Myocardial perfusion and sympathetic innervation in patients with hypertrophic cardiomyopathy

OBJECTIVE This study assessed left ventricular myocardial perfusion and sym pathetic innervation and function in hypertrophied and nonhypertrophied myo cardial regions of patients with hypertrophic cardiomyopathy (HCM). BACKGROUND Patients with HCM often have clinical findings consistent with i ncreased cardiac sympathetic outflow. Little is known about the status of s ympathetic innervation specifically in hypertrophic regions. METHODS We conducted positron emission tomographic (PET) scanning using the perfusion imaging N-13-ammonia ((NH3)-N-13) and the sympathoneuronal imagi ng agent 6-[F-18]agent fluorodopamine (F-18-FDA) in 8 patients with HCM and 15 normal volunteers. Positron emission tomographic data corrected for att enuation and the partial volume effect were analyzed using the region-of-in terest technique. RESULTS Myocardial (NH3)-N-13-derived radioactivity was similar in hypertro phied and nonhypertrophied regions of patients with HCM and in normal volun teers. At all time points, the F-18:N-13 ratio was lower in hypertrophied t han in nonhypertrophied regions of HCM patients and in the F-18-FDA-derived radioactivity over time septum of normal volunteers (p = 0.001). Trends in were normal in both hypertrophied and nonhypertrophied myocardium. CONCLUSIONS The results are consistent with decreased neuronal uptake of ca techolamines in hypertrophied but not in nonhypertrophied myocardium of pat ients with HCM. Other aspects of cardiac sympathoneural function seem norma l. Decreased neuronal uptake could reflect local relative hypoinnervation, decreased numbers of neuronal uptake sites, or metabolic limitations on cel l membrane transport. By enhancing norepinephrine delivery to adrenoceptors for a given amount of sympathetic nerve traffic, decreased neuronal uptake can explain major clinical features of HCM. (J Am Coll Cardiol 2000;35:186 7-73) (C) 2000 by the American College of Cardiology.