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Myocardial perfusion and sympathetic innervation in patients with hypertrophic cardiomyopathy
S T Li1, C J Tack, L Fananapazir
1Clinical Neurocardiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892, USA. lisht@box-1.nih.gov
Insights
Hypertrophic cardiomyopathy (HCM) patients show reduced catecholamine uptake in hypertrophied heart regions, suggesting local hypoinnervation. This may explain key clinical features of HCM by altering norepinephrine delivery to adrenoceptors.
Area of Science:
- Cardiology
- Nuclear Medicine
- Medical Imaging
Background:
- Patients with hypertrophic cardiomyopathy (HCM) often exhibit signs of increased cardiac sympathetic activity.
- The specific status of sympathetic innervation within hypertrophied myocardial regions in HCM is not well understood.
Purpose of the Study:
- To assess left ventricular myocardial perfusion and sympathetic innervation in hypertrophied and nonhypertrophied regions of HCM patients.
- To compare these parameters with those in normal volunteers.
Main Methods:
- Positron emission tomographic (PET) scanning was performed on 8 HCM patients and 15 normal volunteers.
- The perfusion agent 13N-ammonia (13NH3) and the sympathoneuronal agent 6-[18F]-fluorodopamine (18F-FDA) were utilized.
- PET data were analyzed using region-of-interest techniques after corrections for attenuation and partial volume effects.
Main Results:
- Myocardial perfusion (13NH3) was comparable across hypertrophied, nonhypertrophied regions in HCM patients, and normal volunteers.
- The ratio of sympathoneuronal to perfusion tracer uptake (18F:13N) was significantly lower in hypertrophied HCM regions compared to nonhypertrophied regions and normal volunteer septa (p=0.001).
- Trends in sympathoneuronal tracer (18F-FDA) uptake over time were normal in all myocardial regions studied.
Conclusions:
- Results suggest decreased neuronal catecholamine uptake in hypertrophied myocardium of HCM patients, potentially indicating local hypoinnervation or transport limitations.
- Other aspects of cardiac sympathoneural function appear normal in HCM patients.
- Reduced neuronal uptake may explain clinical manifestations of HCM by influencing norepinephrine delivery to adrenoceptors.
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.