Michael Oneglia
A growing body of evidence points towards the involvement of myocardial steatosis in the development of left ventricular diastolic dysfunction, although conclusive proof in humans is hampered by complicating coexisting conditions. To address this, we employed a 48-hour food restriction protocol to induce an acute elevation in Myocardial Triglyceride (mTG) content quantified using 1H magnetic resonance spectroscopy in a cohort of 27 young and healthy volunteers (comprising 13 men and 14 women). The results of the fasting regimen exhibited a remarkable over threefold rise in mTG content (P<0.001). Interestingly, the early diastolic circumferential strain rate (CSRd), a marker of diastolic function, remained unaffected following the 48-hour fasting intervention. However, a noteworthy elevation in systolic circumferential strain rate was observed (P<0.001), indicating a decoupling between systolic and diastolic phases. This phenomenon of uncoupling was further substantiated by an additional experiment involving 10 individuals, where the administration of low-dose dobutamine (2 μg/kg/min) resulted in a similar alteration in systolic circumferential strain rate as the one observed during the 48-hour food restriction. Moreover, this change was accompanied by a proportionate increase in CSRd, thereby preserving the synchronization between the two metrics. The collective findings of this study underscore the role of myocardial steatosis in instigating diastolic dysfunction by disrupting the coupling between diastole and systole in the context of healthy adult subjects. Furthermore, these findings postulate a potential contributory role of steatosis in the progression of cardiovascular ailments.
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