 |
 |

Rapid Down-regulation of Thyroid Hormones in Acute Myocardial Infarction
Is It Cardioprotective in Patients With Angina?
Leif Friberg, MD;
Sigbritt Werner, MD, PhD;
Gösta Eggertsen, MD, PhD;
Staffan Ahnve, MD, PhD, FACP
Arch Intern Med. 2002;162:1388-1394.
Background In severe illness of any cause, down-regulation of the thyroid hormone
system may occur. How this affects patients with acute myocardial infarction
(AMI) is largely unknown.
Objective To investigate changes in serum levels of the thyroid hormones during
AMI and their association with cardiac function and outcome.
Methods Forty-seven consecutive euthyroid patients with AMI were studied prospectively
during the first 5 days and again 6 and 12 weeks later. Time from pain onset
was used in all analyses.
Results The thyroid hormone system was rapidly down-regulated with maximal changes
24 to 36 hours after onset of symptoms. The mean level of the hormone total
triiodothyronine (T3) decreased 19% (P
= .02), the inactive metabolite reverse T3 (rT3) levels
increased 22% (P = .01), and thyrotropin levels declined
51% (P<.001) between the first 6-hour and the
24- to 36-hour period. The prohormone free thyroxine was largely unchanged.
Patients with poor heart function or more intense inflammatory reaction showed
more pronounced down-regulation of the thyroid system. No correlation was
found with cardiac enzymes. Patients with prior angina pectoris had lower
T3 levels in early samples, smaller infarctions, and higher levels
of C-reactive protein and the proinflammatory cytokine interleukin 6 on admittance.
Peak levels of interleukin 6 correlated negatively with T3 (P = .005) and positively with rT3 (P<.05), suggesting that down-regulation before AMI may be cardioprotective.
However, mortality was high among patients with the most pronounced thyroid
level depression, indicating that down-regulation after AMI may be maladaptive.
Conclusions The thyroid hormone system is rapidly down-regulated in AMI. This may
be beneficial during acute ischemia. Patients with angina had higher levels
of interleukin 6 and C-reactive protein and more depressed thyroid hormone
system in early samples. Thyroid level depression in patients with angina
may possibly have been present before the infarction process started. This
novel finding needs further evaluation in large studies to sort out cause-and-effect
relationships.
From the Department of Cardiology (Drs Friberg and Ahnve), Center of
Metabolism and Endocrinology (Dr Werner), and Department of Clinical Chemistry
(Dr Eggertsen), Karolinska Institute at Huddinge University Hospital, and
Division of Preventive Medicine, Karolinska Hospital (Dr Ahnve), Stockholm,
Sweden.
CiteULike Connotea Del.icio.us Digg Reddit Technorati Twitter
What's this?
RELATED ARTICLE
Archives of Internal Medicine Reader's Choice: Continuing Medical Education
Arch Intern Med. 2002;162(12):1424.
FULL TEXT
THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES
Thyroid Function Disturbance and Type 3 Iodothyronine Deiodinase Induction after Myocardial Infarction in Rats A Time Course Study
Olivares et al.
Endocrinology 2007;148:4786-4792.
ABSTRACT
| FULL TEXT
Acute Effects of Triiodothyronine on Endothelial Function in Human Subjects
Napoli et al.
J. Clin. Endocrinol. Metab. 2007;92:250-254.
ABSTRACT
| FULL TEXT
Thyroid Hormone Action in the Heart
Kahaly and Dillmann
Endocr. Rev. 2005;26:704-728.
ABSTRACT
| FULL TEXT
Endocrine Changes in Critical Illness
Nylen and Muller
J Intensive Care Med 2004;19:67-82.
ABSTRACT
|