Introduction
Amyloidosis is a constellation of diseases characterized by misfolded
proteins deposited in target organs1. Cardiac
involvements were thought to be very rare previously but are now
understood to be underdiagnosed2. Acquired monoclonal
immunoglobulin light-chain (AL); hereditary, mutated
transthyretin-related (ATTRm); and wild-type transthyretin-related
(ATTRwt) are considered as three major types of cardiac
amyloidosis3. Light chains cardiac amyloidosis (AL-CA)
progresses much faster than other types of amyloidosis, and appropriate
treatment is capable of prolonging survival time substantially1,4.
Traditionally, AL-CA can be diagnosed by pathologic confirmation of
immunoglobulin light chain amyloid in extracardiac tissue and cardiac
imaging consistent with cardiac amyloidosis (CA)5.
Echocardiography often provides first clues to the presence of CA, and
is helpful for prompting a low threshold for further multimodality
assessment2,6.
Cardiac amyloid can virtually infiltrate all cardiac
chambers7,8. Previous studies have shown the
significant enlargement of LA and reduction of left atrial strain in CA
patients9-14. Possible mechanisms include restrictive
LV physiology with elevated filling pressure resulting from
intramyocardial amyloid infiltration and intrinsic LA failure due to
direct amyloid infiltration10. Similarly, increased LA
volume is a marker of hypertensive heart disease (HHD), and significant
reduction of LA strain occurs in HHD patients15. A
study containing 11 AL-CA patients, 33 ATTR-CA patients, and 25 HHD
patients showed that HHD group had significantly higher left atrial
strain values than the amyloid cases9. However, the
number of AL-CA patients in that study was small. Meanwhile, patients
with atrial fibrillation (AF) had reduced left atrial strain values,
which were not studied separately in that study9. The
aim of this study was to evaluate the differences in left atrial strain
between patients with AL-CA and those with HHD.