Heart Disease

Heart Disease

3.1 Ischemic Heart Disease

Giora Landesberg

Ischemic heart disease (IHD) has a major impact on perioperative mortality and morbidity. It is important to understand the different presentations of IHD, how to assess the severity of IHD, when to order specialized tests, when to request cardiology consultation, what specifically to ask the cardiologist, or to determine if additional coronary interventions are warranted before proceeding with major surgery. Published guidelines and consensus documents for preoperative cardiac evaluation can assist the practitioner (1,2,3).


In order to prevent perioperative cardiac complications, it is important to understand the pathophysiology of cardiac complications. The most recent Third Universal Definition of Myocardial Infarction defines myocardial infarction (MI) by a rise and/or fall of cardiac biomarkers, preferably cardiac troponin, with at least one value >99th percentile upper reference limit and >1 of the following: ischemic symptoms, new ischemic electrocardiogram (ECG) changes or imaging evidence of new nonviable myocardium or new regional wall motion abnormalities (WMAs). Electrocardiographically there are two types of MI:

Unlike NSTEMI, STEMI patients benefit from immediate (within 3 hours) coronary intervention, usually with percutaneous coronary intervention (PCI) or thrombolysis. NSTEMI patients usually undergo coronary angiography within days of their symptom onset, after initiation of medical treatment and risk stratification. This difference is because there is typically a culprit coronary lesion causing a STEMI, while often there are multiple lesions without a clear culprit in a patient with an NSTEMI. Postoperatively, STEMI is rare and NSTEMI is ≥15 times more common than STEMI (4,5). It is unusual to have postoperative patients who require urgent coronary intervention.

The Universal Definition of MI recognizes two main pathophysiologic types of MI (6):

  • Type 1 is a spontaneous MI related to ischemia due to a primary event such as plaque erosion, rupture, fissuring, or dissection.

  • Type 2 is an MI with ischemia due to an imbalance between myocardial oxygen supply and demand resulting from prolonged tachycardia, coronary spasm, anemia, or hypotension.

A type 1 event can lead to STEMI and NSTEMI, whereas type 2 events lead almost exclusively to NSTEMI. Postoperative MIs are mostly type 2 MIs and mostly NSTEMIs. This differentiation is important for preoperative cardiac assessment because type 1 MIs are spontaneous, unpredictable, and occur even in arteries with <50% occlusion. Plaque stabilization, such as provided with statin therapy, is expected to have the greatest impact on type 1 MIs (7,8). Importantly, acute stent thrombosis results in type 1 MI that is preventable (Fig. 3.1). In contrast, the more common type 2 MI occurs mainly with severe yet stable coronary artery disease (CAD). Even chronic total occlusions with poor collaterals are associated with type 2 postoperative MI, morbidity, and mortality (9,10).


Postoperative MI occurs in up to 8% of very high-risk patients, but troponin elevations occur in >20% of high-risk patients. Many of the postoperative troponin elevations are asymptomatic, without evidence of ischemia on ECG, and can therefore be termed myocardial injuries. Perioperative myocardial injury is associated with significantly increased 30-day and up to 5-year postoperative mortality (11,12). Routine postoperative troponin measurements in high-risk patients have been advocated with the hope that better management will reduce morbidity and mortality (3,13). To date, neither routine monitoring with troponins nor interventions to lower risk are substantiated by evidence (5). The pathophysiology of silent troponin elevations is unclear; it is the bias of this author that it is similar to silent type 2 MI and occurs mainly in patients with significant, yet stable CAD who sustain postoperative prolonged myocardial oxygen supply-demand imbalance (14,15).


The main symptom of heart failure (HF) is shortness of breath (SOB). There are two types of HF:

  • Systolic HF or HF with reduced ejection fraction

  • Diastolic HF or HF with normal (or preserved) ejection fraction

In ischemic HF, systolic and diastolic HF can be chronic, or acute (as a result of acute ischemia). Severe chronic HF is often associated with sustained troponin elevation, and acute HF is often accompanied by acute troponin release (as in type 2 MI). Both are markers of worse prognosis. Echocardiography is the most important tool for diagnosing systolic and diastolic HF. See Chapter 3.4 for more discussion of HF.


Some patients present for elective surgery with overt IHD with a history of stable angina, an abnormal stress test or angiography, previous MI or coronary revascularization. Others have silent IHD, typically with risk factors for CAD, but no clear history of ischemia. These patients are more likely to be diabetic, elderly, or have vascular disease. Patients with silent IHD have the same risk of perioperative complications as patients with overt IHD with a similar extent of CAD. The perioperative significance of CAD is determined based on the patient’s risk factors, functional capacity, planned procedure, and additional diagnostic tests.

Figure 3.1 Pathophysiology of perioperative myocardial infarction. (Adapted from Landesberg G, Beattie WS, Mosseri M, et al. Perioperative myocardial infarction. Circulation. 2009;119:2936-2944.)

A patient who presents with an acute MI, unstable (recent onset or crescendo) angina, decompensated HF, or serious, life-threatening arrhythmias is considered to have an acute coronary syndrome (ACS). These patients are not suitable for elective surgery and are referred for cardiac consultation and stabilization. Elective surgery is best delayed if possible for 60 days post-MI per the ACC/AHA guidelines (1).

Some patients will have undergone recent coronary revascularization with either PCI or coronary artery bypass grafting (CABG). Timing of surgery depends on several parameters including urgency and type of planned surgery and the conditions of revascularization. Patients who underwent successful CABG may proceed with noncardiac surgery after 30 days, or less if the surgery is urgent. Patients having angioplasty without stenting benefit from 2 weeks of dual antiplatelet therapy (DAPT) before having surgery (16). Those receiving bare-metal stents (BMS) may undergo surgery after 4 weeks of DAPT, if no myocardial damage has occurred. Delay surgery for 6 months in patients who receive drug-eluting stents (DES) to complete the required course of DAPT. See Chapter 3.2 for a detailed discussion of stents. Success and completeness of revascularization, the location of stents in the coronary tree, and left ventricular function are among the important factors that determine the associated risk of non-cardiac surgery.


In most cases, decisions can be made based on a careful history and physical examination, which includes assessment of the following:

  • Angina pectoris—a determination of whether it is stable or unstable, occurs with exertion or at rest, and the Canadian Cardiovascular Society (CCS) grade of angina (Table 3.1) (17). Associated symptoms such as radiation of the pain, nausea, near syncope, SOB, and the level of exertion precipitating chest pain are important.

  • History of MI—determining the number of MIs and dates of occurrence, and the location of MI by information from an ECG, echocardiography, stress test, or angiography. Documenting the ejection fraction (EF), the amount of myocardial damage during the MI, residual coronary lesions, and the therapeutic regimen is necessary.

  • Determining coronary angiography and interventions; number and dates of CABG or PCI, use of DES or BMS, including which coronary arteries were treated, and recurrence of symptoms after last intervention are important.

    TABLE 3.1 CCS Grading of Angina Pectoris

    • Class I—Angina only during strenuous or prolonged physical activity

    • Class II—Slight limitation, with angina only during vigorous physical activity

    • Class III—Symptoms with everyday living activities, i.e., moderate limitation

    • Class IV—Inability to perform any activity without angina or angina at rest, i.e., severe limitation

    Class 0 has also been proposed as an asymptomatic category (1).

    From Canadian Cardiovascular Society (CCS) grade of angina. Used with permission from The Canadian Journal of Cardiology and the Canadian Cardiovascular Society.

    TABLE 3.2 NYHA Classification of Heart Failure

    NYHA Class



    Cardiac disease, but no symptoms and no limitation in ordinary physical activity (e.g., no shortness of breath when walking, climbing stairs)


    Mild symptoms (mild shortness of breath or angina) with slight limitation during ordinary activity


    Marked limitation in activity due to symptoms, even during less than ordinary activity (e.g., walking short distances such as 20-100 meters). Comfortable only at rest


    Severe limitations. Experiences symptoms even while at rest. Mostly bedbound patients

    From Yancy CW, Jessup M, Bozkurt B, et al. 2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. 2013;128:e240.

  • History of HF—determine whether HF is systolic, diastolic, or a combination, the degree of HF based on the New York Heart Association (NYHA) classification (Table 3.2) and EF (18). Exploring whether the patient has been hospitalized for HF, the exercise capacity and treatments are important. Examining the patient for pulmonary edema and signs of left or right HF is needed.

  • Functional capacity—by asking a very simple question: “Can you climb two flights of stairs without stopping and without chest pain or SOB?” the examiner can get an estimate of the functional capacity of the patient. Those with an average functional capacity, defined as ≥4 metabolic equivalents (METs), have a low risk of MACE during the vast majority of moderate- to high-risk operations. Being able to exercise without symptoms does not rule out CAD, but if present, the CAD is not likely to be severe. Patients who are asymptomatic with ≥4 METs of activity (e.g., climbing two flights of stairs or walking two to four blocks on a level surface) typically have enough cardiac and coronary reserves for most major operations. This is a strong predictor but not helpful in patients with functional limitations due to noncardiac conditions. Another conundrum is the patient with SOB. This nonspecific symptom may indicate myocardial ischemia but also poor physical fitness or deconditioning and other comorbidities such as obesity, HF, or pulmonary dysfunction. In these situations, more specific tests may be needed (see Chapters 2.4 and 13.2.)


The risk factors for IHD are well known: older age, hypertension, diabetes mellitus, smoking, hyperlipidemia, and a family history of IHD. Numerous studies used multivariate models to develop cardiac risk indices based on simple preoperative clinical findings that predict cardiac morbidity and mortality following noncardiac surgery. Some of the most important are summarized in Table 3.3. Lee’s Revised Cardiac Risk

Index (RCRI) is based on six preoperative predictors (19). The risk of perioperative MACE increases with increasing number of predictors present: 0 predictors, 0.4%; 1 predictor, 0.9%; 2 predictors, 6.6%; ≥3 predictors, 11%. Despite its limitations, the RCRI is currently the most important metric in practice guidelines and research to assess high-risk patients before noncardiac surgery and for deciding who may benefit from further noninvasive testing. Wijeysundera found that noninvasive testing was associated with harm in low-risk patients (RCRI 0), no benefit in patients who were at intermediate risk of MACE (RCRI 1-2), and only beneficial for those at high risk (RCRI 3-6). The risk calculator developed from the National Surgical Quality Improvement Program (NSQIP) is designed to predict not only MACE but also allcause perioperative morbidity and mortality (20).

