There is circumstantial clinical evidence to suggest that patients with hypertrophic cardiomyopathy (HCM) have disordered regulation of intra-cellular calcium. The hypercontractile myocardium with poor diastolic relaxation could be explained, for example, by increased cytosolic Ca+2 in the cardiac myocyte. Given that some forms of HCM are genetically transmitted, we postulated that a disorder of cytosolic calcium metabolism might be present in other, non-cardiac tissue. To study this, we isolated platelets from the plasma of patients with HCM and normals and measured intra-cellular calcium levels using the fluorescent indicator QuinII. Our preliminary results (on only a small number of patients and controls) indicates that resting Ca+2 levels are the same in these populations. When the cells are stimulated with vasopressin -- which causes both intra- cellular calcium mobilization and Ca+2 influx -- some patients appear to have a blunted response to this stimulant. Whether this is an epiphenomenon still remains to be determined, but if these results are substantiated, they point to wide-spread Ca+2 dysregulation. The mechanism of this could be determined and might give us an important clue as to the etiology of this disease.
