Pulmonary and systemic hemodynamics in patients with hyperthyroidism.

Grave's disease Pulmonary hypertension blood pressure amplification central blood pressure hemodynamics in hyperthyroidism hyperthyroidism

Journal

The American journal of medicine
ISSN: 1555-7162
Titre abrégé: Am J Med
Pays: United States
ID NLM: 0267200

Informations de publication

Date de publication:
15 Dec 2023
Historique:
received: 04 11 2023
revised: 28 11 2023
accepted: 29 11 2023
medline: 18 12 2023
pubmed: 18 12 2023
entrez: 17 12 2023
Statut: aheadofprint

Résumé

There is an association between hyperthyroidism and pulmonary hypertension. However, the prevalence of pulmonary hypertension in hyperthyroidism and the underlying mechanisms are incompletely defined. Consecutive patients with severe hyperthyroidism, mostly due to Grave's disease, were included in this single-center study. Echocardiographic assessment of pulmonary hemodynamics was performed at of the time hyperthyroidism diagnosis (baseline) and after normalization of thyroid hormones (follow-up; median 11 months). In a subset of patients, right heart catheterization and non-invasive assessment of central hemodynamics was performed. Among all 99 patients, 31% had PH at baseline. The estimated systolic pulmonary artery pressure correlated significantly with the estimated left ventricular filling pressure (E/e'). The invasively measured systolic pulmonary artery pressure correlated well with the estimated systolic pulmonary artery pressure. Cardiac output, E/e', left and right ventricular dimensions were significantly reduced from baseline to follow-up, whereas the estimated pulmonary vascular resistance did not differ. Diastolic blood pressure was significantly higher at follow up with no change in systolic blood pressure. The central systolic blood pressure, however, exhibited a trend for a reduction at follow up, whilst the pulse wave velocity was significantly lower at follow-up. Approximately one third of patients with hyperthyroidism have evidence of pulmonary hypertension. Our data suggest that an increased cardiac output and left ventricular filling pressure are the main mechanisms underlying the elevated systolic pulmonary artery pressure in hyperthyroidism, whereas there is no evidence of significant pulmonary vascular disease.

Sections du résumé

BACKGROUND AND AIMS OBJECTIVE
There is an association between hyperthyroidism and pulmonary hypertension. However, the prevalence of pulmonary hypertension in hyperthyroidism and the underlying mechanisms are incompletely defined.
METHODS METHODS
Consecutive patients with severe hyperthyroidism, mostly due to Grave's disease, were included in this single-center study. Echocardiographic assessment of pulmonary hemodynamics was performed at of the time hyperthyroidism diagnosis (baseline) and after normalization of thyroid hormones (follow-up; median 11 months). In a subset of patients, right heart catheterization and non-invasive assessment of central hemodynamics was performed.
RESULTS RESULTS
Among all 99 patients, 31% had PH at baseline. The estimated systolic pulmonary artery pressure correlated significantly with the estimated left ventricular filling pressure (E/e'). The invasively measured systolic pulmonary artery pressure correlated well with the estimated systolic pulmonary artery pressure. Cardiac output, E/e', left and right ventricular dimensions were significantly reduced from baseline to follow-up, whereas the estimated pulmonary vascular resistance did not differ. Diastolic blood pressure was significantly higher at follow up with no change in systolic blood pressure. The central systolic blood pressure, however, exhibited a trend for a reduction at follow up, whilst the pulse wave velocity was significantly lower at follow-up.
CONCLUSIONS CONCLUSIONS
Approximately one third of patients with hyperthyroidism have evidence of pulmonary hypertension. Our data suggest that an increased cardiac output and left ventricular filling pressure are the main mechanisms underlying the elevated systolic pulmonary artery pressure in hyperthyroidism, whereas there is no evidence of significant pulmonary vascular disease.

Identifiants

pubmed: 38104644
pii: S0002-9343(23)00760-X
doi: 10.1016/j.amjmed.2023.11.023
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

Copyright © 2023. Published by Elsevier Inc.

Déclaration de conflit d'intérêts

Declaration of Competing Interest None

Auteurs

Roman Brenner (R)

Department of Cardiology, Kantonsspital, St. Gallen, Switzerland. Electronic address: Roman.brenner@kssg.ch.

Tilman Drescher (T)

Department of Endocrinology, Kantonsspital, St.Gallen, Switzerland.

Rebecca Locher (R)

Department of Endocrinology, Kantonsspital Graubünden, Chur, Switzerland.

Stefan Bilz (S)

Department of Endocrinology, Kantonsspital, St.Gallen, Switzerland.

Hans Rickli (H)

Department of Cardiology, Kantonsspital, St. Gallen, Switzerland.

Michael Brändle (M)

Department of Endocrinology, Kantonsspital, St.Gallen, Switzerland.

Daniel Nobel (D)

Department of internal medicine, Spital Wil, Switzerland.

Daniel Weilenmann (D)

Department of Cardiology, Kantonsspital, St. Gallen, Switzerland.

Peter Ammann (P)

Department of Cardiology, Kantonsspital, St. Gallen, Switzerland.

Micha T Maeder (MT)

Department of Cardiology, Kantonsspital, St. Gallen, Switzerland; University of Basel.

Classifications MeSH