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Published on: April 17, 2021
Enterovirus Causing Progression of Heart Failure in a Patient with a History of Myocardial Infarction
Agnieszka Pawlak1, Maciej Przybylski, Malgorzata Frontczak-Baniewicz
1Department of Invasive Cardiology, Central Clinical Hospital of the Ministry of Interior, Warsaw, Poland.
Insights
Human enteroviruses (HEV) can cause heart failure (HF) after myocardial infarction (MI). This study suggests HEV may worsen HF progression, and treatment with interferon- improved a patient's condition.
Area of Science:
- Cardiology
- Virology
- Molecular Biology
Background:
- Human enteroviruses (HEV) are linked to myocarditis and dilated cardiomyopathy (DCM).
- HEV presence in myocardium is documented in various heart conditions.
- The role of HEV in heart failure (HF) post-myocardial infarction (MI) is largely unexplored.
Observation:
- A case study of a 54-year-old female patient with a history of MI and progressive HF.
- Investigations were conducted to identify potential causes for HF progression.
Findings:
- The study identified HEV as a potential etiological factor contributing to HF progression in the patient.
- The presence of the HEV genome in the myocardium was investigated in the context of HF post-MI.
Implications:
- This suggests HEV could be a significant factor in HF development and progression after MI.
- Interferon- treatment showed clinical improvement, supporting the hypothesis of HEV involvement.
- Further research into HEV's role in post-MI cardiac dysfunction is warranted.
Abstract:
Human enteroviruses (HEV) are an important cause of myocarditis and are associated with the pathogenesis of dilated cardiomyopathy (DCM). Current polymerase chain reaction studies in human myocardium have provided evidence that HEV are present in acute and chronic myocarditis as well as in DCM. To our knowledge, the presence of the HEV genome in the myocardium of human patients with heart failure (HF) after myocardial infarction (MI) has not been reported, nor have HEV been implicated as a factor affecting HF progression in patients after MI. Information about the presence of HEV in the heart tissue seems to be clinically important, since HEV infection is a frequent cause of HF and increased mortality. We present the case of a 54-year-old woman with a history of MI and HF progression. Our investigations suggested HEV as a possible cause of HF progression. Successful treatment with interferon- improved the patient's clinical status, apparently confirming our hypothesis.
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