Drs. Mantzoros and Ravi suggest the possibility of a beneficial response to thyroxine rather than to intravenous triiodothyronine. The following observations argue against any significant therapeutic contribution from the thyroxine: After 7 days of thyroxine therapy, the patient had hemodynamic measurements indicating cardiogenic shock; on day 8, both serum thyroxine and triiodothyronine levels were still abnormally low; and ". since T3 (triiodothyronine) has approximately three times the metabolic potency of T4 (thyroxine), virtually all of the metabolic action of T4 can be ascribed to the action of the T3 that it gives rise to" [1]. We believe thyroxine could not give rise to triiodothyronine in our patient because of impaired conversion. These points, along with dramatic improvement 16 hours after administering intravenous triiodothyronine, with a then normal serum triiodothyronine level, support the belief that parenteral triiodothyronine was the definitive hormone therapy.

We agree with Drs. Mantzoros and Ravi that cautious thyroid hormone replacement therapy should be used if coronary ischemic heart disease is suspected. In our case report, we emphasize that heart failure caused by hypothyroidism is rare, but when it exists and is severe, intravenous triiodothyronine therapy is recommended. We are not proposing this treatment for patients with heart failure due to other causes who are concurrently hypothyroid.

We agree with Dr. Klein that the differential diagnosis of hypopituitarism should include lymphocytic hypophysitis. This disorder frequently is associated with elevated prolactin levels [2]. In the case we reported, the patient was unable to lactate after her last pregnancy, and she had an undetectable prolactin level. To completely resolve this question would require microscopic examination of the patient's pituitary gland.

Dr. Klein's comments about the potential role of triiodothyronine in lowering systemic vascular resistance are most intriguing [3]. Other variables contributing to the falling systemic vascular resistance included decreased catecholamine levels after intubation with improved oxygenation and decreased work of breathing; and a reflex decrease in systemic vascular resistance after triiodothyronine-mediated improvement in myocardial contractility leading to improved cardiac output.

We agree with Dr. Klein about underlying left ventricular dysfunction in patients with heart failure and hypothyroidism. Given the return to normal of left ventricular systolic function with thyroid hormone replacement therapy and the absence of another etiologic factor, the cause could have been entirely hypothyroidism. The lag between establishment of normal serum thyroid hormone levels and recovery of normal left ventricular systolic performance suggests that significant time is required to re-establish normal myosin isoenzymes along with intracellular calcium kinetics [4, 5].