Non-Cardiac Surgery After Percutaneous Coronary Intervention Saurabh Sanon, MD, and Charanjit S. Rihal, MD* Perioperative management of patients after percutaneous coronary intervention presents physicians with unique challenges and dilemmas. Although newer generation drug-eluting stents, transcatheter-based therapies, and minimally invasive surgical techniques have changed the medical landscape, guidelines for managing perioperative patients after percutaneous intervention are based largely on expert opinion and inconsistent data from an earlier era. In conclusion, the aims of this review are to summarize the data pertinent to managing patients after percutaneous coronary intervention in the perioperative period and to explore future perspectives. Ó 2014 Elsevier Inc. All rights reserved. (Am J Cardiol 2014;114:1613e1620) Approximately 600,000 percutaneous coronary interventions (PCIs) are performed annually in the United States.1,2 The incidence of noncardiac surgery (NCS) after PCI has been reported to range from 4% to 11% in the first year and from 7% to 34% in the first 2 years after index PCI.3e5 With an aging population, the incidence of coronary disease and the use of PCI may further increase, resulting in a greater incidence of NCS after PCI. Clear understanding of the characteristics of the post-PCI and perioperative states and the effects of overlap of the 2 states is imperative for the optimal management of this patient group. Unique Characteristics of the Postoperative State Contrary to the common belief that the risk for perioperative myocardial ischemia is greatest during anesthesia induction or intraoperatively, studies have revealed that the risk peaks 2 to 3 days after NCS, unless there is significant left main coronary artery or multivessel disease.6e8 Surgical stress results in sympathetic activation, with release of norepinephrine, epinephrine, cortisol, and renin. Plasminogen activator inhibitor levels increase and endogenous tissue plasminogen activator levels decrease, causing decreased fibrinolysis, while procoagulant factors increase.9e11 The cumulative result is an intensely prothrombotic, proinflammatory, and catabolic state. Consequently, the risk for thrombosis in the setting of newly deployed nonendothelized stents is enhanced. Coupled with cessation of antiplatelet therapy, as might occur in preparation for surgery, the thrombotic risk is further increased, especially in the first 6 to 8 weeks after stent implantation, when the stent may not be endothelized.12 Furthermore, this metabolically active state can cause coronary spasm and increase shear stress on coronary plaques, leading to plaque disruption. Dawood et al7 performed histopathologic analysis on the coronary arteries of 42 patients who had Division of Cardiovascular Diseases, Mayo Clinic, Rochester, Minnesota. Manuscript received July 21, 2014; revised manuscript received and accepted August 12, 2014. See page 1618 for disclosure information. *Corresponding author: Tel: (507) 284-4554; fax: (507) 255-2550. E-mail address: [email protected] (C.S. Rihal). 0002-9149/14/$ - see front matter Ó 2014 Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.amjcard.2014.08.023

perioperative myocardial infarctions (MIs) and reported plaque erosion or acute plaque disruption as the predominant pathology in this group. Additionally, fluid shifts, tachycardia, and increased cardiac output may result in myocardial demand-supply disparity, predisposing to ischemia and infarction.13 The unique pathophysiologic milieu of the postoperative state can lead to myocardial ischemia, even in patients without underlying coronary artery disease, but the risk is almost quadrupled in the setting of known coronary disease.6 The incidence of postoperative myocardial ischemia has been reported to range from 0.8% to 4.1%6 and is associated with mortality as high as 17% to 70%.14,15 It is therefore important to recognize the finite baseline risk for perioperative MI, even for apparently lowrisk patients without known coronary disease. Unique Characteristics of the Post-PCI State Stent implantation results in denudation of the endothelial surface, exposing the highly thrombogenic subendothelial surface while introducing a foreign object (the stent) into the milieu. The endothelium heals by reendothelization and neointima formation that occurs 6 to 8 weeks after bare-metal stent (BMS) implantation.12,16 In contrast, drug-eluting stents (DESs) consist of a metal stent platform, a polymer, and an antirestenotic drug. The controlled release of the antirestenotic agent prevents neointimal hyperplasia but also causes inflammation and endothelial dysfunction and predisposes to a longer period of thrombotic vulnerability (Figure 1).17 Angioscopic studies have demonstrated delayed neointimal coverage of DES struts compared with BMS struts, and this has been associated with a longer period of higher thrombotic risk.18,19 Studies have revealed no overall difference in the frequency of stent thrombosis between DES and BMS, but a clear temporal variation has been described. The incidence of stent thrombosis peaks in the first 6 months after BMS and later with DES (late stent thrombosis [LST], occurring at 31 days to 1 year).20 The frequency of very late stent thrombosis (VLST; occurring after 1 year) was also reported to be higher after firstgeneration DESs. Second-generation DESs have been shown to have higher average tissue coverage thickness and a lower degree of uncovered struts, malapposed struts, www.ajconline.org

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Figure 1. DES and BMS: scanning electron microscopic images revealing differential levels of strut coverage at 28 and 90 days after implantation in a rabbit iliac artery model. There is notably less endothelization in the DESs (Cypher and Taxus) compared with the BMSs (BX Velocity and Express). Arrows indicate overlapping stent regions.58 Figure reproduced with permission.

thereby underscoring the overwhelming effect of the thrombogenic postsurgical state. Numerous patient and procedural factors have been associated with stent thrombosis, including advanced age, diabetes, renal insufficiency, premature discontinuation of DAPT, smaller stent diameter, overlapping stent segments, bifurcation stenting, and longer stent lengths.4 The pathogenesis of stent thrombosis includes platelet activation and aggregation, leading to the development of an occlusive thrombus (Figure 3).27 It is therefore reasonable to conclude that the key to preventing stent thrombosis is continuation of DAPT, if feasible, and certainly continuation of aspirin monotherapy at the minimum. Noncardiac Surgery After Coronary Intervention

Figure 2. Angiogram demonstrating acute right coronary artery stent thrombosis in a patient presenting with an inferior ST-segment elevation MI.

inflammation, and less fibrin deposition compared with firstgeneration stents.21,22 All of these factors may theoretically protect against LST and VLST in second-generation stents. Although stent thrombosis has a low reported incidence of

Non-cardiac surgery after percutaneous coronary intervention.

Perioperative management of patients after percutaneous coronary intervention presents physicians with unique challenges and dilemmas. Although newer ...
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