A case of severe onset of Pulmonary Hypertension
resolved after treatment
of COVID-19 Pneumonia
Introduction
COVID-19 is a disease caused by the virus SARS-CoV-2, with a broad clinical presentation. Growing evidence in this rapidly evolving literature suggests significant morbidity and mortality of this disease is caused by a cytokine release syndrome (CRS)1. Amongst other effects, CRS causes a hyperinflammatory, hypercoagulable state, and predisposes patients to thromboembolic events including pulmonary embolism (PE) reported in up to 20-30% of ICU patients 2. PE contributes to increased mortality in hospitals, but there is concern that macro and microvascular thrombosis can contribute to the development of mid- and long-term complications such as pulmonary hypertension (PH), and right ventricular dysfunction3. This article is relevant as it relates the case of a patient treated for COVID 19 in ICU due to rapid development of severe PH and resulting right heart failure likely secondary to COVID-19 infection4 who had complete normalization of her pulmonary artery pressure after treatment of the infection.
Case Presentation
This is a 77-year-old man with a history of hypertension, atrial flutter and, hypothyroidism who presented to our institution due to worsening dyspnea for 3 days. The patient was found to be positive for COVID-19 pneumonia and developed hypoxemic respiratory failure requiring intubation. He then received supportive therapy including antiviral, antimicrobial and anti-inflammatory agents. The patient had a long ICU course during which an echocardiogram was performed and showed findings of an RVSP of 73 mmHg and secondary/functional tricuspid regurgitation suggestive of severe pulmonary hypertension. The patient had been previously worked up in another hospital for a syncopal episode three months before this admission and the report described an RVSP of 45 mmHg at that time, RA and RV dilatation and, low/normal RV systolic function with mild to moderate tricuspid regurgitation.
The patient right heart catheterization was deferred, and he was started on Sildenafil and continuous Nitric Oxide for 48 hours. After a week, the patient showed an overall improvement of his respiratory and hemodynamic status and was transferred out of the ICU. He was retested for SARS-CoV-2 RNA and was negative three weeks after the initial positive result. A repeat echocardiogram was performed to evaluate response to treatment and his RVSP was markedly improved at 28 mmHg. A RHC was scheduled for the next day and it confirmed the improvement of hemodynamics with the following pressures: RV pressures 24/3 mmHg, PA 24/12 mmHg (mean 16 mmHg), PCWP 13mm Hg.
Discussion
COVID-19 can cause extensive microvascular damage to the lungs through immune thrombotic and complement-mediated pathways, which can progress to PE 5,6. There is rising concern that damage to the lungs can cause chronic morbidity, including PH and right ventricular dysfunction.
In this patient, there was no documented history of PH on previous admissions and the development of symptoms was dazzling. He did not have an autoimmune disease or reported use of high-risk medications, suggesting group I PH is unlikely etiology. The patient had a history of HTN, but no other indications that this was group II (left heart disease) or group V (multifactorial) pulmonary hypertension. Given the temporality of symptoms and objective findings with severe COVID-19, there is a strong argument that this is group IV PH (pulmonary artery obstruction). In light of this association, it suggests that PH can be a complication of COVID 19. Unique to this case is the fact that the patient had rapid improvement of PH with the treatment of the virus.
Conclusion
The sequelae of COVID-19 are not fully elucidated. This case suggests that PH is a serious comorbid condition and can be reversed if the disease is treated rapidly. Awareness of PH as a potential complication of covid19 infection and the need to treat these patients aggressively are warranted. Further case reports or case studies need to corroborate this hypothesis.
References
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2.Iba T, Levy JH, Levi M, Connors JM, Thachil J. Coagulopathy of Coronavirus Disease 2019 [published online ahead of print, 2020 May 27]. Crit Care Med. 2020;10.1097/CCM.0000000000004458. doi:10.1097/CCM.0000000000004458
3.Park JF, Banerjee S, Umar S. In the eye of the storm: the right ventricle in COVID-19. Pulm Circ. 2020;10(3):2045894020936660. Published 2020 Jul 2. doi:10.1177/2045894020936660
4. van Dongen CM, Janssen MT, van der Horst RP, et al. Unusually Rapid Development of Pulmonary Hypertension and Right Ventricular Failure after COVID-19 Pneumonia. Eur J Case Rep Intern Med. 2020;7(7):001784. Published 2020 Jun 17. doi:10.12890/2020_001784
5. Magro C, Mulvey JJ, Berlin D, et al. Complement associated microvascular injury and thrombosis in the pathogenesis of severe COVID-19 infection: A report of five cases. Transl Res. 2020;220:1-13. doi:10.1016/j.trsl.2020.04.007
6. Ackermann M, Verleden SE, Kuehnel M, et al. Pulmonary Vascular Endothelialitis, Thrombosis, and Angiogenesis in Covid-19. N Engl J Med. 2020;383(2):120-128. doi:10.1056/NEJMoa2015432
Affiliations:
1-Columbia University Division of Cardiology at Mount Sinai Medical Center
2-Boston University Division of Cardiology
Garly St Croix MD, Michel Ibrahim MD