Comparative hemodynamics of ATTR and AL amyloidosis with exercise-induced pulmonary hypertension: A retrospective analysis [version 1; peer review: awaiting peer review]
Background Cardiac amyloidosis, characterized by the deposition of amyloid proteins in the heart tissue, presents in two main types: transthyretin (ATTR) and light-chain (AL) amyloidosis. The hemodynamic response to exercise and the relationship with pulmonary hypertension (PH) in these patients is...
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Published in | F1000 research Vol. 13; p. 769 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
2024
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Subjects | |
Online Access | Get full text |
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Summary: | Background
Cardiac amyloidosis, characterized by the deposition of amyloid proteins in the heart tissue, presents in two main types: transthyretin (ATTR) and light-chain (AL) amyloidosis. The hemodynamic response to exercise and the relationship with pulmonary hypertension (PH) in these patients is not well understood.
Methods
This retrospective study analyzed 100 patients diagnosed with either ATTR or AL amyloidosis. We assessed the prevalence of PH at rest and its induction during exercise stress tests. Hemodynamic parameters were measured to identify differences in the cardiac response to exercise between the two subtypes.
Results
A higher prevalence of PH was noted in the ATTR group compared to the AL group. Exercise stress tests induced significant PH, particularly in the ATTR subgroup. Subtle yet clinically relevant hemodynamic differences were observed between the amyloidosis subtypes.
Conclusions
Our findings suggest that the amyloidosis subtype is an important factor in the management of PH. There is a need for tailored clinical approaches to address the distinct pathophysiological mechanisms in ATTR and AL amyloidosis. This study contributes to a better understanding of the hemodynamic changes during exercise in cardiac amyloidosis and underscores the importance of subtype-specific management strategies. |
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ISSN: | 2046-1402 2046-1402 |
DOI: | 10.12688/f1000research.148652.1 |