[Estimation of intracellular free calcium concentration in patients undergoing digitalis treatment and in patients presenting digitalis toxicity].

Delayed afterdepolarizations occur under conditions in which there are large increase in the intracellular Ca and may be considered as one of the important mechanisms for digitalis-induced arrhythmias. Intraplatelet free calcium (Ca2i+) was measured in 25 patients, using the fluorescent indicator Quin-2. The patients included 15 with glycosides treatment (Group A) and 10 with arrhythmias indicating the presence of digitalis intoxication (Group B). The average Ca2i+ level in Group A was higher than the normal value but did not reach a statistical significance (170.8 +/- 9.09 vs 161.6 +/- 30.2, NS). The Ca2i+ level during digitalis toxicity in Group B was significantly higher than that in Group A (201.7 +/- 17.65 vs 170.18 +/- 91.09, P less than 0.01) as well as the normal value (P less than 0.01). With the disappearance of digitalis toxicity the Ca2i+ level was significantly decreased from 201.7 +/- 17.65 to 171.4 +/- 14.08 (P less than 0.001). Following the elimination of digitalis toxicity the increased digoxin concentration also declined. However, the decline of digoxin concentration did not correlate well with the decline of Ca2i+ (r = -0.57, P greater than 0.05). There is a close association between digitalis-induced arrhythmias and the change of Ca2i+ level, compatible with the tentative mechanism of delayed after depolarization (triggered activity). The poor correlation between the Ca2i+ level and digoxin concentration during the process of digitalis toxicity may suggest the presence of factors other than glycosides concentration to cause increased Cai2+ and arrhythmias.