Left Ventricular Structure and Function in Transthyretin-Related Versus Light-Chain Cardiac Amyloidosis
Key result
Wild-type and light-chain cardiac amyloidosis show similarly depressed longitudinal strain, worse than mutant TTR.
- P=0.54
- n=172
Why the study?
Does left ventricular structure and function differ between transthyretin-related and light-chain cardiac amyloidosis?
Population
172 patients with cardiac amyloidosis (AL amyloidosis, n=80; ATTRm, n=36; ATTRwt, n=56)
Design
Cohort
Authors
Discussion
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Implication
Similar strain impairment in wild-type TTR and AL amyloidosis despite differing outcomes supports additional AL mechanisms; leaves open causal inference.
Study Design
Type
Observational (n=172)
Structured PICO
Does left ventricular structure and function differ between transthyretin-related and light-chain cardiac amyloidosis?
P
Population
172 patients with cardiac amyloidosis (AL amyloidosis, n=80; ATTRm, n=36; ATTRwt, n=56)
C
Comparator
Comparison between AL amyloidosis, ATTRm, and ATTRwt
O
Outcome
Cardiac structure and function assessed by standard echocardiography and 2-dimensional speckle-tracking imaging-derived left ventricular (LV) longitudinal (LS), radial, and circumferential strains, and survivalsurrogate
Main Result
Absolute Event Rate: -11% vs -12%
p-value: p=0.54
Patients with ATTRwt cardiac amyloidosis have greater wall thickness but lower mortality than those with AL amyloidosis despite similar degrees of longitudinal strain impairment, suggesting additional mechanisms like light-chain toxicity in AL amyloidosis.
Cite This Study
Quarta et al. (2014) conducted an observational in Cardiac amyloidosis (n=172). Transthyretin-related cardiac amyloidosis (ATTRwt) vs. Light-chain cardiac amyloidosis (AL) was evaluated on Left ventricular longitudinal strain (LS) (p=0.54). Wild-type transthyretin and light-chain cardiac amyloidosis showed similarly depressed left ventricular longitudinal strain (-11±3% vs -12±4%, P=0.54), which was worse than in mutant TTR (-15±4%).