Up to 60% of patients undergoing vascular surgery have significant CAD. Two major mechanisms underlie perioperative myocardial infarction: Surgery-induced procoagulant state may lead to coronary thrombosis over a ruptured or even a non-ruptured lesion, particularly if the stenosis is tight with a low flow state. Overall, each one of the two mechanisms is primarily responsible for ~50% of postoperative MIs.1 A combination is likely responsible for MI in a substantial proportion of patients. Most events occur in the first 24–48 hours postoperatively, the period of highest sympathetic tone. The infarct is most commonly NSTEMI/non-Q-wave MI. In a series of 21 patients who underwent preoperative coronary angiography and developed postoperative MI after vascular surgery, slightly over half of the infarcts corresponded to the territory of a totally occluded coronary artery, in which collaterals could not provide enough supply during a period of high stress; additionally, those patients had severe multivessel disease, potentially impairing collateral flow.3 The remaining infarcts occurred in the territory of a non-significant lesion, in patients who nonetheless had extensive atherosclerosis. This highlights not only the frequency of demand/supply mismatch, but also the fact that plaque rupture may very well occur at non-obstructive sites. The overall extent of CAD correlates with the risk of events and plaque rupture; however, the infarct does not necessarily occur at the actual site of severe stenosis. In fact, a non-obstructive lesion may be vulnerable (high plaque burden, thin cap). This explains why revascularization does not prevent postoperative MI. According to the ACC/AHA 2014 preoperative guidelines,4 the cardiac evaluation for noncardiac surgery is based on the assessment of (1) active cardiac conditions, (2) known cardiovascular disease and cardiac risk factors, and (3) functional capacity in metabolic equivalents (METs). Active cardiac conditions: These patients need to have their cardiac condition treated before surgery, depending on the urgency of the surgery (PCI for ACS, medical therapy for HF, surgical therapy for symptomatic, severe valvular disease). In case of an emergent surgery, proceed to the high-risk surgery with maximal medical therapy. The Lee index includes six factors:5 Note that preoperative testing is mainly useful to assess how risky the surgery will be and to see whether it should be avoided or altered, if possible. Testing is only performed if it will change management, i.e., if surgery can be deferred. Preoperative testing is, therefore, much less useful in patients who require a necessary, vital surgery (e.g., cancer surgery). A high-risk finding on preoperative testing indicates preoperative coronary angiography only if preoperative revascularization is feasible, i.e., surgery can be deferred and the patient can tolerate an antithrombotic regimen. If extensive CAD is present (left main or multivessel CAD), revascularization, typically CABG, should generally be performed before a non-vital elective surgery (class I recommendation). This revascularization is mainly meant to improve the long-term cardiac risk of the patient. Outside ACS or left main disease, preoperative revascularization does not clearly change the operative cardiac risk (CARP trial), even in high-risk ischemic patients with at least five abnormal segments on stress imaging (LV being divided into 17 segments).5,6 There is no evidence that PCI of a single- or two-vessel disease improves perioperative outcomes, outside ACS. The surgery is classified into one of three risk categories: The risk of perioperative major cardiac events (death or MI) is generally ≤1% with low-risk surgery, regardless of the underlying patient’s risk; and is generally 1–5% with intermediate-risk surgery and 5% with high-risk surgery, although the actual risk of intermediate- and high-risk surgeries also depends on the patient’s intrinsic risk (Lee risk score). For example, a low-risk patient undergoing major vascular surgery has <2–5% risk of major cardiac events. In the presence of an active cardiac condition (Section I.B, above), the patient is a high-risk patient. In the absence of an active condition, a Lee risk score ≥3 identifies high-risk stable patients, a score of 2 identifies intermediate-risk patients, while a score of 0 or 1 identifies low-risk patients. The risk of postoperative major adverse cardiac events (MACE) (MI, VF or primary cardiac arrest, or definite pulmonary edema) in high-, intermediate-, and low-risk patients is ≥9%, 4–5%, and 0.5–1.3%, respectively.7 A high-risk stress test result (stress echo or nuclear stress test) is associated with a 10–25% risk of perioperative death or MI, while a normal stress test result is associated with