Thread by @ZdenekVrozina

This study suggests that in some patients, COVID-19 triggers a long-term process of vascular and cardiac injury that can gradually increase pulmonary pressure, strain the right ventricle, and raise the risk of death in the following years🧵

The study followed 480 hospitalized patients (240 moderate, 240 severe) for one year after discharge. It assessed heart function using echocardiography and measured biomarkers of vascular inflammation.

In severe COVID-19, right-ventricular function was already significantly worse at the first study examination. Over the following year, pulmonary artery pressure increased by 17.8% in severe cases and 7.1% in moderate cases!

Two year mortality reached 16.9%. The main risk factors were common cardiometabolic conditions. Hypertension, diabetes, dyslipidemia, and structural signs of cardiac strain.

The most affected structure was not the left, but the right side of the heart. The right ventricle pumps blood into the lungs. When its function worsens, it usually means increased resistance in the pulmonary vessels.

The study found reduced right-ventricular contraction (lower TAPSE) and impaired coupling between the right ventricle and pulmonary circulation. This pattern appears when pulmonary vessels are narrowed, inflamed, or affected by microthrombi.

In other words - this is not only a lung infection. In severe COVID-19, the study points to a vascular disease of the lungs that places a chronic load on the right heart.

This suggests that in some patients, the process was not limited to an acute injury. The vascular changes may continue even after the infection subsides, gradually burdening the right ventricle.

Two biomarkers - endothelin-1 and FeNO - had strong prognostic value. Both are linked to endothelial dysfunction and inflammation.

Elevated endothelin-1 indicates constricted vessels and damaged endothelium. Elevated FeNO points to an active inflammatory process and impaired regulation of vascular tone.

The study suggests that severe COVID-19 may act as a trigger for long-term cardiovascular decompensation. These findings fit into a broader body of research describing post-COVID patterns of endothelial dysfunction, microvascular injury, and rising pulmonary pressures.

The cohort spanned multiple pandemic waves and variants from 2020 to 2023. It describes long-term cardiovascular changes in previously hospitalized patients in general, regardless of the specific variant.

Süleymanoglu at al., Integrated Echocardiographic and Biomarker Assessment Reveal Progressive Cardiovascular Injury After Moderate and Severe COVID-19. onlinelibrary.wiley.com/doi/abs/10.111…

What are @CzechCardiology @szupraha @ZdravkoOnline if long-term risks after COVID-19 were minimized or pushed aside for years? No clear guidance, no follow-up, no fair public communication.