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Related Concept Videos

Myocarditis I: Introduction01:21

Myocarditis I: Introduction

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...
Cardiomyopathy I: Introduction and Classification01:25

Cardiomyopathy I: Introduction and Classification

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...
Cardiomyopathy II: Dilated Cardiomyopathy01:30

Cardiomyopathy II: Dilated Cardiomyopathy

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,...
Cardiomyopathy III: Hypertrophic Cardiomyopathy01:29

Cardiomyopathy III: Hypertrophic Cardiomyopathy

Hypertrophic cardiomyopathy, or HCM, is an autosomal dominant genetic disorder characterized by asymmetric left ventricular hypertrophy without ventricular dilation. It is more common in men and is typically diagnosed in young, athletic adults.EtiologyHCM is primarily genetic and is caused by mutations in genes encoding sarcomeric proteins. Researchers have identified over 1400 mutations across at least 11 different genes. Among these, the most frequently occurring mutations are found in the...
Cardiomyopathy IV: Restrictive Cardiomyopathy01:29

Cardiomyopathy IV: Restrictive Cardiomyopathy

Restrictive cardiomyopathy (RCM) is a rare heart muscle disease characterized by impaired ventricular filling due to stiffened ventricular walls, leading to significant diastolic dysfunction.EtiologyRestrictive cardiomyopathy can arise from both inherited and acquired diseases, many of which are systemic. It is categorized into four main types: infiltrative, storage, non-infiltrative, and endomyocardial diseases.Infiltrative diseases, such as amyloidosis, lead to RCM by depositing amyloid...
Cardiomyopathy V: Interprofessional Care01:29

Cardiomyopathy V: Interprofessional Care

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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Magnetic Resonance Derived Myocardial Strain Assessment Using Feature Tracking
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Characterisation of Post-Sepsis Cardiomyopathy Using Cardiovascular Magnetic Resonance.

Samuel Malomo1, Thomas Oswald1, Edward Stephenson1

  • 1Sussex Cardiac Centre, Royal Sussex County Hospital, Brighton BN2 5BE, UK.

Diagnostics (Basel, Switzerland)
|May 1, 2025
PubMed
Summary

Post-sepsis cardiomyopathy often involves left ventricular (LV) enlargement and dysfunction, with evidence of myocardial fibrosis but not significant edema weeks after sepsis recovery. This understanding is crucial for developing new treatments for this condition.

Keywords:
cardiomyopathycardiovascular imagingcardiovascular magnetic resonanceheart failuresepsis

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Area of Science:

  • Cardiology
  • Intensive Care Medicine
  • Medical Imaging

Background:

  • Post-sepsis cardiomyopathy (PSC) is linked to poor cardiovascular outcomes but is poorly understood, hindering therapeutic development.
  • Characterizing PSC is essential for advancing treatment strategies and improving patient prognosis.
  • Cardiovascular magnetic resonance (CMR) imaging offers a detailed method for assessing cardiac structure and function in PSC.

Purpose of the Study:

  • To characterize the cardiac manifestations of post-sepsis cardiomyopathy (PSC) using cardiovascular magnetic resonance (CMR) imaging.
  • To investigate the presence of myocardial fibrosis and edema in patients recovering from sepsis.
  • To provide insights into the pathophysiology of PSC for future therapeutic interventions.

Main Methods:

  • A cohort of 22 patients with acute sepsis and suspected cardiac injury underwent CMR (cines, T1/T2-mapping, LGE) 47 days (IQR: 22-122) post-admission.
  • Age- and gender-matched healthy controls (n=16) were included for comparison.
  • CMR parameters assessed included left ventricular (LV) volumes, ejection fraction, and myocardial tissue characterization (native T1/T2, LGE).

Main Results:

  • 59% of post-sepsis patients exhibited left ventricular (LV) dilatation with significantly elevated LV volumes compared to controls.
  • 50% of patients had LV systolic dysfunction (ejection fraction < 50%), with most showing non-ischaemic late gadolinium enhancement (LGE).
  • Elevated septal native T1 values indicated myocardial fibrosis, while similar T2 values suggested minimal myocardial edema weeks post-sepsis.

Conclusions:

  • Post-sepsis cardiomyopathy is characterized by LV dilatation, systolic dysfunction, and non-ischaemic myocardial fibrosis.
  • Significant myocardial edema is not a prominent feature several weeks after sepsis recovery.
  • Further multi-center studies are required to validate these findings and develop targeted therapies for PSC.