tetano
Editor, Senior Moderator
ESC Heart Fail
. 2020 Nov 15.
doi: 10.1002/ehf2.13049. Online ahead of print.
Sudden cardiogenic shock mimicking fulminant myocarditis in a surviving teenager affected by severe acute respiratory syndrome coronavirus 2 infection
Giovanni Garau[SUP] 1 [/SUP], Sabrina Joachim[SUP] 2 [/SUP], Guy-Loup Duliere[SUP] 2 [/SUP], Maria Melissopoulou[SUP] 1 [/SUP], Sandrine Boccar[SUP] 2 [/SUP], Vincent Fraipont[SUP] 2 [/SUP], Christophe Dugauquier[SUP] 1 [/SUP], Pierre Troisfontaines[SUP] 1 [/SUP], Olivier Hougrand[SUP] 3 [/SUP], Philippe Delvenne[SUP] 3 [/SUP], Etienne Hoffer[SUP] 1 [/SUP]
Affiliations
Abstract
In the context of the coronavirus disease 2019 pandemic, myocardial injury is a relatively frequent finding. Progression to cardiogenic shock has been rarely described, especially in healthy young patients. The underlying mechanisms are to date controversial. A previously healthy 18-year-old female teenager affected by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) developed fulminant cardiogenic shock requiring a prompt extracorporeal membrane oxygenation support. Cardiac involvement was predominant compared with the pulmonary one. Myocardial biopsies were performed; and in order to clarify the pathophysiology of the acute heart failure, optical and transmission electron microscopy study was realized. Two additional immunohistology techniques were developed in order to (i) detect a SARS-CoV-2 recombinant fusion nucleoprotein by using a specific antibody and (ii) study fractalkine expression induced by activated endothelium because this molecule is well known to be elevated in patients with severe cytokine release syndrome. SARS-CoV-2 genome was not detected in the myocardium. Even if the clinical presentation, laboratory markers, and cardiac imaging techniques strongly suggested fulminant myocarditis, histology and immunohistology were not fully consistent with this diagnosis according to the Dallas criteria. Although rare suspected coronavirus particles were found by transmission electron microscopy in the cardiac endothelium, neither significant immunoreactivity for the viral nucleocapsid protein nor image suggestive of endotheliitis was detected. Intense endothelial immunoreactivity pattern for fractalkine expression was observed. From a clinical point of view, the left ventricular systolic function gradually improved, and the patient survived after a long stay in the intensive care unit. Our observations suggest that a massive cytokine storm induced by SARS-CoV-2 infection was the main cause of the cardiogenic shock, making a direct viral injury pathway very unlikely.
Keywords: Cardiogenic shock; Cytokine storm; Extracorporeal membrane oxygenation; Myocardial injury; SARS-CoV-2; Teenager.
. 2020 Nov 15.
doi: 10.1002/ehf2.13049. Online ahead of print.
Sudden cardiogenic shock mimicking fulminant myocarditis in a surviving teenager affected by severe acute respiratory syndrome coronavirus 2 infection
Giovanni Garau[SUP] 1 [/SUP], Sabrina Joachim[SUP] 2 [/SUP], Guy-Loup Duliere[SUP] 2 [/SUP], Maria Melissopoulou[SUP] 1 [/SUP], Sandrine Boccar[SUP] 2 [/SUP], Vincent Fraipont[SUP] 2 [/SUP], Christophe Dugauquier[SUP] 1 [/SUP], Pierre Troisfontaines[SUP] 1 [/SUP], Olivier Hougrand[SUP] 3 [/SUP], Philippe Delvenne[SUP] 3 [/SUP], Etienne Hoffer[SUP] 1 [/SUP]
Affiliations
- PMID: 33190387
- DOI: 10.1002/ehf2.13049
Abstract
In the context of the coronavirus disease 2019 pandemic, myocardial injury is a relatively frequent finding. Progression to cardiogenic shock has been rarely described, especially in healthy young patients. The underlying mechanisms are to date controversial. A previously healthy 18-year-old female teenager affected by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) developed fulminant cardiogenic shock requiring a prompt extracorporeal membrane oxygenation support. Cardiac involvement was predominant compared with the pulmonary one. Myocardial biopsies were performed; and in order to clarify the pathophysiology of the acute heart failure, optical and transmission electron microscopy study was realized. Two additional immunohistology techniques were developed in order to (i) detect a SARS-CoV-2 recombinant fusion nucleoprotein by using a specific antibody and (ii) study fractalkine expression induced by activated endothelium because this molecule is well known to be elevated in patients with severe cytokine release syndrome. SARS-CoV-2 genome was not detected in the myocardium. Even if the clinical presentation, laboratory markers, and cardiac imaging techniques strongly suggested fulminant myocarditis, histology and immunohistology were not fully consistent with this diagnosis according to the Dallas criteria. Although rare suspected coronavirus particles were found by transmission electron microscopy in the cardiac endothelium, neither significant immunoreactivity for the viral nucleocapsid protein nor image suggestive of endotheliitis was detected. Intense endothelial immunoreactivity pattern for fractalkine expression was observed. From a clinical point of view, the left ventricular systolic function gradually improved, and the patient survived after a long stay in the intensive care unit. Our observations suggest that a massive cytokine storm induced by SARS-CoV-2 infection was the main cause of the cardiogenic shock, making a direct viral injury pathway very unlikely.
Keywords: Cardiogenic shock; Cytokine storm; Extracorporeal membrane oxygenation; Myocardial injury; SARS-CoV-2; Teenager.