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Synopsis of Adult Cardiac Surgical Disease

It is essential that all individuals involved in the assessment and management of patients with cardiac surgical disease have a basic understanding of the disease processes that are being treated. This chapter presents the spectrum of adult cardiac surgical disease that is encountered in most cardiac surgical practices. The pathophysiology, indications for surgery, specific preoperative considerations, and surgical options for various diseases are presented. Diagnostic techniques and general preoperative considerations are presented in the next two chapters. Issues related to cardiac anesthesia and postoperative care specific to most of the surgical procedures presented in this chapter are discussed in Chapters 4 and 8, respectively. The most current guidelines for the evaluation and management of patients with cardiac disease can be obtained from the American College of Cardiology website (www.acc.org).

I. Coronary Artery Disease

1. Pathophysiology. Coronary artery disease (CAD) results from the progressive blockage of the coronary arteries by atherothrombotic disease. Significant risk factors include hypertension, dyslipidemia (especially high LDL, low HDL, elevated Lp(a) or apoB, or triglycerides), diabetes mellitus, obesity (a combination of the above being termed metabolic syndrome), cigarette smoking, and a family history of premature CAD. Clinical syndromes result from an imbalance of oxygen supply and demand resulting in inadequate myocardial perfusion to meet metabolic demand (ischemia). Progressive compromise in luminal diameter producing supply/demand imbalance usually produces a pattern of chronic stable angina, commonly referred to as “stable ischemic heart disease (SIHD). Plaque rupture with superimposed thrombosis is responsible for most acute coronary syndromes (ACS), which include classic “unstable angina”, non‐ST‐elevation myocardial infarctions (non‐STEMI), and ST‐elevation infarctions (STEMI). Paradoxically, plaque rupture more commonly occurs in coronary segments that are not severely stenotic. Endothelial dysfunction has become increasingly recognized as a contributing factor to worsening ischemic syndromes. Generalized systemic inflammation, indicated by elevated C‐reactive protein levels, is usually noted in patients with ACS, and appears to be associated with adverse outcomes.
2. Primary prevention of cardiovascular disease entails control of modifiable risk factors. Notably, statins are generally not recommended for patients with normal cholesterol levels (unless there is a family history of premature CAD) or for patients at low risk for atherosclerotic cardiovascular disease (ASCVD) based on the ASCVD risk calculator (available at https://clincalc.com/cardiology/ascvd/pooledcohort.aspx). Furthermore, aspirin, which had been widely utilized for primary prevention in the past, has received only a level IIb recommendation for patients age 40–70 with higher ASCVD risk, but not at increased bleeding risk, and was considered contraindicated on a routine basis in patients >age 70 or in any patient with an increased risk of bleeding according to a 2019 ACC report.1
3. Management strategies in stable ischemic heart disease (SIHD)
   1. Symptomatic coronary disease is initially treated with medical therapy, including aspirin, nitrates, ß‐adrenergic blockers, and calcium‐channel blockers (CCBs). Ranolazine may be added as a second‐line drug for symptomatic relief in patients with refractory angina. It inhibits inward sodium currents in the heart muscle, leading to a reduction in intracellular calcium levels, which reduces myocardial wall tension and oxygen requirements. It does not cause bradycardia and hypotension, which occasionally are limiting factors with the use of other antianginal drugs. Statins should be given to control dyslipidemias and are effective for plaque stabilization. Angiotensin‐converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) are given to patients with depressed left ventricular (LV) function (ejection fraction [EF] <40%) and to those with hypertension and diabetes. P2Y12 inhibitors (clopidogrel, ticagrelor) generally do not provide benefit to patients with SIHD.
   2. Optimal medical therapy should be the initial management strategy for patients with SIHD, since studies have not shown that proceeding to percutaneous coronary intervention (PCI) reduces the risk of death, infarction or other major adverse cardiovascular events.2 Thus, the decision to proceed with cardiac catheterization should be based on the rationale that the patient’s symptoms are disabling enough or the degree of ischemia is significant enough to warrant an intervention to revascularize the heart. Risk stratification with noninvasive functional testing is important to provide objective evidence of inducible ischemia, using exercise stress testing, nuclear imaging, or dobutamine stress echocardiography.
