Myocardial fibrosis

Last revised by Joachim Feger on 26 Nov 2021

Myocardial fibrosis refers to an increase in collagen volume within the extracellular interstitium of the myocardium 1-3.

Myocardial fibrosis leads to diastolic and or systolic dysfunction and patients can present with symptoms associated with cardiac insufficiency arrhythmias such as dyspnea, orthopnea, edema, etc.

Fibrosis can be diffuse or focal and can be as a result of different mechanisms 1:

  • reactive interstitial fibrosis
  • infiltrative interstitial fibrosis
  • replacement fibrosis and myocardial scarring

A progressive increase of the extracellular matrix leads to diastolic and systolic dysfunction and an increase of adverse cardiovascular events 1. In end-stage heart failure, myocardial fibrosis is always present 1.

Myocardial fibrosis can occur as a result of various cardiac diseases 1 (classified by subtypes):

due to accelerated collagen synthesis as a result of different stimuli

progressive deposit of protein or glycosphingolipids

Due to cell damage or necrosis, an intense inflammatory response is induced, which leads to degradation of the normal interstitial matrix and generation of new matrix fragments thus an alteration of tissue composition 1,2.

Fibrosis leads to an increase in extracellular volume (ECV), thus to an increased volume of distribution for contrast agents and an increased shortening in postcontrast T1 1.

  • T2/STIR: normal
  • IRGE/PSIR: It can be seen as a late gadolinium enhancement (LGE) in focal disease. Due to the “nulling” of the myocardium in inversion-recovery sequences, it will be difficult to detect diffuse fibrosis 1.
  • T2 mapping: normal T2 [ms]
  • T1 mapping: increased T1 [ms] 1
  • ECV: increased 1

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Cases and figures

  • Case 1: midwall fibrosis apical HCM
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