Ischemic Heart Disease and Noncardiac Surgery

Shamsuddin Akhtar

Paul G. Barash

A. Medical Disease and Differential Diagnosis

What are the preoperative predictors for major adverse cardiac events (MACE) perioperatively?
What are the determinants of myocardial oxygen demand? How are they measured clinically?
What factors determine myocardial oxygen supply?
What is the mechanism of perioperative myocardial ischemia and infarction?
What is the incidence of perioperative reinfarction for noncardiac surgery?
State the perioperative medical therapy you would employ to reduce the incidence of myocardial ischemia.
Based on his MI, would you recommend that the surgery be postponed for a certain period of time? If so, why?
Would you recommend that this elective colectomy be postponed, if the patient underwent placement of a right coronary artery, second-generation DES, and is taking aspirin and clopidogrel (Plavix)?

B. Preoperative Evaluation and Preparation

How would you evaluate the patient’s cardiac condition? What laboratory tests would you like to order?
Would you recommend further cardiac testing or coronary revascularization before surgery?
How would you classify the cardiac risk according to the type of surgery?
What is the role of exercise or pharmacologic stress test for this patient?
Would you discontinue any medication before surgery?
How would you premedicate this patient?
Is there a role for α₂-agonist in premedication?

C. Intraoperative Management

What are the intraoperative predictors for perioperative MACE?
How would you monitor the patient in the operating room?
What electrocardiogram (ECG) leads would you monitor? Why V₅?
Would you use a pulmonary artery catheter (PAC)?
Would you use transesophageal echocardiography (TEE) as a monitor?
Is regional anesthesia better than general anesthesia for patients with cardiac disease?
How will you induce general anesthesia?
Would you induce anesthesia with etomidate? Why?
What is the best choice of anesthetic agents for maintenance of anesthesia? Why?
You notice a new 3-mm ST-segment depression in lead V₅. How would you treat it?
Would you give prophylactic intravenous NTG to prevent myocardial ischemia?
What is the significance of tight control of the heart rate intraoperatively?
When would you extubate the trachea in this patient? What could you do to prevent hypertension and tachycardia during extubation and emergence?

D. Postoperative Management

What are the postoperative predictors of perioperative MACE?
How would you control postoperative pain?
Is postoperative anemia associated with adverse cardiac outcome?
Is postoperative hypothermia associated with postoperative myocardial ischemia?
How would you make a diagnosis of perioperative myocardial infarction (PMI)?
How would you manage the patient with a suspected PMI?

A. Medical Disease and Differential Diagnosis

A.1. What are the preoperative predictors for major adverse cardiac events (MACE) perioperatively?

Perioperative myocardial infarction or injury (PMI) is one of the most important predictors of short- and long-term mortality and morbidity associated with noncardiac surgery. Therefore, the prevention of PMI can improve postoperative outcomes. Numerous risk indices and predictors for perioperative cardiac morbidity (PCM) have been published over the last 40 years.

In 1999, Lee et al. revised the Goldman Cardiac Risk Index, now called the Revised Cardiac Risk Index (RCRI), utilizing six independent predictors of cardiac risk, which are as follows:

High-risk type of surgery
History of ischemic heart disease (IHD)
History of congestive heart failure (CHF)
History of cerebrovascular disease
Preoperative treatment of diabetes mellitus with insulin
Preoperative serum creatinine greater than 2.0 mg per dL

They concluded that the rate of major cardiac complications (MI, pulmonary edema, ventricular fibrillation, and primary cardiac arrest) with 0, 1, 2, and more than or equal to 3 predictors, were 0.5%, 1.3%, 4%, and 9%, respectively.