TABLE 3.3 Cardiac and Surgical Risk Indices

Goldman Index of Cardiac Risk (1977)

Revised Cardiac Risk Index (1999)

NSQIP Perioperative Ml and Cardiac Arrest (MICA) Risk Calculator (2011)

NSQIP Universal Surgical Risk Calculator (2013)


  • Jugular venous distention or a third heart sound on auscultation

  • Ml within 6 months

  • ≥5 PVCs per min

  • Non-sinus cardiac rhythm or PACs on preoperative ECG

  • Age >70 years

  • Aortic stenosis

  • Intraperitoneal, intrathoracic, or aortic surgery

  • Any emergency surgery

  • Cerebrovascular disease

  • Ischemic heart disease

  • History of heart failure

  • Insulin therapy for diabetes mellitus

  • Serum creatinine ≥2.0 mg/dL

  • Planned highrisk procedure (intraperitoneal, intrathoracic, or major vascular surgery)

  • Age

  • ASA class

  • Creatinine ≥1.5 mg/dL

  • Preoperative functional status

  • Procedure type (anorectal surgery, aortic, bariatric, brain, breast, cardiac, ENT (except thyroid/parathyroid), foregut/hepatopancreatobiliary, gallbladder/appendix/adrenal/spleen, hernia, intestinal, Neck (thyroid/parathyroid) obstetric/gynecologic, Orthopedic and non-vascular Extremity, other abdominal, peripheral vascular, skin, spine, non-esophageal thoracic, urology, vein)

  • Age

  • Sex

  • Functional status

  • Emergency case

  • ASA class

  • Steroid use for chronic condition

  • Ascites within 30 days

  • System sepsis within 48 hours

  • Ventilator dependent

  • Disseminated cancer

  • Diabetes mellitus

  • Hypertension requiring medication

  • Heart failure in 30 days

  • Dyspnea

  • Current smoker within 1 year

  • Severe COPD

  • Dialysis

  • Acute renal failure

  • BMI class

  • CPT-specific linear risk


Intraoperative/postoperative Ml, pulmonary edema, VT, cardiac death

Ml, pulmonary edema, ventricular fibrillation, complete heart block, cardiac death

Intraoperative/postoperative Ml or cardiac arrest within 30 days

Cardiac arrest, Ml, all-cause mortality within 30 days

Derivation set ROC



0 88

0.90 (cardiac arrest or Ml), 0.94 (mortality)

Validation set ROC




Not reported

ASA, American Society of Anesthesiologists; BMI, body mass index; C0PD, chronic obstructive pulmonary disease; CPT, current procedural terminology; ECG, electrocardiogram; ENT, ear nose and throat; Ml, myocardial infarction; NSQIP, National Surgical Quality Improvement Program; ROC, area under the receiver operating characteristic curve (C statistic); PAC, premature atrial contractions; PVC, premature ventricular contraction; and VT, ventricular tachycardia

From 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.


Preoperative Resting ECG

Although chronic pathologic ECG changes are associated with risk for perioperative cardiac events, they do not independently predict events. A preoperative ECG may be indicated in patients with risk factors or history of CAD, abnormal heart rates, arrhythmias, or conduction defects. In IHD patients, an ECG offers prognostic information and is predictive of long-term outcome, independent of clinical findings and perioperative ischemia (21). The ECG has not been shown to independently predict perioperative MACE. An ECG may be normal or nonspecific in patients with myocardial ischemia or even with infarction. Most ECG changes represent chronic patterns of injury or aging.

Suspected new ECG changes require comparison with an older ECG. Pathologic Q-waves represent old MI, and the more ECG leads with Q-waves, the wider is the territory of infarcted myocardium. Q-waves on resting preoperative ECG were an important part of the definition of IHD in Lee’s RCRI criteria, however they did not independently predict risk. Tall R waves and wide QRS complexes with or without ST-T changes and inverted T-waves may indicate myocardial hypertrophy or dilatation. Left ventricular hypertrophy and baseline ST segment depression on 12-lead ECGs are important markers of increased risk for MACE after major vascular surgery (22). Left bundle branch block (LBBB) has been shown to predict death or cardiac events following noncardiac surgery but had no added value over clinical predictors (23).

Recommendations from major guidelines vary on preoperative ECGs:

  • The 2014 ACC/AHA guidelines—preoperative resting 12-lead ECG is reasonable for patients with known coronary heart disease, significant arrhythmia, peripheral arterial disease, cerebrovascular disease, or other significant structural heart disease, except for those undergoing low-risk surgery (class IIa indication, level of evidence B) (1).

  • The 2014 European Society of Cardiology/European Society of Anaesthetists (ESC/ESA) guidelines—preoperative ECG is recommended for patients who have risk factor(s) and are scheduled for intermediate- or high-risk surgery (class I indication, level of evidence C) (2).

  • The 2017 Canadian Cardiovascular Society (CCS) guidelines do not recommend preoperative ECGs be done (3).

Despite the guidelines, it is the experience of this author that resting ECG is useful in males age above 40 or females above 50 who are scheduled for major surgery, in whom important, previously unrecognized ECG abnormalities are not infrequent.
In any case, clinical decisions and the need for additional preoperative tests are based on comprehensive clinical judgment that includes a patient’s history, physical examination, and functional capacity.


Routine preoperative echocardiography is not recommended. It is indicated to address a specific clinical question arising from the history, physical findings, ECG, or chest radiography (e.g., cardiomegaly). Echocardiography is indicated before major surgery to evaluate the significance of suspected:

  • Valvular disease, particularly aortic stenosis or mitral disease

  • Left or right ventricular systolic and/or diastolic dysfunction

  • Pulmonary hypertension

  • Cardiomyopathies (e.g., hypertrophic obstructive cardiomyopathy)

Resting echocardiography is not useful to evaluate CAD or the risk of perioperative myocardial ischemia or infarction. Echocardiography can provide valuable information in patients with poor functional capacity or define significant myocardial dysfunction or valvular disease. Regional WMAs on echocardiography are strong evidence for IHD and previous MI, even without a previous history.

Exercise Stress Test

An exercise stress test (EST) is a physiologic test to detect myocardial ischemia based on a defined protocol with a patient gradually increasing physical exertion on a treadmill or cycle ergometer. The test determines a patient’s functional capacity in METs, the hemodynamic response to exercise including maximally achieved heart rate, duration of exertion, and detects ischemia on continuous ECG or by imaging when combined with tomography or echocardiography. If a patient is able to exercise sufficiently without symptoms or ischemic ECG changes to achieve 85% of predicted heart rate which is required for completion of an EST, then further testing before planned surgery would is not indicated. The accuracy of an exercise ECG varies widely among studies and in populations with different pretest probability for CAD. A meta-analysis showed a low sensitivity (74%) and specificity (69%) for EST with ECG alone. The main disadvantage is its unsuitability for patients with low effort capacity such as patients with vascular, orthopedic, or neurologic problems, or an abnormal baseline ECG. The most recent 2014 ACC/AHA guidelines designate only a class IIb recommendation for preoperative EST (level of evidence: B) (1).

Myocardial Perfusion Imaging (MPI)

Myocardial perfusion imaging (MPI) using single photon emission tomography (SPECT) with thallium-201 or technetium-based agents is the most widely used noninvasive test for CAD. The test can be performed with physiologic (exercise on a treadmill or cycle ergometer) or pharmacologic (dipyridamole or adenosine) stress. Cardiac images acquired in a resting state are compared with the stressed state to differentiate fixed (e.g., infarct) from reversible (e.g., ischemia) perfusion defects detected by myocardial tracer uptake. The sensitivity and specificity of SPECT for detecting CAD with ≥50% stenosis are 88% and 61%, respectively (24). SPECT has a value in predicting long-term risk in patients with suspected CAD. SPECT also provides calculation of left ventricular ejection fraction (LVEF) during stress and rest. Transient LV
dilatation as well as increased lung uptake during stress indicate higher cardiac risk. A meta-analysis found that reversible ischemia in <20% of the myocardial segments did not change the likelihood of perioperative complications, but greater extents of reversibility of perfusion defects were associated with increased MACE in patients having vascular surgery (25). A normal SPECT scan may occur in up to 15% of patients (falsenegative rate) with left main disease or multivessel disease because of balanced ischemia. False-positive tests can occur due to attenuation artifacts in patients who are obese, have a left elevated diaphragm, or breast tissue.

Stress Echocardiography

Stress echocardiography assesses global and regional WMA during stress that is induced by increasing doses of dobutamine (DSE) or exercise. The great advantage of stress echocardiography is that it provides data on cardiac structure and function, both at rest and during maximum stress. However, numerous baseline WMAs or BBBs may cause difficulty in interpreting echocardiogram results. In a meta-analysis, the sensitivity of DSE was 83% in patients without prior MI but decreases to 74% in patients with prior MI (26). The specificity of DSE for detecting significant CAD is approximately 80%. A recent meta-analysis by Beattie and coworkers compared the value of DSE versus MPI in predicting postoperative MI or in-hospital death (27). This report included 25 studies (3373 patients) of mainly DSE, and 50 MPI studies with marked variability in results among the studies. The likelihood ratio for positive test was greater for DSE than for MPI, 4.1 vs. 1.8, respectively and the area under the ROC curve for the tests was 0.8 and 0.75, respectively. The 2014 ACC/AHA guidelines designate a class IIa recommendation for preoperative cardiac pharmacologic testing: “It is reasonable for patients who are at an elevated risk for non-cardiac surgery and have poor functional capacity (<4 METs) to undergo noninvasive pharmacological stress testing (either DSE or MPI) if it will change management (level of evidence: B)” (1).

