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Surgery_Schwartz. decreases angina burden when added to CABG in patients who cannot be revascularized by CABG alone.90 The current STS guidelines support the consideration of TMR in patients with ischemic myocardial territories that cannot be revascularized by PCI or CABG.91 Because of equivocal late results at most centers, this therapeutic strategy has not gained widespread acceptance, and ACC/AHA guidelines give TMR a class IIb recommendation for treatment of refractory angina.39New DevelopmentsRegenerative Medicine and Tissue Engineering. Provoca-tive investigations are being performed on the level of signaling molecules, gene therapy, stem cells, and tissue engineering to regenerate or replace damaged tissue in patients with ischemic heart disease. Growth factors, such as fibroblast growth fac-tor (FGF) and vascular endothelial growth factor (VEGF), are receiving attention due to their ability to induce growth of new vessels. Although concerns regarding systemic administration of these pleiotropic


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Surgery_Schwartz. and vascular endothelial growth factor (VEGF), are receiving attention due to their ability to induce growth of new vessels. Although concerns regarding systemic administration of these pleiotropic signaling molecules exist, early placebo-controlled clinical trials have shown some promising results with administration of these agents.92,93 Adenoviral transfection of diseased tissue with transgenes for growth factors and tran-scription factors has been attempted with variable results.Research in tissue engineering has been directed at cre-ation of vascular conduits that are resistant to atherosclerosis. Stem cells have also been infused directly into the site of injury or in the generation of new tissue around a biodegradable scaffold.94 Despite their potential, these technologies are still in their infancy, and significant progress will be needed before more widespread clinical adoption.VALVULAR HEART DISEASEGeneral PrinciplesThe number of patients undergoing surgical management of


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Surgery_Schwartz. in their infancy, and significant progress will be needed before more widespread clinical adoption.VALVULAR HEART DISEASEGeneral PrinciplesThe number of patients undergoing surgical management of valvular heart disease has increased over the last decade, from a total of 26,547 isolated aortic or mitral valve procedures reported to the STS Adult Cardiac Surgery Database in 2006 to 45,253 such procedures in 2015.95 In 2016, valve procedures represented over 50% of the cases performed at our institution. Although congenital and inherited etiologies represent impor-tant clinical entities, age-associated and acquired conditions still represent the primary causes of valvular heart disease and are the focus of this section.The most common screening method for valvular heart disease is cardiac auscultation, with murmurs classified based primarily on their timing in the cardiac cycle, but also on their configuration, location and radiation, pitch, intensity, and dura-tion (Table 21-6).96


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Surgery_Schwartz. auscultation, with murmurs classified based primarily on their timing in the cardiac cycle, but also on their configuration, location and radiation, pitch, intensity, and dura-tion (Table 21-6).96 Although some systolic murmurs are related to normal physiologic increases in blood flow, some may indi-cate cardiac disease, such as valvular aortic stenosis (AS), that are important to diagnose, even when asymptomatic. Diastolic and continuous murmurs, on the other hand, are frequently Brunicardi_Ch21_p0801-p0852.indd 81401/03/19 5:32 PM 815ACQUIRED HEART DISEASECHAPTER 21Table 21-7Hemodynamic alterations in cardiac murmur intensityINTERVENTIONEFFECTRespirationRight-sided murmurs increase with inspiration. Left-sided murmurs increase with expiration.Valsalva maneuverMost murmurs decrease in length and intensity. The murmur of HCM becomes louder, and the murmur of MVP becomes louder and longer.ExerciseBenign flow murmurs and murmurs caused by stenotic valves become louder with isotonic


Surgery_Schwartz

Surgery_Schwartz. length and intensity. The murmur of HCM becomes louder, and the murmur of MVP becomes louder and longer.ExerciseBenign flow murmurs and murmurs caused by stenotic valves become louder with isotonic and isometric exercise. The murmurs of MR, VSD, and AI also increase with isometric exercise.Positional changesMost murmurs decrease with standing; the murmur of HCM becomes louder, and the murmur of MVP becomes louder and longer. Brisk squatting and passive leg raising increases most murmurs; the murmurs of HCM and MVP diminish.Postventricular premature beat or atrial fibrillationBenign flow murmurs and stenosis at the semilunar valves increase in intensity following a ventricular premature beat or a long cycle length in atrial fibrillation. Systolic murmurs of atrioventricular valve regurgitation do not change.Pharmacologic interventionsThe initial hypotensive phase following inhalation of amyl nitrate decreases the murmurs of MR, VSD, and AI, and increases the murmur of AS. The later


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Surgery_Schwartz. do not change.Pharmacologic interventionsThe initial hypotensive phase following inhalation of amyl nitrate decreases the murmurs of MR, VSD, and AI, and increases the murmur of AS. The later tachycardic phase following inhalation of amyl nitrate increases right-sided murmurs and the murmur of MS. The response in MVP is biphasic (softer then louder than control).Transient arterial occlusionTransient external compression of the upper extremity increases the murmurs of MR, VSD, and AI.AI = aortic insufficiency; AS = aortic stenosis; HCM = hypertrophic cardiomyopathy; MR = mitral regurgitation; MS = mitral stenosis; MVP = mitral valve prolapse; VSD = ventricular septal defect.pathologic in nature. Dynamic cardiac auscultation provides further evidence as to the significance and origin of many mur-murs (Table 21-7).96Although auscultation may provide initial evidence to the existence of valvular disease, associated signs and symptoms may help narrow the diagnosis. Abnormalities in the


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Surgery_Schwartz. many mur-murs (Table 21-7).96Although auscultation may provide initial evidence to the existence of valvular disease, associated signs and symptoms may help narrow the diagnosis. Abnormalities in the splitting of the heart sounds and additional heart sounds should be noted, as should the presence of pulmonary rales. Peripheral pulses should be checked for abnormal intensity or timing, and the presence of a jugular venous wave should be documented. Addi-tionally, symptoms of syncope, angina pectoris, heart failure, and peripheral thromboembolism are important and may help guide diagnosis and management.Several imaging examinations are also available to aid in the diagnosis and classification of various valvular disorders. Electrocardiograms may provide information regarding ven-tricular hypertrophy, atrial enlargement, arrhythmias, conduc-tion abnormalities, prior myocardial infarction, and evidence of active ischemia that would prompt further workup. Posteroan-terior and lateral chest


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Surgery_Schwartz. atrial enlargement, arrhythmias, conduc-tion abnormalities, prior myocardial infarction, and evidence of active ischemia that would prompt further workup. Posteroan-terior and lateral chest X-rays are also easy to obtain and may yield information regarding cardiac chamber size, pulmonary blood flow, pulmonary and systemic venous pressure, and cardiac calcifications. The gold standard for the evaluation of valvular heart disease is transthoracic echocardiography (TTE), which is helpful in the noninvasive evaluation of valve mor-phology and function, chamber size, wall thickness, ventricu-lar function, pulmonary and hepatic vein flow, and pulmonary artery pressures. Specialized examinations based on the specific findings of TTE examinations are discussed in the following sections.Regardless of the etiology, valvular heart disease can pro-duce a myriad of hemodynamic derangements. Left untreated, valvular stenosis and insufficiency can produce significant pressure and volume overload on


Surgery_Schwartz

Surgery_Schwartz. of the etiology, valvular heart disease can pro-duce a myriad of hemodynamic derangements. Left untreated, valvular stenosis and insufficiency can produce significant pressure and volume overload on the affected cardiac chamber, respectively, with mixed disease consequently causing mixed pathology. Although the heart can initially compensate for alter-ations in cardiac physiology, cardiac function eventually dete-riorates, leading to heart failure, decreased patient functional status, ventricular dysfunction, and eventually death. In order to optimize long-term survival, surgery or transcatheter therapeu-tics are recommended in various forms of valvular heart disease and in an increasing number of elderly and high-risk patients.Surgical OptionsAlthough valve repair is increasingly indicated, especially in patients with aortic, mitral or tricuspid insufficiency, valve replacement is appropriate in certain patient populations. Valve replacement can be accomplished with either mechanical


Surgery_Schwartz

Surgery_Schwartz. especially in patients with aortic, mitral or tricuspid insufficiency, valve replacement is appropriate in certain patient populations. Valve replacement can be accomplished with either mechanical or bio-logical prostheses, and the choice of valve depends on many patient-specific factors such as age, health status, and desire for future pregnancy. Preexisting indications or contraindications to anticoagulation therapy also influence the choice of mechanical versus tissue valve prosthesis.Current options for mechanical valve replacement include either tilting disc valves or bileaflet valves. Although mechanical valves are highly durable, they require perma-nent anticoagulation to mitigate the risk of valve thrombosis and thromboembolic sequelae.97 Due to the concordant risk of hem-orrhagic complications, patient characteristics such as debility, lifestyle, and contraindications to systemic anticoagulation therapy may preclude mechanical valve replacement. Moreover, young women who are


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Surgery_Schwartz. complications, patient characteristics such as debility, lifestyle, and contraindications to systemic anticoagulation therapy may preclude mechanical valve replacement. Moreover, young women who are planning future pregnancies cannot take warfarin due to its teratogenic potential. Conversely, patients with other indications for systemic anticoagulation, such as other risk factors for thromboembolism (i.e., atrial fibrillation), or the presence of a mechanical prosthetic valve in place in another position, may benefit from mechanical valve replace-ment. Current ACC/AHA guidelines recommend a shared-decision-making process between patient and physician when determining the choice of valve prosthesis, with the use of 3Brunicardi_Ch21_p0801-p0852.indd 81501/03/19 5:32 PM 816SPECIFIC CONSIDERATIONSPART IIFigure 21-5. SJM Regent mechanical heart valve. (SJM Regent and St. Jude Medical are trademarks of St. Jude Medical, LLC or its related companies. Reproduced with permission of St.