The 2014 American College of Cardiology (ACC)/American Heart Association (AHA) guidelines categorize the patients into two groups, namely, low risk and elevated risk based on the presence of clinical risk factors and risk of surgical procedures. Patients with less than 1% chance of MACE are categorized as low risk, whereas patients with cumulative risk of MACE more than 1% are categorized as elevated risk. Patients who have two or more RCRIs are considered at elevated risk. The other two indices are the American College of Surgeons National Surgical Quality Improvement Program (NSQIP) Myocardial Infarction and Cardiac Arrest (MICA), and American College of Surgeons NSQIP Surgical Risk Calculator (http://riskcalculator.facs.org). Both are readily available on the web to evaluate patients. The European Society of Cardiology (ESC) guidelines define surgical risk procedures as low-(<1%),
intermediate-(1% to 5%), and high-risk procedures (>5%). By ACC guideline criteria, this patient will be considered elevated risk, scheduled to undergo an intermediate-risk procedure (by ESC guidelines).

Although the new guidelines do not categorize the clinical predictors of MACE into major, intermediate, and minor factors, in addition to the RCRI mentioned earlier, the following clinical factors significantly increase the risk of perioperative MACE.

Unstable coronary syndromes: Acute (MI ≤7 days before examination) or recent MI (>7 days but ≤1 month) with evidence of important ischemic risk by clinical symptoms or noninvasive study. A study using discharge summaries demonstrated that the postoperative MI rate decreased substantially as the length of time from MI to operation increased (0 to 30 days = 32.8%; 31 to 60 days = 18.7%; 61 to 90 days = 8.4%; and 91 to 180 days = 5.9%), as did the 30-day mortality rate. However, risk was modified by coronary intervention. It is suggested that more than 60 days should elapse after MI before noncardiac surgery is undertaken in the absence of coronary intervention.
Unstable or severe angina (Canadian class III): marked limitation of ordinary physical activity; walking one to two blocks on the level and climbing one flight of stairs in normal conditions at normal pace; and Canadian class IV: inability to carry on any physical activity without discomfort—anginal syndrome may be present at rest
Decompensated heart failure (HF): Patients with active HF have significantly higher risk of postoperative death than do patients with coronary artery disease (CAD). Survival after surgery for those with a left ventricular ejection fraction (LVEF) less than 30% is significantly worse than for those with an LVEF ≥30%.
Severe valvular disease (severe aortic stenosis [AS] with valve area less than 1 cm² or symptomatic) have a two to three times higher risk of 30-day mortality than patients without AS. Similar observations have been noted for severe mitral stenosis. Left-sided regurgitant lesions convey increased cardiac risk during noncardiac surgery but are better tolerated than stenotic valvular disease.
Significant arrhythmias, such as high-grade atrioventricular block, Mobitz type II atrioventricular block, third-degree heart block, or unanticipated symptomatic supraventricular and ventricular arrhythmias, increase operative risk. Risk of other supraventricular and ventricular arrhythmias seems to be lower than reported before.
Age is considered a risk factor especially when it is associated with frailty. However, its exact role still needs to be defined further.
Pulmonary hypertension: Patients with pulmonary artery hypertension are at an increased risk of cardiopulmonary complications after noncardiac surgery. Mortality rates of 4% to 26% and cardiorespiratory morbidity rates of 6% to 42% have been reported.

Fleisher LA, Fleischmann KE, Auerbach AD, et al. 2014 ACC/AHA guideline on perioperative cardiovascular evaluation and management of patients undergoing noncardiac surgery: a report of the American College of Cardiology/American Heart Association Task Force on practice guidelines. J Am Coll Cardiol. 2014;64:e77-e137.

Kristensen SD, Knuuti J, Saraste A, et al. 2014 ESC/ESA guidelines on non-cardiac surgery: cardiovascular assessment and management: the Joint Task Force on non-cardiac surgery: cardiovascular assessment and management of the European Society of Cardiology (ESC) and the European Society of Anaesthesiology (ESA). Eur Heart J. 2014;35:2383-2431.

Lee TH, Marcantonio RE, Mangione CM, et al. Derivation and prospective validation of a simple index for prediction of cardiac risk of major noncardiac surgery. Circulation. 1999;100:1043-1049.

