We would like to thank Casian et al. for their interest in our article,1 and we will try to address some of the issues raised.

Although the family study in the first 2 cases did not identify more carriers, the TNNC1 p.Ala8Val and MYL3 p.Met173Val variants have been reported in other families with hypertrophic cardiomyopathy and functional studies have been reported that support their pathogenicity.2,3

False positives of cardiac scintigraphy occur mostly in other types of amyloid cardiomyopathy, but also in recent myocardial infarction or hydroxychloroquine cardiotoxicity. Blood pool could be interpreted as a false positive, and consequently single photon emission computed tomography is recommended to confirm uptake.4 We acknowledge that false positive cases have been reported in hypertrophic cardiomyopathy,5 but unlike ours, those did not show the red flags or imaging findings expected in cardiac transthyretin amyloidosis, such as apical sparing in speckle-tracking or high T1/extracellular volume.4 Our first case had a chronic coronary syndrome but not recent myocardial infarction, and transthyretin amyloidosis deposits were confirmed in endomyocardial biopsy.1 Currently, a noninvasive diagnosis of cardiac transthyretin amyloidosis is accepted when the clinical picture is compatible and there is grade ≥ 2 uptake in cardiac scintigraphy in the absence of monoclonal gammopathy.4

Finally, tafamidis 61mg was initiated in the first and second cases. In the third case, it was not initiated because the patient refused to attempt histological confirmation.