Positron Emission Tomography

Cardiac positron emission tomography (PET) is a newer, more expensive modality that is not widely available. PET includes dual perfusion and metabolic imaging. Mismatch between perfusion and metabolism suggests viable ischemic areas, while matched reduction in both blood flow and metabolism suggest a nonviable infarct area. One meta-analysis showed that PET had a sensitivity of 92% and a specificity of 85% for detecting significant CAD (28). Its main utility is in symptomatic patients who have had coronary revascularization(s), and a question remains as to whether there is additional underperfused but viable myocardial tissue worth an intervention.

Cardiac Magnetic Resonance Imaging

Cardiac magnetic resonance imaging (MRI) may become the standard preoperative test in the future. Unlike SPECT and PET, cardiac MRI has excellent spatial resolution and can provide accurate information on transient (ischemia) or fixed (infarction) hypoperfusion and scar tissue, even in small areas of the subendocardium. Myocardial perfusion is imaged during the first pass of a bolus of gadolinium at rest, during “stress” (achieved by adenosine or dipyridamole), and late gadolinium enhancement. In a meta-analysis, cardiac MRI was shown to have better sensitivity (89%) and specificity (76%) than SPECT for detecting significant CAD (29). Contraindications to cardiac MRI include implanted metals; hypersensitivity to gadolinium; severe renal insufficiency with GFR
<30 mL/min/1.73 m2; severe asthma or chronic obstructive pulmonary disease; or sensitivity to the vasodilating agents, adenosine, and dipyridamole.

Computed Tomography Coronary Angiography

Computed tomography coronary angiography (CTCA) is an established noninvasive method for evaluating coronary anatomy and myocardial function. Studies show that CTCA has a high diagnostic accuracy for detecting coronary artery stenosis. A meta-analysis showed the sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) were 97%, 91%, 93%, and 96% compared with conventional coronary angiography (30). However, the specificity drops significantly (66%) in patients with coronary calcifications. One prospective study found that a higher RCRI, a coronary artery calcium score (CACS) >113, the presence of significant coronary artery stenosis, and multivessel CAD on CTCA are strong predictors of postoperative MACE (31). In another study of CTCA before noncardiac surgery, the risk of perioperative MACE was 14.0% in patients with significant CTCA findings (>3 lesions), as compared with 2.2% of patients without significant findings on CTCA regardless of their RCRI (32). CTCA may become a viable tool to rule out significant CAD (e.g., left main, proximal left anterior descending, or three-vessel disease) before major surgery. The utility of CTCA is limited in patients with renal dysfunction (creatinine clearance <40 mL/min/1.73 m2) due to the need for contrast, although with the faster CTCAs (256 slices/sec or higher), or when there is a significant amount of calcium in the coronaries the amount of contrast needed is reduced significantly.

Preoperative Coronary Angiography and Revascularization

If significant CAD is suspected by noninvasive testing in a patient scheduled for major surgery, the next question is whether to proceed with coronary angiography. One must weigh the potential benefits of a subsequent intervention (PCI or CABG) versus the risks and costs associated with the intervention and delaying the noncardiac surgery. Some retrospective studies suggested that preoperative coronary revascularization for patients having vascular surgery was associated with improved postoperative and long-term survival (33). The Coronary Artery Revascularization Prophylaxis (CARP) trial screened patients for cardiac risk before major vascular surgery and randomized 510 patients with ≥1 major coronary vessel with ≥70% stenosis present on angiography to either PCI or CABG or no revascularization (34). Patients were followed for a mean of 2.5 years after surgery, and there was no difference in survival among the groups. This trial had two important limitations. The screening process did not follow the ACC/AHA guidelines, and only a minority of the patients had evidence of severe ischemia on noninvasive testing, and those with left main CAD or severely reduced LVEF were excluded. Nevertheless, this trial had a strong impact worldwide on perioperative patient management by shifting the paradigm toward fewer coronary investigations and interventions before major noncardiac surgery. Moreover, this trial coincided with the COURAGE trial which showed that PCI in patients with stable CAD does not confer survival benefit over optimal medical treatment (35). Together, these studies supported that prophylactic PCI is not warranted before surgery in patients with stable CAD.

Subsequent publications utilizing the CARP data reported that patients who had CABG with more complete coronary revascularization had better survival than those
revascularized by PCI (36). Additionally, patients with left main disease, who were excluded from the trial, had markedly better survival with revascularization (37). Later, Monaco randomized patients with RCRI ≥2 scheduled for elective abdominal aortic surgery to either a “selective strategy” with coronary angiography only if their stress test was positive or to a “systematic strategy” with routine coronary angiography (38). The systematic strategy discovered 50% more patients with significant CAD than the selective strategy, who subsequently had more revascularizations (58% vs. 40%, respectively) and was associated with significantly improved long-term survival and freedom from MACE. While this small study supports prophylactic preoperative angiography and revascularization in patients at high clinical risk (RCRI ≥2), routine angiography without prior noninvasive screening is currently not an acceptable practice. Another large retrospective study suggested that patients with an MI within 3 years before surgery benefited from preoperative revascularization, and that CABG improved outcomes more than PCI with stents, especially when noncardiac surgery is necessary within 1 month of the revascularization (39).

The 2014 ACC/AHA update on Perioperative Cardiovascular Evaluation and Management of Patients Undergoing Noncardiac Surgery states: “Revascularization before non-cardiac surgery is recommended in circumstances in which revascularization is indicated according to existing clinical practice guidelines (CPGs).” (Class I indication, Level of Evidence: C) (1). The guidelines also state that: “It is not recommended that routine coronary revascularization be performed before noncardiac surgery exclusively to reduce perioperative cardiac events.” (Class III indication, Level of Evidence: B) (1).


Cardiac Troponins

Studies have shown that even minor elevations in troponins before surgery is associated with worse postoperative prognosis, although not as strongly as postoperative elevations (40). Some high-risk patients may have elevated serum levels of troponin, especially with the high-sensitivity troponin assay even before the stress of surgery. These are very elderly patients, patients with renal failure, HF, diabetes, or stable IHD (41). It is suggested therefore that the delta increase of troponin from baseline preoperative level be used to determine postoperative elevation.

Natriuretic Peptides

Similar to troponin, pre- and postoperative BNP or N-terminal (NT-proBNP) elevations are significantly associated with postoperative cardiac morbidity and mortality (3). Several meta-analyses show that among patients undergoing major vascular or nonvascular surgery, elevated natriuretic peptides independently predict MACE at 30 days and are better than the RCRI (42). As with troponin, postoperative natriuretic peptides are more predictive of MACE than the preoperative values (43). Authors suggest that a single preoperative elevation in BNP or NT-proBNP is highly predictive of MACE after noncardiac surgery, greater even than the RCRI. An NT-proBNP >300 ng/L and BNP ≥92 mg/L have been identified as significant thresholds associated with an increased risk of MACE. In particular, normal BNP or NT-proBNP levels have a very high negative predictive
value. Preoperative noninvasive and invasive testing in otherwise high-risk patients is deemed unnecessary in those with normal BNP or NT-proBNP level (3).


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25. Etchells E, Meade M, Tomlinson G, et al. Semiquantitative dipyridamole myocardial stress perfusion imaging for cardiac risk assessment before noncardiac vascular surgery: a meta-analysis. J Vasc Surg. 2002;36:534-540.

26. Geleijnse ML, Krenning BJ, van Dalen BM, et al. Factors affecting sensitivity and specificity of diagnostic testing: dobutamine stress echocardiography. J Am Soc Echocardiogr. 2009;22:1199-1208.

27. Beattie WS, Abdelnaem E, Wijeysundera DN, Buckley DN: A meta-analytic comparison of preoperative stress echocardiography and nuclear scintigraphy imaging. Anesth Analg. 2006;102:8-16.

28. Nandalur KR, Dwamena BA, Choudhri AF, et al. Diagnostic performance of positron emission tomography in the detection of coronary artery disease: a meta-analysis. Acad Radiol. 2008;15:444-451.

29. Gargiulo P, Dellegrottaglie S, Bruzzese D, et al. The prognostic value of normal stress cardiac magnetic resonance in patients with known or suspected coronary artery disease: a meta-analysis. Circ Cardiovasc Imaging. 2013;6:574-582.

30. Abdulla J, Abildstrom SZ, Gotzsche O, et al. 64-multislice detector computed tomography coronary angiography as potential alternative to conventional coronary angiography: a systematic review and meta-analysis. Eur Heart J. 2007;28:3042-3050.

31. Ahn JH, Park JR, Min JH, et al. Risk stratification using computed tomography coronary angiography in patients undergoing intermediate-risk noncardiac surgery. J Am Coll Cardiol. 2013;61:661-668.

32. Hwang JW, Kim EK, Yang JH, et al. Assessment of perioperative cardiac risk of patients undergoing noncardiac surgery using coronary computed tomographic angiography. Circ Cardiovasc Imaging. 2015;8:e002582. doi: 10.1161/CIRCIMAGING.114.002582.

33. Landesberg G, Mosseri M, Wolf YG, et al. Preoperative thallium scanning, selective coronary revascularization, and long-term survival after major vascular surgery. Circulation. 2003;108:177-183.

34. McFalls EO, Ward HB, Moritz TE, et al. Coronary artery revascularization before elective major vascular surgery. N Engl J Med. 2004;351:2795-2804.

35. Boden WE, O’Rourke RA, Teo KK, et al. Optimal medical therapy with or without PCI for stable coronary disease. N Engl J Med. 2007;356:1503-1516.

36. Ward HB, Kelly RF, Thottapurathu L, et al. Coronary artery bypass grafting is superior to percutaneous coronary intervention in prevention of perioperative myocardial infarctions during subsequent vascular surgery. Ann Thorac Surg. 2006;82:795-801.

37. Garcia S, Moritz TE, Ward HB, et al. Usefulness of revascularization of patients with multivessel coronary artery disease before elective vascular surgery for abdominal aortic and peripheral occlusive disease. Am J Cardiol. 2008;102:809-813.