A.2. What are the determinants of myocardial oxygen demand? How are they measured clinically?

The three major determinants of myocardial oxygen demand are (1) myocardial left ventricular (LV) wall tension (LV preload and afterload), (2) cardiac contractility, and (3) heart rate.

A.3. What factors determine myocardial oxygen supply?

The factors determining myocardial oxygen supply include cardiac output, arterial oxygen content, heart rate, aortic diastolic pressure, LV end-diastolic pressure, patency of coronary arteries, and coronary vascular tone.

A.4. What is the mechanism of perioperative myocardial ischemia and infarction?

Myocardial ischemia occurs whenever myocardial oxygen supply does not match myocardial oxygen demand. Intraoperative ischemia can be precipitated by increases in myocardial oxygen demand caused by tachycardia, hypertension, anemia, surgical stress, sympathomimetic drugs, or discontinuation of β-blockers. Potential etiologies for decreased supply include hypotension, tachycardia, increased cardiac filling pressures, anemia, hypoxemia, and decreased cardiac output. In one study, ischemia occurred (67%) at the end of anesthesia or immediately after surgery, during a period characterized by high sympathetic output, hypercoagulability, hypertension, and tachycardia. Ischemia in this period is usually silent, with only ST-segment depression as a marker. And in at least one-third of the patients, this ST-segment depression goes unnoticed. Hypotension is strongly correlated with PMI. In addition, internal factors such as acute coronary artery thrombosis and spasm may also play a role.

PMI is one of the most important predictors of short- and long-term morbidity and mortality associated with noncardiac surgery. Unfortunately, the exact nature of PMI remains uncertain and a subject of debate and controversy. The interaction between morphologic and functional factors is unpredictable. Some older pathologic and angiographic studies suggested that the etiology of PMI resembles that in the nonsurgical setting, that is, plaque rupture was the cause of PMI in 50% of the cases. However, newer analysis suggests that myocardial oxygen supply/demand imbalance predominates in the first 3 to 4 postoperative days and patients suffer PMI from demand ischemia. In PMI, the severity of underlying coronary artery stenosis does not necessarily predict the infarct territory. The high incidence of histologically confirmed transmural infarctions seems to be contradictory to the ECG finding of almost exclusively non-Q-wave PMIs. On the other hand, the presence of subendocardial PMIs is consistent with a myocardial oxygen supply/demand mismatch being the main trigger of myocardial injury. However, myocardial oxygen supply/demand mismatch and plaque rupture are not mutually exclusive mechanisms, and PMIs may be developed by different mechanisms at different locations in the same patient.

Most PMIs occur early after surgery (0 to 4 days) and 90% occur within 7 days, are asymptomatic, of the non-Q-wave type (60% to 100%), and are commonly preceded by ST-segment depression rather than ST-segment elevation. Long duration (single duration >20 to 30 minutes or cumulative duration >1 to 2 hours intraoperatively or postoperatively) rather than just the presence of postoperative ST-segment depression seems to be the important factor associated with adverse cardiac outcome.

Biccard BM, Rodseth RN. What evidence is there for intraoperative predictors of perioperative cardiac outcomes? A systematic review. Perioper Med (Lond). 2013;2:14.

Cheung C, Martyn A, Campbell N, et al. Predictors of intraoperative hypotension and bradycardia. Am J Med. 2015;128:532-538.

Galal W, Hoeks SE, Flu WJ, et al. Relation between preoperative and intraoperative new wall motion abnormalities in vascular surgery patients: a transesophageal echocardiographic study. Anesthesiology. 2010;112:557-566.

Landesberg G, Beattie WS, Mosseri M, et al. Perioperative myocardial infarction. Circulation. 2009;119:2936-2944.

Lonjaret L, Lairez O, Minville V, et al. Optimal perioperative management of arterial blood pressure. Integr Blood Press Control. 2014;7:49-59.

Subramaniam B, Subramaniam K. Not all perioperative myocardial infarctions can be prevented with preoperative revascularization. Anesthesiology. 2010;112:524-526.

