# Transthyretin Amyloidosis—One of the Causes of Heart Failure in Patients with Severe Clinical Course of COVID-19

**Authors:** Zarina Gioeva, Liudmila Mikhaleva, Nikita Gutyrchik, Nikolay Shakhpazyan, Valentina Pechnikova, Konstantin Midiber, Andrej Kontorshchikov, Elizaveta Zentsova, Lev Kakturskij

PMC · DOI: 10.3390/ijms26199806 · International Journal of Molecular Sciences · 2025-10-09

## TL;DR

This study shows that pre-existing heart amyloidosis can worsen the severity of COVID-19, leading to rapid heart failure and poor outcomes.

## Contribution

The study identifies wild-type transthyretin amyloidosis as a previously underdiagnosed contributor to severe COVID-19 outcomes.

## Key findings

- ATTR amyloidosis was confirmed in all 19 patients with severe COVID-19.
- SARS-CoV-2 RNA was detected in 53% of myocardium and lung autopsy specimens.
- Heart damage, including cardiosclerosis and myocarditis, was common in these patients.

## Abstract

Wild-type transthyretin amyloidosis is an underdiagnosed condition that significantly contributes to mortality in the elderly population. This histopathological study describes autopsy findings in patients with severe clinical course of COVID-19 and ATTR not identified during life. Autopsy findings in the myocardium were analyzed in 19 patients with pre-existing ATTR who died from severe COVID-19. RT PCR was used for pre- and post-mortem detection of SARS-CoV-2 RNA. Immunohistochemical typing was performed with a broad panel of antibodies against different amyloid types. Autopsy specimens from the myocardium and lungs were positive for SARS-CoV-2 RNA in 10 (53%) cases. Microscopic examination of the myocardium revealed focal cardiosclerosis and cardiomyocyte dissociation in 15 (68%) cases, hypertrophy and atrophy of cardiomyocytes in 17 (77%) and 7 (32%), respectively, and myocarditis in 4 (18%) cases. Immunohistochemical analysis determined ATTR amyloidosis in all cases. In patients with rapidly progressive heart failure, the postmortem examination revealed multiple sites of interstitial amyloid deposits and focal cardiosclerosis in the myocardium. Pre-existing cardiac amyloidosis contributes to the aggressive clinical course of COVID-19. Coupled with the toxic effect of the SARS-CoV-2 virus on the myocardium, the disease may lead to progressive heart failure and poor outcomes.

## Linked entities

- **Diseases:** amyloidosis (MONDO:0019065), heart failure (MONDO:0005252), COVID-19 (MONDO:0100096)

## Full-text entities

- **Diseases:** died (MESH:D003643), hypertrophy (MESH:D006984), amyloid (MESH:C000718787), Transthyretin Amyloidosis (MESH:C567782), myocarditis (MESH:D009205), atrophy (MESH:D001284), cardiac amyloidosis (MESH:D000686), Heart Failure (MESH:D006333), COVID-19 (MESH:D000086382)
- **Species:** Severe acute respiratory syndrome coronavirus 2 (no rank) [taxon 2697049], Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

6 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12524381/full.md

## References

34 references — full list in the complete paper: https://tomesphere.com/paper/PMC12524381/full.md

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Source: https://tomesphere.com/paper/PMC12524381