The major factor of left ventricular systolic dysfunction in patients with cardiac amyloidosis: Amyloid overload or

Jianyao Lu1, Peijun Zhao1,2, Jinhan Qiao1

  • 1Department of Radiology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

Insights

In cardiac amyloidosis, increased amyloid in the heart muscle is the main cause of left ventricular systolic dysfunction. Microcirculation impairment is less significant in this condition.

Area of Science:

  • Cardiology
  • Cardiovascular Imaging
  • Cardiac Amyloidosis

Background:

  • Cardiac amyloidosis (CA) involves amyloid deposition in the heart, potentially impairing left ventricular (LV) function.
  • Both amyloid overload and microcirculation impairment can affect LV systolic function, but their relative contributions in CA are unclear.

Purpose of the Study:

  • To determine whether amyloid overload or microcirculation impairment is the primary driver of LV systolic dysfunction in CA patients.
  • To investigate the major factor of LV functional remodeling using cardiac magnetic resonance imaging (CMR).

Main Methods:

  • Forty CA patients and 20 healthy controls underwent CMR, including cine, T1 mapping, and first-pass perfusion.
  • CA patients were stratified by left ventricular ejection fraction (LVEF) into reduced (rLVEF) and preserved (pLVEF) subgroups.
  • Correlation analyses assessed relationships between LVEF and CMR-derived mapping and perfusion parameters.

Main Results:

  • Higher native T1 values (indicating greater amyloid deposition) were found in rLVEF patients compared to pLVEF patients.
  • Reduced LVEF correlated negatively with native T1 values, suggesting amyloid burden is a key factor.
  • No significant correlation was observed between LVEF and microcirculation parameters (perfusion).

Conclusions:

  • Amyloid overload in the myocardial interstitium is likely the dominant factor causing LV systolic dysfunction in CA patients.
  • Microcirculation impairment appears to play a lesser role in LV systolic dysfunction in this cohort.
Abstract

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