A.5. What is the incidence of perioperative reinfarction for noncardiac surgery?

The risk assessment for noncardiac surgery of patients with CAD is based upon the time interval between the MI and surgery. Using a discharge database of more than half million patients, it was shown that postoperative MI rate for the recent MI cohort decreased substantially as the length of time from MI to operation increased (0 to 30 days = 32.8%; 31 to 60 days = 18.7%; 61 to 90 days = 8.4%; and 91 to 180 days = 5.9%), as did 30-day
mortality (0 to 30 days = 14.2%; 31 to 60 days = 11.5%; 61 to 90 days = 10.5%; and 91 to 180 days = 9.9%). MI within 30 days of an operation was associated with a highest risk of postoperative MI. However, with improvements in perioperative care, this difference has become blurred. The importance of the timing of the MI in relation to the proposed surgical procedure may no longer be valid in the era of thrombolytics, angioplasty, and risk stratification. Although many patients with a history of an MI may continue to have myocardium at risk, others may not. If a stress test does not indicate residual myocardium at risk, the likelihood of reinfarction is low. The current AHA/ACC guidelines for perioperative cardiovascular evaluation suggests that more than 60 days should elapse after MI, before noncardiac surgery is undertaken in the absence of coronary intervention. Landesberg et al. reported that early mortality after PMI ranges from 3.5% to 25% and is higher among patients with marked troponin elevation compared with patients with minor troponin elevation (0% to 7%). This is in contrast to older data that reported a very high incidence of mortality.

Landesberg G, Beattie WS, Mosseri M, et al. Perioperative myocardial infarction. Circulation. 2009;119: 2936-2944.

Li SL, Wang DX, Wu XM, et al. Perioperative acute myocardial infarction increases mortality following noncardiac surgery. J Cardiothorac Vasc Anesth. 2013;27:1277-1281.

Livhits M, Ko CY, Leonardi MJ, et al. Risk of surgery following recent myocardial infarction. Ann Surg. 2011;253:857-864.

A.6. State the perioperative medical therapy you would employ to reduce the incidence of myocardial ischemia.

β-Adrenergic Antagonists (Esmolol, Atenolol, Metoprolol, Bisoprolol)

These drugs reduce myocardial oxygen consumption, improve coronary blood flow by prolonging diastolic perfusion period, improve supply/demand ratio, stabilize cellular membranes, improve oxygen dissociation from hemoglobin, and inhibit platelet aggregation. β-Blockers suppress perioperative tachycardia and appear most efficacious in preventing perioperative myocardial ischemia. In view of their beneficial effects, prophylactic use of β-blocker to decrease PMI has been explored in many trials. Mangano et al. reported a beneficial effect of atenolol in a randomized double-blind, placebo-controlled trial on overall survival and cardiovascular morbidity in noncardiac surgery patients with or at risk for CAD. Poldermans et al. reported that the β-blocker, bisoprolol, reduced the perioperative incidence of death from cardiac causes and nonfatal MI in vascular surgical patients with known CAD. Bisoprolol, started before noncardiac surgery (30 days), can substantially reduce perioperative cardiac complications in all but the highest risk patients. However, results of subsequent large trials have not shown efficacy of high-dose, acutely administered, perioperative β-blockers to reduce overall mortality in patients undergoing noncardiac surgery. The largest of these trials, the PeriOperative ISchemic Evaluation (POISE) study, did show better perioperative cardiac outcomes with β-blocker use; however, increased mortality and stroke rate also was noted in the β-blocker group. ACC/AHA has conducted a systematic review on the topic, and the main findings are (1) preoperative use of β-blockers was associated with a reduction in cardiac events in the studies examined, but few data support the effectiveness of preoperative administration of β-blockers to reduce the risk of surgical death; and (2) a clear association exists between β-blocker administration and adverse outcomes, such as bradycardia and stroke. Currently, the only class I recommendation for perioperative β-blockers use is to continue their use in the patients who are already on β-blockers (class I, level of evidence B). β-Blockers can be used in patients with elevated risk, such as ischemia during preoperative stress testing or in patients with three or more RCRI risk factors (class IIb, level of evidence B). Although there are some differences between the ESC and the AHA guidelines, both recommend that if β-blockers are used for prophylactic purposes, they should be slowly titrated (2 to 7 days prior to elective surgery) and acute administration of high-dose β-blockers in high-risk patients undergoing low-risk surgery is not recommended (class III, level of evidence B).

