Pathophysiology and prevalence of high output heart failure in group 1 pulmonary hypertension - PubMed
3 days ago
- #pulmonary hypertension
- #high output heart failure
- #vasodilators
- Pulmonary vasodilators increase cardiac output (CO) in group 1 pulmonary hypertension (PH), sometimes leading to high CO with unclear implications.
- In a study of 449 group 1 PH participants, 9% had high output (CO>8 L·min⁻¹ or CI>4 L·min⁻¹·m⁻²), associated with intensive vasodilator use and lower pulmonary vascular resistance (PVR).
- High output was linked to the lowest systemic vascular resistance, greater left ventricular (LV) and left atrial (LA) enlargement, and increased LV and right ventricular (RV) workload at rest and during exercise.
- Despite higher oxygen delivery during exercise, peripheral oxygen utilization was impaired, with no functional or survival benefit compared to normal output PH.
- High output PH had a higher adjusted risk of death or transplant (HR 2.1) compared to normal output PH.
- In a validation cohort, 93% had normal CO at diagnosis, with high output developing after vasodilator initiation.
- Conclusions suggest that 1 in 10 group 1 PH patients develop high output, linked to vasodilator intensity, adverse cardiac remodeling, and increased myocardial workload.
- Further studies are needed to optimize vasodilator dosing and explore therapeutic interactions with vasodilator-sparing therapies like sotatercept.