ABSTRACT
Closure of the left atrial appendage is a common procedure for patients with atrial fibrillation undergoing cardiac surgery. The technique of left atrial appendage occlusion (LAAO) by an extracardiac clip (AtriClip) is established as a reliable method. Acute coronary obstruction of the circumflex artery has already been described after minimally invasive LAAO. Here, we report a case of delayed circumflex artery obstruction after open-heart surgery. A patient who had mitral and tricuspid valve surgery in combination with AtriClip implantation suffered from myocardial infarction 24 h after clip implantation. Cardiac catheterization showed that the circumflex artery was obstructed on the level of the AtriClip device. The stenosis was treated by percutaneous coronary intervention with stent implantation. In conclusion, the surgeon should consider placing the AtriClip device slightly far away from the base of the left atrial appendage to avoid coronary obstruction.
Subject(s)
Atrial Appendage , Atrial Fibrillation , Cardiac Surgical Procedures , Stroke , Atrial Appendage/diagnostic imaging , Atrial Appendage/surgery , Atrial Fibrillation/etiology , Cardiac Catheterization , Humans , Treatment OutcomeABSTRACT
Atrial fibrillation (AF) is accompanied by intracellular calcium overload. The purpose of this study was to assess the role of calcium-dependent calpains and cytokines during AF. Atrial tissue samples from 32 patients [16 with chronic AF and 16 in sinus rhythm (SR)] undergoing open heart surgery were studied. Atrial expression of calpain I and II, calpastatin, troponin T (TnT), troponin C (TnC), and cytokines [interleukin (IL)-1 beta, IL-2, IL-6, IL-8, IL-10, transforming growth factor (TGF)-beta 1, and tumor necrosis factor-alpha] were determined. Expression of calpain I was increased during AF (461 +/- 201% vs. 100 +/- 34%, P < 0.05). Amounts of calpain II and calpastatin were unchanged. Total calpain enzymatic activity was more than doubled during AF (35.2 +/- 17.7 vs. 12.4 +/- 9.2 units, P < 0.05). In contrast to TnC, TnT levels were reduced in fibrillating atria by 26% (P < 0.05), corresponding to the myofilament disintegration seen by electron microscopy. Small amounts of only IL-2 and TGF-beta 1 mRNA and protein were detected regardless of the underlying cardiac rhythm. In conclusion, atria of patients with permanent AF show evidence of calpain I activation that might contribute to structural remodeling and contractile dysfunction, whereas there is no evidence of activation of tissue cytokines.