38. Monaco M, Stassano P, Di Tommaso L, et al. Systematic strategy of prophylactic coronary angiography improves long-term outcome after major vascular surgery in medium- to highrisk patients: a prospective, randomized study. J Am Coll Cardiol. 2009;54:989-996.

39. Livhits M, Gibbons MM, de Virgilio C, et al. Coronary revascularization after myocardial infarction can reduce risks of noncardiac surgery. J Am Coll Surg. 2011;212:1018-1026.

40. Maile MD, Jewell ES, Engoren MC. Timing of preoperative troponin elevations and postoperative mortality after noncardiac surgery. Anesth Analg. 2016;123:135-140.

41. Everett BM, Brooks MM, Vlachos HE, et al. Troponin and cardiac events in stable ischemic heart disease and diabetes. N Engl J Med. 2015;373;610-620.

42. Rodseth RN, Lurati Buse GA, Bolliger D, et al. The predictive ability of pre-operative B-type natriuretic peptide in vascular patients for major adverse cardiac events: an individual patient data meta-analysis. J Am Coll Cardiol. 2011;58:522-529.

43. Rodseth RN, Biccard BM, Le Manach Y, et al. The prognostic value of pre-operative and post-operative B-type natriuretic peptides in patients undergoing noncardiac surgery: B-type natriuretic peptide and N-terminal fragment of pro-B-type natriuretic peptide: a systematic review and individual patient data meta-analysis. J Am Coll Cardiol. 2014;63:170-180.

3.2 Recent Coronary Revascularization

Zdravka Zafirova

Significant coronary artery disease (CAD) identified before surgery necessitates the initiation or escalation of comprehensive medical management. Controversies persist in the literature regarding the appropriateness of preoperative revascularization. Decisions regarding which patients with high-risk CAD may benefit from revascularization, which route is optimal, with either coronary artery bypass grafting (CABG) or percutaneous intervention (PCI), with or without stenting, require a multidisciplinary approach (1,2). Optimal stent choice, with either bare metal stent (BMS) or drug eluting stent (DES), remains uncertain (3,4). The necessity, urgency, and magnitude of the planned surgery and patient comorbidities impact these decisions.


Patients undergoing surgery shortly after revascularization have an increased risk of MACE compared with nonsurgical patients. MACE and mortality are more common when noncardiac surgery is performed within 2 to 4 weeks after CABG. Worse outcomes may be related to the comorbidities of the patients or the urgent nature of the surgeries rather than the timing of the CABG (6,7). MACE are more likely in patients having surgery within 6 weeks to 6 months of PCI compared to a nonsurgical cohort. After 6 months, the risk difference levels off (7,8). The pattern is likely similar for BMS and DES, when optimal APT is used—studies suggest that while the risk of MACE with BMS may be slightly lower within 6 weeks, between 6 weeks and 6 months, DES may have lower MACE (5,8,9). The risk is highest within 7 days after the noncardiac surgery but persists up to 30 days postoperatively. When the indication for PCI is an ACS, compared to stable CAD, the incidence of MACE is substantially higher, especially within 3 months of stent placement (10). Urgent surgery increases the risk of MACE after recent revascularization, while minor surgical procedures do not have a significant impact past the high-risk period (6,8,11) (Table 3.4).

TABLE 3.4 Timing of Noncardiac Surgery After Revascularization

Revascularization Type




Timing of noncardiac surgery after revascularization

≥1 month

≥12 months

≥1 month

Consider 6 months with new generation DES if risk of postponing outweighs the cardiac risk. BMS, bare-metal stent; DES, drug-eluting stent; CABG, coronary artery bypass surgery


Restenosis, disease progression at unstented sites, stent thrombosis, and microvascular dysfunction contribute to symptoms and MACE after revascularization. The indications, timing, and benefits of preoperative cardiac testing are more challenging to identify after revascularization, compared to the primary evaluation of CAD. The American Heart Association (AHA) guidelines for management of PCI discourage routine follow-up testing and suggest it is indicated only for new symptoms of ischemia or before starting a cardiac rehabilitation program (12).

In patients with persistent or atypical symptoms after revascularization, stress testing has high negative predictive and low positive predictive value. A negative test is reassuring and no further intervention is advised (13,14). An abnormal stress test correlates with increased cardiac events and overall mortality. Consensus opinions recommend that coronary imaging in asymptomatic patients is rarely appropriate within 2 years after PCI and 5 years after CABG (15). Studies demonstrate, however, that stress testing and myocardial perfusion imaging performed for risk stratifying asymptomatic patients may identify ischemia as early as 12 months after revascularization, and the presence of ischemia correlates with increased MACE, including mortality (14,16,17,18,19). The clinical status of the patient predicts outcomes and directs further evaluation (16,17,18). Factors predicting increased risk include incomplete revascularization, multivessel disease, prior acute MI, older age, dyslipidemia, diabetes mellitus, smoking, and female gender (16,17,20). Ischemia on testing does not consistently result in repeat catheterization or revascularization, and the superiority of revascularization over medical management is not evident (14,16,18).

Asymptomatic patients on optimal medical management, with good exercise tolerance, within 2 years after PCI or 5 years after CABG, without significant clinical risk factors, are unlikely to benefit from preoperative testing or revascularization. Testing may be considered in asymptomatic patients with significant risk factors and poor exercise tolerance within 2 years of PCI. However, the effect of testing and revascularization on clinical outcomes is uncertain (22). Cardiology evaluation and stress testing may be indicated for patients with symptoms or limited exercise tolerance after revascularization.


The preoperative encounter is an opportune moment to underscore lifestyle modifications and ascertain control of metabolic and endocrine conditions, including
diabetes mellitus and dyslipidemia. Practitioners need to emphasize exercise, tobacco cessation, diet regulation, and optimal medication management (23,24). Aggressive reduction of low-density lipoprotein (LDL) and triglycerides is indicated. Preoperative statin administration, even in patients with normal cholesterol levels and in those >80 years old, reduces disease progression in native and revascularized coronary beds, improves venous graft patency, and reduces MACE (25). High-intensity statin therapy with atorvastatin 40 to 80 mg or rosuvastatin 20 to 40 mg is recommended throughout the perioperative period. Withdrawal of statins may pose particularly high risk. Lower doses may be used in older patients, those with intolerance or at elevated risk from high-dose statin. Starting at a lower dose and titrating up may be associated with fewer side effects. Alternative lipid-control medications are used if there is a contraindication to statins (26). Control of hypertension is a persistent goal after revascularization to reduce MACE, including stroke and death (26). The optimal blood pressure (BP) target is <140/90 mm Hg with cardiovascular risk to realize significant outcome benefits. Slightly better outcomes occur with BP <130/80 mm Hg (27,28). Studies suggest a “J-curve effect,” whereupon BP <120/75 mm Hg may reduce coronary and cerebral perfusion and increase MACE (29). Preoperative optimization aims to achieve control of BP with goals of systolic BP 120 to 140 mm Hg and diastolic BP 75 to 85 mm Hg.

While the preoperative initiation of beta blockade in all patients at risk for CAD is not recommended, beta blockers for secondary prevention after MI have an important role in reducing MACE. Furthermore, these agents aid in the management of hypertension, arrhythmias, and HF (30). In the absence of contraindications, these agents should be administered in advance prior to the surgery and continued throughout the perioperative period without interruption; hypotension should be avoided (26). See Chapter 3.3 “Risk reduction with medications preoperatively” for additional discussion.

Blockade of the renin-angiotensin system (RAS) reduces the incidence of MACE after revascularization. Angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) are used long term, particularly in high-risk patients with diabetes or HF (31). Initiation of ACEIs or ARBs immediately after CABG is controversial (32). See Chapter 18.5 for discussion of ACEI and ARB.

Antiplatelet agents are an essential therapy in revascularized patients. After CABG, single antiplatelet agent therapy (SAPT) consisting of aspirin 81 mg is continued indefinitely in the absence of contraindications. An alternative agent is clopidogrel. There may be a benefit of dual DAPT after CABG to overcome platelet inhibition resistance and reduce progression of native lesions, but the added bleeding risk may not be justified (33). DAPT is more common after off-pump CABG (34).

APT after PCI is crucial, and premature discontinuation strongly correlates with stent thrombosis and significant morbidity and mortality, especially in the perioperative period. Recommended regimens include aspirin 81 mg and P2Y12 inhibitors such as clopidogrel 75 mg, prasugrel 10 mg, or ticagrelor 90 mg. SAPT is continued indefinitely (35,36). Patients with BMS after ACS and DES have reduced risk of MACE and death with DAPT duration of at least 12 months. Patients with high thrombotic potential and lower bleeding risk may benefit from DAPT beyond 12 months. However, new generations of DES are associated with less thrombosis risk, and DAPT duration may be able to be reduced to 3 to 6 months (36).

The bleeding risk depends on SAPT versus DAPT and the surgery. APT is associated with some increase in perioperative blood loss and transfusion rates, particularly
DAPT and P2Y12 inhibitors. However, many procedures, including major vascular and major orthopedic, can be performed on aspirin therapy without major impact on morbidity, mortality, or hospital length of stay; most vascular procedures are consistently performed on SAPT and DAPT (38,39).

Neurosurgical and orthopedic spine and possibly posterior eye chamber procedures have a significant morbidity and mortality associated with even minor bleeding. Discontinuation of antiplatelet agents is prudent in these procedures for 7 days preoperatively (40).

If premature discontinuation of DAPT is necessary, consultation with an interventional cardiologist familiar with stenting is recommended. Bridging with in-patient intravenous GPIIb/IIIa inhibitors (eptifibatide), P2Y12 inhibitors, or direct thrombin inhibitors (bivalirudin) is considered in patients at high risk for stent thrombosis (41,42). Heparin and its derivatives are not considered an adequate bridging strategy.