a 0–4% (~2%) risk of death or MI.4 Therefore, a low-risk stress test steps down the risk in a patient with a high Lee index, but the absolute risk may remain significant. The CARP and DECREASE V trials have shown that patients with established but stable CAD, including multivessel/triple-vessel CAD, who are undergoing high-risk vascular surgery, do not benefit from revascularization preoperatively. In the CARP trial, 509 intermediate-to-high-risk patients (by Lee risk score or stress testing) undergoing vascular surgery (33% AAA) and found to have CAD on coronary angiography were randomized to medical therapy or coronary revascularization (59% CABG, 41% PCI). Surgery was delayed a median of 6 weeks after revascularization. The postoperative risk of death was ~3% in both groups, and MI rate was ~8% (high MACE risk not modified by revascularization).6 In DECREASE V trial of patients with extensive baseline ischemia (≥ 5/17 segments), the MACE risk was high but unchanged with revascularization. This is related to the fact that postoperative MI in a CAD patient may result from a plaque rupture occurring at the site of an obstructive lesion but also frequently a non-obstructive one. Moreover, preoperative revascularization is associated with its own set of complications, such as stent thrombosis. Therefore, the usefulness of preoperative coronary revascularization in patients not having active ACS is not established, even in high-risk subgroups with strongly positive stress tests.7 Preoperative coronary testing may be useful to show the general prognosis of the patient. A high surgical risk based on preoperative stress testing may lead to a change in management but not necessarily revascularization. It should lead to a risk/benefit discussion with the patient, with a potential cancellation of non-vital surgery and consideration of percutaneous angioplasty for PAD or endovascular repair of abdominal aortic aneurysm, even if the result is expected to be inferior to surgery. Preoperative coronary testing is much less useful in patients who require a vital surgery, such as cancer surgery. The highest-risk patients are those with MI in the last month with persistent ischemia clinically or on stress testing. Stenting, however, is associated with several pitfalls: Surgery soon after stenting (2 weeks) may lead to catastrophic results, with a high risk of death and MI. In one analysis, death (mostly secondary to stent thrombosis, and partly secondary to bleeding) occurred in 32% of patients who underwent surgery <2 weeks after stenting, and in four out of five patients who underwent surgery 1 day after stenting.11 One or both antiplatelet agents were only briefly interrupted before surgery (~1 day), and interruption of antiplatelet therapy may therefore not have been solely responsible for this high rate of stent thrombosis. Bleeding was also very common, and early post-PCI bleeding is known to be associated with MI and stent thrombosis. If percutaneous revascularization needs to be performed preoperatively, dual antiplatelet therapy is given and surgery is postponed for at least 1 month after bare-metal stent (BMS) and 3 months, preferably 6 months, after drug-eluting stent (DES) (class I for antiplatelet interruption at 6 months, IIb at 3 months). Three trials suggest that interruption of ADP-receptor antagonist at 1 month is as safe with DES as with BMS ; 2 other trials suggest that, after DES, interruption at 1 month is as safe as 6 months (Chapter 1, VI). Hence, the preference for BMS in this setting is obsolete . If surgery is needed more urgently (<4 weeks), balloon angioplasty is performed without any stenting if possible, and stenting is only done as a bailout for complicated angioplasty. Surgery can be performed 2–4 weeks after balloon angioplasty; there is a risk of acute vessel thrombosis with earlier surgery.
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Preoperative Cardiac Evaluation
I. Steps in preoperative evaluation
A. First step: if the surgery is emergent, no cardiac workup is performed preoperatively
B. Second step: if the surgery is not emergent, evaluate for active cardiac conditions
C. Third step: in the absence of active cardiac conditions, look for clinical risk factors, and use the revised cardiac risk index or Lee index
II. Surgical risk: surgery’s risk and patient’s risk
A. Classification of the surgery’s risk
B. Classification of the patient’s overall risk (integrates the surgery’s risk with the patient’s risk factors)
C. Risk of MACE according to stress testing results
III. CARP and DECREASE V trials
Caveats
IV. Only the highest-risk coronary patients require revascularization preoperatively
V. Preoperative percutaneous revascularization
VI. Surgery that needs to be performed soon after stent placement