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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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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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Congestive Hepatopathy.

José Ignacio Fortea1,2,3, Ángela Puente1,2,3, Antonio Cuadrado1,2,3

  • 1Gastroenterology and Hepatology Department, University Hospital Marqués de Valdecilla, 39008 Santander, Spain.

International Journal of Molecular Sciences
|December 16, 2020
PubMed
Summary
This summary is machine-generated.

Congestive hepatopathy (CH), a liver disease from heart failure (HF), causes fibrosis and cirrhosis due to venous congestion. Improved heart treatments increase CH prevalence, complicating patient management.

Keywords:
cirrhosisheart failureheart transplantationportal hypertension

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Area of Science:

  • Cardiology
  • Hepatology
  • Internal Medicine

Background:

  • Heart failure (HF) can lead to liver disease, termed cardiac hepatopathy.
  • Congestive hepatopathy (CH), a form of cardiac hepatopathy, arises from chronic right-sided HF and passive venous congestion.
  • The etiology of CH has shifted towards ischemic cardiomyopathy and congenital heart disease, differing from historical associations with rheumatic valvular disease.

Purpose of the Study:

  • To describe the current spectrum and pathological characteristics of congestive hepatopathy.
  • To highlight the progression of liver damage in CH, including fibrosis, cirrhosis, and hepatocellular carcinoma.
  • To discuss the implications of improved HF survival on the incidence and clinical relevance of CH.

Main Methods:

  • Review of existing literature and clinical data on cardiac hepatopathy and congestive hepatopathy.
  • Analysis of pathological changes associated with chronic venous congestion in the liver.
  • Evaluation of the diagnostic challenges and prognostic factors in CH.

Main Results:

  • Chronic passive congestion in CH leads to sinusoidal hypertension, centrilobular fibrosis, and potentially cardiac cirrhosis and hepatocellular carcinoma.
  • Fibrosis in CH exhibits a unique "reversed lobulation" pattern, with inflammation playing a minimal role, unlike in primary liver diseases.
  • Non-invasive diagnostic tests for liver fibrosis show poor performance in the context of CH.

Conclusions:

  • Advances in HF management have increased patient survival, leading to a rise in liver complications like CH.
  • CH can become a significant clinical issue, potentially rivaling the cardiac condition in complexity and management challenges.
  • Early recognition and understanding of CH are crucial for managing patients with advanced heart disease.