Pulmonary beta adrenoceptor density in arrhythmogenic right ventricular cardiomyopathy and idiopathic tachycardia

Objective. In recent in vivo studies using positron emission tomography (PE T) our group demonstrated that: the myocardial beta adrenoceptor (PAR) dens ity is reduced in arrhythmogenic right ventricular cardiomyopathy (ARVC) an d idiopathic right ventricular outflow tract tachycardia (RVO-VT) associate d with an increased presynaptic catecholamine washout. It was hypothesised that the reduction of myocardial PAR density is secondary to an increase of local catecholamines in the myocardium resulting from the presynaptic dysf unction since circulating plasma catecholamines were demonstrated to be unc hanged in these conditions. To further prove this hypothesis of an organ-li mited adrenergic nervous dysfunction of the heart, this study aimed to inve stigate PAR density in another thoracic organ, the lung. Methods. Pulmonary and myocardial PAR density was measured in 7 ARVC patients, 8 RVO-VT patie nts and in a group of healthy controls (n = 13) using the non-selective bet a -blocker [C-11]-CGP 12177 and PET. Results. Pulmonary PAR density was sim ilar in controls (12.4 +/- 1.7 pmol/g tissue), ARVC (11.6 +/- 1.7 pmol/g ti ssue, p = ns) and RVO-VT (12.8 +/- 2.0 pmol/g tissue, p = ns), whereas myoc ardial PAR density was significantly reduced in ARVC (6.3 +/- 1.1 pmol/g ti ssue, p = 0.006) and RVO-VT (6.8 +/- 1.2 pmol/g tissue, p=0.02) as compared to controls (8.8+/-1.5 pmol/g tissue). Conclusion. The unchanged pulmonary PAR density in the presence of a previously described significant reductio n in myocardial PAR density in the same patient principally supports our pa thophysiological hypothesis that the myocardial PAR density may be reduced in ARVC and RVO-VT because of an increase in local synaptic catecholamine l evels due to an organ-limited presynaptic adrenergic dysfunction of the hea rt. Since in the present study only pulmonary PAR density was measured, fut ure functional studies excluding pulmonary PAR desensitisation are required to finally prove the unchanged pulmonary sympathetic innervation in ARVC a nd RVO-VT.