High SERCA 2a activity, co-expressed with the myosin heavy chain isoform V1, is hypothesized to facilitate spontaneous ventricular defibrillation by preventing intracellular calcium overload.
Does high SERCA 2a activity and V1 MHC expression facilitate spontaneous ventricular defibrillation in mammals?
The paper proposes that spontaneous termination of ventricular fibrillation depends on high SERCA 2a activity and V1 myosin heavy chain isoform expression to prevent intracellular calcium overload.
The present paper deals with spontaneous ventricular defibrillation in mammals and the possibility to facilitate its occurrence. Clinical and experimental evidence suggest that in the majority of cases, ventricular fibrillation (VF) is permanent, requiring defibrillation by electric shock. However, a growing number of reports show that VF can terminate spontaneously in various mammals, including human beings. The mechanisms involved in spontaneous ventricular defibrillation are controversial. Available reports imply that intracellular Ca2+ overload is the key event triggering VF and preventing its reversal. Since the sarcoplasmatic reticulum is the main intracellular Ca2+ regulating organelle and the activity of the cardiac SR Ca2+ ATPase (SERCA 2a) is its prime element of Ca2+ sequestration, spontaneous ventricular defibrillation likely requires high level of SERCA 2a activity. We suggest that mammalian hearts with high SERCA 2a activity defibrillate spontaneously and those with low activity only after its enhancement. Since high SERCA 2a activity is co-expressed with the myosin heavy chain (MHC) isoform V1, we assumed that those hearts preferentially expressing V1 MHC are able to defibrillate spontaneously. Hearts with small amounts of V1 MHC and correspondingly lower level of SERCA 2a activity can only defibrillate following administration of compounds that augment SERCA 2a activity and prevent intracellular Ca2+ overload.
Manoach et al. (Mon,) conducted a review in Ventricular fibrillation. High SERCA 2a activity and myosin heavy chain isoform V1 vs. Low SERCA 2a activity and small amounts of V1 MHC was evaluated on Spontaneous ventricular defibrillation. High SERCA 2a activity, co-expressed with the myosin heavy chain isoform V1, is hypothesized to facilitate spontaneous ventricular defibrillation by preventing intracellular calcium overload.