AbstractAimsThis paper proposes to explain the mechanism of M-cells, particularly its role in the T-wave generation and its contribution to arrhythmogenesis in short QT syndrome 2 (SQTS2).MethodsA 2D transmural anisotropic ventricular model made up of three principal cell types were developed. Different setups in which: a) entire column of mid-myocardial (mid) cells, b) single island of cells c) two island of cells within the mid-layer d) single island of cells in endocardial (endo)-mid layer were considered as M-cells. These setups are stimulated to explain i) contribution of M-cells in T-wave morphology ii) arrhythmia generation phenomena under SQTS2 heterozygous gene mutation by creating pseudo ECGs from the tissue.ResultsFindings infer that setups with an entire layer of M-cells and a higher percentage of epicardial (epi) cells exhibit positive T-waves. Increasing the size of the island in M-cell island setups results in an increased positive T-peak. Placing the M-cell island in the bottom of the mid-layer produced low amplitude T-waves. Further, in two M-cell islands setup, a higher T-wave amplitude was observed when the islands are placed closer than far apart. Moving the M-cell island slightly into the endo layer increases the amplitude of the T-wave. Lastly, on including SQTS2 conditions and pacing with premature beats, an arrhythmia occurs only in those setups containing a layer of M-cells compared to M-cells island setup.ConclusionThese simulation findings paved the way for a better understanding of the M-cells functionality in T-wave morphology as well as promoting arrhythmogenesis under SQTS2 condition.
Do M-cells contribute significantly in T-wave morphology during normal and arrhythmogenesis conditions like short QT Syndrome?