Myocardial cGMP-PKG1α dysregulation contributes to VT pathogenesis in type II diabetes and metabolic syndrome.

Background: Type-II diabetes (DMII) and metabolic syndrome increase ventricular arrhythmia and sudden cardiac death risk.

Objectives: To identify signaling mechanisms through which DMII and metabolic syndrome promote ventricular tachycardia (VT).

Methods: We performed ventricular programmed stimulation on leptin receptor mutant (Db/Db) mice with DMII, high fat high sucrose (HFHS)-fed mice with metabolic syndrome, and cGMP-dependent Protein Kinase 1α (PKG1α) leucine zipper mutant (LZM) mice, which do not have DMII or metabolic syndrome but have disrupted PKG1α signaling.