Fulminant myocarditis associated with pandemic H1N1 influenza A virus

Abstract

Fulminant myocarditis associated with influenza A virus is exceedingly rare, with only a few cases reported in the literature. We describe a previously healthy 10-year-old boy, with a three-day history of flu-like symptoms without antiviral treatment. He was hospitalized with dehydration and hypothermia in the context of persistent vomiting, when he suddenly developed heart failure secondary to fulminant myocarditis. Despite aggressive management, including circulatory support and cardiopulmonary resuscitation measures, the patient died of cardiogenic shock. The postmortem histopathology was compatible with a multisystem viral infection with myocarditis and pulmonary involvement, and H1N1v polymerase chain reaction was positive. The prevalence of influenza-associated fulminant myocarditis remains unknown. Findings reported in the literature raise the possibility that the novel H1N1 influenza A virus is more commonly associated with a severe form of myocarditis than previously encountered influenza strains.

Reporte de casos por infección de virus de Influenza A H1N1: Hallazgos de autopsia

“…Los pacientes desarrollan neumonía, que se caracteriza por la presencia de septos interalveolares ampliados, hemorragias intersticiales, abundante edema intra-alveolar con deposición de membranas hialinas y un infiltrado de células mononucleares 18 , tal y como se encontró en este caso, que al examen microscópico mostro daño alveolar difuso caracterizado por neumonía, hemorragia, edema y presencia de membrana hialina, con abundantes colonias bacterianas. Ha sido ampliamente descrito que los virus de la Influenza A predisponen a las infecciones bacterianas; en un estudio histopatológico de casos de autopsia realizado en la epidemia de 1917, se encontró que el porcentaje de coinfección oscilaba entre el 92% y 96%, constituyéndose además como la principal causa de muerte de los casos estudiados 17 .…”

“…Ha sido ampliamente descrito que los virus de la Influenza A predisponen a las infecciones bacterianas; en un estudio histopatológico de casos de autopsia realizado en la epidemia de 1917, se encontró que el porcentaje de coinfección oscilaba entre el 92% y 96%, constituyéndose además como la principal causa de muerte de los casos estudiados 17 . Otra complicación descrita es la miopericarditis 11 , tal y como lo observamos en este caso; aunque el mecanismo fisiopatológico aún no es claro, se estima que obedece a la citólisis inducida por el virus; estudios de autopsias han reportado que todos los casos con miopericarditis, también presentaron neumonía severa y compromiso multi orgánico, implicando que la miopericarditis podría ser un estadio terminal de la infección por influenza 18 .…”

Risk Factors Associated with Severe Clinical Outcomes of Pandemic H1N1 Infection

“…While the main cause of death was usually acute respiratory distress syndrome (ARDS) in patients with an underlying co-morbidity, there have been several reported cases of critical illness or death in patients, resulting from myocarditis, with no underlying condition [25][26][27][28][29][30][31][32][33].…”

“…With the exception of 0-1 year old group in general the severity of clinical outcome appeared to be directly proportional to age [5,7,9,10,12,13]. Other key risk factors leading to severe clinical outcomes were asthma, COPD and obesity [10][11][12][13][14][15]although there were a number of severe clinical cases with no known underlying condition [7,[25][26][27][28][29][30][31][32][33]. …”

To: Fulminant myocarditis associated with the H1N1 influenza virus: case report and literature review

“…( 5 ) defined lymphocytic infiltration of the myocardium at autopsy as one of the criteria for fulminant myocarditis. Cabral et al ( 6 ) described the case of a 10-year-old boy with fulminant myocarditis associated with influenza A virus infection; the histopathological findings at autopsy were multifocal infiltrates comprising mostly lymphocytes. You suggest that the degeneration of some myocytes described in our report differs from the cardiomyocyte necrosis that has been observed previously; however, we believe that our findings are similar to previous findings and that a translation error may have been to blame for any perceived difference.…”