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Related Concept Videos

Heart Failure II: Pathophysiology01:29

Heart Failure II: Pathophysiology

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Systolic Heart Failure and Compensatory MechanismsSystolic heart failure (also termed HFrEF, Heart Failure with Reduced Ejection Fraction) is the most prevalent type of heart filure. It results in a decreased volume of blood being pumped from the ventricle. The aortic arch and carotid sinuses have baroreceptors that detect reduced blood pressure, triggering the sympathetic nervous system (SNS) to release epinephrine and norepinephrine. Initially, this response aims to boost heart rate and...
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Pathophysiology of Heart Failure01:17

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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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Heart Failure I: Introduction01:27

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Heart failure refers to a clinical syndrome caused by structural or functional cardiac disorders that prevent the heart from pumping an adequate amount of blood to meet the body's metabolic needs. This condition often arises from myocardial infarction or ischemia, leading to decreased cardiac output, reduced tissue perfusion, impaired gas exchange, fluid volume imbalance, and decreased functional ability.Heart failure can result from disruptions in the mechanisms that regulate cardiac output...
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Introduction to the Human Microbiota01:22

Introduction to the Human Microbiota

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Microorganisms colonize various regions of the human body, including the mouth, nasal passages, throat, stomach, intestines, urogenital tract, and skin. The total number of microbial cells is estimated to range from 10¹³ to 10¹⁴—comparable to, or exceeding, the number of human somatic cells. This host–microbiome relationship has led to the conceptualization of humans as supraorganisms, wherein microbial communities perform vital roles in development, immunity,...
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Development of Human Microbiota01:30

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The human microbiota begins developing at birth and undergoes continual change as we age. Infancy marks a critical period of microbial sensitivity, offering a “window of opportunity” during which beneficial microbes help mature the immune system. By age three, children typically develop a more stable and diverse microbial community. Newborns acquire microbes from their immediate environment; vaginal delivery favors maternal vaginal microbes, while cesarean births favor microbes from...
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Heart Failure III: Clinical Manifestations01:26

Heart Failure III: Clinical Manifestations

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Heart failure (HF) manifests primarily as dyspnea, fatigue, and fluid retention, resulting in peripheral and pulmonary edema. Symptoms may vary depending on which ventricle is more affected, left or right.Left-Sided Heart FailureAlso known as left ventricular failure, this condition results from the left ventricle's inability to fill or eject sufficient blood into the systemic circulation. It leads to pulmonary congestion, which occurs when the left ventricle fails to eject blood effectively...
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Murine Fecal Isolation and Microbiota Transplantation
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Exploring the Microbiome in Heart Failure.

Takeshi Kitai1, Jennifer Kirsop2, W H Wilson Tang3,4,5

  • 1Department of Cardiovascular Medicine, Heart and Vascular Institute, Cleveland Clinic, Cleveland, OH, USA.

Current Heart Failure Reports
|February 18, 2016
PubMed
Summary
This summary is machine-generated.

Gut microbiota changes, known as dysbiosis, impact heart failure (HF) and cardiovascular disease. Trimethylamine N-oxide (TMAO) from gut bacteria contributes to HF and chronic kidney disease (CKD) pathogenesis.

Keywords:
Cardiorenal syndromeCardiovascular diseaseChronic kidney diseaseGut microbiotaHeart failureTrimethylamine N-oxide

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Area of Science:

  • Microbiology
  • Cardiology
  • Nephrology

Background:

  • The human gut microbiota significantly influences cardiovascular (CV) health, including heart failure (HF).
  • Gut dysbiosis, an imbalance in microbial composition, can lead to systemic inflammation implicated in HF pathophysiology.
  • Trimethylamine N-oxide (TMAO), a metabolite from gut bacteria, is increasingly recognized as a key factor in CV disease development.

Purpose of the Study:

  • To explore the role of gut microbiota and TMAO in the pathogenesis of heart failure (HF) and chronic kidney disease (CKD).
  • To investigate the bidirectional relationship between HF and CKD mediated by gut microbiota and TMAO.
  • To identify potential novel therapeutic targets for cardiorenal syndrome.

Main Methods:

  • Review of current literature on gut microbiota, TMAO, HF, and CKD.
  • Analysis of studies linking dysbiosis, TMAO levels, and cardiorenal outcomes.
  • Examination of proposed mechanisms for TMAO's role in cardiovascular disease.

Main Results:

  • Elevated TMAO levels are associated with adverse outcomes in patients with HF and CKD.
  • Gut dysbiosis contributes to increased TMAO production and uremic toxin generation, potentially worsening HF and CKD.
  • A bidirectional relationship exists between HF and CKD, potentially mediated by gut microbiota.

Conclusions:

  • The gut microbiota and its metabolite TMAO play a significant role in the cardiorenal syndrome.
  • Understanding the mechanisms linking gut microbiota, TMAO, and cardiorenal disease is crucial for developing new therapies.
  • Further research is needed to elucidate the direct effects of TMAO on cardiovascular pathophysiology and renal handling.