2
3
4
5
6
7
lial function: report of six subjects with normal coronary
arteriograms. Chest 2000; 118:756 –760
Seiler C, Suter TM, Hess OM. Exercise-induced vasomotion
of angiographically normal and stenotic coronary arteries
improves after cholesterol-lowering drug therapy with benzafibrate. J Am Coll Cardiol 1995; 26:1615–1622
Evans M, Anderson RA, Graham J, et al. Ciprofibrate therapy
improves endothelial function and reduces postprandial lipemia and oxidative stress in type 2 diabetes mellitus. Circulation 2000; 101:1773–1779
Ridker PM, Rifai N, Miles JS, et al. Lovastatin 20 – 40 mg/day
lowers high sensitivity C-reactive protein levels in AFCAPS/
TexCAPS [abstract]. Circulation 2000; 102:II833
Shepherd J, Cobbe SM, Ford I, et al. Prevention of coronary
heart disease with pravastatin in men with hypercholesterolemia: West of Scotland Coronary Prevention Study Group.
N Engl J Med 1995; 333:1301–1307
Sacks FM, Pfeffer MA, Moye LA, et al. The effect of
pravastatin on coronary events after myocardial infarction in
patients with average cholesterol levels. N Engl J Med 1996;
335:1001–1009
Rosenson RS, Tangney CC. Antiatherothrombotic properties
of statins: implications for cardiovascular event reduction.
JAMA 1998; 279:1643–1650
Pulmonary Arterial Hypertension and
Thyroid Disease
To the Editor:
We have been following with interest the articles by Curnock et al1 and Nakchbandi et al2 commenting on the associa-
tion of thyroid disease and primary pulmonary hypertension
(PPH). We would like to draw attention to our recent
observations of thyroid disease and pulmonary artery hypertension (PAH).3
Although an increased prevalence of thyroid disease has
been reported in patients with PAH, whether long-term
treatment with prostacyclin (PGI2) plays a role is unclear. We
performed a retrospective analysis of thyroid function studies
in 134 adults (112 with PPH and 22 with connective tissue
disease [CTD]) with PPH or PAH associated with CTD, and in
78 children with PPH (Fig. 1). The objective of our study was
to determine if long-term therapy with PGI2 “induces” or
“unmasks” thyroid disease in patients with PAH. Twenty of the
26 adult patients (16 with PPH and 10 with CTD) with thyroid
disease were treated with long-term PGI2 therapy, and 11
patients (all with PPH) of these 20 developed thyroid disease
after starting PGI2 therapy. Five of these 11 patients had
thyrotoxicosis at the time of evaluation. The remaining nine
patients with thyroid disease prior to starting long-term PGI2
therapy were all hypothyroid, as were the six patients who
were never treated with PGI2. Eight of the 78 PPH children
had thyroid disease, and 6 of the 8 children developed the
disease after starting PGI2.
Although our data on prevalence of patients with hypothyroidism and PPH (9% in adults and 6.5% in children) are
similar to finding of previously published reports, prior reports
of hyperthyroidism with PPH have only included single case
reports4 and one case series of four patients with PAH in
whom the PAH resolved in all four patients when their
hyperthyroidism was treated.5 The increased occurrence in
our study of hyperthyroid disease in PPH patients receiving
long-term PGI2 therapy raises the possibility that PGI2 treat-
Figure 1. Results of thyroid function studies. M ⫽ male; F ⫽ female; CREST ⫽ calcinosis, Reynaud’s
syndrome, esophageal motility disorders, sclerodactyly, and telangiectasia; Labs ⫽ laboratory findings;
SLE ⫽ systemic lupus erythematosus; TSH ⫽ thyroid stimulating hormone; T4⫽thyroxine.
1980
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Communications to the Editor
ment may be a trigger to the development of thyroid disease;
further investigation is warranted.
Anne Ferris, MD
Thomas Jacobs, MD
Allison Widlitz, MS, PA
Robyn J. Barst, MD
Jane H. Morse, MD
Columbia University
New York, NY
Correspondence to: Robyn J. Barst, MD, Columbia University,
College of Physicians and Surgeons, 3959 Broadway BH-262N,
New York, NY 10032
References
1 Curnock AL, Dweik RA, Higgins BH, et al. High prevalence
of hypothyroidism in patients with primary pulmonary hypertension. Am J Med Sci 1999; 318:289 –292
2 Nakchbandi IA, Wirth JA, Inzucchi SE. Pulmonary hypertension caused by Grave’s thyrotoxicosis: normal pulmonary
hemodynamics restored by 131I treatment. Chest 1999; 116:
1483–1485
3 Ferris AM, Morse JH, Barst RJ, et al. Thyroid disease and
pulmonary arterial hypertension (PAH) in patients treated
with prostacyclin [abstract]. Circulation 2000; 102:18(suppl
II):426
4 Okura H, Takatsu Y. High-output heart failure as a cause of
pulmonary hypertension. Intern Med 1994; 33:363–365
5 Thurnheer R, Jenni R, Russi EW, et al. Hyperthyroidism and
pulmonary hypertension. J Intern Med 1997; 242:185–188
One of the surgeons at the meeting, who stressed the forceful
expansile properties of the emphysematous lung pushing down
the diaphragm, claimed support for his theory by observing the
bulging of the emphysematous lung through a thoracotomy
incision at the time of lung volume reduction surgery. When this
point of view was presented to Dr. Jerry Mead during his
“Distinguished Lecture in Physiology—Thoracic Kinetics,” he
thought this was due to the pressure involved in the administration of the anesthesia.
