFrEF, although its mechanisms and impacts vary between the two. In HFpEF, sympathetic overactivity, often linked to comorbid conditions like hypertension, leads to augmented β-adrenergic signaling [115]. This signaling increases cAMP levels, leading to enhanced PKA activity.…”

Section: Ca 2+ Sensitivity Changes In Hfpef and Hfrefmentioning

confidence: 99%

Altering Calcium Sensitivity in Heart Failure: A Crossroads of Disease Etiology and Therapeutic Innovation

Saad,

Mashali,

Repas

et al. 2023

IJMS

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Heart failure (HF) presents a significant clinical challenge, with current treatments mainly easing symptoms without stopping disease progression. The targeting of calcium (Ca2+) regulation is emerging as a key area for innovative HF treatments that could significantly alter disease outcomes and enhance cardiac function. In this review, we aim to explore the implications of altered Ca2+ sensitivity, a key determinant of cardiac muscle force, in HF, including its roles during systole and diastole and its association with different HF types—HF with preserved and reduced ejection fraction (HFpEF and HFrEF, respectively). We further highlight the role of the two rate constants kon (Ca2+ binding to Troponin C) and koff (its dissociation) to fully comprehend how changes in Ca2+ sensitivity impact heart function. Additionally, we examine how increased Ca2+ sensitivity, while boosting systolic function, also presents diastolic risks, potentially leading to arrhythmias and sudden cardiac death. This suggests that strategies aimed at moderating myofilament Ca2+ sensitivity could revolutionize anti-arrhythmic approaches, reshaping the HF treatment landscape. In conclusion, we emphasize the need for precision in therapeutic approaches targeting Ca2+ sensitivity and call for comprehensive research into the complex interactions between Ca2+ regulation, myofilament sensitivity, and their clinical manifestations in HF.

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Coupling of β-adrenergic and Hippo pathway signaling: Implications for heart failure pathophysiology and metabolic therapy

Du,

She,

et al. 2024

Mitochondrion

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The Sympathetic Nervous System in Hypertensive Heart Failure with Preserved LVEF

Cited by 3 publications

References 115 publications

Ion channel trafficking implications in heart failure

Ion channel trafficking implications in heart failure

Altering Calcium Sensitivity in Heart Failure: A Crossroads of Disease Etiology and Therapeutic Innovation

Coupling of β-adrenergic and Hippo pathway signaling: Implications for heart failure pathophysiology and metabolic therapy

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