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Recent research has revealed that infiltrating Adipose Tissue (inFAT) co localizes with scar in infarcted hearts and may be a factor in Ventricular Arrhythmias (VAs), a potentially fatal cardiac rhythm problem. The impact of inFAT on VA hasn't been well demonstrated, though. With the help of a combined prospective clinical and mechanistic computational study, we examined the function of inFAT versus scar in VA. We show that inFAT, rather than scar, are a primary driver of arrhythmogenic propensity and are frequently present in crucial areas of the VA circuit by using individualised computational heart models and comparing the outcomes of simulations of VA dynamics with measured electrophysiological abnormalities during the clinical procedure. We came to the conclusion that inFAT, not scar is primarily responsible for conduction slowing in crucial sites within the VA circuitry, thereby mechanistically promoting VA. Our findings challenge preconceived notions and pave the way for previously unconsidered anti-arrhythmic approaches by implicating inFAT as a key player in infarct related VA.
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