α₂-Adrenergic Agonist (Clonidine)

α₂-Agonist (clonidine) decrease sympathetic outflow, blood pressure, and heart rate. Although older studies suggested possible beneficial effect of α₂-agonists, the most recent POISE-2 trial that enrolled 10,010 patients did not show any statistically beneficial effect of clonidine. Clonidine did not reduce the rate of 30-day risk of all-cause death or nonfatal MI in patients with or at risk of atherosclerotic disease who were undergoing noncardiac surgery. Clonidine did increase the rate of nonfatal cardiac arrest and clinically important hypotension. Based on the ACC/AHA guidelines, α₂-agonists for prevention of cardiac events are not recommended in patients who are undergoing noncardiac surgery (class III, level of evidence B).

Nitrovasodilators (Nitroglycerin, Isosorbide Dinitrate)

Nitrates are associated with the following:

Decreased LV preload (low dose)
- Systemic venous dilation
- Pulmonary arterial bed dilation
- Pulmonary vein dilation
- Decreased LV filling pressure
- Decrease in LV diastolic compressive forces
- Decreased LV diastolic chamber size
Decreased LV afterload (high dose)
- Decreased systolic pressure
- Decreased systemic vascular resistance
- Decreased aortic impedance
Coronary circulation
- Coronary artery and arteriolar dilation (high dose)
- Spasm reversal or prevention
- Stenosis dilation
- Increased collateral flow
- Improvement of regional subendocardial ischemia

NTG, one of the oldest antianginal therapies, has had very few trials in noncardiac surgery to evaluate its role in perioperative ischemia reduction. However, there are no significant studies within the past 10 years examining the effect of prophylactic NTG on perioperative myocardial ischemia. Prior studies yielded conflicting results, were small (<50 patients), and not blinded. The current guidelines do not recommend the use of prophylactic intravenous NTG to reduce myocardial ischemia undergoing noncardiac surgery.

Calcium Channel Blockers (Verapamil, Diltiazem, Nifedipine, Nicardipine)

Calcium channel blockers reduce myocardial oxygen demand by depression of myocardial contractility and dilation of coronary and collateral vessels, which improves blood flow. However, the most important effect may be the prevention of sympathetically mediated coronary vasoconstriction.

A meta-analysis of perioperative calcium channel blockers in noncardiac surgery (11 studies involving 1,007 patients) showed significantly reduced ischemia and postoperative supraventricular tachycardia. The beneficial effects were mostly due to the use of diltiazem, whereas the use of a 1,4-dihydropyridine (DHP) derivative nifedipine was associated with ischemia. Another study in 1,000 patients having acute or elective aortic aneurysm surgery showed that DHP calcium channel blocker use was independently associated with an increased incidence of perioperative mortality. The use of short-acting DHP, in particular nifedipine capsules, should be avoided. The AHA makes no specific recommendations for the prophylactic use of calcium channels blockers. Routine use of calcium channel blockers to reduce the risk of perioperative cardiovascular complications is not recommended (class III).

