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Mitochondrial Function in Transthyretin Amyloidosis

NCT03328338 · Status: TERMINATED · Type: OBSERVATIONAL · Enrollment: 12

Last updated 2023-08-28

No results posted yet for this study

Summary

Hereditary (familial) amyloidosis arising from the misfolding of a mutated or variant transthyretin, is the most frequent form of amyloid cardiomyopathy in the Caribbean basin. Affected organs invariably harbor extracellular amyloid deposits in the myocardium. Circulating or pre-fibrillar amyloidogenic proteins are implicated in the disruption of cell function. The investigators aim is to demonstrate that transthyretin mediated amyloid disease alter the mitochondrial function of cardiac cells.

Conditions

  • Cardiac Amyloidosis

Sponsors & Collaborators

  • University Hospital Center of Martinique

    lead OTHER

Principal Investigators

  • Jocelyn INAMO, MD-PhD · CHU de Martinique

Eligibility

Min Age
18 Years
Sex
ALL
Healthy Volunteers
No

Timeline & Regulatory

Start
2018-07-17
Primary Completion
2019-09-30
Completion
2019-12-29

Countries

  • Martinique

Study Locations

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Read the full study record

This page highlights key information. For complete eligibility criteria, study locations, investigator contacts, and the full protocol, visit the original record on ClinicalTrials.gov.

View NCT03328338 on ClinicalTrials.gov