Myocardial perfusion and sympathetic innervation in patients with hypertrophic cardiomyopathy.

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.