TABLE 3.5 Duration of Antiplatelet Therapy and Perioperative Management

Duration of DAPT

Duration of SAPT

Perioperative Management

High Bleeding Risk

Low/Moderate Bleeding Risk


≥4-6 weeks


<4 weeks: bridgeb

>4 weeks: hold 7 days

<4 weeks: bridgeb

>4 weeks: continue SAPT


≥6-12 monthsa


<3-6 months: bridgeb

≥6 months: hold

<3-6 months: bridgeb

≥6 months: continue SAPT

ACS with any stent

≥12 months


<12 months: bridgeb

>12 months: hold

<12 months: SAPT +/- bridging

>12 months: continue SAPT


? in very high risk


>1-12 months: hold

Continue SAPT


≥1 month


>1-12 months: hold

Continue SAPT

a >12 months in high thrombosis risk situations.

b Bridge with GPIIb/IIIa inhibitors (eptifibatide), P2Y12 inhibitors, or direct thrombin inhibitors (bivalirudin); heparin and its derivatives are not adequate for bridging.

ACS, acute coronary syndrome; BMS, bare-metal stent; CABG, coronary artery bypass grafting; DAPT, dual antiplatelet therapy; DES; drug-eluting stent; OPCAB, off-pump coronary artery bypass surgery; SAPT, single antiplatelet therapy

Aspirin and P2Y12 inhibitors, particularly clopidogrel, have variability in platelet inhibition among patients due to genetic factors and comorbidities. Platelet function testing may have utility in the perioperative period to balance adequate antithrombotic protection with bleeding risk, anticipate transfusion requirements, and guide individualized antiplatelet therapies (43).

  • Perioperative antiplatelet therapy management

    • Aspirin (81 to 100 mg): continue

    • P2Y12 inhibitor may be continued for low bleeding risk procedures if aspirin is contraindicated

    • High bleeding risk surgery: discontinue aspirin or P2Y12 inhibitor 7 days preoperatively (5 days for ticagrelor)

    • DES >6 months: may be able to discontinue P2Y12 inhibitors if the risk of surgical delay outweighs the risk of stent thrombosis (Table 3.5)


1. McFalls EO, Ward HB, Moritz TE, et al. Coronary-artery revascularization before elective major vascular surgery. N Engl J Med. 2004;351:2795-804.

2. Illuminati G, Schneider F, Greco C, et al. Long-term results of a randomized controlled trial analyzing the role of systematic pre-operative coronary angiography before elective carotid endarterectomy in patients with asymptomatic coronary artery disease. Eur J Vasc Endovasc Surg. 2015;49:366-374.

3. Bangalore S, Silbaugh TS, Normand SL, et al. Drug-eluting stents versus bare metal stents prior to noncardiac surgery. Catheter Cardiovasc Interv. 2015;85:533-541.

4. Bønaa KH, Mannsverk J, Wiseth R, et al; NORSTENT Investigators. Drug-eluting or bare-metal stents for coronary artery disease. N Engl J Med. 2016;375:1242-1252.

5. Tokushige A, Shiomi H, Morimoto T, et al; CREDO-Kyoto PCI/CABG Registry Cohort-2 Investigators. Incidence and outcome of surgical procedures after coronary artery bypass grafting compared with those after percutaneous coronary intervention: a report from the Coronary Revascularization Demonstrating Outcome Study in Kyoto PCI/CABG Registry Cohort-2. Circ Cardiovasc Interv. 2014;7:482-491.

6. Mookadam F, Carpenter SD, Thota VR, et al. Risk of adverse events after coronary artery bypass graft and subsequent noncardiac surgery. Future Cardiol. 2011;7:69-75.

7. Breen P, Lee JW, Pomposelli F, et al. Timing of high-risk vascular surgery following coronary artery bypass surgery: a 10-year experience from an academic medical centre. Anaesthesia. 2004;59:422-427.

8. Holcomb CN, Graham LA, Richman JS, et al. The incremental risk of noncardiac surgery on adverse cardiac events following coronary stenting. J Am Coll Cardiol. 2014; 64(25):2730-2739.

9. Hawn MT, Graham LA, Richman JS, et al. Risk of major adverse cardiac events following noncardiac surgery in patients with coronary stents. JAMA. 2013;310(14):1462-1472.

10. Holcomb CN, Hollis RH, Graham LA, et al. Association of coronary stent indication with postoperative outcomes following noncardiac surgery. JAMA Surg. 2016;151(5):462-469.

11. Brilakis ES, Cohen DJ, Kleiman NS, et al. Incidence and clinical outcome of minor surgery in the year after drug-eluting stent implantation: results from the Evaluation of Drug-Eluting Stents and Ischemic Events Registry. Am Heart J. 2011;161(2):360-366.

12. Levine GN, Bates ER, Blankenship JC, et al; American College of Cardiology Foundation; American Heart Association Task Force on Practice Guidelines; Society for Cardiovascular Angiography and Interventions. 2011 ACCF/AHA/SCAI Guideline for percutaneous coronary intervention. A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines and the Society for Cardiovascular Angiography and Interventions. J Am Coll Cardiol. 2011;58(24):e44-e122.

13. Joshi FR, Biasco L, Pedersen F, et al. Invasive angiography and revascularization in patients with stable angina following prior coronary artery bypass grafting: results from the East Denmark heart registry. Catheter Cardiovasc Interv. 2017;89:341-349.

14. Harb SC, Marwick TH. Prognostic value of stress imaging after revascularization: a systematic review of stress echocardiography and stress nuclear imaging. Am Heart J. 2014;167:77-85.

15. Douglas PS, Garcia MJ, Haines DE, et al. 2011 Appropriate Use Criteria for Echocardiography. A Report of the American College of Cardiology Foundation Appropriate Use Criteria Task Force, American Society of Echocardiography, American Heart Association, American Society of Nuclear Cardiology, Heart Failure Society of America, Heart Rhythm Society, Society for Cardiovascular Angiography and Interventions, Society of Critical Care Medicine, Society of Cardiovascular Computed Tomography, Society for Cardiovascular Magnetic Resonance American College of Chest Physicians. J Am Soc Echocardiogr. 2011;24:229-267.

16. Rossi A, Moccetti T, Faletra F, et al. Dipyridamole stress echocardiography stratifies outcomes of asymptomatic patients with recent myocardial revascularization. Int J Cardiovasc Imaging. 2008;24(5):495-502.

17. Huqi A, Morrone D, Guarini G, et al. Stress testing after complete and successful coronary revascularization. Can J Cardiol. 2016;32(8):986.e23-e29.

18. Harb SC, Cook T, Jaber WA, et al. Exercise testing in asymptomatic patients after revascularization: are outcomes altered?. Arch Intern Med. 2012;172(11):854-861.

19. Acampa W, Petretta M, Florimonte L, et al. Prognostic value of exercise cardiac tomography performed late after percutaneous coronary intervention in symptomatic and symptom-free patients. Am J Cardiol. 2003;91:259-263.

20. Zellweger MJ, Fahrni G, Ritter M, et al; BASKET Investigators. Prognostic value of “routine” cardiac stress imaging 5 years after percutaneous coronary intervention: the prospective long-term observational BASKET (Basel Stent Kosteneffektivitäts Trial) LATE IMAGING study. JACC Cardiovasc Interv. 2014;7(6):615-621.

21. Erne P, Schoenenberger AW, Burckhardt D, et al. Effects of percutaneous coronary interventions in silent ischemia after myocardial infarction: the SWISSI II randomized controlled trial. JAMA. 2007;297(18):1985-1991.

22. Acampa W, Petretta MP, Daniele S, et al. Myocardial perfusion imaging after coronary revascularization: a clinical appraisal. Eur J Nucl Med Mol Imaging. 2013;40(8):1275-1282.

23. Lee HY, Kim JH, Kim BO, et al. Regular exercise training reduces coronary restenosis after percutaneous coronary intervention in patients with acute myocardial infarction. Int J Cardiol. 2013;167(6):2617-2622.

24. Iqbal J, Zhang YJ, Holmes DR, et al. Optimal medical therapy improves clinical outcomes in patients undergoing revascularization with percutaneous coronary intervention or coronary artery bypass grafting: insights from the Synergy Between Percutaneous Coronary Intervention with TAXUS and Cardiac Surgery (SYNTAX) trial at the 5-year follow-up. Circulation. 2015;131(14):1269-1277.

25. Natsuaki M, Morimoto T, Furukawa Y, et al; CREDO-Kyoto PCI/CABG Registry Cohort-2 Investigators. Effect of statin therapy on cardiovascular outcomes after coronary revascularization in patients ≥80 years of age: observations from the CREDO-Kyoto Registry Cohort-2. Atherosclerosis. 2014;237(2):821-828.

26. Kulik A, Ruel M, Jneid H, et al; American Heart Association Council on Cardiovascular Surgery and Anesthesia. Secondary prevention after coronary artery bypass graft surgery: a scientific statement from the American Heart Association. Circulation. 2015;131(10): 927-964.

27. Zanchetti A, Thomopoulos C, Parati G. Randomized controlled trials of blood pressure lowering in hypertension: a critical reappraisal. Circ Res. 2015;116(6):1058-1073.

28. Thomopoulos C, Parati G, Zanchetti A. Effects of blood pressure lowering on outcome incidence in hypertension: 3. effects in patients at different levels of cardiovascular risk— overview and meta-analyses of randomized trials. J Hypertens. 2014;32:2305-2314.

29. Lu W. Could intensive anti-hypertensive therapy produce the “J-curve effect” in patients with coronary artery disease and hypertension after revascularization? Eur Rev Med Pharmacol Sci. 2016;20(7):1350-1355.

30. Bangalore S, Makani H, Radford M, et al. Clinical outcomes with β-blockers for myocardial infarction: a meta-analysis of randomized trials. Am J Med. 2014;127(10):939-953.

31. Bertrand ME, Fox KM, Remme WJ, et al. Angiotensin-converting enzyme inhibition with perindopril in patients with prior myocardial infarction and/or revascularization: a subgroup analysis of the EUROPA trial. Arch Cardiovasc Dis. 2009;102(2):89-96.

32. Rouleau JL, Warnica WJ, Baillot R, et al; IMAGINE (Ischemia Management with Accupril post-bypass Graft via Inhibition of the coNverting Enzyme) Investigators. Effects of angiotensin-converting enzyme inhibition in low-risk patients early after coronary artery bypass surgery. Circulation. 2008;117(1):24-31.

