Extract
Cardiac amyloidosis (CA) originates primarily from the accumulation of insoluble misfolded protein deposits within the myocardial interstitium [1–3]. While more than 30 proteins are known to be capable of aggregating as amyloid in vivo, non-mutated (ATTRwt) and variant transthyretin (ATTRv) are the most frequent amyloidogenic proteins impacting the heart. Both ATTRwt and ATTRv cardiac amyloidosis can elicit restrictive cardiomyopathy leading to poor outcomes including heart failure and death [1–3]. While myocardial dysfunction is often cited as the predominant mechanism for dyspnea and exercise intolerance in CA patients, growing evidence suggest that extracardiac causes, including abnormal lung function, may be responsible for these clinical symptoms [1–3].
Footnotes
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Conflict of interest: Rishika Banydeen has nothing to disclose.
Conflict of interest: Giuseppe Vergaro has nothing to disclose.
Conflict of interest: Antoine Deney has nothing to disclose.
Conflict of interest: Astrid Monfort has nothing to disclose.
Conflict of interest: Michele Emdin has nothing to disclose.
Conflict of interest: Olivier Lairez has nothing to disclose.
Conflict of interest: Anna Gaelle Giguet has nothing to disclose.
Conflict of interest: Jocelyn Inamo has nothing to disclose.
Conflict of interest: Remi Neviere has nothing to disclose.
- Received September 8, 2021.
- Accepted December 9, 2021.
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