Affiliations: Cleveland Clinic Foundation
Yale University School of Medicine
New Haven, CT
Maine Medical Center
South Portland, ME
Correspondence to: Alejandro C. Arroliga, MD, FCCP, Director, Fellowship Program, Cleveland Clinic Foundation, 9500 Euclid Avenue, Dept G62, Cleveland, OH 44195-0001; e-mail: firstname.lastname@example.org
To the Editor:
We read with interest the article of Nakchbandi et al (November
1999).1We agree that an association exists between
primary pulmonary hypertension (PPH) and thyroid disease. Our group
recently reported a cohort of 40 patients with PPH, in whom the
prevalence of hypothyroidism was 22.5%.2
The association between hyperthyroidism and pulmonary hypertension has
been described since the early 1980s.3 We recently treated
two patients with moderate and severe pulmonary hypertension documented
by echocardiography and Grave’s disease, in which the pulmonary
hypertension improved after treatment of the hyperthyroid state.
Nakchbandi et al suggested that pulmonary hypertension in a patient
with hyperthyroidism was probably caused by a high cardiac output,
endothelial damage/dysfunction, or increased metabolism of intrinsic
pulmonary vasodilating substances. We offer an alternative explanation
for the presence of pulmonary hypertension in some patients with
The relationship between the hyperthyroid state and the sympathoadrenal
system is a complex one.4Electrical stimulation of the
sympathetic nerves causes pulmonary vasoconstriction, reduction of
pulmonary artery compliance, and increase in pulmonary vascular
resistance.5–7 In some studies, acetylcholine can induce
pulmonary vasodilator response,8 but in the presence of
hyperthyroidism, it is possible that the cholinergic output
is decreased and the vasodilator response is diminished. The final
result is an increase in the pulmonary artery pressure and pulmonary
vascular resistance in some patients with hyperthyroid state. Our
proposed explanation is consistent with the transient nature of
pulmonary hypertension as documented by Nakchbandi et al.1
We appreciate the comments made by Arroliga et al. Our report
describes a patient with thyrotoxicosis and resultant secondary
pulmonary hypertension. As we noted in our article, evaluation of
thyroid function should be considered in patients with unexplained
The possible explanation offered by Arroliga et al about the
pathophysiology of the association is intriguing. The study of
pulmonary vascular changes in patients with thyrotoxicosis has been
confounded by the involvement of the cardiovascular
system.1The fact that β-adrenergic receptor blockade
ameliorates some of the manifestations of thyrotoxicosis suggests that
catecholamines play a key role in their pathogenesis. This is most
likely a result of enhanced catecholamine sensitivity, responsiveness,
or both, because plasma concentrations of catecholamines have been
demonstrated to be normal in these patients.2
We know of no direct evidence of decreased cholinergic output in
hyperthyroidism. In actively hyperthyroid patients with myasthenia
gravis, there is no correlation between the dose of anticholinesterase
medication required and the level of circulating thyroid
hormones.3–5 Further investigation is needed to establish
the precise pathophysiology of the association between pulmonary
hypertension and hyperthyroidism.
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