33. Une D, Al-Atassi T, Kulik A, et al. Impact of clopidogrel plus aspirin versus aspirin alone on the progression of native coronary artery disease after bypass surgery: analysis from the Clopidogrel After Surgery for Coronary Artery DiseasE (CASCADE) randomized trial. Circulation. 2014;130(11 Suppl 1):S12-S18.

34. Mannacio VA, Di Tommaso L, Antignan A, et al. Aspirin plus clopidogrel for optimal platelet inhibition following off-pump coronary artery bypass surgery: results from the CRYSSA (prevention of Coronary arteRY bypaSS occlusion After off-pump procedures) randomised study. Heart. 2012;98(23):1710-1715.

35. Fleisher LA, Fleischmann KE, Auerbach AD, et al; American College of Cardiology.; American Heart Association. 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(22):e77-e137.

36. Bittl JA, Baber U, Bradley SM, et al. Duration of dual antiplatelet therapy: a systematic review for the 2016 ACC/AHA guideline focused update on duration of dual antiplatelet therapy in patients with coronary artery disease: a report of the American College of Cardiology/American Heart Association Task Force on clinical practice guidelines. J Am Coll Cardiol. 2016;68:1116-1139.

37. Wassef AW, Khafaji H, Syed I, et al. Short duration vs standard duration of dual-antiplatelet therapy after percutaneous coronary intervention with second-generation drug-eluting stents—a systematic review, meta-analysis, and meta-regression analysis of randomized controlled trials. J Invasive Cardiol. 2016;28:E203-E210.

38. Ito T, Derweesh IH, Ginzburg S, et al. Perioperative outcomes following partial nephrectomy performed on patients remaining on antiplatelet therapy. J Urol. 2017;197:31-36.

39. Chechik O, Thein R, Fichman G, et al. The effect of clopidogrel and aspirin on blood loss in hip fracture surgery. Injury. 2011;42(11):1277-1282.

40. Park JH, Ahn Y, Choi BS, et al. Antithrombotic effects of aspirin on 1- or 2-level lumbar spinal fusion surgery: a comparison between 2 groups discontinuing aspirin use before and after 7 days prior to surgery. Spine. 2013;38:1561-1565.

41. Warshauer J, Patel VG, Christopoulos G, et al. Outcomes of preoperative bridging therapy for patients undergoing surgery after coronary stent implantation: a weighted meta-analysis of 280 patients from eight studies. Catheter Cardiovasc Interv. 2015;85(1):25-31.

42. Morici N, Moja L, Rosato V, et al. Bridge with intravenous antiplatelet therapy during temporary withdrawal of oral agents for surgical procedures: a systematic review. Intern Emerg Med. 2014;9(2):225-235.

43. Corredor C, Wasowicz M, Karkouti K, et al. The role of point of-care platelet function testing in predicting postoperative bleeding following cardiac surgery: a systematic review and meta-analysis. Anaesthesia. 2015;70:715-731.

3.3 Cardiac Risk Reduction With Medications

Zdravka Zafirova

The multifactorial nature of ischemic heart disease (IHD) necessitates therapeutic regimens aimed at the various components of the disease. Lifestyle modifications include physical fitness, smoking cessation, and dietary alterations to control excess weight, diabetes mellitus, dyslipidemia, and blood pressure. Medications are an integral part of the management of IHD to modify risk and improve long-term outcomes.


The utility of antiplatelet therapy (APT) for reduction of MACE in high-risk patients has been consistently demonstrated. However, their use has to be weighed against increased bleeding, particularly in the perioperative period (1,2). When these agents are taken for primary prevention, the perioperative bleeding risk is felt to be higher than potential benefits and APT is stopped for most procedures. On the contrary, after coronary revascularization, APT is essential. Depending on the timing of revascularization dual APT (DAPT) with aspirin and a P2Y12 inhibitor such as clopidogrel 75 mg, prasugrel 10 mg, or ticagrelor 90 mg twice a day may be indicated. After percutaneous coronary intervention (PCI) with stenting lifelong monotherapy with aspirin or P2Y12 inhibitor is indicated. Patients having surgery should continue aspirin 75 to 100 mg, except in surgeries with very high adverse events from bleeding. Perioperative continuation of DAPT may be indicated in a high-thrombosis risk time period after PCI (3). See Chapter 3.2 for additional discussion.

Decisions regarding APT with IHD without revascularization continue to present a challenge in the perioperative period. APT, especially aspirin, is associated with reduction in lifelong MACE with IHD. Early trials suggested worse outcomes with perioperative aspirin withdrawal (4), but more recent results have failed to demonstrate clear benefits of perioperative aspirin continuation (5). Perioperative risks and benefits of aspirin in IHD in the absence of revascularization remain incompletely clarified. The POISE-2 trial excluded high-risk patients (recent PCI) and had a low number of patients with IHD (25%), therefore the interpretation of the results is problematic (5). Practitioners must weigh the benefits and risks of specific clinical situations and individualize perioperative APT regimens (Table 3.5 in Chapter 3.2).


The use of statins in patients with elevated cardiovascular risk reduces MACE, including the need for revascularization, the incidence of major coronary and ischemic cerebrovascular events, and death (6). The benefits are seen across gender, age groups, and lipid levels (7,8). After revascularization, statins attenuate disease progression in native and grafted vessels and improve long-term graft patency (8). More intense lipid control and higher doses of statins confer incremental benefits. Therefore, if tolerated, statins are utilized in high doses (atorvastatin 40-80 mg, simvastatin 40-80 mg, or rosuvastatin 20-40 mg) in patients with IHD. Preoperative patients benefit from therapy initiation, even within short periods of time before surgery. Intolerance to high-dose statins may be solved by lowering the dose. Statins are continued in the
perioperative period without interruption. Alternative medications to control lipids, such as bile acid sequestrants, niacin, fibrates, or ezetimibe, are considered if statins are not tolerated or contraindicated, or as a second agent (9). In patients with IHD, lipid-lowering targets are triglycerides ≤200 mg/dL, LDL-C <100 mg/dL, or, in very high-risk patients, LDL-C <70 mg/dL (9).


Blood pressure control reduces the risk of MACE, particularly in patients at higher cardiovascular risk (12). The role of beta-adrenergic antagonists has been controversial. The utility of beta blockade in IHD for secondary prevention is endorsed by the AHA (9). A recent meta-analysis of clinical trials has questioned benefits of beta blockers in patients with IHD and MI (11). While there is short-lived reduction in MI and angina, there is increased incidence of cardiogenic shock and HF, without mortality benefits, in the setting of reperfusion therapy (11). Prospective studies support a reduction in all-cause mortality and MACE with beta blockade after ACS and PCI (12). At present, the long-term use of beta blockers such as metoprolol, carvedilol, and bisoprolol, is advisable in patients with IHD, especially following revascularization. Continuation of already established beta antagonist regiment is important perioperatively. Short-term initiation before surgery is not recommended, due to evidence of increased risk of stroke, MACE, and all-cause mortality (13).

Blockade of the renin-angiotensin-aldosterone system (RAAS) with ACEIs and ARBs results in a demonstrable reduction in the incidence of MACE and cerebrovascular events, particularly in patients with IHD with reduced ejection fraction, diabetes, or renal disease (9,14). There appears to be synergistic benefit from combined therapy with beta-adrenergic and RAAS blockade (15). When ACEI and ARB are continued immediately preoperatively, hypotension has been consistently demonstrated with general anesthesia (16). The degree of hypotension depends on the anesthetic regimen. The clinical implications of this hypotension are unclear. Some studies have shown an increased need for vasopressors, while others have contradicting results or have shown that optimization of fluids is sufficient for hemodynamic control (16,17,18). Practitioners should take into account the clinical situation when deciding to continue or withhold RAAS blockade on the day of surgery. Table 3.6 lists clinical scenarios which may prompt discontinuation of RAAS 12 to 24 hours before surgery.

Another component of RAAS inhibition is aldosterone antagonism, which may have a role in secondary prevention of IHD, particularly in addition to beta-antagonists, ACEI, and ARB (9,19).

A large trial of the alpha-2-adrenergic agonist clonidine failed to demonstrate outcome improvement in patients with atherosclerotic disease undergoing noncardiac surgery, while noting an increase in adverse events (20). Patients already taking clonidine should continue to avoid withdrawal.

Multimodal pharmacotherapy in patients with IHD reduces long-term cardiovascular morbidity and mortality. In the perioperative period, most components of established therapy are continued. However, certain medications including APT, ACEI, and ARB may need to be held before surgery. Decisions regarding specific regimens and timing are arrived at by consensus among the surgeon, the anesthesiologist, the patient, the primary physician, and specialists considering the benefits and the potential risks.

TABLE 3.6 Potential Indications for Preoperative Discontinuation of RAAS Therapy

Multiple antihypertensive medications

Well-controlled hypertension

Use of potent loop diuretics

Risk for stroke

Absence of significant heart failure

Lengthy surgical procedure

Procedures involving significant blood loss

Spine or intracranial procedures, especially in prone position

General anesthesia


1. Antithrombotic Trialists’ Collaboration. Collaborative meta-analysis of randomized trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients. BMJ. 2002;324:71-86.

2. Baigent C, Blackwell L, Collins R, et al. Aspirin in the primary and secondary prevention of vascular disease: collaborative meta-analysis of individual participant data from randomized trials. Lancet. 2009;373:1849-1860.

3. Bittl JA, Baber U, Bradley SM, et al. Duration of dual antiplatelet therapy: a systematic review for the 2016 ACC/AHA guideline focused update on duration of dual antiplatelet therapy in patients with coronary artery disease: a report of the American College of Cardiology/American Heart Association Task Force on clinical practice guidelines. J Am Coll Cardiol. 2016;68:1116-1139.

4. Burger W, Chemnitius JM, Kneissl GD, et al. Low-dose aspirin for secondary cardiovascular prevention—cardiovascular risks after its perioperative withdrawal versus bleeding risks with its continuation—review and meta-analysis. J Intern Med. 2005;257:399-414.

