COVID-19 and rhinovirus infections showed high rates of echo-defined pulmonary hypertension (53% and 78%), similar to non-viral controls (68%), with no significant differences in RV parameters.
Cohort (n=86)
No
Does viral infection (COVID-19 or rhinovirus) worsen echocardiographic markers of pulmonary hypertension compared to no viral infection?
Viral infections like COVID-19 and rhinovirus did not significantly alter echocardiographic markers of pulmonary hypertension severity compared to non-viral patients in a referred PH cohort.
Absolute Event Rate: 53% vs 68%
Abstract Rationale Viral infection can impact the severity of pulmonary hypertension (PH) both acutely and chronically. Some viruses, like rhinovirus, may cause transient increases in pulmonary pressure that resolve, while others (like COVID-19) might have long-term effects. Identifying which patients develop PH during illness, retain PH post-recovery, or experience clinical worsening is critical. Echocardiography is essential for early detection of PH, with tricuspid regurgitant velocity (TRV, 2.8 m/s) serving as a key marker of severity. We hypothesize that viruses may influence PH risk and progression through distinct mechanisms. Methods Patients referred to The Ohio State University PH program with an echocardiographic exam were retrospectively identified (N = 1560). Patients with prior viral panels were identified (N = 559). Chart review was conducted on the subset of patients with positive viral panels to identify patients with COVID-19 or rhinovirus infections. Patients with a negative viral panel (non-viral) or rhinovirus infection were selected as control and viral-infection comparator groups, respectively. Echocardiography data was collected within 90 days post viral panel. Markers of PH were collected including tricuspid annual plane systolic excursion (TAPSE 1.7 cm), TAPSE/SPAP (systolic pulmonary artery pressure) ratio (0.5 mm/mmHg), RVSP (35 mmHg), and TRV (2.8 m/s). Statistical analysis was conducted using Excel and R. Results In the identified patients, 32 patients had COVID-19 infections, 23 had rhinovirus infections, and 31 had negative viral panels. Overall, the cohort was primarily female (64% female) with no significant difference in sex between groups. The median time from viral test to echocardiography was 2 0, 4.5 days and 3 1, 34 days in the non-viral and rhinovirus groups, respectively, but increased to 11 3, 36 days in the COVID-19 group (P 0.05). Based on a TRV 2.8 m/s, the majority of patients met the criteria for echo-derived PH (COVID-19: 17 (53%), Rhinovirus: 18 (78%), non-viral: 21 (68%). However, there were no significant differences in TAPSE, TAPSE/SPAP or RVSP between groups (P 0.05). Patients in the rhinovirus or non-viral groups were referred to the PH clinic 2 -76, 9 or 208 -546, -5 days prior to viral testing compared to the COVID-19 group that was referred 22 -55.5, 347 days after viral testing (P = 0.005). Conclusion Preliminary analysis shows that the incidence of echo-defined PH was high in patients with a positive viral panel regardless of the referral to the PH clinic. Further study is planned to evaluate the longitudinal changes in pre- and post-viral impacts on PH severity. This abstract is funded by: None
Saldivar et al. (2026) conducted a cohort in Pulmonary hypertension (n=86). COVID-19 or Rhinovirus infection vs. Negative viral panel was evaluated on Echo-derived pulmonary hypertension (TRV >2.8 m/s). COVID-19 and rhinovirus infections showed high rates of echo-defined pulmonary hypertension (53% and 78%), similar to non-viral controls (68%), with no significant differences in RV parameters.