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Surgery_Schwartz. 21-5. SJM Regent mechanical heart valve. (SJM Regent and St. Jude Medical are trademarks of St. Jude Medical, LLC or its related companies. Reproduced with permission of St. Jude Medical, ©2017. All rights reserved.)bioprosthetic valves in all patients who have a contraindication to lifelong anticoagulation or who are unwilling to receive it.98The potential to avoid the hazards of serious bleeding com-plications spurred the development of valve prostheses using biological materials, which obviate the need for systemic anti-coagulation therapy. As tissue valves are naturally less throm-bogenic, the attendant yearly risks of both thromboembolic and anticoagulation-related complications are considerably less than with mechanical valves.99 Consequently, tissue valve replace-ment is generally recommended for patients averse to systemic anticoagulation therapy, with potential concerns regarding com-pliance or follow-up while taking anticoagulant medications, and in the case of reoperation


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Surgery_Schwartz. recommended for patients averse to systemic anticoagulation therapy, with potential concerns regarding com-pliance or follow-up while taking anticoagulant medications, and in the case of reoperation for a thrombosed mechanical valve. However, biological valves are more prone to degenera-tion, especially when implanted in the mitral position, and in younger patients, and those in renal failure, on hemodialysis, or with hypercalcemia.99 Improved manufacturing methods have made currently available tissue valves more durable than previ-ous versions, and valve replacement with a biological prosthesis is generally preferred in patients without other indications for anticoagulation therapy who are >60 years of age for the aortic position and >70 years of age for the mitral position. The avail-ability of transcatheter aortic valves for re-replacement, has resulted in patients and surgeons preferring bioprosthetic aortic valves in patients even <60 years of age in many centers.Mechanical


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Surgery_Schwartz. of transcatheter aortic valves for re-replacement, has resulted in patients and surgeons preferring bioprosthetic aortic valves in patients even <60 years of age in many centers.Mechanical Valves. The first bileaflet mechanical valve was introduced in 1977. Bileaflet valves are comprised of two semi-circular leaflets that open and close, creating one central and two peripheral orifices (Fig. 21-5). Bileaflet mechanical valves have demonstrated excellent flow characteristics, low risk of late valve-related complications, including valve failure, and are currently the most commonly implanted type of mechanical valve prosthesis in the world.100Although mechanical valves necessitate systemic antico-agulation, careful monitoring of the International Normalized Ratio (INR) reduces the risk of thromboembolic events and hemorrhagic complications and improves overall survival.101 Patients undergoing mechanical aortic valve replacement gen-erally have a target INR of 2 to 3 times normal;


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Surgery_Schwartz. of thromboembolic events and hemorrhagic complications and improves overall survival.101 Patients undergoing mechanical aortic valve replacement gen-erally have a target INR of 2 to 3 times normal; however, after a randomized study, one of the mechanical aortic valves has been improved for an INR range of 1.5 to 2.0.102 Patients undergoing mechanical mitral valve replacement frequently have increased left atrial size, concomitant atrial fibrillation, and are at higher risk for thromboembolism that those undergoing aortic valve replacement and are thus recommended to have a target INR 2.5 to 3.5 times normal. When managed appropriately, the yearly risk of major bleeding is <1.4%. Patients with mechanical mitral valve prostheses have nearly twice the thromboembolic risk of those with mechanical aortic valve prostheses (1.3% vs. 0.8% per year).103Tissue Valves. A xenograft valve is one implanted from another species, such as porcine xenograft valves, or manufac-tured from tissue such as


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Surgery_Schwartz. aortic valve prostheses (1.3% vs. 0.8% per year).103Tissue Valves. A xenograft valve is one implanted from another species, such as porcine xenograft valves, or manufac-tured from tissue such as bovine pericardium. A variety of xeno-graft tissue valves exist and are primarily differentiated by the presence or absence of a mounting stent. Stented valves are the most commonly implanted, and the most popular valve in the United States is a stented bovine pericardial valve.104The more traditional stented valves are attached to a sew-ing ring, which decreases the technical complexity of valve replacement compared with stentless valves (Fig. 21-6). The chief disadvantage of stented tissue valves is a smaller effective orifice area, which increases the transvalvular gradient. This phenomenon is referred to as patient prosthetic mismatch. This effect is most pronounced in patients with small prosthetic valve areas, specifically <0.85 cm2 valve area per square meter body surface area and may


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Surgery_Schwartz. referred to as patient prosthetic mismatch. This effect is most pronounced in patients with small prosthetic valve areas, specifically <0.85 cm2 valve area per square meter body surface area and may affect survival, symptomatic improve-ment, and the hemodynamic response to exercise following surgery.105Stentless porcine xenograft valves were developed in order to minimize the limitations in flow characteristics seen in patients with small prosthetic valve areas and have demon-strated an increase in effective valve area of approximately 10% over stented xenografts of equivalent size.100 They can result in improved hemodynamics, both at rest and with exercise.106 The absence of a stent and sewing ring both increases the techni-cal complexity of valve replacement and takes advantage of the biologic mobility of the aortic valve apparatus. Though results with stentless valves seem promising, some stentless valves have been shown to have poor durability,107 and stentless valves have not


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Surgery_Schwartz. biologic mobility of the aortic valve apparatus. Though results with stentless valves seem promising, some stentless valves have been shown to have poor durability,107 and stentless valves have not been widely adopted due to the technical complexity of implantation.Recently, rapid deployment valves have been introduced to further decrease the complexity and time required for aortic valve replacement. Two of these valves are on the market in the United States. The Perceval valve by LivaNova is the only sutureless, stentless valve available.108 These rapid deployment valves have shown improved hemodynamics, particularly in patients with small annuli, and shorter implantation times. In some series, these benefits have been shown to reduce early morbidity.108Homografts. Homograft valves from human cadavers, also known as allografts, have been used for aortic valve replace-ment since the technique was originally described over 50 years ago.109 Since that time, homografts have typically


Surgery_Schwartz

Surgery_Schwartz. human cadavers, also known as allografts, have been used for aortic valve replace-ment since the technique was originally described over 50 years ago.109 Since that time, homografts have typically been used for aortic and pulmonary valve replacements and have been successfully harvested from brain dead organ donors and the Brunicardi_Ch21_p0801-p0852.indd 81601/03/19 5:32 PM 817ACQUIRED HEART DISEASECHAPTER 21Figure 21-6. Carpentier-Edwards PERIMOUNT Magna Ease stented porcine bioprosthesis. (Edwards Lifesciences LLC, Irvine, CA. Additionally, it should be noted that Edwards, Edwards Lifesciences, the stylized E logo, Carpentier-Edwards, Carpentier-Edwards Classic, Magna, Magna Ease, Magna Mitral Ease are trademarks of Edwards Lifesciences Corporation.)explanted hearts of heart transplant recipients. Following har-vest, these valves are sterilized using an antibiotic solution and subsequently stored in fixative or cryopreservation solution.Like other types of tissue valves, the


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Surgery_Schwartz. recipients. Following har-vest, these valves are sterilized using an antibiotic solution and subsequently stored in fixative or cryopreservation solution.Like other types of tissue valves, the risk of thrombo-embolic complications with homograft valves is low, and sys-temic anticoagulation therapy is not required. Additionally, the structure of homograft valves is naturally low-profile, allow-ing for larger effective valve orifices and lower postoperative transvalvular gradients compared with stented xenograft valves. Additionally, they have been shown to have some advantages in patients with endocarditis.110The major shortcoming of homograft valves is their lim-ited long-term durability due to tissue degeneration. Within one year of implantation, these valves undergo substantial loss of cellular components and subsequent structural compro-mise, which may ultimately lead to valve failure.111 Although enhanced preservation techniques has improved cellular viabil-ity, which approaches


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Surgery_Schwartz. cellular components and subsequent structural compro-mise, which may ultimately lead to valve failure.111 Although enhanced preservation techniques has improved cellular viabil-ity, which approaches the 15-year viability of xenograft valves, the limited availability of these valves and techniques has lim-ited the use of homograft tissue valves.Autografts. In 1967, Donald Ross described a procedure in which the diseased aortic valve was replaced using the patient’s native pulmonary valve as an autograft, which was in turn replaced with a homograft in the pulmonic position.112 The pro-cedure resulted in minimal transvalvular gradients and favor-able left ventricular mechanics, both at rest and during exercise. Known as the Ross procedure, this operation has been shown to be particularly beneficial in children, as the pulmonary trunk grows with the child and long-term anticoagulation is not required.113The late results of the Ross procedure are discussed later in this chapter. In


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Surgery_Schwartz. beneficial in children, as the pulmonary trunk grows with the child and long-term anticoagulation is not required.113The late results of the Ross procedure are discussed later in this chapter. In addition to potential concerns with durability, performance of the Ross procedure has also been limited by its technical complexity and the increased surgical risk associated with double valve replacement.Valve Repair. Valve repair offers a number of advantages over valve replacement, due in large part to the preservation of the patient’s native valvular and subvalvular apparatus. In mitral valve (MV) surgery, preservation of the mitral apparatus has been shown to lead to better postoperative left ventricular func-tion and survival.114,115 Additionally, as there is no implanted prosthesis, the patient avoids the risks of chronic anticoagula-tion, infection, thromboembolic complications, and prosthetic valve failure after surgery.In the case of MV repair, freedom from reoperation and


