The etiopathogenetic mechanisms of metabolic syndrome that affect cardiac electrophysiology and lead to myocardial remodelling are numerous. Cardiomyocyte changes induced by metabolic and proinflammatory factors impair repolarization, exacerbate the heterogeneity of the transmural dispersion of repolarization, and prolong the Tpeak-end interval. Tpeak-Tend interval has been described as a marker of arrhythmogenicity that is more sensitive than the standard QT interval. Multiple pathological conditions and their effect on myocardial repolarisation have been studied – coronary artery disease, sleep apnea, arterial hypertension, Brugada syndrome and other channelopathies, systemic sclerosis, endocrinological diseases such as hypothyroidism, diabetes mellitus, acromegaly, hypertrophic cardiomyopathy, sudden cardiac death, familial hypercholesterolemia, etc. Currently, the most widely accepted theory of the mechanism of formation of Tp-e the interval and its dynamics are transmural myocardial heterogeneity/dispersion repolarisation. For the clinician, this is an additional tool for assessment of arrhythmogenicity through easy and accessible electrocardiographic markers in dail
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