5. Devereaux PJ, Mrkobrada M, Sessler DI, et al; POISE-2 Investigators. Aspirin in patients undergoing noncardiac surgery. N Engl J Med. 2014;370:1494-1503.

6. Bulbulia R, Bowman L, Wallendszus K, et al; Heart Protection Study Collaborative Group. Effects on 11-year mortality and morbidity of lowering LDL cholesterol with simvastatin for about 5 years in 20,536 high-risk individuals: a randomised controlled trial. Lancet. 2011;378:2013-2020.

7. Fulcher J, O’Connell R, Voysey M, et al; Cholesterol Treatment Trialists’ (CTT) Collaboration. Efficacy and safety of LDL-lowering therapy among men and women: meta-analysis of individual data from 174,000 participants in 27 randomised trials. Lancet. 2015;385:1397-1405.

8. Natsuaki M, Morimoto T, Furukawa Y, et al; CREDO-Kyoto PCI/CABG Registry Cohort-2 Investigators. Effect of statin therapy on cardiovascular outcomes after coronary revascularization in patients ≥ 80 years of age: observations from the CREDO-Kyoto Registry Cohort-2. Atherosclerosis. 2014;237:821-828.

9. Smith SC Jr., Benjamin EJ, Bonow RO, et al; World Heart Federation and the Preventive Cardiovascular Nurses Association. AHA/ACCF secondary prevention and risk reduction therapy for patients with coronary and other atherosclerotic vascular disease: 2011 update: a guideline from the American Heart Association and American College of Cardiology Foundation. Circulation. 2011;124:2458-2473.

10. Blood Pressure Lowering Treatment Trialists’ Collaboration. Predicted cardiovascular risk can inform decisions to lower blood pressure with drugs: evidence from an individual patient data meta-analysis. Lancet. 2014;384:591-598.

11. Bangalore S, Makani H, Radford M, et al. Clinical outcomes with β-blockers for myocardial infarction: a meta-analysis of randomized trials. Am J Med. 2014;127:939-953.

12. Li C, Sun Y, Shen X, et al. Relationship between β-Blocker therapy at discharge and clinical outcomes in patients with acute coronary syndrome undergoing percutaneous coronary intervention. J Am Heart Assoc. 2016;5:e004190.

13. Wijeysundera DN, Duncan D, Nkonde-Price C, et al. Perioperative beta blockade in noncardiac surgery: a systematic review for the 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;64:2406-2425.

14. Thomopoulos C, Parati G, Zanchetti A. Effects of blood pressure lowering on outcome incidence in hypertension: 4. Effects of various classes of antihypertensive drugs-overview and meta-analyses. J Hypertens. 2015;33:195-211.

15. Bertrand ME, Ferrari R, Remme WJ, et al. Perindopril and β-blocker for the prevention of cardiac events and mortality in stable coronary artery disease patients: a EUropean trial on Reduction Of cardiac events with Perindopril in stable coronary Artery disease (EUROPA) subanalysis. Am Heart J. 2015;170:1092-1098.

16. Rajgopal R, Rajan S, Sapru K, et al. Effect of pre-operative discontinuation of angiotensin-converting enzyme inhibitors or angiotensin II receptor antagonists on intra-operative arterial pressures after induction of general anesthesia. Anesth Essays Res. 2014;8:32-35.

17. Vijay A, Grover A, Coulson TG, et al. Perioperative management of patients treated with angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers: a quality improvement audit. Anaesth Inten Care. 2016;44:346-352.

18. Roshanov P, Rochwerg B, Patel A, et al. Withholding versus continuing angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers before noncardiac surgery: an analysis of the vascular events in noncardiac surgery patients cohort evaluation prospective cohort. Anesthesiology. 2017;126:16-27.

19. Pitt B, Remme W, Zannad F, et al; Eplerenone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival Study Investigators. Eplerenone, a selective aldosterone blocker, in patients with left ventricular dysfunction after myocardial infarction. N Engl J Med. 2003;348:1309-1321.

20. Devereaux PJ, Sessler DI, Leslie K, et al; POISE-2 Investigators. Clonidine in patients undergoing noncardiac surgery. N Engl J Med. 2014;370:1504-1513.

3.4 Heart Failure

Rachel Eshima McKay

Heart failure (HF) describes a clinical syndrome caused by impaired ventricular filling or limited ventricular ejection, where cardiac output declines below the minimum needed to meet the metabolic demands of the body. HF has a variety of underlying structural and functional causes, and may primarily involve one or both sides of the heart (1). Diagnosis of HF is made clinically, on the basis of characteristic symptoms and physical findings—most importantly dyspnea, fatigue, and congestion.

Although inadequate cardiac output is the initiating factor, the syndrome is driven by secondary counterregulatory responses, including sodium and water retention,
with persistent activation of sympathetic and renin-angiotensin-aldosterone system (RAAS), creating a spiraling process of vasoconstriction, edema, arrhythmia, and further impairment of cardiac output. Compensatory ventricular remodeling follows one of two typical patterns: concentric hypertrophy develops to overcome the increase in wall tension that occurs from chronic pressure overload, creating susceptibility to ischemia due to unfavorable oxygen supply-demand balance; or eccentric hypertrophy develops in response to volume overload, causing dilatation, impaired contractility, and susceptibility to arrhythmia.


HF is categorized by left ventricular (LV) ejection fraction (EF), with heart failure with preserved ejection fraction (HFpEF) signifying normal LVEF, versus heart failure with reduced ejection fraction (HFrEF) signifying reduced LVEF (Table 3.7). Previously, “systolic HF” was used to describe HFrEF, and “diastolic HF” to describe HFpEF. The premise is that these entities are clinically distinct. Recently, more discriminating analytical tools and broad population data suggest a continuum of findings and considerable overlap of abnormal systolic and diastolic parameters in both categories of HF. The term “congestive heart failure” has also fallen out of favor, because features of congestion and volume overload may be minimal or absent in affected patients (2).

Approximately 50% of all patients with HF fall into the category of HFpEF. Diastolic dysfunction indicates delayed or limited LV relaxation (an active process),
and/or decreased LV compliance, both leading to impaired LV filling. Diagnosis of diastolic dysfunction is complex. Values of individual parameters used to assess diastolic function may overlap between patients with HFpEF versus patients who are elderly or otherwise normal. Therefore, a set of diagnostic criteria are considered, where a majority of values outside normative ranges is needed to establish a diagnosis of diastolic dysfunction. The clinical significance of diastolic dysfunction is influenced by stage and estimated left atrial (LA) filling pressures, including mitral inflow velocities. These values should be reported in a formal echocardiogram, and are useful to determine stability and guide management of an individual patient, especially when previous studies are available for comparison (3). Although diastolic dysfunction is the major mechanism underlying HFpEF, it is also observed frequently in the HFrEF population, where its presence often correlates with symptom severity. A major distinguishing feature of HFrEF is ventricular dilatation and eccentric remodeling.

TABLE 3.7 Classification of Heart Failure Based on Ejection Fraction


Ejection Fraction (%)


Heart failure with reduced ejection fraction (HFrEF)


  • Systolic heart failure

Heart failure with preserved ejection fraction (HFpEF)


  • Diastolic heart failure

  • Diagnosed after excluding alternative causes of symptoms and when ≥3 of 4 parameters are present on echo:

    1. LA volume index >34 mL/m2

    2. Septal e’ velocity <7 cm/s; or lateral e’ velocity <10 cm/s

    3. Average E/e’ ratio >14

    4. TR velocity >2.8 m/s

Preserved or low-normal ejection fraction


  • Poor functioning

  • Borderline status

Preserved responders


  • Previously failing but responsive to treatment

LA, left atrial; TR, tricuspid regurgitation


  • Identify previously recognized HF, and assess the current degree of compensation relative to baseline.

  • Establish the underlying cause of HF.

  • Identify and address coexisting conditions that may precipitate HF during the perioperative period.

  • Exclude or confirm a new HF diagnosis in patients with dyspnea, fatigue, edema, congestion, or arrhythmias.

  • Pursue alternative or coexisting diagnoses that may cause or contribute to the symptoms of dyspnea, fatigue, or congestion.

  • Document the level of activity that elicits HF symptoms.

  • Confirm adherence to therapy, and appropriate response to medications.

  • Determine the stability of HF. New or acutely decompensated HF warrants optimization, specialist referral, and sometimes hospitalization to stabilize perfusion, oxygenation, volume status, and symptoms in a safe, expeditious manner.

  • A discussion of the risks and timing of surgery must take place between the surgeon, perioperative physician, and the primary care physician or HF specialist.

  • Coordination and planning with physicians who will care for the patient during and after surgery should take place in advance.


Clinicians may fail to recognize HF because most of its signs and symptoms are nonspecific. Dyspnea and pulmonary congestion from fluid overload frequently characterize acute or decompensated HF, although these features may be subtle or absent. Over time, elevated pulmonary venous pressure increases venous capacitance, attenuating the accumulation of alveolar fluid transudation, although pleural effusion may develop. Clinical symptoms of HF such as fatigue, anorexia, muscle weakness, and peripheral edema characterize chronic, long-standing HF and reflect decreased cardiac output, vasoconstriction, and inadequate splanchnic and skeletal muscle perfusion.

The classification system based on the degree of functional limitation imposed by HF was developed by the New York Heart Association (NYHA) (2). Patients are assigned to one of four functional categories, depending on the minimum effort needed to elicit HF symptoms:

  • Class I—Patients with heart disease without resulting limitation of physical activity. Ordinary physical activity does not cause HF symptoms such as fatigue or dyspnea.

  • Class II—Patients with heart disease resulting in slight limitation of physical activity. Symptoms of HF develop with ordinary activity but there are no symptoms at rest.

  • Class III—Patients with heart disease resulting in marked limitation of physical activity. Symptoms of HF develop with less than ordinary physical activity but there are no symptoms at rest.

  • Class IV—Patients with heart disease resulting in the inability to carry on any physical activity without discomfort. Symptoms of HF may occur even at rest.

NYHA Class III and IV confers 3.5 times greater risk of mortality compared to NHYA Class I and II, independent of LVEF (11).