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Surgery_Schwartz. the patient avoids the risks of chronic anticoagula-tion, infection, thromboembolic complications, and prosthetic valve failure after surgery.In the case of MV repair, freedom from reoperation and valve-related complications has been excellent in certain patient populations, even at 20-year follow-up.116 It has also been dem-onstrated that patients undergoing MV surgery with moder-ate functional tricuspid regurgitation (TR) do not experience increased perioperative complication rates when a concomitant tricuspid valve (TV) repair is performed.117 Midterm results in this group are encouraging, with greater than 98% freedom from reoperation reported by some groups at 5 years, suggesting fur-ther indications for valve repair.Despite its advantages for the patient, valve repair is gen-erally more technically demanding than valve replacement and may occasionally fail. Both the suitability of the patient for valve repair and the skill and expertise of the surgeon perform-ing the operation


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Surgery_Schwartz. more technically demanding than valve replacement and may occasionally fail. Both the suitability of the patient for valve repair and the skill and expertise of the surgeon perform-ing the operation are important when considering valve repair in the individual patient.MITRAL VALVE DISEASEMitral StenosisEtiology. Acquired mitral stenosis (MS) is most often caused by rheumatic fever, with approximately 60% of patients with pure MS presenting with a clinical history of rheumatic heart disease.96 Rarely, other conditions can cause obstruction to fill-ing of the left ventricle (LV), mimicking MS. Acquired causes of MV stenosis include left atrial myxoma, prosthetic valve thrombosis, mucopolysaccharidosis, previous chest radiation, and severe annular calcification.Pathology. Although rheumatic heart disease is associated with a transmural pancarditis, pathological fibrosis of the valves Brunicardi_Ch21_p0801-p0852.indd 81701/03/19 5:32 PM 818SPECIFIC CONSIDERATIONSPART IIFigure


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Surgery_Schwartz. heart disease is associated with a transmural pancarditis, pathological fibrosis of the valves Brunicardi_Ch21_p0801-p0852.indd 81701/03/19 5:32 PM 818SPECIFIC CONSIDERATIONSPART IIFigure 21-7. Mitral stenosis. The thickened, fused leaflets of the diseased mitral valve are viewed through a left atriotomy. (Reproduced with permission from Centers for Disease Control and Prevention, Edwin P. Ewing, Jr.)Table 21-8Data from ACC/AHA guidelines for the classification of the severity of mitral valve disease in adultsMITRAL STENOSISINDICATORMILDMODERATESEVEREMean gradient (mmHg)a< 55–10>10Pulmonary artery systolic pressure (mmHg)< 3030–50> 50Valve area (cm2)>1.51.0–1.5< 1.0MITRAL REGURGITATIONQUALITATIVEMILDMODERATESEVEREAngiographic grade1+2+3+Color Doppler jet areaSmall, central jet (< 4 cm2 or < 20% left atrial area)More than mild criteria, but no severe criteria presentVena contracta width > 0.7 cm with large central jet (area > 40% of left atrial area) or with a wall-impinging jet


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Surgery_Schwartz. or < 20% left atrial area)More than mild criteria, but no severe criteria presentVena contracta width > 0.7 cm with large central jet (area > 40% of left atrial area) or with a wall-impinging jet of any size, swirling in left atriumDoppler vena contracta width (cm)< 0.30.3–0.69≥ 0.7QUANTITATIVE (CATH OR ECHO)Regurgitant volume (ml per beat)< 3030–59≥ 60Regurgitant fraction (%)< 3030–49≥ 50Regurgitant orifice area (cm2)0.20.2–0.39≥ 0.4ADDITIONAL ESSENTIAL CRITERIALeft atrial size EnlargedLeft ventricular size EnlargedaValve gradients are flow dependent and when used as estimates of severity of valve stenosis should be assessed with knowledge of cardiac output or forward flow across the valve.results primarily from the endocarditic process. The damage caused by endocardial inflammation and fibrosis is progressive, causing commissural fusion, subvalvular shortening of the chor-dae tendineae, and calcification of the valvular and subvalvu-lar apparatus.118 The resulting stenotic MV has


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Surgery_Schwartz. fibrosis is progressive, causing commissural fusion, subvalvular shortening of the chor-dae tendineae, and calcification of the valvular and subvalvu-lar apparatus.118 The resulting stenotic MV has a funnel shape, with doming of the leaflets, and a significantly narrowed orifice caused by interchordal and commissural fusion (Fig. 21-7). The degree of mitral stenosis should be determined preoperatively, as these pathological features may help determine the timing and type of intervention to perform.96Pathophysiology. As the normal MV area of 4.0 to 5.0 cm2 is reduced by the rheumatic process, blood can flow from the left atrium to the left ventricle only if it is propelled by an ever-increasing pressure gradient. This increased left atrial pressure causes left atrial enlargement and eventually pulmonary hyper-tension and decreased exercise tolerance. Patients with diastolic valve doming, usually accompanied by a history of rheumatic fever, are defined as having stage A MS, even with


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Surgery_Schwartz. pulmonary hyper-tension and decreased exercise tolerance. Patients with diastolic valve doming, usually accompanied by a history of rheumatic fever, are defined as having stage A MS, even with normal trans-mitral flow velocities. Stage B MS is defined by an increased transmitral flow velocity with mitral valve area greater than 1.5 cm2. This condition is associated with mild to moderate left atrial enlargement but normal pulmonary arterial pressure. Stage C MS consists of a severely stenotic valve (mitral valve area ≤1.5 cm2) without symptoms. This is frequently associated with commissural fusion and diastolic doming of the leaflets as well as a pulmonary arterial pressure of >30 mmHg. Stage D MS is defined as the aforementioned criteria with the onset of decreased exercise tolerance and/or dyspnea on exertion (Table 21-8).98The onset of symptoms is due to the evolution of patho-physiological processes, beginning with an elevation in left atrial pressure. The increased left atrial


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Surgery_Schwartz. dyspnea on exertion (Table 21-8).98The onset of symptoms is due to the evolution of patho-physiological processes, beginning with an elevation in left atrial pressure. The increased left atrial pressure is subsequently transmitted to the pulmonary venous system, causing pulmo-nary edema as the hydrostatic pressure in the vessels exceeds the plasma oncotic pressure. Decreased pulmonary venous compli-ance exacerbates the pulmonary venous hypertension, though a concomitant decrease in microvascular permeability may Brunicardi_Ch21_p0801-p0852.indd 81801/03/19 5:32 PM 819ACQUIRED HEART DISEASECHAPTER 21preclude pulmonary edema in the chronic setting.119 Patients may also develop pulmonary arterial hypertension, owing to vasoconstriction, intimal hyperplasia, and medial hypertrophy of the pulmonary arterioles in response to the increased pul-monary venous pressure. The secondary obstruction to flow caused by reactive pulmonary arterial hypertension may serve to protect against


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Surgery_Schwartz. of the pulmonary arterioles in response to the increased pul-monary venous pressure. The secondary obstruction to flow caused by reactive pulmonary arterial hypertension may serve to protect against pulmonary edema, but it also exacerbates the intractable decrease in cardiac output that develops as stenosis worsens.120Throughout the process, the left atrium becomes dilated and hypertrophied due to increased work in filling the ventricle against a fixed obstruction. Atrial fibrillation (AF) may develop, exacerbating the patient’s symptoms and increasing the risk of left atrial thrombus and subsequent embolization. Left ventricu-lar structure and function are typically preserved owing to the protective effect of the stenotic valve.Clinical Manifestations. The sudden opening of the thick-ened, nonpliable valve with left atrial contraction produces an opening snap, followed by a diastolic rumble caused by rapid entry of blood into the left ventricle. When diastole is complete, the MV


Surgery_Schwartz

Surgery_Schwartz. nonpliable valve with left atrial contraction produces an opening snap, followed by a diastolic rumble caused by rapid entry of blood into the left ventricle. When diastole is complete, the MV subsequently closes very rapidly, causing an increased first heart sound. The murmur, classically known as the aus-cultatory triad, is best heard at the apex. Associated mitral and tricuspid insufficiencies are heard as a pansystolic murmur radi-ating to the axilla and a systolic murmur at the xiphoid process, respectively.The first clinical signs of MS are those associated with pulmonary venous congestion, namely exertional dyspnea, decreased exercise capacity, orthopnea, and paroxysmal noctur-nal dyspnea. Hemoptysis and pulmonary edema may develop as the venous hypertension worsens. Advanced MS can also cause pulmonary arterial hypertension and subsequent right heart fail-ure, manifested as jugular venous distention, hepatomegaly, ascites, and lower extremity edema.2As mentioned previously,


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Surgery_Schwartz. can also cause pulmonary arterial hypertension and subsequent right heart fail-ure, manifested as jugular venous distention, hepatomegaly, ascites, and lower extremity edema.2As mentioned previously, atrial fibrillation may develop as left atrial pathology worsens, causing atrial stasis and subse-quent thromboembolism. Patients with MS may initially present with signs of arterial embolization, even rarely with angina from coronary occlusion.2Diagnostic Studies. All patients with a clinical history and physical exam suggestive of MS should have an electrocardio-gram (ECG) and chest X-ray. Abnormalities in the ECG may include atrial fibrillation, left atrial enlargement, or right axis deviation. Chest X-ray findings may include enlargement of the left atrium and pulmonary artery, creating a double contour behind the right atrial shadow and obliterating the normal con-cavity between the aorta and left ventricle. Findings consistent with pulmonary congestion may also be present.2The


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Surgery_Schwartz. a double contour behind the right atrial shadow and obliterating the normal con-cavity between the aorta and left ventricle. Findings consistent with pulmonary congestion may also be present.2The diagnostic tool of choice is TTE, which not only con-firms the diagnosis of MS, but also rules out other concomi-tant myocardial or valvular heart disease.121 Two-dimensional TTE can be used to calculate the MV area and to determine the morphology of the MV apparatus, including leaflet mobility and flexibility, leaflet thickness and calcification, subvalvular fusion, and the appearance of the commissures. Doppler TTE can also be used in combination with various equations to esti-mate the hemodynamic severity of MS in terms of the mean transmitral pressure gradient, the MV area, and the pulmonary artery systolic pressure.In most cases, further examinations are not necessary. A preoperative TEE may be utilized to rule out left atrial appendage thrombus, when the patient is being considered for


