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Quantification of Mouse Heart Left Ventricular Function, Myocardial Strain, and Hemodynamic Forces by Cardiovascular Magnetic Resonance Imaging
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Quantification of Mouse Heart Left Ventricular Function, Myocardial Strain, and Hemodynamic Forces by Cardiovascular Magnetic Resonance Imaging

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Myocardial T1 mapping and extracellular volume quantification in patients with left ventricular non-compaction

José A B Araujo-Filho1, Antonildes N Assuncao1, Marcelo D Tavares de Melo2

  • 1Department of Radiology and Oncology, Heart Institute (InCor), University of Sao Paulo Medical School, Cardiovascular Magnetic Resonance and Computed Tomography Sector, Av. Dr. Enéas de Carvalho Aguiar, 44, Andar AB, Cerqueira César, São Paulo, 05403-000 SP, Brazil.

European Heart Journal. Cardiovascular Imaging
|March 9, 2018
PubMed

Insights

Left ventricular non-compaction cardiomyopathy (LVNC) shows diffuse myocardial fibrosis, indicated by expanded extracellular volume (ECV). This fibrosis is linked to impaired ejection fraction and ventricular arrhythmias in LVNC patients.

Area of Science:

  • Cardiology
  • Biomedical Imaging
  • Pathophysiology

Background:

  • Left ventricular non-compaction cardiomyopathy (LVNC) is a complex condition with ongoing debates regarding its pathophysiology, risk stratification, and management.
  • Cardiovascular magnetic resonance (CMR) offers advanced imaging techniques for characterizing myocardial tissue.

Purpose of the Study:

  • To characterize myocardial T1 mapping and extracellular volume (ECV) fraction using CMR in patients with LVNC.
  • To investigate the relationship between these biomarkers, left ventricular ejection fraction (LVEF), and ventricular arrhythmias (VA) in LVNC.

Main Methods:

  • A CMR study was conducted on 36 LVNC patients and 18 healthy controls, including T1 mapping.
  • Extracellular volume (ECV) was quantified in segments without late gadolinium enhancement (LGE) to assess diffuse myocardial fibrosis.

Main Results:

  • LVNC patients exhibited higher native T1 values and significantly expanded ECV compared to controls.
  • ECV was independently associated with reduced LVEF.
  • In patients without LGE, higher ECV correlated with the presence of VA.

Conclusions:

  • T1 mapping and ECV quantification in LVNC suggest extracellular expansion due to diffuse fibrosis in non-infarcted myocardium.
  • This diffuse fibrosis is associated with myocardial dysfunction and VA in LVNC.
  • The extent of fibrosis, as measured by ECV, was not correlated with the degree of non-compaction.
Abstract

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