[en] Myocardial scintigraphy was performed on 24 patients with hypertrophic cardiomyopathy (HCM), 5 with essential hypertension (EHT) and 7 normal controls at rest by means of simultaneous dual energy data acquisition following an intravenous injection of ¹²³I-metaiodobenzylguanidine (MIGB) and ²⁰¹Tl-chloride (Tl). The myocardial uptake rates of both tracers were measured in the planar images by taking into account the myocardial and pulmonary attenuation. The regional myocardial distributions of the tracers were also studied in the SPECT images. In planar images, the rate of loss of ¹²³I-MIBG from the myocardium of HCM subjects was significantly higher than of control subjects 15 min to 3 hr after injection. No significant difference was observed from 3 hr to 5 hr and from the 5 hr to 21 hr periods. In the SPECT images, the rate of loss of ¹²³I-MIBG from the myocardium of HCM subjects was significantly higher than of control subjects in all segments of myocardium through a 15 min to 5 hr observation period. The results suggested that the uptake-release mechanism of ¹²³I-MIBG in the neuronal vesicles was impaired in HCM subjects in two different ways: (1) normal release in delayed phase associated with low uptake in early phase or (2) accelerated release in early phase. Moreover, the sympathetic dysfunction may spread through the all segments of myocardium of HCM subjects. The apical lesion showed an extremely high rate of loss up to 5 hr after injection in SPECT images. This was quite different from that of the septal lesion. This indicated that the apical lesion of HCM subjects may have a different sympathetic abnormality. In EHT subjects, no abnormal regional distribution of ¹²³I-MIBG was observed. This suggested that the sympathetic innervation was maintained although an abnormal distribution of blood flow was frequently observed in ²⁰¹Tl scintigraphy. (author)