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Surgery_Schwartz. artery systolic pressure.In most cases, further examinations are not necessary. A preoperative TEE may be utilized to rule out left atrial appendage thrombus, when the patient is being considered for percutane-ous balloon mitral commissurotomy, or if the preoperative TTE is insufficient for diagnosis. Exercise TTE is indicated when resting TTE parameters are discordant with symptom sever-ity.122 Routine coronary angiography is usually performed prior to valve surgery,98 except in young patients (≤30 years of age) with no risk factor for coronary artery disease.Indications for Operation. Depending on the severity and the morphology of the diseased MV (see Table 21-8), balloon commissurotomy, surgical repair, or MV replacement may be indicated for the treatment of MS (Table 21-9).98Mitral RegurgitationEtiology. The most important cause of MR in the United States is myxomatous degenerative disease of the MV, which occurs in 2% to 3% of the population.123 Other important causes of MR


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Surgery_Schwartz. RegurgitationEtiology. The most important cause of MR in the United States is myxomatous degenerative disease of the MV, which occurs in 2% to 3% of the population.123 Other important causes of MR include rheumatic heart disease, infective endocarditis, ischemic heart disease, and dilated cardiomyopathies. Less frequently, MR can be caused by collagen vascular diseases, trauma, pre-vious chest radiation, hypereosinophilic syndrome, carcinoid disease, and exposure to certain drugs.96Pathology. The MV apparatus consists of the mitral leaflets, chordae tendineae, papillary muscles, and mitral annulus, and abnormalities in any one of these components has the potential to cause MR.124 The system for classifying MR proposed by Carpentier focuses on the functional and anatomic characteris-tics of the MV pathology and proposes three basic types of dis-eased valves based on the motion of the free edge of the leaflet relative to the plane of the mitral annulus.125In Type I MR, valvular


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Surgery_Schwartz. of the MV pathology and proposes three basic types of dis-eased valves based on the motion of the free edge of the leaflet relative to the plane of the mitral annulus.125In Type I MR, valvular insufficiency occurs secondary to annular dilatation or leaflet perforation, and normal leaflet motion is maintained. Type II MR is seen in patients with mitral valve prolapse and is due to prolapse of often thickened exces-sive leaflet tissue that gives the valve a “billowing” appearance, in addition to ruptured or elongated chordae tendineae caus-ing increased leaflet motion. Type III insufficiency, as seen in patients with rheumatic and ischemic heart disease, occurs from restricted leaflet motion, either during systole and diastole (Type IIIA) or during systole alone (Type IIIB).Pathophysiology. The basic pathophysiologic abnormality of MR is the retrograde flow of a portion of the LV stroke volume into the left atrium during systole due to an incompetent MV or dilated MV annulus.Acute


Surgery_Schwartz

Surgery_Schwartz. basic pathophysiologic abnormality of MR is the retrograde flow of a portion of the LV stroke volume into the left atrium during systole due to an incompetent MV or dilated MV annulus.Acute severe MR can result from ruptured chordae ten-dineae, a ruptured papillary muscle, or infective endocarditis and causes a sudden volume overload of both the left atrium and ventricle.96 Although an acute increase in preload provides a modest increase in overall stroke volume, the left atrium and ventricle are unable to fully accommodate the regurgitant vol-ume or maintain forward stroke volume in the acute setting due to a lack of remodeling.Chronic MR generally has a more indolent course, with increasing volume overload of the left atrium and ventricle as the effective regurgitant orifice size becomes larger. The result-ing increase in left atrial and ventricular volume initially allows for an increase in the total stroke volume by Starling’s law and accommodation of the regurgitant volume, thus


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Surgery_Schwartz. larger. The result-ing increase in left atrial and ventricular volume initially allows for an increase in the total stroke volume by Starling’s law and accommodation of the regurgitant volume, thus maintaining forward cardiac output and alleviating pulmonary congestion during the compensatory phase of chronic MR.126 However, as the left atrium becomes more dilated, the development of AF becomes more likely, disrupting atrioventricular synchrony and Brunicardi_Ch21_p0801-p0852.indd 81901/03/19 5:32 PM 820SPECIFIC CONSIDERATIONSPART IITable 21-9Data from ACC/AHA guidelines for MV surgery in specific clinical contextsCLINICAL SETTINGCLASS OF RECOMMENDATIONLEVEL OF EVIDENCEBalloon Valvotomy for Mitral Stenosis• Symptomatic patients (NYHA II, III, IV) with moderate or severe MS and favorable valve morphology, without left atrial thrombus or moderate to severe MR• Asymptomatic patients with moderate or severe MS, favorable valve morphology, and pulmonary hypertension (PASP > 50 mmHg at


Surgery_Schwartz

Surgery_Schwartz. valve morphology, without left atrial thrombus or moderate to severe MR• Asymptomatic patients with moderate or severe MS, favorable valve morphology, and pulmonary hypertension (PASP > 50 mmHg at rest, > 60 mmHg with exercise), without left atrial thrombus or moderate to severe MR• Symptomatic patients (NYHA III, IV) with moderate or severe MS and favorable valve morphology, who are high risk or not candidates for surgery• Asymptomatic patients with moderate or severe MS, favorable valve morphology, and new onset atrial fibrillation, without left atrial thrombus or moderate to severe MR• Symptomatic patients (NYHA II, III, IV) with MV area > 1.5 cm2 if there is evidence of hemodynamically significant MS (PASP > 60 mmHg, PAWP ≥ 25 mmHg, mean MV gradient >15 mmHg during exercise)• Symptomatic patients (NYHA III, IV) with moderate or severe MS and favorable valve morphology, as an alternative to surgery• Patients with mild MS• Patients with moderate to severe MR or left atrial


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Surgery_Schwartz. patients (NYHA III, IV) with moderate or severe MS and favorable valve morphology, as an alternative to surgery• Patients with mild MS• Patients with moderate to severe MR or left atrial thrombusIIIIaIIbIIbIIbIII – HarmIII – HarmACCCCCCCSurgery for Mitral Stenosisa• Symptomatic patients (NYHA III, IV) with moderate or severe MS when:Balloon valvotomy is unavailableBalloon valvotomy is contraindicated due to thrombus or MRValve morphology is not favorable for balloon valvotomy• Symptomatic patients with moderate to severe MS who also have moderate to severe MR• Mildly symptomatic patients (NYHA I, II) with severe MS and severe pulmonary hypertension (PASP > 60 mmHg)• Asymptomatic patients with moderate or severe MS and recurrent embolic events while receiving adequate anticoagulation, when the likelihood of successful MVr is high• MVr in the setting of mild MS• Closured commissurotomy in the setting of MVr; open commissurotomy should be performedIIIIaIIbIII – HarmIII –


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Surgery_Schwartz. when the likelihood of successful MVr is high• MVr in the setting of mild MS• Closured commissurotomy in the setting of MVr; open commissurotomy should be performedIIIIaIIbIII – HarmIII – HarmBCCCCCSurgery for Mitral Regurgitationa• Symptomatic patients with acute severe MR• Symptomatic patients (NYHA II, III, IV) with chronic severe MR without LV dysfunction (LVEF < 0.30) and/or end-systolic dimension > 55 mm• Asymptomatic patients with chronic severe MR and mild to moderate LV dysfunction (LVEF 0.30–0.60) and/or end-systolic dimension ≥ 40 mm• Asymptomatic patients with chronic severe MR and preserved LV function (LVEF > 0.60, end-systolic dimension < 40 mm), when the likelihood of successful MVr is > 90%• Asymptomatic patients with chronic severe MR, preserved LV function, and 1) New onset atrial fibrillation, 2) Pulmonary hypertension (PASP > 50 mmHg at rest, > 60 mmHg with exercise)• Symptomatic patients (NYHA III, IV) with chronic severe MR due to a primary abnormality of the


Surgery_Schwartz

Surgery_Schwartz. onset atrial fibrillation, 2) Pulmonary hypertension (PASP > 50 mmHg at rest, > 60 mmHg with exercise)• Symptomatic patients (NYHA III, IV) with chronic severe MR due to a primary abnormality of the mitral apparatus and severe LV dysfunction (LVEF < 0.30, end-systolic dimension > 55 mm), when the likelihood of successful MVr is high• Symptomatic patients (NYHA III, IV) with chronic severe MR secondary to severe LV dys-function (LVEF < 0.30) who remain symptomatic despite optimal medical management for heart failure, including biventricular pacing• Asymptomatic patients with MR and preserved LV function (LVEF > 0.60, end-systolic dimension < 40 mm), when the likelihood of successful repair is low• Isolated MV surgery in the setting of mild or moderate MRIIIIIaIIaIIaIIbIII – HarmIII – HarmBBBBCCCCCLV = left ventricular; LVEF = left ventricular ejection fraction; MR = mitral regurgitation; MS = mitral stenosis; MV = mitral valve; MVr = mitral valve repair; MVR = mitral valve


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Surgery_Schwartz. – HarmBBBBCCCCCLV = left ventricular; LVEF = left ventricular ejection fraction; MR = mitral regurgitation; MS = mitral stenosis; MV = mitral valve; MVr = mitral valve repair; MVR = mitral valve replacement; NYHA = New York Heart Association; PASP = pulmonary artery systolic pressure; PAWP = pulmonary artery wedge pressure; a = mitral valve repair should be performed when possible in this population.Brunicardi_Ch21_p0801-p0852.indd 82001/03/19 5:32 PM 821ACQUIRED HEART DISEASECHAPTER 21predisposing to thrombus formation. Additionally, chronic vol-ume overload may lead to LV contractile dysfunction, result-ing in impaired ejection and end-systolic volume increases. LV dilatation and elevated LV end-diastolic pressures may also worsen throughout the progression of MR, reducing cardiac output and causing congestion of the pulmonary vasculature. These changes herald LV decompensation and heart failure and often indicate irreversible myocardial injury.Clinical Manifestations. In cases


