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. 2020 Jul 2;13(8):1857–1858. doi: 10.1016/j.jcmg.2020.06.015

The Authors Reply:

Karan Sud, Jagat Narula, Edgar Argulian
PMCID: PMC7330584  PMID: 32762890

We thank Drs. Tsolaki and Zakynthinos for their interest in our study (1) and their insights into possible underlying mechanisms of right ventricular (RV) dilation in patients with coronavirus disease-2019 (COVID-19) infection. The authors summarize the underlying pathophysiology of the interplay of mechanical ventilation, pulmonary vascular resistance, and consecutive changes in hemodynamics as one of the many possible mechanisms of RV dilation in these patients. They also postulate that mechanical ventilation by itself, especially with high levels of positive end-expiratory pressure (PEEP), may be a major contributor to the observed findings. In our study, 31 patients (30% of the study population) were mechanically ventilated at the time of echocardiography. Among these patients, 14 patients had RV dilation (44% of all patients with RV dilation). Interestingly, the median PEEP was 10 cm H2O (interquartile range: 8 to 14 cm H2O) among patients with RV dilation compared with 12 cm H2O (interquartile range: 6 to 14 cm H2O) among patients without RV dilation, with no significant difference (p = 0.98) and no meaningful correlation between PEEP and RV dimensions. Of note, 24% of the remaining nonventilated patients had RV dilation. We acknowledge that these findings are derived from a small sample size and are observational in nature with inherent limitations.

Although mechanical ventilation and ventilation settings are possibly contributory, RV dilation is likely a multifactorial phenomenon. Other echocardiographic studies reported high rates of RV dilation and dysfunction in patients with COVID-19 infection. One study reported RV dilation in 41% of 74 patients, of whom 78% were mechanically ventilated at the time of echocardiography (2). Another study described RV dilation and dysfunction in 39% of 100 patients, of whom only 10% were mechanically ventilated at the time of echocardiography (3). Importantly, on follow-up echocardiogram, RV enlargement and dysfunction were common in deteriorating patients in that study.

The underlying mechanisms of RV dilation in patients with COVID-19 infection extend beyond mechanical ventilation and possibly include pulmonary thromboembolism, microthrombi in pulmonary vasculature, persistent hypoxic pulmonary vasoconstriction, and direct viral damage. Dedicated studies to understand these underlying mechanisms will provide more insights into the complex pathophysiology of this disease.

Footnotes

Please note: The authors have reported that they have no relationships relevant to the contents of this paper to disclose.

The authors attest they are in compliance with human studies committees and animal welfare regulations of the authors’ institutions and Food and Drug Administration guidelines, including patient consent where appropriate. For more information, visit the JACC: Cardiovascular Imagingauthor instructions page.

References

  • 1.Argulian E., Sud K., Vogel B. Right ventricular dilation in hospitalized patients with COVID-19 infection. J Am Coll Cardiol Img. 2020 May 15 doi: 10.1016/j.jcmg.2020.05.010. [E-pub ahead of print] [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 2.Mahmoud-Elsayed H.M., Moody W.E., Bradlow W.M., Khan-Kheil A.M., Hudsmith L.E., Steeds R.P. Echocardiographic findings in Covid-19 pneumonia. Can J Cardiol. 2020 May 28 doi: 10.1016/j.cjca.2020.05.030. [E-pub ahead of print] [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 3.Szekely Y., Lichter Y., Taieb P. The spectrum of cardiac manifestations in coronavirus disease 2019 (COVID-19)—a systematic echocardiographic study. Circulation. 2020 May 29 doi: 10.1161/CIRCULATIONAHA.120.047971. [E-pub ahead of print] [DOI] [PMC free article] [PubMed] [Google Scholar]

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