Objective: The objective of this study was to highlight the impact of increased cardiac output (CO) and/or pulmonary vascular resistance (PVR) on the occurrence and evolution of pulmonary hypertension (PH) in hyperthyroidism and to follow their evolution in patients under therapy.
Methods: Our study group consisted of 142 women with hyperthyroidism of different severities and etiologies. We divided our patients into three groups: groups A (overt hyperthyroidism), B (recurrent disease), and C (subclinical forms). We performed echocardiography to determine echocardiographically estimated systolic pulmonary arterial pressure (eePAP), CO, and PVR before and at 3, 6, and 12 months after treatment with thyroid suppression therapy and beta-blockers.
Results: In our study group we documented PH of various severities in 73 patients (51.4%). Increased CO, induced mostly by hyperthyroidism-specific tachycardia, was frequently detected in overt hyperthyroidism and also augmented PVR, as documented in 43.66% of patients with severe and recurrent forms. For all patients with PH, we emphasized a strong correlation between eePAP and PVR level (r=0.854, p<0.0001) and a moderate one with CO (r=0.437, p<0.0001) and with hyperthyroidism duration (r=0.545, p<0.0001). Under therapy, CO rapidly normalized and PVR significantly decreased in groups A and C. In group B, the reduction was modest and statistically significant.
Conclusion: The pathophysiological mechanisms responsible for the occurrence of PH are elevated CO and PVR. While increased CO is rapidly alleviated under therapy, elevated eePAP and PVR persist in recurrent cases and are responsible for the perpetuation of PH.