Surgery_Schwartz

Surgery_Schwartz. and causing congestion of the pulmonary vasculature. These changes herald LV decompensation and heart failure and often indicate irreversible myocardial injury.Clinical Manifestations. In cases of acute severe MR, patients are often symptomatic and present with pulmonary congestion and reduced forward stroke volume. In severe cases, patients may present with cardiogenic shock.2 Because the LV has not remodeled in the acute setting, a hyperdynamic apical impulse may not be present in the precordium. The typical sys-tolic murmur of MR may be holosystolic or absent, with a third heart sound and/or diastolic flow murmur being the only aus-cultatory findings.In cases of chronic MR, patients may remain asymptom-atic for long periods of time due to the compensatory mecha-nisms of the remodeled LV. However, once the LV begins to fail, patients become increasingly symptomatic from exertional dyspnea, decreased exercise capacity, orthopnea, and eventu-ally pulmonary hypertension and right heart


Surgery_Schwartz

Surgery_Schwartz. However, once the LV begins to fail, patients become increasingly symptomatic from exertional dyspnea, decreased exercise capacity, orthopnea, and eventu-ally pulmonary hypertension and right heart failure.2 Physical examination may demonstrate displacement of the LV apical impulse due to cardiac enlargement from chronic volume over-load, a third heart sound, or an early diastolic flow rumble. The characteristic auscultatory findings also include an apical sys-tolic murmur, which is variably transmitted to the axilla or the left sternal border, depending on the location of the pathology. As mentioned previously, patients may present with AF due to dilatation of the left atrium. Findings consistent with pulmonary hypertension frequently indicate late-stage disease.Diagnostic Studies. In the setting of acute heart failure, TTE should be performed and may demonstrate the anatomical loca-tion and severity of the MV pathology. However, TTE may underestimate lesion severity due to


Surgery_Schwartz

Surgery_Schwartz. the setting of acute heart failure, TTE should be performed and may demonstrate the anatomical loca-tion and severity of the MV pathology. However, TTE may underestimate lesion severity due to inadequate views of the color flow jet. In this case, severe MR should be suspected if hyperdy-namic systolic function of the LV is visualized, and TEE may be used to confirm the diagnosis and direct repair strategies.127In cases of chronic MR, ECG and chest X-ray are per-formed to assess rhythm status and the degree of pulmonary vascular congestion.96,98 An initial 2D and Doppler TTE should be performed for a baseline estimation of LV and left atrial size, LV systolic function, pulmonary artery pressure, MV morphol-ogy, and MR severity.128 A central color flow jet in the setting of a structurally normal MV on TTE suggests functional MR, which may be due to LV dilatation or tethering of the posterior leaflet in patients with ischemic heart disease. In the setting of organic MR (i.e., rheumatic


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Surgery_Schwartz. normal MV on TTE suggests functional MR, which may be due to LV dilatation or tethering of the posterior leaflet in patients with ischemic heart disease. In the setting of organic MR (i.e., rheumatic and degenerative MR), which is suggested by the presence of an eccentric color flow jet and morphological abnormalities in the MV apparatus on TTE, the presence of calcium in the annulus or leaflets, the redundancy of the leaflets, and the anatomy of the MV pathology should be assessed. Follow-up TTE is indicated on an annual or semian-nual basis in patients with asymptomatic moderate to severe MR in order to assess changes from baseline parameters and direct the timing of surgery. Any abrupt change in signs or symp-toms in a patient with chronic MR is also an indication for TTE examination.98Additional preoperative studies are variably indicated in certain patient populations. Preoperative TEE is indicated in patients with indications for surgery or poor windows on TTE in order to


Surgery_Schwartz

Surgery_Schwartz. preoperative studies are variably indicated in certain patient populations. Preoperative TEE is indicated in patients with indications for surgery or poor windows on TTE in order to determine the severity and anatomic basis of MR and to evaluate LV systolic function.96 Preoperative TEE is also indicated in cases when a discrepancy exists between a patient’s functional status and the severity of MR on TTE. It is helpful for preoperative planning when assessing the feasibility of repair in the individual patient. Exercise stress-echocardiography may also be useful to detect LV systolic dysfunction in well-compensated patients, who may not demonstrate a rise in the end-systolic dimension of the heart or a drop in ejection fraction on routine TTE.129 Coronary angiography should be performed prior to valve surgery in patients with evidence of ischemia, decreased LV systolic function, a history of coronary artery dis-ease or coronary risk factors, including postmenopausal status and age ≥40


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Surgery_Schwartz. to valve surgery in patients with evidence of ischemia, decreased LV systolic function, a history of coronary artery dis-ease or coronary risk factors, including postmenopausal status and age ≥40 in men and premenopausal women.98Indications for Operation. Based on the etiology, morphol-ogy, and severity of MR (see Table 21-8), MV repair, MV replacement with preservation of part or all of the mitral apparatus may be variably performed for the treatment of MR. As the intraoperative findings may dictate MV replacement whenever a MV repair is planned, current recommendations are for MV surgery in general (see Table 21-9).98Mitral Valve Operative Techniques and ResultsMitral valve surgery is performed on the arrested heart with the assistance of cardiopulmonary bypass. Traditionally, a median sternotomy incision has been used; however, the left atrium can also be approached via minimally invasive incisions, such as a right thoracotomy, or a fully endoscopic approach. The MV is commonly


Surgery_Schwartz

Surgery_Schwartz. sternotomy incision has been used; however, the left atrium can also be approached via minimally invasive incisions, such as a right thoracotomy, or a fully endoscopic approach. The MV is commonly exposed through a left atrial incision placed poste-rior and parallel to the intra-atrial groove or via a transseptal approach through the right atrium.Commissurotomy. Upon opening the left atrium, the MV is visualized and the left atrium is examined for thrombus. A nerve hook or right-angle clamp is subsequently introduced beneath the commissures and used to evaluate the MV apparatus for leaflet mobility, commissural fusion, and subvalvular chordal abnormalities. The commissure is then carefully incised in a slightly anterior direction 2 to 3 mm at a time, making sure with each extension of the incision that the chordae tendineae remain attached to the commissural leaflets. The commissurotomy is generally stopped 1 to 2 mm from the annulus where the leaf-let tissue thins, indicating the


Surgery_Schwartz

Surgery_Schwartz. the incision that the chordae tendineae remain attached to the commissural leaflets. The commissurotomy is generally stopped 1 to 2 mm from the annulus where the leaf-let tissue thins, indicating the transition to normal commissural tissue. The papillary muscles are subsequently examined and incised as necessary in order to maximize the mobility of the leaflets.After the commissurotomy is complete and the associated chordae tendineae and papillary muscles are mobilized, leaflet mobility is assessed. The anterior leaflet is grasped with forceps and brought through its complete range of motion. If subvalvu-lar restriction or leaflet rigidity is identified, further division or excision of fused chordae and debridement of calcium may be necessary. Occasionally, the leaflets can be debrided carefully to increase mobility. In rheumatic patients, the thickened leaf-lets can be thinned by careful dissection.130 Valve replacement may be more appropriate if extensive secondary mobilization is


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Surgery_Schwartz. to increase mobility. In rheumatic patients, the thickened leaf-lets can be thinned by careful dissection.130 Valve replacement may be more appropriate if extensive secondary mobilization is required. At the end of the procedure, competence of the valve is assessed with injection of cold saline into the ventricle.Open surgical commissurotomy has an operative risk of <1%, and has been shown to have good long-term results, with freedom from reoperation as high as 88.5%, 80.3%, and 78.7% at 10, 20, and 30 years, respectively.131 The incidence of 4Brunicardi_Ch21_p0801-p0852.indd 82101/03/19 5:32 PM 822SPECIFIC CONSIDERATIONSPART IIFigure 21-8. Mitral valve replacement. A St. Jude bileaflet mechanical valve is viewed through a left atriotomy.postoperative thromboembolic complications is generally <1% per patient-year, and the lack of required systemic anticoagula-tion precludes the development of hemorrhagic complications long term.132 In some institutions, balloon valvuloplasty has


Surgery_Schwartz

Surgery_Schwartz. generally <1% per patient-year, and the lack of required systemic anticoagula-tion precludes the development of hemorrhagic complications long term.132 In some institutions, balloon valvuloplasty has replaced commissurotomy.Mitral Valve Replacement. After exposing the valve, an inci-sion is made in the anterior mitral leaflet, in the midline. The chordal attachments are preserved if possible, with leaflet tis-sue being excised as needed. Attempts are made to preserve the annular and subvalvular apparatus when possible. If it is necessary to excise the anterior leaflet and chordae, the papil-lary muscles can be reattached to the annulus with PTFE suture. If possible, the posterior leaflet along with its associated sub-valvular structures are preserved. The annulus is subsequently sized, and an appropriate mitral prosthesis is implanted using pledgeted horizontal mattress sutures. The annular sutures may be placed from the atrial to the ventricular side, seating the valve


Surgery_Schwartz

Surgery_Schwartz. sized, and an appropriate mitral prosthesis is implanted using pledgeted horizontal mattress sutures. The annular sutures may be placed from the atrial to the ventricular side, seating the valve intra-annularly, or from the ventricular to the atrial side, seating the valve in a supra-annular position. When placing the mattress sutures, care must be taken to stay within the annular tissue, as excessively deep bites may cause injury to critical structures such as the circumflex coronary artery posterolaterally, the atrioventricular node anteromedially, or the aortic valve antero-laterally. The sutures are subsequently placed through the sew-ing ring, and the valve prosthesis is lowered onto the annulus, where it is secured (Fig. 21-8).The factors associated with increased operative risk for MV replacement include age, left ventricular systolic dys-function, emergent procedure status, NYHA functional status, previous cardiac surgery, associated coronary artery disease, and concomitant