An important distinction in patients with HF relates to the pattern of symptoms. Compensated HF implies a previously recognized, currently well-managed condition associated with stable body weight and symptoms. In contrast, new or acutely decompensated HF is characterized by sudden, worsening, or previously unexplained dyspnea or fatigue accompanied by abrupt elevation in LV filling pressure. Distinguishing between these clinical presentations is critical during patient evaluation, since the latter confers very high risk of adverse postoperative events without appropriate preoperative management.

The following are frequently reported in patients with HF:

  • Symptoms caused by decreased perfusion

    • Fatigue

    • Weakness

    • Anorexia

  • Symptoms caused by fluid retention

    • Dyspnea on exertion

    • Dyspnea at rest

    • Paroxysmal nocturnal dyspnea

    • Orthopnea

    • Peripheral edema

    • Unexplained weight gain

    • Abdominal pain

    • Nausea from hepatic congestion

  • Symptoms caused by tachyarrhythmia

    • Palpitations

    • Light-headedness

The following issues are evaluated on examination:

  • Precordial apical impulse that is prolonged suggests LV dysfunction. Apical impulse palpable lateral to the midclavicular line raises suspicion of LV enlargement.

  • Elevated jugular venous pressure is usually seen when HF is responsible for peripheral edema, since high venous and capillary pressures drive intravascular fluid into interstitial tissue compartments.

  • Third heart sound (S3) is highly specific as an indicator of elevated left ventricular end diastolic pressure (LVEDP), elevated LA pressure, and HF. However, sensitivity is low, and considerable variability exists among clinicians in the ability to hear and recognize a third heart sound.

  • Rales (basilar crackles) indicate pulmonary congestion, and are more often seen in acute HF.

  • Peripheral edema is caused by ongoing sodium retention, or may be caused by right HF.

  • Hepatojugular reflux, with abdominal distention and right upper quadrant tenderness, provides further evidence of volume overload due to HF.

  • Resting sinus tachycardia without an obvious alternative cause (i.e., fever) may accompany HFrEF.

  • Narrow pulse pressure (<25 mm Hg), if present, should raise suspicion of HF.

  • Cool extremities indicate peripheral vasoconstriction, a sign of secondary adaptation to low cardiac output.

  • Precordial lift should raise suspicion of right ventricular enlargement.

  • Murmurs may signify rapid flow through a stenotic valve or regurgitation, which can be a cause or result of HF. The murmur of aortic stenosis is best heard at the right upper sternal border, and frequently radiates to the neck.


HF arises from a variety of causes (see Table 3.8), and the onset may be acute or insidious. A majority of cases are preceded by a period of elevated afterload or increased blood volume. Increases in venous and capillary pressures in the pulmonary and systemic beds lead to pulmonary congestion, generalized edema, and hepatic enlargement.

TABLE 3.8 Etiology of Heart Failure

Mechanism of Heart Failure

Cause or Associated Condition


Acute or chronic volume overload

Ventricular dilatation, with eccentric remodeling

Ischemic heart disease

Valvular heart disease (MR, AI, critical AS)

Toxin exposure (ethanol, cocaine, chemotherapy)

Infectious causes (viral, parasitic)



Congenital heart disease

Severe, labile hypertension

Renal failure



Chronic pressure overload

Ventricular hypertrophy with concentric remodeling


Long-standing hypertension

Myocardial ischemia



Aortic stenosis

Sleep-disordered breathing


Ventricular under filling

Pericardial disease

Mitral stenosis

HFrEF, heart failure with reduced ejection fraction; MR, mitral regurgitation; AI, aortic insufficiency; AS, aortic stenosis; HFpEF, heart failure with preserved ejection fraction

New or acutely decompensated HF often coincides with one or more precipitating events, such as ACS, arrhythmia, pulmonary thromboembolism, conditions that increase oxygen demand (i.e., sepsis, infection, anemia, thyrotoxicosis), or nonadherence to chronic HF treatment. Myocardial ischemia due to underlying coronary artery disease (CAD) should be considered in patients with acute or newly decompensated HF. A stress test or angiograpy is considered reasonable (Class IIA) in patients with de novo HF, unless the patient is ineligible for revascularization. Valvular heart disease (VHD) is a common underlying cause of HF, usually indicating advanced disease warranting repair or replacement. Valvular disease also occurs as a result of HF. As ventricular dilation worsens, mitral or tricuspid regurgitation develops, often causing further deterioration. Whether primary or secondary, correction of valvular disease can improve HF symptoms.


Laboratory Data

Blood chemistry should be measured, and electrolyte abnormalities corrected (potassium, magnesium). Stability of renal function is assessed by current and trended creatinine and blood urea nitrogen values. Liver function tests and PT may be abnormal if hepatic congestion is present. Anemia confers twofold greater risk of postoperative mortality for patients with HFrEF or HRpEF (12).

Natriuretic Peptides

BNP is released from the myocardium in response to increased wall stress during conditions of pressure overload, volume expansion, or ischemia. N-terminal proBNP (NT-proBNP) is a cleaved product of BNP. Natriuretic peptide (NP) measurements are recommended by the ACC/AHA guidelines for management of HF and to help exclude an HF diagnosis in patients with dyspnea when uncertainty exists about the underlying cause (2). BNP, the biologically active of the two molecules, induces myocardial relaxation and counteracts the impact of sympathetic and RAAS activation that occurs in the setting of decreased cardiac output, inducing natriuresis, diuresis, and vasodilatation. The circulating half-lives are 20 minutes for BNP and 120 minutes for NT-proBNP. Both peptides become elevated as glomerular filtration rate falls below 60 mL/min. The thresholds listed in Table 3.9 have been suggested for determining the probability of HF in a patient with dyspnea. NP values below specific limits have high negative predictive (NPV) value. BNP <100 pg/mL is 95% to 98% specific in excluding HF as cause of dyspnea (13). NT-proBNP <300 pg/mL has 98% NPV in excluding HF independent of age. Peptide values above higher thresholds add supportive evidence to a diagnosis of HF, but are not conclusive given interindividual variability and numerous sources of confounding. Data are currently lacking to support preoperative strategies targeting lowering of BNP levels in hopes of improving postoperative outcomes, although data from a combination of trials suggest improvement in all-cause mortality when BNP-guided HF therapy, as opposed to standard care, is used in the management of hospitalized patients.

Several large studies have demonstrated an association between preoperative NP elevation, above various threshold values, and increased risk of 30-day MACE and all-cause mortality after noncardiac surgery. Elevated preoperative NP levels above a
diagnostic threshold (BNP ≥372 pg/mL) are independently associated with increased likelihood of 30-day postoperative MACE after vascular surgery (Table 3.9). BNP values, used in conjunction with RCRI, provide superior prognostic value for predicting MACE and 30-day postoperative mortality in patients having both vascular and nonvascular surgery, compared to use of RCRI alone, especially for reclassification of patients in intermediate RCRI risk categories (14). The recently published guidelines from the Canadian Cardiovascular Society on perioperative cardiac risk assessment and management recommend NP measurement in patients with ≥1 RCRI risk factor ≥65 years of age with planned surgery requiring at least one overnight hospital stay (15). If preoperative NP levels exceed specific threshold values, postoperative electrocardiogram (ECG) and daily troponin measurements for 48 to 72 hours are recommended.

TABLE 3.9 Interpretation of Natriuretic Peptide Levels Under Various Conditions

Natriuretic Peptide

BNP (pg/mL)

NT-proBNP (pg/mL)

Range in which HF is unlikely



Level above which HF is likely


Age <50: 450

Age 50-75: 900

Age >75: 1,800

Values may be ELEVATED for reasons not directly related to HF

Reduced GFR

Yes (moderate)

Yes (significant)

Pulmonary embolus



Myocardial ischemia



Sacubitril (neprilysin inhibitor)



Sepsis or high output state






Recent cardioversion




Yes (small)

Yes (moderate)

Values may be misleadingly LOW even in the presence of HF with these conditions




HF caused by inflow obstruction: mitral stenosis, pericardial constriction, tamponade



BNP, B-type natriuretic peptide; NT-proBNP, N-terminal-proBNP; HF, heart failure; GFR, glomerular filtration rate


An ECG identifies or confirms the presence of arrhythmias that may be an instigator or consequence of HF, and is useful in the setting of an abnormal heart rate (HR)
or rhythm. Pathologic Q waves, ST depression, or findings suggestive of injury raise suspicion of HF caused by myocardial infarction. A normal ECG is rarely seen in patients with HFrEF. However, abnormal ECG findings have poor specificity as supportive evidence of HF, especially in older patients, so “routine” ECG is not helpful or recommended.

Chest Radiography

HF consensus guidelines recommend chest radiographs (CXR) in patients with new, suspected, or decompensated HF (2,5). CXR may show specific findings that are highly characteristic of HF—pulmonary congestion, Kerley-B lines, prominence or cephalization of pulmonary vascular markings, cardiac chamber enlargement, and pleural effusion. On the other hand, patients with HF often have nonspecific or normal CXR findings, including lack of congestion and appearance of normal heart size. Therefore, a normal CXR does not exclude a diagnosis of HF. However, the CXR may provide diagnostic value in determining an alternative or contributory cause of clinical symptoms.


Consensus guidelines from the ACC/AHA recommend echocardiogram for (5):

  • Patients with signs and symptoms possibly caused by HF but without previous diagnosis.

  • Patients with previously diagnosed HF who experience increasing symptoms, change in clinical management, or new conditions with possible impact on heart function.

  • Patients with previous HF after a stable interval may be considered.

The 2011 Appropriate Use Criteria for Echocardiography states an echocardiogram is warranted in the following circumstances (16):

  • Suspected pulmonary hypertension (PH)

  • Reassessment of patients with known PH after a change in clinical status

  • Surveillance in patients with previously established PH in whom most recent assessment occurred >1 year earlier.


The following strategies to prolong survival and reduce hospitalization in patients with HFpEF and HFrEF are supported by evidence:

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Nov 14, 2018 | Posted by in ANESTHESIA | Comments Off on Heart Disease
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