Aspirin

Aspirin (acetylsalicylic acid) inhibits platelet aggregation by blocking the production of thromboxane A₂. Observational data suggest that preoperative withdrawal of aspirin increases thrombotic complications. However, the value of aspirin in nonstented patients in preventing
ischemic complications is uncertain. The Pulmonary Embolism Prevention (PEP) trial, which randomized 13,356 patients undergoing hip surgery to 160 mg aspirin or placebo, did not show benefit of aspirin. The POISE-2 trial randomized 10,010 patients who were undergoing noncardiac surgery to aspirin 200 mg or placebo. Aspirin did not have a protective effect for MACE or death in patients either continuing aspirin or starting aspirin. However, aspirin increased the chance of major bleeding especially in the first 5 days after surgery. This is supported by a previous large meta-analysis, including 41 studies in 49,590 patients, which compared periprocedural withdrawal versus bleeding risks of aspirin, concluded that the risk of bleeding complications was increased by 1.5, but that aspirin did not lead to higher severity levels of bleeding complications. Initiation of aspirin is not beneficial in patients undergoing elective noncardiac, noncarotid surgery who have not had previous coronary stenting, unless the risk of ischemic events outweighs the risk of surgical bleeding.

Statins

Statins are primarily used for their lipid-lowering effects and are widely prescribed in patients with or at risk for IHD. Statins also induce coronary plaque stabilization by decreasing lipid oxidation, inflammation, matrix metalloproteinase, and cell death. These so-called non-lipid or pleiotropic effects may prevent plaque rupture and subsequent MI in the perioperative period. A meta-analysis of 223,010 patients from 12 retrospective and 3 prospective trials showed that statins reduced mortality significantly by 44% in noncardiac surgery and by 59% in vascular surgery. The accumulated evidence to date suggests a protective effect of perioperative statin use on cardiac complications during noncardiac surgery. Most of the data come from observational studies. The time of initiation of statin therapy and the duration of therapy are often unclear in the observational trials. Randomized clinical trials are limited in patient numbers and types of noncardiac surgery. Both the AHA and ESC guidelines recommend continuing statin therapy for patients currently taking statins and scheduled for noncardiac surgery (class I). ESC recommends that preoperative statin therapy should be considered in patients undergoing vascular surgery and initiated at least 2 weeks before surgery.

Devereaux PJ, Mrkobrada M, Sessler DI, et al. Aspirin in patients undergoing noncardiac surgery. N Engl J Med. 2014;370(16):1494-1503.

Devereaux PJ, Sessler DI, Leslie K, et al. Clonidine in patients undergoing noncardiac surgery. N Engl J Med. 2014;370(16):1504-1513.

Devereaux PJ, Yang H, Yusuf S, et al. Effects of extended-release metoprolol succinate in patients undergoing non-cardiac surgery (POISE trial): a randomised controlled trial. Lancet. 2008;371:1839-1847.

Mangano DT, Layug EL, Wallace A, et al. Effect of atenolol on mortality and cardiovascular morbidity after noncardiac surgery. N Engl J Med. 1996;335:1713-1720.

Poldermans D, Boersma E, Bax JJ, et al; for Dutch Echocardiographic Cardiac Risk Evaluation Applying Stress Echocardiography Study Group. The effect of bisoprolol on perioperative mortality and myocardial infarction in high-risk patients undergoing vascular surgery. N Engl J Med. 1999;341:1789-1794.

Prevention of pulmonary embolism and deep vein thrombosis with low dose aspirin: pulmonary embolism prevention (PEP) trial. Lancet. 2000;355:1295-1302.

Schouten O, Boersma E, Hoeks SE, et al. Fluvastatin and perioperative events in patients undergoing vascular surgery. N Engl J Med. 2009;361:980-989.

Wallace AW, Galindez D, Salahieh A, et al. Effect of clonidine on cardiovascular morbidity and mortality after noncardiac surgery. Anesthesiology. 2004;101:284-293.

A.7. Based on his MI, would you recommend that the surgery be postponed for a certain period of time? If so, why?