Surgery_Schwartz

Surgery_Schwartz. MV replacement include age, left ventricular systolic dys-function, emergent procedure status, NYHA functional status, previous cardiac surgery, associated coronary artery disease, and concomitant disease in another valve. However, for most patients, MV replacement is associated with an operative mor-tality between 2% to 6%, and 65% to 70% 5-year survival.133,134 Although preservation of the mitral apparatus during MV replacement is important for subsequent left ventricular func-tion, there was no difference between complete and partial preservation with respect to 30-day and 5-year mortality.133 Mechanical valves are associated with increased durability compared to bioprosthetic valves, and they have demonstrated a freedom from reoperation of 98% vs. 79% at 15 years, respectively.135 Despite these findings, the choice of prosthetic valve depends on many factors and should be decided on a patient-by-patient basis.Mitral Valve Repair. There are many techniques available for MV repair


Surgery_Schwartz

Surgery_Schwartz. these findings, the choice of prosthetic valve depends on many factors and should be decided on a patient-by-patient basis.Mitral Valve Repair. There are many techniques available for MV repair that are variably used depending on the preoperative and intraoperative assessment of valvular pathology. On open-ing the atrium, the endocardium is examined for a jet lesion, a roughened area caused by a regurgitant jet striking the wall, in order to better localize the area of valvular insufficiency. The commissures are examined for evidence of prolapse, fusion, and malformation. The subvalvular apparatus and individual leaflets are subsequently examined, and areas of prolapse, restriction, fibrosis, and calcification are identified. Leaflet perforations are generally repaired primarily, or with a pericardial patch. The degree of annular dilation is also noted. The basic components of MV repair based on this assessment may include resection of the posterior and/or anterior leaflet, chordal


Surgery_Schwartz

Surgery_Schwartz. a pericardial patch. The degree of annular dilation is also noted. The basic components of MV repair based on this assessment may include resection of the posterior and/or anterior leaflet, chordal shortening, chordal transposition, artificial chordal replacement, and annuloplasty. Recent trends have been toward leaflet preservation.One of the mainstays of MV repair is triangular resection of the posterior leaflet. Excision of the diseased leaflet tissue extends down towards but generally not to the mitral annulus. After repair has been completed, valvular competency is evalu-ated by injecting saline into the ventricle with a bulb syringe and assessing leaflet mobility and apposition. If focal insufficiency is identified in other areas, additional procedures are performed.The anterior leaflet may be repaired via chordal shorten-ing, chordal transposition, artificial chordal replacement, and triangular resection of the anterior leaflet. Chordal shortening has generally been abandoned


Surgery_Schwartz

Surgery_Schwartz. may be repaired via chordal shorten-ing, chordal transposition, artificial chordal replacement, and triangular resection of the anterior leaflet. Chordal shortening has generally been abandoned in favor of chordal replacement. During chordal transposition, a resected portion of the posterior leaflet with attached chordae is transposed onto the prolapsed portion of the anterior leaflet to provide structural support, and this is followed by posterior leaflet repair, as described pre-viously. The procedure of artificial chordal replacement uses polytetrafluoroethylene sutures to attach the papillary muscle to the free edge of the prolapsing anterior leaflet. Triangular resection with primary repair of the anterior leaflet removes the prolapsing segment of the anterior MV leaflet, while preserv-ing adjacent chordal tissue, and may be especially helpful in patients with a ruptured chord or large amount of redundant anterior leaflet tissue.Annular dilation is generally corrected using a MV


Surgery_Schwartz

Surgery_Schwartz. adjacent chordal tissue, and may be especially helpful in patients with a ruptured chord or large amount of redundant anterior leaflet tissue.Annular dilation is generally corrected using a MV annu-loplasty device, such as a ring or partial band. Annuloplasty is known to improve the durability of all types of MV repair (Fig. 21-9).136 A number of devices are available and include rigid or semirigid rings that geometrically remodel the annulus, flexible rings or bands that restrict annular dilation while main-taining the physiologic sphincter motion of the annulus, and semirigid bands that provide a combination of annular remodel-ing and support of physiologic motion.Another technique known as the “double-orifice” or “edge-to-edge” repair was introduced by Alfieri in 1995, and it involves tacking the free edge of the anterior leaflet to the opposing free edge of the posterior leaflet.137 This procedure effectively gives the valve a double-orifice “bow tie” configura-tion, and it has


Surgery_Schwartz

Surgery_Schwartz. tacking the free edge of the anterior leaflet to the opposing free edge of the posterior leaflet.137 This procedure effectively gives the valve a double-orifice “bow tie” configura-tion, and it has been used as both a primary repair technique and an adjunct to other repair techniques, usually in cases of anterior leaflet pathology or Barlow’s disease. While some groups report excellent late results, its use remains controversial, and it is used mainly as a bail-out procedure of last resort in many centers.Brunicardi_Ch21_p0801-p0852.indd 82201/03/19 5:32 PM 823ACQUIRED HEART DISEASECHAPTER 21Figure 21-9. Mitral valve repair. The narrow arrow indicates the posterior leaflet repair, and the wide arrow indicates the ring annu-loplasty as viewed through a left atriotomy.Figure 21-10. Aortic stenosis. The aorta has been removed to demonstrate the thickened, fused aortic valve leaflets associated with rheumatic heart disease. (Reproduced with permission from Centers for Disease Control


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Surgery_Schwartz. stenosis. The aorta has been removed to demonstrate the thickened, fused aortic valve leaflets associated with rheumatic heart disease. (Reproduced with permission from Centers for Disease Control and Prevention, Edwin P. Ewing, Jr.)Due to the variety in operations and etiologies of MV dis-ease, there is heterogeneity in outcomes following MV repair. In general, the operative risk for elective, younger patients undergoing MV repair is <1%, and late results across a broad range of patients have demonstrated benefits in survival and valve-related complications, such as thromboembolic events, infective endocarditis, and anticoagulation-related hemorrhage, compared to MV replacement.116,138 Patients with MR due to degenerative disease have especially encouraging outcomes, demonstrating rates of survival and freedom from reoperation of >50% and >94% at 20 years, respectively.116 Historically, isolated anterior leaflet prolapse increased the risk of reopera-tion fivefold in this population.


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Surgery_Schwartz. survival and freedom from reoperation of >50% and >94% at 20 years, respectively.116 Historically, isolated anterior leaflet prolapse increased the risk of reopera-tion fivefold in this population. However, increasing experi-ence and the expanded use of chordal replacement has greatly improved these results in recent series.139 Independent predic-tors of mortality have included higher NYHA class, lower left ventricular ejection fraction, renal dysfunction, and age. Older patients have demonstrated slightly worse outcomes overall, with an operative mortality of approximately 4%, and a 10-year survival of 54% in patients ≥65 years of age. However, the superiority of repair over replacement persists even for patients >80 years of age.134Patients with rheumatic disease have demonstrated slightly worse outcomes, with one study showing significantly better freedom from operation at 10 years in patients with non-rheumatic MV disease (88% vs. 73%, P <0.005).140 Similarly, in patients with MR


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Surgery_Schwartz. worse outcomes, with one study showing significantly better freedom from operation at 10 years in patients with non-rheumatic MV disease (88% vs. 73%, P <0.005).140 Similarly, in patients with MR secondary to myocardial ischemia, there is growing recent evidence that mitral valve replacement may be significantly more durable than repair.141,142 Despite these differ-ences in outcomes, MV repair remains the procedure of choice for the majority of patients with amenable MV disease.Transcatheter Mitral Valve Repair and Replace-ment. Since the successful introduction of transcatheter aortic valve replacement, efforts have been made to translate the les-sons learned to treatment of the mitral valve. The first device to receive FDA approval for repair of severe mitral regurgitation due to degenerative mitral disease was the MitraClip (Abbott, Abbott Park, IL), introduced in 2003. This device allows a sur-geon or cardiologist to grasp the anterior and posterior leaflets of the mitral valve


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Surgery_Schwartz. mitral disease was the MitraClip (Abbott, Abbott Park, IL), introduced in 2003. This device allows a sur-geon or cardiologist to grasp the anterior and posterior leaflets of the mitral valve together, approximating the Alfieri double-orifice repair technique.143 Transcatheter mitral valve repair is now in clinical use in patients with chronic severe primary MR in whom surgery would be too great a risk, as judged by a heart team approach including a cardiologist skilled in structural heart intervention and an experienced mitral valve surgeon (see Table 21-9). In a recent randomized controlled trial comparing trans-catheter mitral valve repair to open surgical mitral valve repair, 20.1% (n = 37) of patients who received transcatheter mitral valve repair (n = 184) underwent second intervention with sur-gical mitral valve repair or replacement within 12 months com-pared with 2% (n = 2) of patients who underwent surgical repair (n = 95) (P <0.001).143,144 Surgical repair was associated


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Surgery_Schwartz. with sur-gical mitral valve repair or replacement within 12 months com-pared with 2% (n = 2) of patients who underwent surgical repair (n = 95) (P <0.001).143,144 Surgical repair was associated with higher rates of blood transfusion and mechanical ventilation >48 hours but had otherwise equivalent safety. Other transcatheter techniques, including transcatheter mitral valve replacement, have begun clinical trials. This is an area of active research; however, at present, open surgical repair or replacement remains the standard of care for most patients.AORTIC VALVE DISEASEAortic StenosisEtiology. The most common cause of adult aortic stenosis (AS) is calcification of a normal trileaflet or congenital bicuspid aortic valve, particularly in patients >70 years of age. Another important cause of AS is rheumatic heart disease, which is par-ticularly common in developing countries (Fig. 21-10).Pathology. Calcific aortic valve disease, also known as senile or degenerative disease, is an


