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Related Concept Videos

Myocarditis I: Introduction01:21

Myocarditis I: Introduction

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Myocarditis is inflammation of the myocardium, which is the muscular layer of the heart.EtiologyMyocarditis has a diverse etiology, including a wide range of infectious and non-infectious causes:Infectious CausesViral: Common viruses include Coxsackie A and B, adenovirus, parvovirus B19, enteroviruses, and influenza A.Bacterial: Examples include infections caused by Streptococcus, Staphylococcus, and Mycoplasma species.Rickettsial: Infections like Rocky Mountain spotted fever can result in...
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Cardiomyopathy II: Dilated Cardiomyopathy01:30

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Dilated cardiomyopathy, or DCM, is a progressive myocardial disorder characterized by ventricular chamber dilation and contractile dysfunction.EtiologyVarious factors can cause DCM, including hypertension and heavy alcohol intake, which contribute to the weakening and enlargement of the heart muscle. Viral infections, such as Coxsackievirus B, adenoviruses, and influenza, can lead to DCM by causing inflammation and damage to heart tissue. Certain chemotherapeutic agents, including daunorubicin,...
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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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Imbalances in Cardiac Output01:26

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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...
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Cardiomyopathy V: Interprofessional Care01:29

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Managing cardiomyopathy involves addressing underlying or precipitating causes, treating heart failure with medications, and implementing dietary changes and a balanced exercise and rest regimen.Lifestyle ModificationsCardiomyopathy patients should adopt a low-sodium diet to reduce fluid retention and manage heart failure. A personalized exercise and rest plan helps maintain physical fitness without overstraining the heart. Avoiding alcohol and tobacco is essential to prevent further damage to...
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Cardiomyopathy I: Introduction and Classification01:25

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Cardiomyopathy, or CMP, is a group of diseases affecting the myocardial structure, impairing its ability to pump blood effectively. This condition can lead to arrhythmias, heart failure, or sudden cardiac death.Cardiomyopathies are classified into primary and secondary categories:Primary Cardiomyopathy refers to conditions involving only the heart muscle that are often idiopathic (of unknown cause) or genetic. They primarily affect the myocardium without the involvement of other systemic...
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Scanning Electron Microscopy of Macerated Tissue to Visualize the Extracellular Matrix
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Circulating Factors Induce Cardiomyopathy after Burn Injury.

Susana Fortich1, Jake J Wen1, Jana E Dejesus1

  • 1From the Departments of Surgery (Fortich, Wen, Dejesus, and RS Radhakrishnan), University of Texas Medical Branch, Galveston, TX.

Journal of the American College of Surgeons
|March 26, 2026
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Summary
This summary is machine-generated.

Burn injury releases circulating factors that damage heart cells and mitochondria. Sildenafil (SIL) treatment reversed this damage in vitro, suggesting a therapeutic potential for burn-induced cardiac dysfunction.

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Area of Science:

  • Cardiovascular Research
  • Cellular Biology
  • Burn Injury Pathophysiology

Background:

  • Burn injury can lead to cardiac dysfunction via the phosphodiesterase type 5 (PDE5)-cyclic guanosine monophosphate-protein kinase G pathway.
  • The role of circulating factors in post-burn cardiac damage and the potential of PDE5A inhibitors in vitro remain unclear.

Purpose of the Study:

  • To investigate if circulating factors from burn injury cause mitochondrial damage in cardiomyocytes in vitro.
  • To determine if PDE5A inhibitors can reverse this damage.

Main Methods:

  • Human cardiomyocyte cell line (AC16) treated with serum from sham-injured rats, 24-hour post-burn (24hpb) rats, sildenafil (SIL) alone, or 24hpb serum with SIL.
  • Analyses included ELISA, mitochondrial function assays, fluorescence microscopy, gene analysis, and Illumina RNA sequencing.

Main Results:

  • 24hpb serum decreased cyclic guanosine monophosphate and increased cTN1 levels; SIL treatment reversed these changes.
  • 24hpb serum induced cardiomyocyte cytotoxicity, apoptosis, and mitochondrial dysfunction (decreased ATP, impaired respiration).
  • SIL treatment restored cardiomyocyte viability and mitochondrial function to near sham levels.

Conclusions:

  • Circulating factors released post-burn injury contribute to cardiomyocyte mitochondrial damage.
  • Sildenafil demonstrates potential in reversing burn-induced cardiac dysfunction by protecting mitochondria and improving cellular function in vitro.