LETTER
Treatment of Myxedema-Associated Cardiogenic Shock
Irwin Klein
15 July 1993 | Volume 119 Issue 2 | Pages 168-169
TO THE EDITOR:
MacKerrow and colleagues [1] reported on the ability of triiodothyronine to treat cardiogenic shock resulting from severe hypothyroidism (myxedema); however, certain points must be clarified.
First, the authors conclude that their patient had Sheehan syndrome because she was unable to lactate after her last pregnancy. In the absence of significant hemorrhage or obstetrical trauma, an equally likely diagnosis would be lymphocytic hypophysitis [2], which would account for secondary adrenal and thyroid failure.
That the patient failed to improve and, in fact, worsened over the first 5 days while receiving therapy with oral L-thyroxine, 50 µg/d, is not surprising. As they suggest, hypothyroidism may impair the absorption of orally administered thyroid hormone. In addition, the doses of thyroxine were less than those usually required for inducing rapid cellular and clinical responses. This is confirmed by the failure of the serum thyroxine level to increase after 8 days of treatment.
Much of the hemodynamic improvement after triiodothyronine treatment can be explained by decreases in systemic vascular resistance. Recent observations suggest that one of the major sites of action of thyroid hormone is in the peripheral circulation and specifically at the level of regulating tone of vascular smooth muscle cells [3, 4]. If indeed these direct effects are relatively specific for triiodothyronine, then the current case would suggest that intravenous triiodothyronine may be the treatment of choice in severe hypothyroidism associated with impaired cardiac performance. Known or suspected coexistent ischemic heart disease, however, requires that the triiodothyronine dose be at physiologic replacement levels and that the patient be carefully monitored.
That the patient continued to manifest left ventricular dysfunction long after both the adrenal insufficiency and hypothyroidism were treated is consistent with our observation that true heart failure accompanying hypothyroidism should suggest underlying left ventricular dysfunction [5].
1. MacKerrow SD, Osborn LA, Levy H, Eaton RP, Economou P. Myxedema-associated cardiogenic shock treated with intravenous triiodothyronine. Ann Intern Med. 1992; 117:1014-5.
2. Portocarrero CJ, Robinson AG, Taylor AJ, Klein I. Lymphoid hypophysistis: an unusual cause of hyperprolactinemia and enlarged sella turcica. J Am Med Assoc. 1981; 246:1811-3.
3. Klein I. Thyroid hormone and high blood pressure. In: Laragh JH, Brenner BM, Kaplan NM, eds. Endocrine Mechanisms in Hypertension. v. 2. New York: Raven Press; 1989:61-80.
4. Ojamaa K, Balkman C, Klein I. Acute effects of T3 on arterial smooth muscle cells. Ann Thorac Surg. 1993; (In press).
5. Klein I. Thyroid hormone and the cardiovascular system. Am J Med. 1990; 88:642-7.
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