ESC Guidelines on the diagnosis and treatment of peripheral artery diseases Document covering atherosclerotic disease of extracranial carotid and vertebral, mesenteric, renal, upper and lower extremity arteries The Task Force on the Diagnosis and Treatment of Peripheral Artery Diseases of the European Society of Cardiology (ESC)

Among patients with unstable angina or myocardial infarction without ST-segment elevation, prasugrel did not significantly reduce the frequency of the primary end point, as compared with clopidogrel, and similar risks of bleeding were observed. (Funded by Eli Lilly and Daiichi Sankyo; TRILOGY ACS ClinicalTrials.gov number, NCT00699998.).

Postoperative CK-MB and troponin, even at low cutoff levels, are independent and complementary predictors of long-term mortality after major vascular surgery.

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...