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Surgery_Schwartz. of AS is rheumatic heart disease, which is par-ticularly common in developing countries (Fig. 21-10).Pathology. Calcific aortic valve disease, also known as senile or degenerative disease, is an age-related disorder characterized by lipid accumulation, proliferative and inflammatory changes, upregulation of angiotensin-converting enzyme activity, oxidative stress, and infiltration of macrophages and T lymphocytes.145 This process, which closely resembles atherosclerotic vascular calcification, initially results in bone formation within the base of the cusps, reducing leaflet motion. Calcification progresses to involve the leaflets, and eventually results in obstructive Brunicardi_Ch21_p0801-p0852.indd 82301/03/19 5:32 PM 824SPECIFIC CONSIDERATIONSPART IITable 21-10Data from ACC/AHA guidelines for the classification of the severity of aortic valve disease in adultsAORTIC STENOSISINDICATORMILDMODERATESEVEREJet velocity (m per s)< 303.0–4.0> 40Mean gradient (mmHg)a< 2525–40> 4.0Valve


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Surgery_Schwartz. for the classification of the severity of aortic valve disease in adultsAORTIC STENOSISINDICATORMILDMODERATESEVEREJet velocity (m per s)< 303.0–4.0> 40Mean gradient (mmHg)a< 2525–40> 4.0Valve area (cm2)> 1.51.0–1.5< 1.0Valve area index (cm2 per m2) < 0.6AORTIC REGURGITATIONQUALITATIVEMILDMODERATESEVEREAngiographic grade1+2+3–4+Color Doppler jet widthCentral jet, width < 25% of left ventricular outflow tractGreater than mild, but no signs of severe regurgitationCentral jet, width >65% of left ventricular outflow tractDoppler vena contracta width (cm)< 0.30.3–0.6> 0.6QUANTITATIVE (CATH OR ECHO)Regurgitant volume (ml per beat)< 3030–59≥ 60Regurgitant fraction (%)< 3030–49≥ 50Regurgitant orifice area (cm2)< 0.10.1–0.29≥ 0.3ADDITIONAL ESSENTIAL CRITERIALeft ventricular size EnlargedaValve gradients are flow dependent and when used as estimates of severity of valve stenosis should be assessed with knowledge of cardiac output or forward flow across the valve.disease, with a reduced


Surgery_Schwartz

Surgery_Schwartz. gradients are flow dependent and when used as estimates of severity of valve stenosis should be assessed with knowledge of cardiac output or forward flow across the valve.disease, with a reduced effective valve area without signs of leaflet fusion.Pathophysiology. In general, once moderate AS is present, the average rate of progression includes an increase in jet velocity of 0.3 m/s per year, an increase in mean pressure gradient of 7 mmHg per year, and a decrease in valve area of 0.1 cm2 per year (Table 21-10).96 In most adult patients with AS, obstruction develops gradually and includes a long latent period free from symptoms. During this time, the LV typically hypertrophies in response to systolic pressure overload, and normal intracavi-tary volume is maintained.146 Afterload, which is defined as left ventricular systolic wall stress, and thus ejection fraction remain normal early in this process as the increase in myocardial thickness is usually enough to counter the increased


Surgery_Schwartz

Surgery_Schwartz. is defined as left ventricular systolic wall stress, and thus ejection fraction remain normal early in this process as the increase in myocardial thickness is usually enough to counter the increased intracavi-tary systolic pressures. Patients without a typical hypertrophic response to systolic pressure overload or with a depressed con-tractile state of the myocardium do not follow the common clini-cal course, but they experience an early decrease in ejection fraction due to excessively increased afterload without a com-pensatory response.147Concentric LV hypertrophy without chamber dilatation eventually leads to increased end-diastolic pressures and dia-stolic dysfunction. Forceful atrial contraction in the face of elevated end-diastolic pressures becomes an important compo-nent of ventricular filling, even as mean left atrial and pulmo-nary venous pressures remain in the normal range. Disorders such as atrial fibrillation that disrupt atrial contraction can lead to clinical


Surgery_Schwartz

Surgery_Schwartz. of ventricular filling, even as mean left atrial and pulmo-nary venous pressures remain in the normal range. Disorders such as atrial fibrillation that disrupt atrial contraction can lead to clinical deterioration. Although systolic function is gener-ally preserved long into the natural history of the disease, left ventricular decompensation eventually occurs in the setting of longstanding increased afterload and is an indication for surgery even in the absence of other symptoms.Although concentric hypertrophy is a compensatory mech-anism to maintain ejection fraction in the face of high intracavi-tary pressures, the hypertrophied heart becomes increasingly vulnerable to ischemic injury. Coronary blood flow may become inadequate, despite the absence of epicardial coronary artery disease.148 Coronary vasodilation is mitigated by the hypertro-phied myocardium, and the hemodynamic stress of exercise or tachyarrhythmias can lead to subendocardial ischemia and further systolic or


Surgery_Schwartz

Surgery_Schwartz. Coronary vasodilation is mitigated by the hypertro-phied myocardium, and the hemodynamic stress of exercise or tachyarrhythmias can lead to subendocardial ischemia and further systolic or diastolic dysfunction. When ischemic insults occur, patients with ventricular hypertrophy experience larger infarcts and higher mortality rates than those without hypertrophy.149 In some patients, ventricular hypertrophy occurs in excess of what is needed to compensate for increased intra-cavitary pressures, creating a high-output state that is also asso-ciated with increased perioperative morbidity and mortality.150Clinical Manifestations. The characteristic auscultatory findings of AS include a harsh, crescendo-decrescendo systolic murmur at the right second or third intercostal space, often with radiation to the carotid arteries.2 As the disease progresses, aor-tic valve closure may follow pulmonic valve closure, causing paradoxical splitting of the second heart sound. Other physical findings


Surgery_Schwartz

Surgery_Schwartz. to the carotid arteries.2 As the disease progresses, aor-tic valve closure may follow pulmonic valve closure, causing paradoxical splitting of the second heart sound. Other physical findings associated with AS include an apical impulse com-monly described as a “prolonged heave,” and the presence of a narrow and sustained peripheral pulse, known as pulsus parvus et tardus.The classic symptoms of AS are exertional dyspnea, angina, and syncope.2 Although many patients are diagnosed prior to the onset of symptoms, the most common clinical Brunicardi_Ch21_p0801-p0852.indd 82401/03/19 5:32 PM 825ACQUIRED HEART DISEASECHAPTER 21presentation in patients with a known diagnosis of AS is wors-ening exertional dyspnea. Angina occurs in over half of patients with AS and is due to the increased oxygen demand of the hypertrophied myocardium in the setting of reduced oxygen supply secondary to coronary compression. Although some patients may have concomitant coronary disease, angina occurs


Surgery_Schwartz

Surgery_Schwartz. oxygen demand of the hypertrophied myocardium in the setting of reduced oxygen supply secondary to coronary compression. Although some patients may have concomitant coronary disease, angina occurs without significant epicardial coronary artery disease in half of all patients with AS.151 Syncope is most common during exer-tion, as systemic vasodilation in the setting of a fixed cardiac output causes decreased cerebral perfusion. However, at times, it may occur at rest secondary to paroxysmal atrial fibrillation and subsequent loss of atrial booster pump function. Late find-ings of AS include atrial fibrillation, pulmonary hypertension, systemic venous hypertension, and, rarely, sudden death.Diagnostic Studies. Evidence of LV hypertrophy is found in approximately 85% of patients with AS on routine ECG, though the correlation between the absolute electrocardiographic volt-ages in precordial leads and the severity of AS is poor.2 ECG also may demonstrate signs of left atrial enlargement


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Surgery_Schwartz. routine ECG, though the correlation between the absolute electrocardiographic volt-ages in precordial leads and the severity of AS is poor.2 ECG also may demonstrate signs of left atrial enlargement and vari-ous forms and degrees of atrioventricular or intraventricular block due to calcific infiltration of the conduction system. Rou-tine chest X-ray usually demonstrates a normal heart size, with rounding of the left ventricular border and apex. A late finding on chest X-ray is cardiac enlargement, or cardiomegaly, a sign of LV failure.Transthoracic echocardiography is indicated in all patients with a systolic murmur graded ≥2/6, a single second heart sound, or symptoms characteristic of AS.98 Initial TTE examinations are often diagnostic and provide an assessment of left ventricular size and function, the degree of left ventricular hypertrophy, the degree of valvular calcification, and the pres-ence of other associated valvular disease. Doppler evaluation should be performed to define


Surgery_Schwartz

Surgery_Schwartz. function, the degree of left ventricular hypertrophy, the degree of valvular calcification, and the pres-ence of other associated valvular disease. Doppler evaluation should be performed to define the maximum jet velocity, which is a useful measure for following disease severity and predict-ing clinical outcome.2 Additionally, color flow Doppler assesses the severity of the stenotic lesion by allowing calculation of the mean transvalvular pressure gradient and effective valve orifice area (see Table 21-10).98 Follow-up TTE is indicated depending on the severity of AS in order to assess changes from baseline parameters and direct the timing of surgery: yearly for severe AS; every 1 to 2 years for moderate AS; and every 3 to 5 years for mild AS. Any abrupt change in signs or symptoms in a patient with AS is an indication for TTE examination.Additional preoperative studies may be necessary in some patients. Rarely, when TTE images are suboptimal, TEE or fluo-roscopy may be indicated to