A more sophisticated discussion of this can be found in
Chapter 13, “Statics of the Respiratory System” by Emil Agostini
and Jere Mead in Handbook of Physiology, Section 3, Respiration, Vol. I, pages 387– 407 (see pages 390 –391), published by the
American Physiologic Society, Washington, DC, 1964.
Herman F. Froeb, MD, FCCP
La Jolla, CA
Correspondence to: Herman F. Froeb, MD, FCCP, Scripps Memorial Hospital Campus, 9834 Genesee Ave, Suite 416, La Jolla, CA
92037
A Survey of the Use of Herbal Agents
Among Philadelphia Veterans Affairs
Medical Center Pulmonary
Outpatients
To the Editor:
Elastic Recoil of Lung and Lung
Reduction Surgery
To the Editor:
At a recent meeting of the American College of Chest Physicians in San Francisco in October, there were several sessions
concerning lung volume reduction surgery. In two of these
sessions that I attended, the concept of emphysematous lung
“bulging out the chest wall and pushing down the diaphragms
and even compressing the heart” was discussed by surgeons and
pulmonologists present. The beneficial effect of the surgery was
thought to be due to “removal of the bulging emphysematous
lung to allow good lung to expand and to allow the chest to
assume a less distended position and the diaphragms to ascend
once the downward pressure by the bulging lung was relieved.”
Indeed, this does happen, but for an entirely different reason.
It has to do with retractile elastic recoil of the lung being
opposed by the expansive force of the chest wall. When these two
opposing forces equal one another and cancel out, the diaphragms come to rest.
In emphysema, the loss of elastic recoil of the lung allows the
chest wall to expand and hence the diaphragm becomes low. Now
when the surgeon removes the areas of emphysematous lung, the
elastic recoil increases, the chest wall is drawn in, and the
diaphragm rises. This increase in elastic recoil of the lung also
keeps the airways open longer during expiration, and they
become larger on inspiration, improving ventilation/perfusion
ratios and reducing the airway’s resistance and work of breathing.
Another analogy is that of a rubber band with several flabby
sections in it. If these sections are removed, the rubber band has
better elastic recoil.
To appreciate the expansive qualities of the chest wall, consider
the following: if a pneumothorax is present (nontension, noncommunicating) and the chest wall is opened, air rushes in as the
chest wall expands.
Herbal products are used by as many as 20 to 60% of patients
in a variety of practice settings, both in the United States and
abroad.1,2 While the efficacy of many of these agents has not been
demonstrated in scientifically rigorous trials, serious toxicity has
occasionally been described.3,4 However, many health-care providers do not specifically ask patients about use of these agents,
and therefore may not be cognizant of possible toxicities and drug
interactions between herbal products and “conventional” agents
being administered at the same time. In pulmonary medicine, for
example, particular concern has recently focused on an ephedracontaining dietary supplement that may have triggered cardiac
arrest in an asthmatic patient receiving albuterol and theophylline.4
To some extent, the use of herbal products may be fueled by
medically sophisticated or affluent patients, perhaps in concert
with Internet access.1 Meanwhile, the frequency and importance
of the use of herbal remedies in less affluent, urban populations,
and in federal medical facilities is poorly characterized. Therefore, a prospective survey was conducted of patients in a pulmonary outpatient clinic at the Philadelphia Veterans Affairs Medical Center (VAMC). The purpose was to describe the frequency
of herbal drug use and to assess the possibility of potentially
dangerous herbal agent-pulmonary drug interactions or pulmonary toxicity from herbal agents in this setting.
One hundred twenty consecutive veterans attending an outpatient pulmonary clinic staffed by a single practitioner at the
Philadelphia VAMC between June 1, 2000, and October 15,
2000, were queried regarding use of herbal products. The clinic
serves the Philadelphia VAMC, a teaching affiliate of the University of Pennsylvania located in West Philadelphia. The vast
majority of its patients are residents of Philadelphia, although 1 to
5% are referrals from VAMCs in Coatesville, PA, and Wilmington, DE.
The cohort was composed of 117 men and 3 women, 66 African
Americans, and 54 whites. The mean age was 63.7 years (SD, 14
years). The highest level of education achieved was ninth grade or
CHEST / 119 / 6 / JUNE, 2001
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1981