Gait abnormalities in older adults with transthyretin cardiac amyloidosis

Abstract

Background

Transthyretin cardiac amyloidosis (ATTR cardiac amyloidosis) is caused by variant (ATTRv) or wild type (ATTRwt) transthyretin. While gait abnormalities have been studied in younger patients with ATTRv amyloidosis, research on gait in older adults with ATTR cardiac amyloidosis is lacking. Given ATTR cardiac amyloidosis’ association with neuropathy and orthopedic manifestations, we explore the gait in this population.

Methods

Twenty-eight older male ATTR cardiac amyloidosis patients and 11 healthy older male controls walked overground with and without a dual cognitive task. Gait parameters: stride width, length, velocity and stance time percentage were measured using an instrumented mat. ATTR amyloidosis patients were further categorized based on clinical and functional assessments.

Results

We found significant gait differences between ATTR cardiac amyloidosis patients and healthy controls; patients had more variable, slower, narrower and shorter strides, with their feet spending more time in contact with the ground as opposed to in swing. However, the observed gait differences did not correlate with clinical and functional measures of ATTR cardiac amyloidosis severity.

Conclusions

Our results suggest that gait analysis could be a complementary tool for characterizing ATTR cardiac amyloidosis patients and may inform clinical care as it relates to falls, management of anticoagulation, and functional independence.

Keywords:

• ATTRv amyloidosis
• ATTRwt amyloidosis
• cardiac amyloidosis
• gait analysis
• older adults

Disclosure statement

One of our authors has conflicts that they acknowledge related to this manuscript. They have received funding from the National Institutes of Health (HL139671-01, AG R21AG058348 and AG K24AG036778), and consulting income from Akcea, Alnylam, Eidos Therapeutics, Pfizer and Intellia; his institution has also received funding for clinical trials for Alnylam, Eidos Therapeutics, Pfizer and Prothena.

Additional information

Funding

This work was supported by NIH grants; R21AG058348, R01AG081582 and K24AG036778.