Systemic Complications: Cardiac

Myocardial Infarction

One of the most feared complications during, or following, vascular surgery is MI, which occurs in 1.6% to 17% of patients depending on how MI is defined. ^, In 2007 a global task force set out to develop a pathophysiology-based universal definition for MI to align nomenclature used by clinicians and researchers around the world. The Universal Definitions of MI have evolved through the years with the 2018 4th edition dividing the cause of acute cardiac troponin (cTn) leak into two entities: ischemic (“MI”) and nonischemic (“myocardial injury”). ^, The MI category is further divided into five different types. Type IV and V are cTn-positive events following coronary interventional and heart surgical procedures, respectively, and thus not pertinent to this discussion. A “type III MI” occurs when there are typical symptoms or EKG changes suggesting MI followed by cardiac arrest and death before enzymes can be obtained. This diagnosis may be considered in some of our vascular surgery cases depending on the clinical manifestations leading up to a cardiac arrest or sudden death while the patient is still hospitalized. It should be noted that if patients are diagnosed with a type III MI and subsequently found to have vessel thrombosis on autopsy, the diagnosis is then changed to type I MI. The most common Universal Definition cTn positive events following vascular surgery are the MI (type I or II) and “cardiac injury” with associated pathophysiology detailed below.

The type I MI occurs when plaque rupture is triggered by perioperative vessel-wall shear stress, hemodynamic changes, activation of the inflammatory cascade (e.g. interleukin 1 and 6, tumor necrosis factor and C-reactive protein) and perturbation of the clotting cascade. These patients have an associated cTn rise and fall and at least one of the following: symptoms consistent with acute myocardial infarction, new ischemic changes on the EKG, imaging showing new segmental wall motion abnormality or identification of coronary thrombosis on catheterization or autopsy.

The type II MI has very similar requirements as type I but has the absence of coronary thrombosis. Due to the similarities it may be difficult to differentiate a type I and II MI without left heart catheterization or autopsy. In general, patients who have not undergone left heart catheterization and do not have postoperative ST elevation or new LBBB on EKG most often have a type II MI, which is the dominant cause of cardiac enzyme leak after vascular surgery. The diagnosis of type II MI has likely increased as the fidelity (sensitivity and specificity) of cardiac enzymes have improved dramatically. Keep in mind, a type II MI can be caused by increased oxygen demand in the presence of fixed coronary artery occlusive (inadequate flow reserve) in the absence of plaque instability or thrombus. This becomes very important as patients improperly labeled with type I MI are often adjudicated by outside quality peer review analysis in a way that can adversely impact hospital MI outcomes data. ^, Type II MI patients may lack associated significant coronary artery disease but have microvascular disease or other concomitant structural issues within the myocardium that limit tolerance to extreme changes in oxygen demand during major vascular surgery.

To further complicate matters, some patients will have the typical rise and fall of cTn but lack the EKG changes, segmental wall motion changes or other findings to support the diagnosis of a type I or type II MI during or following surgery. In this case, the event is defined as “myocardial injury” due to cardiomyocyte death or injury unrelated to ischemia. We see these types of events when the right or left ventricle is placed under strain that exceeds the boundary conditions predicted by the Frank–Starling curve, resulting in nonischemic stretch injury to cardiac myocytes. It can also be caused by severe metabolic derangements, catecholamine excess and cardioversion.

Many of our surgical and perioperative medicine colleagues have suggested describing the perioperative cardiac enzyme leak (irrespective of MI type) as “myocardial injury after noncardiac surgery” (MINS) or perioperative myocardial injury after surgery (PMI). ^, We believe this adds confusion to the literature since “myocardial injury” is defined differently in the most recent multidiscipline global Universal Definitions described above. However, elevated high-sensitivity cTn is seen in 1 in 7 of patients after noncardiac surgery with an associated 9% and 22% 30-day and 1-year mortality, respectively. There is also a linear relationship between increasing levels of cTn release and 30-day mortality ranging from 0.5% (cTn <20 ng/L) to 29.6% for cTn of >1000 ng/L. Positive high-sensitivity cTn is even more common after vascular surgery (1 in 5 patients) and is associated with an eightfold increase in 30-day mortality. ^{, , ,} It’s unclear today if cTn leak is a predictor of mortality due to the direct impact of the MI/injury or because the presence of positive cardiac enzymes self-selects patients that would ultimately be at the highest risk of mortality. Irrespective, enzyme leaks are proven to be a marker of increased risk of mortality postoperatively and should not be dismissed as a biological epiphenomena. To simplify the different types and causes for cardiac myocyte injury, a modified algorithm for vascular surgery patients is provided with emphasis on the relevant 4th Universal Definition of MI criteria with the inclusion of where MINS fits into this clinical spectrum (see Chapter Algorithm 1).

