Heart failure differentially modulated action potential morphology and ionic currents, increasing action potential duration in RVOT cardiomyocytes but decreasing it in LVOT cardiomyocytes.
Does heart failure differentially affect the electrophysiological characteristics of RVOT and LVOT cardiomyocytes?
Heart failure exerts discrepant effects on the electrophysiological properties of RVOT and LVOT cardiomyocytes, potentially contributing to the mechanisms of ventricular arrhythmias in these regions.
Ventricular arrhythmias commonly arise from the right (RVOT) and left ventricular outflow tracts (LVOT) in patients without structural heart disease. Heart failure (HF) significantly increases the risk of ventricular arrhythmias. The regional differences and how HF affects the electrophysiological characteristics of RVOT and LVOT cardiomyocytes remain unclear. The whole-cell patch-clamp technique was used to investigate the action potentials and ionic currents in isolated single RVOT and LVOT cardiomyocytes from control rabbits and rabbits with HF induced by rapid ventricular pacing. Comparison with control LVOT cardiomyocytes showed that control RVOT cardiomyocytes have a shorter action potential duration (APD), smaller late Na+ currents (INa-late), larger transient outward (Ito) and larger delayed rectifier K+ currents (IKr-tail), but had similar L-type Ca2+ currents (ICa-L) and Na+/Ca2+ exchanger (NCX) current. HF increased APD, INa-late and NCX, but decreased ICa-L and Ito in RVOT cardiomyocytes. In contrast with this, HF decreased APD and ICa-L, but increased Ito and IKr-tail in LVOT cardiomyocytes. In conclusion, RVOT and LVOT cardiomyocytes had distinctive electrophysiological characteristics. HF differentially modulates action potential morphology and ionic currents in RVOT and LVOT cardiomyocytes.
Lu et al. (Wed,) conducted a other in Heart failure. Heart failure (induced by rapid ventricular pacing) vs. Control rabbits was evaluated on Action potentials and ionic currents. Heart failure differentially modulated action potential morphology and ionic currents, increasing action potential duration in RVOT cardiomyocytes but decreasing it in LVOT cardiomyocytes.