   3. The decision to proceed with an intervention must then take into consideration an angiographic assessment of the extent of coronary disease and an invasive assessment of its physiologic significance by fractional flow reserve (FFR)3 or instantaneous flow reserve (iFR)4, which is not dependent on the administration of adenosine. Additional critical information when considering PCI or coronary artery bypass grafting (CABG) includes the patient’s comorbidities, particularly diabetes mellitus, and an assessment of LV function. Multiple studies comparing medical therapy with PCI for patients with SIHD have shown that PCI reduces the incidence of angina, may increase the short‐term risk of myocardial infarction (MI), but does not lower the long‐term risk of MI or improve survival.5 However, PCI does reduce the need for urgent revascularization and may reduce the risk of MI in patients with a large ischemic burden. Superior clinical outcomes are achieved with complete revascularization, which in many patients is better accomplished with CABG than PCI.6 Use of systematic anatomic assessments, such as with the SYNTAX score (see section C.4.a), has been accepted as an adjunct to this decision‐making process.
   4. Appropriate use criteria (AUC) with complex matrices have been set forth for coronary revascularization strategies in patients with SIHD.7 These are subdivided by the number of diseased vessels (1–2–3), the presence of symptoms, the use of antianginal therapy, and whether noninvasive testing indicates the patient is at low, intermediate, or high risk for a cardiac event, or in the absence of testing, by the results of FFR/iFr studies.
      1. The SYNTAX score (http://www.syntaxscore.com) is also incorporated into the AUC guidelines and can be used to determine whether PCI or CABG is preferable for multivessel or left main (LM) disease. This provides an angiographic assessment of coronary disease with an additive score that evaluates the location and degree of stenosis in each vessel, the angiographic complexity of the lesion, vessel diameter and calcification. The SYNTAX trial divided patients into low risk (score of 0–22), intermediate risk (score of 23–32), and high risk (score >32) categories and used a primary end point of major adverse cardiac and cerebrovascular events (MACCE), which includes mortality, myocardial infarction (MI), stroke, and the need for repeat revascularization.
      2. Five‐year follow‐up data from the SYNTAX trial showed that patients in the low‐risk category had similar MACCE rates with PCI or CABG. However, CABG produced superior results in intermediate‐ to high‐risk patients with three‐vessel disease (score >22), and those at high risk with LM disease. In these cohorts, CABG was associated with less MACCE, more complete revascularization, reduced need for repeat revascularization, and improved long‐term benefit.8,9
      3. The FREEDOM trial showed that CABG is superior to PCI in diabetic patients with multivessel disease,10,11 and the presence or absence of diabetes is specifically incorporated into the AUC guidelines for multivessel and LM disease. In these diabetic patients, the SYNTAX score was found to be a predictor of MACCE only with PCI, and therefore was not recommended to guide therapy.12
      4. A “residual SYNTAX” score >8 after PCI for patients in the moderate‐ to high‐risk cohorts, indicative of incomplete revascularization, had worse 30‐day and one‐year survival.13 In fact, in the entire SYNTAX study, PCI resulted in a 10‐fold increase in MI‐related death compared with CABG, but this was mostly accounted for in patients with diabetes, multivessel disease, and high SYNTAX scores.14
      5. One shortcoming of the SYNTAX score was that it correlated only an angiographic assessment with the best revascularization strategy. Because surgery might provide more benefit to patients with significant clinical comorbidities in addition to the anatomical complexity of disease, the SYNTAX II scoring system was devised. This included eight predictors – two anatomic (SYNTAX score and unprotected LM disease), and six clinical predictors (age, creatinine clearance, ejection fraction, female gender, peripheral vascular disease, and chronic obstructive pulmonary disease [COPD]). The SYNTAX II study used second‐generation drug‐eluting stents and intravascular ultrasound imaging with PCI. It showed...