Unfortunately, some patients with poor cardiac reserve or a large burden of perioperative cardiomyocyte insult may face a continuum of pathophysiologic substrates as detailed in Figure 44.1 . For example, patients who are experiencing a large type I infarction, or a new type I infarction superimposed on baseline poor LV function, may subsequently develop an oxygen demand mismatch type II MI due to compensatory changes in the non-infarct zone or from associated poor perfusion due to declining cardiac output. Subsequently, these patients develop compensatory dilation of the left ventricle with progressive LV strain and alongside worsening acidemia there can be direct nonischemic myocardial injury as well. These patients digress into the so-called “spiral” to progressive cardiogenic shock and often do not survive.

Congestive Heart Failure

The pathophysiology and etiology of congestive heart failure (CHF) before, during or following vascular surgery varies significantly and often a single cause is difficult to fully characterize. Any baseline valvular or left ventricular (LV) function abnormality makes the patient vulnerable to perioperative volume shifts and myocardial insult. In the preoperative assessment of patients over age 65 undergoing major noncardiac surgery, CHF was present in 18% of patients. In a Medicare database registry the presence of perioperative CHF was associated with a 63% increase in operative mortality and was a better predictor of re-admission than known coronary artery disease (CAD), although the cause of CHF was not fully elucidated. In other studies, patients who have heart failure with preserved ejection fraction (HFpEF) seem to do better perioperatively whereas the degree of reduced LV function in heart failure with reduced ejection fraction (HFrEF) seems to correlate with worse outcomes. Not surprisingly, in patients undergoing vascular surgery the impact of a preoperative diagnosis of CHF dramatically impacts outcome. For example, patients with CHF compared to patients without CHF undergoing infrainguinal bypass have a >twofold increase in 30-day mortality and prolonged length of stay (>9 days).

Preoperative transthoracic echocardiography (TTE) and natriuretic peptides (NTproBNP or BNP) should be obtained in all patients with known or suspected LV dysfunction. “Brain” natriuretic peptide (BNP) is a misnomer since it was initially discovered in the ventricles of the porcine brain before subsequently noted to be more abundant in LV myocytes. BNP release is directly proportional to LV volume expansion as is the inactive prohormone NT-proBNP. The latter has a slightly longer half-life than BNP but more studies in different patient phenotypes are needed before one of these assays could be suggested over the other. The natriuretic peptides are strong predictors of postoperative MACE and mortality in vascular surgery patients. While the Canadian perioperative guidelines suggest obtaining these studies in all major risk surgery patients with or without history of CHF, many centers still reserve these assays for patients with known or suspected LV dysfunction. ^,

Another potential etiology and risk factor for CHF is valvular disease and this is particularly true of aortic stenosis (AS) since 2% to 3% of patients over 65 years old have calcific aortic valvular stenosis. Unfortunately, many vascular patients with hemodynamic significant aortic stenosis may be asymptomatic due to vascular disease-associated limited activity. It is impractical to screen all patients for AS prior to surgery and the hemodynamic severity of AS cannot be predicted by intensity or harshness of a systolic ejection murmur on exam. The surgeon should be alerted to the presence of significant aortic valve disease if there is delayed carotid or brachial artery upstroke (parvis et tardus) in the presence of a systolic ejection murmur. This finding also can be seen as delayed pulse wave inflection on a radial artery tracing placed at the time of surgery. Severe AS (valve area ≤1 cm ² ) is associated with increased MACE following major noncardiac surgery. While the AS-associated perioperative mortality has decreased it remains high in patients undergoing emergency surgery and is worse in those with concomitant atrial fibrillation or azotemia. Symptomatic regurgitant lesions are generally better tolerated but need to be clinically optimized prior to elective vascular surgery.

