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Spontaneous Multiple Arterial Dissection in a COVID-19-Positive Decedent
Christine James1, Diane C Peterson
1From the Johnson County Medical Examiner's Office, Olathe, KS.
Abstract:
Spontaneous multiple arterial dissection (SMAD) is a rarely reported phenomenon and has been previously linked to connective tissue diseases and specifically the genetic mutations in SMAD3 and COL3A1. Herein we describe a case of SMAD with scattered thrombi in a COVID-19-positive patient with a history of unspecified mitochondrial myopathy. Vasculopathy involved the splenic artery, inferior mesenteric artery, internal mammary arteries, omental arteries, mesenteric arteries, and small renal arteries. Dissections were confirmed by histology in the splenic artery, inferior mesenteric artery, and bilateral renal medullary arteries. Genetic studies were done to rule out SMAD3 and COL3A1 mutations. Because the Smad3 protein has been previously implicated in COVID-19-associated tissue fibrosis, it may play a role in endothelial dysfunction as well.
Insights
Spontaneous multiple arterial dissection (SMAD) is rare, often linked to genetic factors. This case highlights SMAD in a COVID-19 patient with mitochondrial myopathy, suggesting potential roles for Smad3 in viral-induced endothelial dysfunction.
Area of Science:
- Vascular Biology
- Infectious Diseases
- Genetics
Background:
- Spontaneous multiple arterial dissection (SMAD) is a rare vascular condition, typically associated with connective tissue disorders and specific gene mutations (SMAD3, COL3A1).
- Understanding the etiology of SMAD is crucial for diagnosis and management, especially in atypical presentations.
Observation:
- A case of SMAD involving multiple arteries (splenic, mesenteric, renal, etc.) is presented in a patient who was positive for COVID-19.
- The patient had a history of unspecified mitochondrial myopathy, adding complexity to the clinical picture.
- Histological confirmation of arterial dissections was obtained for several affected vessels.
Findings:
- Genetic testing ruled out mutations in SMAD3 and COL3A1, suggesting alternative underlying mechanisms for SMAD in this patient.
- The presence of scattered thrombi within the dissected arteries was noted.
- The patient's COVID-19 positivity is a significant factor in this presentation.
Implications:
- The findings suggest a potential link between COVID-19 infection and the development of SMAD, possibly through endothelial dysfunction.
- The role of the Smad3 protein, previously implicated in COVID-19-associated fibrosis, is explored in the context of endothelial dysfunction and vasculopathy.
- This case broadens the spectrum of potential causes for SMAD and underscores the need for considering infectious triggers.
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