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Related Concept Videos

Pathophysiology of Heart Failure01:17

Pathophysiology of Heart Failure

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Heart failure (HF) is a progressive syndrome involving ventricles that leads to inadequate cardiac output. It can be classified based on location and output or ejection fraction. Ejection fraction (EF) is an essential measurement in the diagnosis and surveillance of HF. Reduced EF corresponds to systolic heart failure (HFrEF). However, HF with preserved ejection fraction (HFpEF) is becoming increasingly prevalent. Also known as diastolic HF, this form of HF is related to aging. The...
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The heart's primary function is to pump blood throughout the body, maintaining a balance between blood sent out (cardiac output) and blood returning (venous return). If this balance is disrupted, it can result in congestive heart failure (CHF), a severe condition where the heart becomes an inefficient pump, leading to inadequate blood circulation.
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Psychoneuroimmunology: Cardiovascular Disease01:27

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Psychoneuroimmunology (PNI) is a multidisciplinary field that examines how psychological factors, particularly stress, interact with the immune system and impact physical health. Research in PNI has shown that chronic or traumatic stress can disrupt both the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system. These disruptions contribute to serious health conditions, including cardiovascular diseases.
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The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
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β-adrenergic antagonists, commonly known as β-blockers, block the effects of sympathetic neurotransmitters such as noradrenaline (NA) and adrenaline (ADR). They have several beneficial effects in heart failure treatment. They reduce heart rate, the force of contraction, and cardiac muscle relaxation. They also slow the atrial-ventricular conduction rate and raise the threshold for arrhythmias. The concentration of β-blockers determines their effects on bronchodilation,...
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Isolation and Identification of Extravascular Immune Cells of the Heart
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Heart failure promotes multimorbidity through innate immune memory.

Yukiteru Nakayama1, Katsuhito Fujiu1,2, Tsukasa Oshima1

  • 1Department of Cardiovascular Medicine, University of Tokyo, Tokyo, Japan.

Science Immunology
|May 24, 2024
PubMed
Summary

Heart failure (HF) triggers changes in hematopoietic stem cells (HSCs), driving recurrent cardiac events and related conditions like kidney disease. These HSCs act as a "stress memory" carrier, linking HF to comorbidities.

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Area of Science:

  • Cardiovascular Biology
  • Hematology
  • Immunology

Background:

  • Heart failure (HF) patients frequently experience recurrent decompensation and develop comorbidities, including chronic kidney disease and frailty.
  • The underlying pathological mechanisms linking these conditions are not well understood.
  • Hematopoietic stem cells (HSCs) are implicated in systemic inflammation and disease progression.

Purpose of the Study:

  • To investigate the role of hematopoietic stem cells (HSCs) in recurrent heart failure (HF) and associated comorbidities.
  • To elucidate the mechanisms by which cardiac stress affects HSC function and systemic health.

Main Methods:

  • Bone marrow transplantation experiments in mice to assess the impact of HF-experienced HSCs.
  • Global chromatin accessibility analysis and single-cell RNA-sequencing (scRNA-seq) in HF mouse models.
  • Assessment of transforming growth factor-beta (TGF-β) signaling in HSCs and its effect on cardiac function.

Main Results:

  • Bone marrow from HF mice induced cardiac dysfunction, fibrosis, and increased susceptibility to kidney and muscle injury in recipients.
  • HF enhanced HSCs' ability to produce proinflammatory macrophages.
  • Suppressed TGF-β signaling in HSCs from HF mice correlated with repressed sympathetic nervous activity and exacerbated cardiac dysfunction upon transplantation.

Conclusions:

  • Cardiac stress epigenetically modifies HSCs, altering their macrophage differentiation capacity.
  • Altered HSCs may serve as a common driver for recurrent HF events and comorbidities by carrying "stress memory."
  • Targeting HSC dysfunction presents a potential therapeutic strategy for managing HF and its associated complications.