The arbitrary delaying of a surgical procedure is not supported by the ACC/AHA guidelines. According to these guidelines, an acute MI (≤7 days) or recent MI (>7 days but ≤1 month) with evidence of important ischemic risk by clinical symptoms or noninvasive study is a
major predictor of PMI. A discharge database analysis showed that patients with a recent MI who were revascularized before surgery had an approximately 50% decreased rate of reinfarction (5.1% vs. 10.0%). Thirty-day (5.2% vs. 11.3%) and 1-year mortality (18.3% vs. 35.8%) was also decreased in the revascularized patients. Current management of MI provides for risk stratification during the convalescence period. If a recent stress test does not indicate residual myocardium at risk, the likelihood of reinfarction after noncardiac surgery is low. Although there are no adequate clinical trials on which to base firm recommendations, it appears reasonable to wait 60 days after MI in a nonrevascularized patient to perform elective surgery due to the decrease in incidence of fatal arrhythmias and ventricular rupture after this period of time. However, the guidelines do not recommend that routine coronary revascularization be performed before noncardiac surgery exclusively to reduce perioperative cardiac events (class III, level of evidence B).

Devereaux PJ, Chan MT, Alonso-Coello P, et al. Association between postoperative troponin levels and 30-day mortality among patients undergoing noncardiac surgery. JAMA. 2012;307:2295-2304.

Fleisher LA, Fleischmann KE, Auerbach AD, et al. 2014 ACC/AHA guideline on perioperative cardiovascular evaluation and management of patients undergoing noncardiac surgery: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2014;130:e278-e333.

A.8. Would you recommend that this elective colectomy be postponed, if the patient underwent placement of a right coronary artery, second-generation DES, and is taking aspirin and clopidogrel (Plavix)?

Coronary stents are particularly predisposed to stent thrombosis. Typically, stent thrombosis is defined according to the time of occurrence: (1) acute, within 24 hours; (2) early, 2 to 30 days; (3) late, >1 month to <1 year; and (4) very late, >1 year. Both bare metal stents (BMS) and DES are predisposed to stent thrombosis and require prolonged DAPT after stent placement: BMS, 4 to 6 weeks; DES, 12 months; and stents placed after acute coronary syndrome (ACS), 12 months. Second-generation DESs may require a minimum of 6 months DAPT after stent placement; however, data in this area is still evolving.

The cumulative incidence of noncardiac surgery after coronary stenting is more than 10% at 1 year and more than 20% at 2 years. Patients with a coronary stent pose a special challenge in the perioperative period. Bleeding is the major risk of continuing DAPT during the perioperative period. Surgical blood loss is increased 2.5% to 20% by aspirin alone and 30% to 50% by aspirin and clopidogrel—but with no increased risk of bleeding-related mortality, except during intracranial surgery. When surgery was performed within 180 days, discontinuation of DAPT was associated with an increased risk of stent thrombosis. Extremely high mortality rates (up to 20%) have been reported secondary to acute stent thrombosis if surgery is performed within weeks after coronary stenting with discontinuation of DAPT. Thus, the risks of stent thrombosis and bleeding should be balanced. Antiplatelet therapy should generally be continued throughout the perioperative period, except in cases where the risk of morbidity or mortality from bleeding significantly outweighs the risk of acute stent thrombosis, as in procedures likely to be associated with “major” blood loss or performed in a closed space.

Current recommendations for DAPT after percutaneous coronary intervention (PCI) with stenting (BMS) is that patients should take aspirin and other P2Y₁₂ platelet inhibitor (clopidogrel, prasugrel, ticagrelor) for at least 30 to 45 days to prevent restenosis and allow reendothelialization of the stent to be completed. Therefore, it is prudent to postpone the elective surgery for a minimum of 30 days and ideally for up to 3 months after BMS implantation (ESC guidelines). Importantly, whenever possible, aspirin should be continued throughout surgery. A large meta-analysis, including 41 studies in 49,590 patients, which compared periprocedural withdrawal versus bleeding risks of aspirin, concluded that the risk of bleeding complications with aspirin therapy was increased by 50%, but that aspirin did not lead to greater severity of bleeding complications. In subjects at risk of—or with proven—IHD, nonadherence/withdrawal of aspirin tripled the risk of MACE.

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