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.
Systolic HF or HF with reduced ejection fraction
Diastolic HF or HF with normal (or preserved) ejection fraction
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.)
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
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.)
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
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).
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.
Valvular disease, particularly aortic stenosis or mitral disease
Left or right ventricular systolic and/or diastolic dysfunction
Cardiomyopathies (e.g., hypertrophic obstructive cardiomyopathy)
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.
<30 mL/min/1.73 m2; severe asthma or chronic obstructive pulmonary disease; or sensitivity to the vasodilating agents, adenosine, and dipyridamole.
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).
value. Preoperative noninvasive and invasive testing in otherwise high-risk patients is deemed unnecessary in those with normal BNP or NT-proBNP level (3).
TABLE 3.4 Timing of Noncardiac Surgery After Revascularization
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.
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).
TABLE 3.5 Duration of Antiplatelet Therapy and Perioperative Management
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)
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).
TABLE 3.6 Potential Indications for Preoperative Discontinuation of RAAS Therapy
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.
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
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.
disease-related hospitalization. Surprisingly, for minor surgical procedures performed on an outpatient basis, 30-day mortality is as high as 4% to 5% in patients with HF, in contrast to 0.8% in patients with IHD. Risk of adverse postoperative outcome is significantly higher for patients after any cardiac-related hospitalization within 4 weeks of surgery (9).
Evidence of severe decompensation
Altered mental status
Declining renal function
Hemodynamically significant arrhythmias
Dyspnea or tachypnea at rest
Suspected transient ischemic attack (TIA) or stroke
Severe electrolyte abnormalities
Recent, repeated delivery of shock from implantable cardioverter defibrillator (ICD)
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.
Symptoms caused by decreased perfusion
Symptoms caused by fluid retention
Dyspnea on exertion
Dyspnea at rest
Paroxysmal nocturnal dyspnea
Unexplained weight gain
Nausea from hepatic congestion
Symptoms caused by tachyarrhythmia
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.
TABLE 3.8 Etiology of Heart Failure
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
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.
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.
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.
PH with normal LVEDP
Chronic lung disease
Consider especially with existing risk factors (malignancy, immobilization, hypercoagulability, or recent orthopedic surgery)
Sleep disordered breathing (SDB)