The impact of COVID‐19 pandemic on pulmonary hypertension: What have we learned?

Abstract

The coronavirus 2019 disease (COVID‐19) pandemic threatened the Spanish health‐care system. Patients with demanding conditions such as precapillary pulmonary hypertension (PH) faced a potentially severe infection, while their usual access to medical care was restricted. This prospective, unicentric study assessed the impact of COVID‐19 on PH patients' outcomes and the operational changes in the PH network. Sixty‐three PH patients (41 pulmonary arterial hypertension [PAH]; 22 chronic thromboembolic pulmonary hypertension [CTEPH]) experienced COVID‐19. Overall mortality was 9.5% without differences when stratifying by hemodynamics or PAH‐risk score. Patients who died were older (73.6 ± 5 vs. 52.2 ± 15.4; p = 0.001), with more comorbidities (higher Charlson index: 4.17 ± 2.48 vs. 1.14 ± 1.67; p = 0.0002). Referrals to the PH expert center decreased compared to the previous 3 years (123 vs. 160; p = 0.002). The outpatient activity shifted toward greater use of telemedicine. Balloon pulmonary angioplasty activity could be maintained after the first pandemic wave and lockdown while pulmonary thromboendarterectomy procedures decreased (19 vs. 36; p = 0.017). Pulmonary transplantation activity remained similar. The COVID‐19 mortality in PAH/CTEPH patients was not related to hemodynamic severity or risk stratification, but to comorbidities. The pandemic imposed structural changes but a planned organization and resource reallocation made it possible to maintain PH patients' care.

Lung perfusion assessment in children with long‐COVID: A pilot study

“…All together, these findings need attention and long term follow-up in children with PCC, as early reports from adult practice suggest a potential link between chronic endothelitis and future development of chronic pulmonary hypertension, if these subclinical conditions are not promptly recognized. [30][31][32][33][34] Even though our pilot study reinforces the presence of unknown microvascular problems in some children with PCC, it is important to interpret cautiously our findings for a few reasons. Although the administrated 99mTc-MAA dose activity was as low as reasonably achievable (ALARA), namely tailored to the children according to the late EANM procedure guidelines, 99m Tc-MAA SPECT/CT involves gamma ray exposure; therefore, its use should be limited to those patients at highest risk of having a pathological test.…”

“…Abnormal perfusion findings on 99m Tc‐MAA SPECT/CT related to a chronic endothelial dysfunction at a small vessel level typically assume a patchy, mottled peripheral pattern, which is associated with no densitometric alterations on co‐registered CT, or with no evidence of abnormal findings on simultaneous ventilation SPECT/CT scan (mismatch) 6 . A similar pattern was described in patients with pulmonary arterial hypertension‐associated microangiopathy, 36,37 further reinforcing that, at least theoretically, such chronic subtle events, if not recognized nor treated, may lead to chronic pulmonary hypertension 29–34 . In our cohort, the pathological perfusion pattern presented with a similar non‐homogenous distribution of 99m Tc‐MAA within both lung parenchyma.…”

“…These results seem to be in line with our larger cohort, showing lung perfusion defects in 6/14 (42.8%) children investigated. All together, these findings need attention and long term follow‐up in children with PCC, as early reports from adult practice suggest a potential link between chronic endothelitis and future development of chronic pulmonary hypertension, if these subclinical conditions are not promptly recognized 30–34 …”

Human Endogenous Retrovirus, SARS-CoV-2, and HIV Promote PAH via Inflammation and Growth Stimulation

“…The reduction in ACE-2 in PAH may prevent SARS-CoV-2 viral entry into the lung [ 63 ]. Patients with PAH with severe hemodynamic features have been found to achieve good outcomes without heart failure [ 65 ]. This may be because the decreased ACE 2 expression in patients with PAH may play a protective role in the early stages of infection from viral entry [ 66 ], alternatively, PAH-associated vasodilator therapy limits the impact of virus-induced endothelial dysfunction [ 9 , 67 ].…”

“…Because PAH patients’ lung function has been impaired, their pulmonary blood vessels have become narrowed, and if they are infected with the SARS-CoV-2 virus, it may lead to a more serious condition. It is generally accepted that the COVID-19 prognosis for patients with PAH is determined by a combination of underlying PAH disease characteristics and risk stratification and other factors such as age, functional status, and comorbidities [ 65 , 76 ].…”