Arrhythmias

The most common perioperative arrhythmia is new-onset atrial fibrillation (AFib) and is seen in 4.7% of patients undergoing vascular surgery. Most often postoperative AFib will spontaneously return to normal sinus rhythm; however, incidental AFib after vascular surgery is associated with significant increases in 30-day MACE, stroke and mortality that is likely explained by the underlying risk factors for this arrhythmia. ^, Atrial fibrillation generally occurs in patients with baseline abnormalities in left atrial architecture (e.g. fibrosis, cellular ultrastructural defects, and contractile protein abnormalities) with associated electrical and autonomic remodeling. Often the atrial pathology predisposing to AFib is driven by long-term injury due to valvular or ventricular dysfunction with pressure overload-associated atrial remodeling. The most common substrate is long-standing hypertension with associated left ventricular diastolic dysfunction. In these patients, atrial fibrillation alone could precipitate perioperative CHF since the loss of atrial contribution to overall cardiac output is much greater in patients with impaired left ventricular relaxation.

Perioperative ventricular arrhythmias are often associated with ischemia, myocardial injury, electrolyte imbalance or catecholamine excess. Non-sustained ventricular tachycardia (VT) can be seen in as many as 1 in 6 vascular surgery patients but sustained VT and ventricular fibrillation (VF) are seen in only 2% and 1% of patients, respectively. Vascular surgery patients with a reduced preoperative ejection fraction have a higher risk of ventricular arrhythmias (VT and VF) and those patients that have perioperative ventricular arrhythmias have a higher risk of sudden cardiac death during follow-up.

Cardiac Risk Indices

The optimal vascular surgery cardiac risk index remains elusive. The Revised Cardiac Risk Index (RCRI) has gained popularity in noncardiac surgery with an overall accuracy ranging between 0.75 and 0.80. The RCRI has been widely used and was adopted by the ACC/AHA and ESC/ESA guideline committees for the preoperative stratification of a patient’s perioperative cardiac risk. However, when limited strictly to studies of vascular surgical populations, a meta-analysis of 24 studies showed that the RCRI had an aggregate sensitivity and specificity of 0.70 and 0.55, suggesting inadequate reliability.

In 2010, the Vascular Study Group of New England (VSGNE) found in a study of over 10,000 patients that the RCRI predicted risk after carotid endarterectomy (CEA) reasonably well, but substantially underestimated risk for low- and higher-risk patients. In a multivariate analysis of the VSGNE cohort, the independent predictors of adverse cardiac events included: increasing age, smoking, insulin-dependent diabetes, CAD, CHF, abnormal cardiac stress test, long-term beta-blocker therapy, COPD, and elevated creatinine. The rates of cardiac complications for patients with zero to three, four, five, and greater than or equal to six VSGNE Cardiac Risk Index (VSG-CRI) risk factors were 3.1%, 5.0%, 6.8%, and 11.6% in the derivation cohort and 3.8%, 5.2%, 8.1%, and 10.1% in the validation cohort, respectively. The authors concluded that the VSG-CRI risk model more accurately predicted the actual risk of cardiac complications in vascular surgery patients than the RCRI.

More recently, the analysis of 88,879 patients in the vascular quality initiative (VQI) registry led to the development of a risk calculator that allowed independent risk assessment for various subtypes of vascular surgery. The procedure-specific models generated by the VQI Cardiac Risk Index (VQI-CRI) demonstrated improved prediction compared with the all-procedure model, with CEA, INFRA, EVAR, and Open AAA. Our team now uses the QxCalculate VQI-CRI app as the preferred risk index assessment model for our vascular surgery patients. However, we anticipate as biomarker assays improve and artificial intelligence matures we will see a movement towards personalized risk assessment based on patient phenotypes, comorbidities, biomarkers and type/urgency of vascular surgery.

Preoperative Blood Work and Risk of MACE

Selection of screening bloodwork before vascular surgery is highly dependent on clinical variables that may impact overall risk, including but not limited to comorbidities and medications (see Ch. 34 , Preoperative Evaluation and Management).