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Published on: February 20, 2017
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.
Purpose:
Amyloid overload and microcirculation impairment are both detrimental to left ventricular (LV) systolic function, while it is not clear which factor dominates LV functional remodeling in patients with cardiac amyloidosis (CA). The purpose of this study was to investigate the major factor of LV systolic dysfunction using cardiac magnetic resonance imaging.
Materials And Methods:
Forty CA patients and 20 healthy controls were included in this study. The CA group was divided into two subgroups by the left ventricular ejection fraction (LVEF): patients with reduced LVEF (LVEF < 50%, rLVEF), and patients with preserved LVEF (LVEF ≥ 50%, pLVEF). The scanning sequences included cine, native and post-contrast T1 mapping, rest first-pass perfusion and late gadolinium enhancement. Perfusion and mapping parameters were compared among the three groups. Correlation analysis was performed to evaluate the relationship between LVEF and mapping parameters, as well as the relationship between LVEF and perfusion parameters.
Results:
Remarkably higher native T1 value was observed in the rLVEF patients than the pLVEF patients (1442.2 ± 85.8 ms vs. 1407.0 ± 93.9 ms, adjusted p = 0.001). The pLVEF patients showed significantly lower slope dividing baseline signal intensity (slope%BL; rLVEF vs. pLVEF, 55.1 ± 31.0 vs. 46.2 ± 22.3, adjusted p = 0.001) and a lower maximal signal intensity subtracting baseline signal intensity (MaxSI-BL; rLVEF vs. pLVEF, 43.5 ± 23.9 vs. 37.0 ± 18.6, adjusted p = 0.003) compared to the rLVEF patients. CA patients required more time to reach the maximal signal intensity than the controls did (all adjusted p < 0.01). There was no significant correlation between LVEF and first-pass perfusion parameters, while significant negative correlation was observed between LVEF and native T1 (r = -0.434, p = 0.005) in CA patients.
Conclusion:
Amyloid overload in the myocardial interstitium may be the major factor of LV systolic dysfunction in CA patients, other than microcirculation impairment.
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