Coronary Stents and Noncardiac Surgery

Riddell, John W.; Chiche, Laurent; Plaud, Benoît; Hamon, Martial

doi:10.1161/circulationaha.107.726992

Cited by 63 publications

(41 citation statements)

References 31 publications

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“…3 To assess the temporal risk of noncardiac surgery according to coronary artery stent type, outcomes were examined categorically for surgical admissions occurring Ͻ42 days, 42 days to 12 months, and Ͼ12 months from coronary stent implantation. These time categories were chosen on the basis of previous data 3,11 and to be consistent with the definition of very late stent thrombosis (Ͼ12 months after implantation). Univariate and multivariable logistical regression analyses were performed to identify variables potentially associated with perioperative ischemic cardiac events.…”

Section: Discussionmentioning

confidence: 99%

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Previous Coronary Stent Implantation and Cardiac Events in Patients Undergoing Noncardiac Surgery

Cruden

Harding

Flapan

et al. 2010

Circ: Cardiovascular Interventions

143

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Section: Discussionmentioning

confidence: 99%

“…3 Treatment of patients with dual antiplatelet therapy (aspirin and thienopyridine) for at least 4 weeks after bare-metal stent implantation has reduced the incidence of stent thrombosis to Ͻ1%. 1 The optimal duration of dual antiplatelet therapy after implantation of a drug-eluting stent remains unknown.…”

Section: Clinical Perspective On P 242mentioning

confidence: 99%

Previous Coronary Stent Implantation and Cardiac Events in Patients Undergoing Noncardiac Surgery

Cruden

Harding

Flapan

et al. 2010

Circ: Cardiovascular Interventions

143

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“…Several studies have reported an inverse relationship between the time after PCI and perioperative major adverse cardiac events. 86 For bare metal stenting, the incidence of in-hospital major adverse cardiac events decreases from 10.5% at Ͻ30 days to 2.8% at Ͼ90 days. 87 For drug-eluting coronary stenting, the risk of perioperative MACE is stable (5.9% to 6.4%) during the first year and declines to 3.3% thereafter.…”

Section: Dual Antiplatelet Therapymentioning

confidence: 98%

Perioperative Myocardial Infarction

et al. 2009

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M ore than 230 million major surgeries are performed annually worldwide, 1 and this number grows continuously. The 30-day mortality associated with moderate-to high-risk noncardiac surgery in recent large cohorts and population-based studies exceeds 2% 2-4 and surpasses 5% in patients at high cardiac risk. 5 Cardiac complications constitute the most common cause of postoperative morbidity and mortality, 4,6 having considerable impact on the length and cost of hospitalization. 7 As our population ages, more high-risk cardiac patients will undergo surgery, and perioperative myocardial infarction (PMI) can be an increasing problem. Redefinition of PMITraditionally, MI was defined by the World Health Organization criteria, ECG criteria, and cardiac enzymes. Defining PMI, however, is often difficult because most PMIs occur without symptoms in anesthetized or sedated patients, ECG changes are subtle and/or transient, and the creatine kinase-MB isoenzyme has limited sensitivity and specificity because of coexisting skeletal muscle injury. 8 Consequently, PMI was often recognized late (postoperative day 3 to 5), resulting in high (30% to 70% 9 ) mortality.Cardiac troponin assays have changed this definition. 10 The recent universal definition of MI 11 is based on a rise and/or fall of cardiac biomarkers (preferably troponin) in the setting of myocardial ischemia: cardiac symptoms, ECG changes, or imaging findings. Studies using serial troponin measurements demonstrate that most PMIs start within 24 to 48 hours of surgery during the greatest postoperative stress. 12-15 Le Manach et al 15 observed early (Ͻ24 hours) and late (Ͼ24 hours) peaks in troponin in 1136 patients after abdominal aortic aneurysmectomy. Yet, 90% of troponin elevations began within Ͻ24 hours. PathophysiologyTwo distinct mechanisms may lead to PMI: acute coronary syndrome and prolonged myocardial oxygen supply-demand imbalance in the presence of stable coronary artery disease (CAD), designated type 1 and type 2 by the universal definition of MI. 11 This distinction is key to therapeutic considerations. Acute Coronary Syndrome (Type 1 PMI)Acute coronary syndrome occurs when an unstable or vulnerable plaque undergoes spontaneous rupture, fissuring, or erosion, leading to acute coronary thrombosis, ischemia, and infarction. Although it is currently widely accepted that intraplaque inflammation plays a pivotal role in plaque instability and spontaneous acute coronary syndrome, 16 external stressors such as those occurring postoperatively are believed to contribute (Figure 1):• Physiological and emotional stresses are known to predispose to MI, likely because of the sympathetic induced hemodynamic, coronary vasoconstrictive, and prothrombotic forces thought to promote plaque disruption. These conditions are common perioperatively. Catecholamines and cortisol increase after surgery 17 and may remain elevated for days. 18 Stress hormones increase with pain, surgical trauma, anemia, and hypothermia. 19,20 Plasma catecholamines correlated with postoperative car...

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“…The interruption of antiplatelet therapy (APT) for surgery is considered to be one of the main reasons for the increased risk (2)(3)(4)(5). The optimal perioperative manage- Figure. Heparin administration according to the local institutional practice guideline.…”

Section: Introductionmentioning

confidence: 99%

Unfractionated Heparin during the Interruption of Antiplatelet Therapy for Non-cardiac Surgery after Drug-eluting Stent Implantation

et al. 2016

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Objective Heparin is not recommended to be administered during the interruption of antiplatelet therapy for non-cardiac surgery. However, there are insufficient data to determine the value. The purpose of the present study was to evaluate the clinical results of the administration of unfractionated heparin during the interruption of antiplatelet therapy in non-cardiac surgery patients who had previously undergone drug-eluting stent (DES) implantation. Methods We retrospectively identified 210 elective non-cardiac surgical procedures that were performed with the administration of unfractionated heparin during interruption of all antiplatelet therapies in patients who had previously undergone DES implantation. Heparin was administered during the perioperative period in accordance with the local practice guideline at out institution. We examined the clinical outcomes within 30 days of surgery. Results The mean number of implanted DESs was 2.1±1.3. No major adverse cardiac events (including cardiac death, definite stent thrombosis, and non-fatal myocardial infarction) occurred in any of the 210 cases within 30 days of surgery. Four of the 210 cases (1.9%) required reoperation for bleeding within 30 days of surgery. Conclusion Our data showed the potential for the perioperative management with unfractionated heparin administration in Japanese patients who had previously undergone DES implantation who required noncardiac surgery with the interruption of all antiplatelet therapies.

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Coronary Stents and Noncardiac Surgery

Cited by 63 publications

References 31 publications

Previous Coronary Stent Implantation and Cardiac Events in Patients Undergoing Noncardiac Surgery

Previous Coronary Stent Implantation and Cardiac Events in Patients Undergoing Noncardiac Surgery

Perioperative Myocardial Infarction

Unfractionated Heparin during the Interruption of Antiplatelet Therapy for Non-cardiac Surgery after Drug-eluting Stent Implantation

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