麻豆传媒

A weakened diaphragm could be related to the persistent shortness of breath some people experience long after COVID-19 hospitalization, a small study suggested.

Whether patients had received ventilation treatment or not, twitch trans-diaphragmatic pressure following posterior cervical magnetic stimulation was significantly impaired in COVID survivors 15 months after hospitalization compared with healthy controls. Furthermore, this measure of diaphragm weakness correlated with severity of dyspnea on exertion.

It may be clinically relevant that investigators identified a possible underlying mechanism for exertional dyspnea in those with long COVID, according to Jens Spiesshoefer, MD, of University Hospital RWTH Aachen, Germany, and coauthors, reporting in the.

"Firstly, it may be reassuring for patients to have a possible explanation for their persistent symptom (dyspnea) after COVID-19. Secondly, respiratory muscle training has been shown to be effective in other groups of patients with diaphragm muscle weakness, and therefore represents a potential therapeutic intervention in this setting," they wrote.

Prior studies exploring the physiology of long COVID have pointed to radiographic evidence of pulmonary pathology, not changes in cardiac structure and function.

Spiesshoefer's group reported that at 15-month follow-up, 28% of COVID survivors reported experiencing mild to no exertional dyspnea, 48% reported moderate exertional dyspnea, and 32% reported severe exertional dyspnea.

Their hypothesis that diaphragm dysfunction may also be related to exertional dyspnea after COVID-19 illness was not supported in the present report. Diaphragm dysfunction was identified via ultrasound in 80% of the study's participants, and did not differ by dyspnea severity or receipt of mechanical ventilation during the index hospitalization.

The study involved 50 patients who had been hospitalized at University Hospital RWTH Aachen from February 2020 and April 2021 as a result of COVID-19. They had a mean age of 58 years, with 28% being women.

Half of these patients met criteria for severe acute respiratory distress syndrome, requiring invasive mechanical ventilation, whereas the other half were only given supplemental oxygen therapy during their hospitalization.

At 15 months, severe exertional dyspnea was reported in 32% of the ventilated group and 16% of peers without ventilation; moderate exertional dyspnea in 40% and 56%, respectively; and mild to no exertional dyspnea in the remaining 28% of both groups.

For the comparison of diaphragm muscle strength, COVID patients were matched 3:1 with controls recruited before the pandemic.

Spiesshoefer and colleagues warned that the observational design of the study cannot prove whether the changes observed in diaphragmatic muscle strength are specifically attributable to COVID-19 or more general post-infection myopathy following an acute lung injury.

Nevertheless, "regardless of the specificity of COVID-19, the extent of diaphragm muscle weakness and its clear association with otherwise unexplained persistent dyspnea is a significant finding, particularly because the large number of post-COVID patients worldwide are likely to impose a considerable burden on modern healthcare systems," they maintained.

Among the other limitations of the study was that patents experiencing comorbidities that could contribute to exertion dyspnea -- namely underlying pulmonary or cardiac diseases -- were not included. Authors also acknowledged that they could not account for the impact of extracorporeal membrane oxygenation and other treatments during hospitalization.

Other factors, including ICU bedding, phrenic nerve neuropathy, use of antiviral drugs, and more could have also led to diaphragm weakness, and according to the authors, warrant further study.

"Specifically designed studies with control subjects who have survived non-COVID pneumonia are required to gain further insights into the pathophysiology," the investigators urged.

Comment