whether the junct ional rhy thm preceded or occurred consequent to the initial hypotension. Normal sinus rhythm re turned with a single dose of epinephrine and was associa ted with some hemodynamic improvement. Ischemia and/or infarction could have caused isolated papil lary muscle dysfunction, but papi l la ry muscle dysfunction was not observed on the t ransesophageal echocardiogram. Transesophageal echocardiography effectively ruled out other possible causes of hemodynamic collapse and confirmed the correct diagnosis. The present case demonstra tes tha t mild HCM without significant outflow t ract gradient, systolic anterior motion of the mitral valve, or mitral regurgitat ion may, under certa in circumstances, progress acutely to a more severe form with a high left ventr icular outflow t ract gradient, systolic anter ior motion of the mitral valve, and severe mitral regurgitation, producing cardiogenic shock and pulmonary edema. The correct management of this condition is problematic. Mit ra l valve replacement for chronic mitral regurgi tat ion in HCM has been described, but no previous studies repor t mitral valve replacement for acute mitral regurgi tat ion in HCM. In light of the unfavorable outcome in our patient , we cannot recommend this approach. However, conventional therapy for cardiogenic shock in our pat ient was likewise ineffective. We speculate tha t therapy directed toward the underlying HCM might have been superior. 9 However, it is difficult to recommend negative inotropic agents and fluid resuscitat ion to pat ients with hypotension and pulmonary edema. Increasing use of t ransesophageal echocardiography in the intensive care uni t may reveal tha t this hemodynamic pa t te rn is more common than previously suspected and may permit analysis of the effects of therapy for HCM in such patients. 9. Lorell BH, Paulus WJ, Grossman W, Wynne J, Cohn PF, Braunwald E. Improved diastolic function and systolic performance in hypertrophic cardiomyopathy after nifedipine. N Engl J Med 1980;303:801.