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CLINICAL STUDIES

Myocardial perfusion and sympathetic innervation in patients with hypertrophic cardiomyopathy

Sheng-Ting Li, MD, PhD^*, Cees J. Tack, MD, Lameh Fananapazir, MD and David S. Goldstein, MD, PhD^*

^* Clinical Neurocardiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892 USA
Department of Internal Medicine, University Hospital, Nijmegen, The Netherlands
Cardiology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892 USA

Manuscript received February 16, 1999; revised manuscript received December 16, 1999, accepted February 9, 2000.

Reprint requests and correspondence: Dr. Sheng-Ting Li, National Institutes of Health, Building 10, Room 6N252, 10 Center Drive, MSC-1620, Bethesda, Maryland 20892-1620
lisht{at}box-1.nih.gov

OBJECTIVES

This study assessed left ventricular myocardial perfusion and sympathetic innervation and function in hypertrophied and nonhypertrophied myocardial regions of patients with hypertrophic cardiomyopathy (HCM).

BACKGROUND

Patients with HCM often have clinical findings consistent with increased cardiac sympathetic outflow. Little is known about the status of sympathetic innervation specifically in hypertrophic regions.

METHODS

We conducted positron emission tomographic (PET) scanning using the perfusion imaging agent ¹³N-ammonia (¹³NH₃) and the sympathoneuronal imaging agent 6-[¹⁸F]-fluorodopamine (¹⁸F-FDA) in 8 patients with HCM and 15 normal volunteers. Positron emission tomographic data corrected for attenuation and the partial volume effect were analyzed using the region-of-interest technique.

RESULTS

Myocardial ¹³NH₃-derived radioactivity was similar in hypertrophied and nonhypertrophied regions of patients with HCM and in normal volunteers. At all time points, the ¹⁸F:¹³N ratio was lower in hypertrophied than in nonhypertrophied regions of HCM patients and in the septum of normal volunteers (p = 0.001). Trends in ¹⁸F-FDA-derived radioactivity over time were normal in both hypertrophied and nonhypertrophied myocardium.

CONCLUSIONS

The results are consistent with decreased neuronal uptake of catecholamines in hypertrophied but not in nonhypertrophied myocardium of patients with HCM. Other aspects of cardiac sympathoneural function seem normal. Decreased neuronal uptake could reflect local relative hypoinnervation, decreased numbers of neuronal uptake sites, or metabolic limitations on cell 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.

Abbreviations and Acronyms   13NH3 = 13N-ammonia   18F-FDA = 6-[18F]-fluorodopamine   HCM = hypertrophic cardiomyopathy   PET = positron emission tomography   ROI = region of interest

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