Ca2+-handling in heart failure – a review focusing on Ca2+ sparks

[Ca ²⁺] _i-transients have been shown to be altered in isolated ventricular myocytes from terminally failing human myocardium. It has been demonstrated that one reason for this alteration is a reduction in the Ca ²⁺ content of the sarcoplasmic reticulum (SR). Further investigations were done to investigate, whether there may be an additional defect of the Ca ²⁺-release mechanisms from the SR. These release mechanisms were investigated through the recording of Ca ²⁺ sparks in single human myocytes. In cardiac myocytes, Ca ²⁺ sparks are elementary units of Ca ²⁺ release, which occur spontaneously, or which are triggered by Ca ²⁺ influx through L-type Ca ²⁺-channels (Ca ²⁺-induced Ca ²⁺ release). Ca ²⁺ sparks have been investigated in various animal models of cardiac hypertrophy and cardiac failure and results were conflicting. Discrepancies may be explained by different species and also by the mechanisms underlying hypertrophy and heart failure. This review summarizes our current knowledge on Ca ²⁺ sparks in heart failure.