AbstractBackground
The impact of left atrial appendage (LAA) exclusion, comparing an epicardial LAA or an endocardial LAA device, on systemic homeostasis remains unknown.
ObjectivesThis study compared the effects of epicardial or endocardial LAA devices on the neurohormonal profiles of patients, emphasizing the roles of the renin-angiotensin-aldosterone system and the autonomic nervous system.
MethodsThis is a prospective, single-center, observational study including 77 patients who underwent LAA closure by an epicardial (n = 38) or endocardial (n = 39) device. Key hormones involved in the adrenergic system (adrenaline, noradrenaline), renin-angiotensin-aldosterone system (aldosterone, renin), metabolic system (adiponectin, free fatty acids, insulin, β-hydroxybutyrate, and free glycerols), and natriuresis (atrial and B-type natriuretic peptides) were assessed immediately before the procedure, immediately after device deployment, at 24 h, and at 3 months follow-up.
ResultsIn the endocardial LAA device group, when compared with baseline blood adrenaline, noradrenaline and aldosterone were significantly lower at 24 h and 3 months (p < 0.05). There was no significant change in levels post-endocardial LAA device implantation. After epicardial LAA device implantation, there were significant increases in adiponectin and insulin, with decreased free fatty acids at 3 months. There was no significant change in these levels post-endocardial LAA device. N-terminal pro-A-type natriuretic peptide and N-terminal pro-B-type natriuretic peptide were significantly decreased in the acute phase after epicardial LAA device implantation, which subsequently normalized at 3 months. Post endocardial LAA device implantation, the levels increased immediately and normalized after 24 h. Systemic blood pressure was also significantly lower at all time points after epicardial LAA device implantation, which was not seen post-endocardial LAA device implantation.
ConclusionsThere are substantial differences in hemodynamics and neurohormonal effects of LAA exclusion with epicardial and endocardial devices. Further studies are required to elucidate the underlying mechanism of these physiological changes.
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