The present study clarified the pathogenesis of disproportional hypertrophy in terms of disturbed coronary microcirculation. Twenty-eight patients with hypertrophic cardiomyopathy (HCM) who had normal coronary angiograms were categorized in four groups according to distributions of disproportional hypertrophy on left ventriculography and biventriculography: (1) Interventricular septal hypertrophy, (2) septal and apico-anterior wall hypertrophy, (3) apico-anterior hypertrophy, and (4) nonspecific hypertrophy of the entire wall. All 28 HCM patients and 10 normal volunteers were tested using exercise myocardial scintigraphy, and the circumferential profiles were processed by computer to relate the washout rate and disproportional hypertrophy. Comparison of the mean curves and mean segmental values of the circumferential profiles of the HCM groups with those of the control group showed that the mean initial uptake values of the HCM groups were to be relatively low in the apical segment and in the lower portion of the anteroseptal segment representing disproportional hypertrophy of these segments. The mean values were significantly elevated in the upper portion of the anteroseptal segment which was projected as the largest amount of the myocardium three-dimensionally. The mean washout rates in the HCM groups were significantly decreased in all segments, especially in those segments which reflected disproportional hypertrophy. This trend was also observed in the segments with increased initial uptakes. On comparing the segmental values of all groups, the segments with initial uptakes and/or washout rates with having the mean value minus 2SD of the control group were observed in the profiles of 12 of the 28 HCM patients. These all had decreased washout rates. In 25 of the total segments of the HCM patients, the initial uptakes and/or washout rates were below the normal limit; 21 of these segments had only decreased washout rates, and 16 of these 21 segments belonged to disproportionally hypertrophic wall. These results indicate that the decreased washout rate in the disproportionally hypertrophic wall is characteristic of HCM. It is suggested that the decreased washout rate with the decreased initial uptake is caused by disturbance of the coronary microcirculation. In addition, the decreased washout rate without a decreased initial uptake is caused not only by disturbance of coronary microcirculation, but by a metabolic disturbance of the myocardial cells as well. Furthermore, both disturbances are closely related to the pathogenesis of disproportional hypertrophy.