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Related Concept Videos

Heart Failure I: Introduction01:27

Heart Failure I: Introduction

1.3K
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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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...
4.6K
Imbalances in Cardiac Output01:26

Imbalances in Cardiac Output

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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.
CHF can occur due to the failure of either side of the heart. Left-side failure leads to pulmonary congestion—the right side continues to send...
3.4K
Heart Failure II: Pathophysiology01:29

Heart Failure II: Pathophysiology

1.4K
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...
1.4K
Heart Failure IV: Classification and Diagnostic Evaluation01:30

Heart Failure IV: Classification and Diagnostic Evaluation

602
Heart failure can be classified in various ways, with the most common classifications based on physical activity limitations, disease progression, severity, and treatment strategies.The Functional Classification of Heart Failure divides patients into four categories based on physical activity limitation due to symptom burden.Class I: Patients in this class have cardiac disease but no physical activity limitations. Ordinary activities like walking, climbing stairs, or routine tasks do not cause...
602
Heart Failure III: Clinical Manifestations01:26

Heart Failure III: Clinical Manifestations

879
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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Related Experiment Video

Updated: Mar 31, 2026

Lumped-Parameter and Finite Element Modeling of Heart Failure with Preserved Ejection Fraction
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Lumped-Parameter and Finite Element Modeling of Heart Failure with Preserved Ejection Fraction

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Heart failure: when form fails to follow function.

Arnold M Katz1, Ellis L Rolett2

  • 1Geisel School of Medicine at Dartmouth, Hanover, NH, USA University of Connecticut School of Medicine, Farmington, CT, USA.

European Heart Journal
|October 27, 2015
PubMed
Summary
This summary is machine-generated.

Heart failure involves impaired cardiac form and function. Systolic heart failure (HFrEF) involves ventricle dilation, while diastolic heart failure (HFpEF) involves thickening, impacting treatment strategies.

Keywords:
Cardiac architectureEjection fractionHeart failureHypertrophic signallingSarcomere addition

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Area of Science:

  • Cardiology
  • Heart Failure Pathophysiology
  • Cardiac Remodeling

Background:

  • Cardiac performance relies on structural and functional adaptations.
  • Heart failure arises from impaired form-function relationships, categorized as systolic (SHF) and diastolic (DHF).
  • Current definitions use ejection fraction (EF), distinguishing heart failure with reduced ejection fraction (HFrEF) and preserved ejection fraction (HFpEF).

Purpose of the Study:

  • To elucidate the distinct structural and functional mechanisms underlying HFrEF and HFpEF.
  • To explain the limitations of ejection fraction as a sole diagnostic index.
  • To explore the molecular basis for differential therapeutic responses in HFrEF versus HFpEF.

Main Methods:

  • Analysis of cardiac architecture, cellular structures, and molecular signaling pathways.
  • Comparison of physiological and biochemical mechanisms regulating cardiac function in health and failure.
  • Review of existing literature defining and differentiating HFrEF and HFpEF.

Main Results:

  • SHF (HFrEF) is characterized by left ventricular (LV) dilation due to sarcomere addition in series, increasing end-diastolic volume (EDV) but impairing ejection.
  • DHF (HFpEF) involves concentric hypertrophy from sarcomere addition in parallel, increasing myocyte thickness, which impairs LV filling.
  • Ejection fraction (EF) is a composite index of stroke volume (function) and EDV (form), potentially masking underlying pathologies.

Conclusions:

  • Distinct structural remodeling processes (dilation vs. hypertrophy) characterize HFrEF and HFpEF.
  • These structural differences influence cardiac mechanics and patient outcomes.
  • Underlying molecular signaling disparities may explain the differential efficacy of therapies for HFrEF and HFpEF.