Ahmed Imdad, Gertner Elie, Nelson William B, House Chad M, Zhu Dennis W X
Department of Medicine, Regions Hospital, 640 Jackson Street, St Paul, MN 55101, USA.
J Interv Card Electrophysiol. 2010 Dec;29(3):203-7. doi: 10.1007/s10840-010-9520-6. Epub 2010 Oct 13.
The aim of this investigation was to determine additional predisposing factors of pocket hematoma formation in patients undergoing anti-arrhythmic device surgery.
Initially, we performed a retrospective chart review of 459 patients on warfarin therapy who underwent anti-arrhythmic device surgery (pacemaker or defibrillator implantation, generator replacement, or lead revision) between April 2004 and September 2008 to determine whether continuation of anticoagulation or cessation of anticoagulation, with or without bridging therapy, was the preferred approach. In those patients who developed pocket hematoma, we then analyzed factors that might predispose to hematoma formation.
The incidence of pocket hematoma in the entire group was 2.2% (n = 10). Forty-eight percent of the patient group was on continued warfarin (n = 220), 27% on bridging therapy with intravenous heparin or subcutaneous enoxaparin (n = 123) and 66% were on antiplatelet therapy (aspirin or clopidegrol or both; n = 303) at the time of device implantation. Twelve percent of the patients had chronic kidney disease (n = 55). In multivariate regression analysis, after adjusting for anticoagulation and antiplatelet agents, chronic kidney disease was found to be a significant risk factor for pocket hematoma formation after ICD and pacemaker placement. An increase of 1.0 mg/dl in creatinine levels was associated with a nearly twofold increase in hematoma formation (OR, 1.99; 95% CI, 1.22-3.21; p = 0.03).
Chronic kidney disease is a significant risk factor for pocket hematoma formation after pacemaker and ICD placement, independent of anticoagulation and antiplatelet agents.
本研究的目的是确定接受抗心律失常器械手术患者发生囊袋血肿形成的其他易感因素。
最初,我们对2004年4月至2008年9月期间接受抗心律失常器械手术(起搏器或除颤器植入、发生器更换或导线修复)的459例接受华法林治疗的患者进行了回顾性病历审查,以确定继续抗凝或停止抗凝(有无桥接治疗)是否为首选方法。在那些发生囊袋血肿的患者中,我们随后分析了可能易导致血肿形成的因素。
整个组中囊袋血肿的发生率为2.2%(n = 10)。在器械植入时,48%的患者组继续使用华法林(n = 220),27%的患者接受静脉肝素或皮下依诺肝素桥接治疗(n = 123),66%的患者接受抗血小板治疗(阿司匹林或氯吡格雷或两者;n = 303)。12%的患者患有慢性肾脏病(n = 55)。在多变量回归分析中,在调整抗凝和抗血小板药物后,发现慢性肾脏病是植入ICD和起搏器后囊袋血肿形成的一个重要危险因素。肌酐水平每增加1.0mg/dl,血肿形成增加近两倍(OR,1.99;95%CI,1.22 - 3.21;p = 0.03)。
慢性肾脏病是起搏器和ICD植入后囊袋血肿形成的一个重要危险因素,独立于抗凝和抗血小板药物。