Estrogen and adenosine triphosphate-sensitive potassium channels.

Potassium Channels To the Editor: We read with interest the publication by Lee et al1 describing the potential mechanisms and effects of intracoronary conjugated estrogens on coronary vasomotion and myocardial ischemia in patients undergoing percutaneous coronary angioplasty. We were surprised at the very high bolus dose of intracoronary Premarin (Wyeth-Ayerst) given—5 mg into the left coronary system (postmenopausal replacement doses, given orally, range from 0.625 to 1.25 mg daily). The initial exposure dose to the coronary circulation would have been enormous; however, the local concentrations of estrogens are not discussed. It is important and relevant to the interpretation of this study to distinguish between acute, pharmacological effects and long-term replacement effects. How can the authors state that physiological levels of estrogen were achieved? They report that “end-study” coronary sinus 17 -estradiol levels were raised in their subjects (mostly male) receiving Premarin, but the levels exceed that reported in women taking oral replacement.2 The authors state that the levels achieved were similar to those of premenopausal women and were, therefore, physiological. The other point to note is that Premarin is a mixture of several conjugated equine estrogens and is not known to contain 17 estradiol. It is metabolized mainly to estrone, which then is converted to other estrogens, including 17 -estradiol.2 The authors, therefore, were wrong in measuring estradiol without also measuring estrone. Blood sampling for measurement of estradiol levels was performed “at the end of the study,” but no time period after administration of Premarin is given. This is vital information for determining whether conversion of Premarin would have occurred. We, therefore, feel that the clinical relevance of this study must be interpreted with caution.