Surgery_Schwartz

Surgery_Schwartz. patient with AS is an indication for TTE examination.Additional preoperative studies may be necessary in some patients. Rarely, when TTE images are suboptimal, TEE or fluo-roscopy may be indicated to assess the degree of valve calcifica-tion and effective valve orifice area. As in other patients with valvular heart disease, coronary angiography should be per-formed prior to aortic valve surgery in most patients.98 Since the symptoms of AS often mimic those of ischemic heart disease, left heart catheterization and coronary angiography may be nec-essary at the initial evaluation in patients with AS. Stress echo-cardiography may also be useful in the asymptomatic patient with AS in order to elicit exercise-induced symptoms or abnor-mal blood pressure responses during exertion. It is also useful in the evaluation of low-gradient AS in patients with depressed LV function.98 However, exercise stress-echocardiography is con-traindicated in patients with ischemic heart disease.98 In patients


Surgery_Schwartz

Surgery_Schwartz. in the evaluation of low-gradient AS in patients with depressed LV function.98 However, exercise stress-echocardiography is con-traindicated in patients with ischemic heart disease.98 In patients with evidence of aortic root disease by TTE, chest computed tomography is useful in evaluating aortic dilatation at several anatomic levels and is necessary for clinical decision making and surgical planning.2Indications for Operation. Based on the severity of AS (see Table 21-10) and the predicted risk with surgical aortic valve replacement (SAVR) determined using the STS risk calculator, SAVR or transcatheter aortic valve replacement (TAVR) may be recommended for the treatment of AS (Table 21-11).98,152 As this field is rapidly evolving, attention to guideline updates and a multidisciplinary heart team approach to risk stratification and treatment selection are mandatory. In patients with severe calcific AS, AVR via either approach is the only effective treat-ment, though controversy exists


Surgery_Schwartz

Surgery_Schwartz. team approach to risk stratification and treatment selection are mandatory. In patients with severe calcific AS, AVR via either approach is the only effective treat-ment, though controversy exists as to the timing of intervention in asymptomatic patients. Balloon aortic valvuloplasty creates a modest hemodynamic effect and temporary symptom improve-ment in patients with calcific AS. However, the procedure has not been shown to affect long-term outcomes and is often used in hemodynamically unstable patients as a bridge to AVR.98Aortic InsufficiencyEtiology. The most common cause of isolated aortic insuffi-ciency (AI) in patients undergoing AVR is aortic root disease, and it represents over 50% of such patients in some studies.2 Other common causes of AI include congenital abnormalities of the aortic valve such as bicuspid aortic valve, calcific degenera-tion, rheumatic disease, infective endocarditis, systemic hyper-tension, myxomatous degeneration, dissection of the ascending aorta,


Surgery_Schwartz

Surgery_Schwartz. the aortic valve such as bicuspid aortic valve, calcific degenera-tion, rheumatic disease, infective endocarditis, systemic hyper-tension, myxomatous degeneration, dissection of the ascending aorta, and Marfan syndrome. Less common causes of AI include traumatic injuries to the aortic valve, ankylosing spondylitis, syphilitic aortitis, rheumatoid arthritis, osteogenesis imperfecta, giant cell aortitis, Ehlers-Danlos syndrome, Reiter’s syndrome, discrete subaortic stenosis, and ventricular septal defects with prolapse of an aortic cusp.96 Although most of these lesions produce chronic aortic insufficiency, rarely acute severe aortic regurgitation can result, often with devastating consequences.Pathology. Regardless of its cause, AI produces volume over-load with dilation and hypertrophy of the left ventricle and sub-sequent dilation of the MV annulus. Depending on the severity of AI, the left atrium may undergo dilation and hypertrophy as well. Frequently, the regurgitant jet causes


Surgery_Schwartz

Surgery_Schwartz. of the left ventricle and sub-sequent dilation of the MV annulus. Depending on the severity of AI, the left atrium may undergo dilation and hypertrophy as well. Frequently, the regurgitant jet causes endocardial lesions at the site of impact on the left ventricular wall.Diseases causing AI can be classified as primary disorders of the aortic valve leaflets and/or disorders involving the wall of the aortic root. Diseases causing dilation of the ascending aorta are a more common indication for AVR due to isolated AI, and they include disorders such as age-related (degenera-tive) aortic dilation, cystic medial necrosis of the aorta as is seen in Marfan syndrome, aortic dilation secondary to bicuspid valves, and aortic dissection, to name a few.153 In these disor-ders, the aortic annulus becomes dilated, causing separation of the valve leaflets and subsequent AI. The diseased aortic wall may dissect secondarily and further escalate regurgitation across the valve, and secondary thickening


Surgery_Schwartz

Surgery_Schwartz. dilated, causing separation of the valve leaflets and subsequent AI. The diseased aortic wall may dissect secondarily and further escalate regurgitation across the valve, and secondary thickening and shortening of the valve cusps may occur due to undue tension placed on the valvular apparatus by the dilated aortic root. As the disease progresses, the valve leaflets become too small to close the aortic orifice, causing further aortic insufficiency and exacerbating dilation of the ascending aorta.There are also many primary valvular diseases that cause AI, generally in association with AS. One such disorder is age-related calcific AS, which causes some degree of AI in up to 75% of patients.154 Infective endocarditis may involve the aortic valve apparatus and cause AI through direct destruction of the valve leaflets, perforation of a leaflet, or formation of vegetations that interfere with proper coaptation of the valve Brunicardi_Ch21_p0801-p0852.indd 82501/03/19 5:32 PM 826SPECIFIC


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Surgery_Schwartz. of the valve leaflets, perforation of a leaflet, or formation of vegetations that interfere with proper coaptation of the valve Brunicardi_Ch21_p0801-p0852.indd 82501/03/19 5:32 PM 826SPECIFIC CONSIDERATIONSPART IITable 21-11Data from ACC/AHA guidelines for AV surgery in specific clinical contextsCLINICAL SETTINGCLASS OF RECOMMENDATIONLEVEL OF EVIDENCEBalloon Valvotomy for Aortic Stenosis• Bridge to surgery in hemodynamically unstable patients with AS at high risk for AVRIIbC• Palliation in adult patients with AS, who are not candidates for AVRIIbC• Alternative to AVR in adult patients with ASIII – HarmBSurgery for Aortic Stenosis• Symptomatic patients with severe ASIB• Severe AS in the setting of1) Concomitant CABG2) Concomitant valvular or aortic surgery3) LV systolic dysfunction (LVEF <0.50)IC• Moderate AS in the setting of1) Concomitant CABG2) Concomitant valvular or aortic surgeryIIaB• Asymptomatic patients with severe AS and• Abnormal response to exercise• High likelihood of


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Surgery_Schwartz. <0.50)IC• Moderate AS in the setting of1) Concomitant CABG2) Concomitant valvular or aortic surgeryIIaB• Asymptomatic patients with severe AS and• Abnormal response to exercise• High likelihood of rapid progression• High likelihood of delay if surgery is withheld until time of symptom onset• Expected operative mortality ≤1.0%IIbC• Mild AS in patients undergoing CABG, when there is high likelihood of rapid progressionIIbC• AVR for prevention of sudden death in asymptomatic patients with AS without any of the findings aboveIII – HarmBSurgery for Aortic Insufficiency• Symptomatic patients with severe AIIB• Asymptomatic patients with chronic severe AI in the setting of1) Concomitant CABG2) Concomitant valvular or aortic surgery3) LV systolic dysfunction (LVEF ≤0.50)ICCB• Asymptomatic patients with severe AI, normal LV systolic function (LVEF >0.50), but severe LV dilatation (end-diastolic dimension >75 mm, end-systolic dimension >55 mm)IIaB• Moderate AI in the setting of1) Concomitant


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Surgery_Schwartz. with severe AI, normal LV systolic function (LVEF >0.50), but severe LV dilatation (end-diastolic dimension >75 mm, end-systolic dimension >55 mm)IIaB• Moderate AI in the setting of1) Concomitant CABG2) Concomitant surgery on the ascending aortaIIbC• Asymptomatic patients with severe AI, normal LV systolic function at rest (LVEF >0.50), and LV dilatation (end-diastolic dimension ≥70 mm, end-systolic dimension ≥50 mm) in the setting of1) Progressive LV dilatation2) Declining exercise tolerance3) Abnormal hemodynamic responses to exerciseIIbC• Asymptomatic patients with mild, moderate, or severe AI and normal LV systolic function (LVEF >0.50), when the degree of LV dilatation is not moderate or severe (end-diastolic dimension <70 mm, end-systolic dimension <50 mm)III – HarmBAS = aortic stenosis; AVR = aortic valve replacement; CABG = coronary artery bypass grafting; LV = left ventricular; LVEF = left ventricular ejection fraction; NYHA = New York Heart Association.cusps. Rheumatic


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Surgery_Schwartz. stenosis; AVR = aortic valve replacement; CABG = coronary artery bypass grafting; LV = left ventricular; LVEF = left ventricular ejection fraction; NYHA = New York Heart Association.cusps. Rheumatic disease causes fibrous infiltration of the valve cusps and subsequent retraction of the valve leaflets, inhibiting apposition of the cusps during diastole and producing a central regurgitant jet. Patients with large ventricular septal defects or membranous subaortic stenosis may develop progressive AI, owing to a Venturi effect that results in prolapse of the aortic valve leaflets.Pathophysiology. The basic pathophysiologic abnormality of AI is the retrograde flow of a portion of the LV stroke volume into the LV during diastole, producing volume overload.Acute severe AI results most commonly from infective endocarditis, acute aortic dissection, or trauma, and it causes a sudden volume overload of the left ventricle.54 Although an acute increase in preload provides a small increase in


Surgery_Schwartz

Surgery_Schwartz. from infective endocarditis, acute aortic dissection, or trauma, and it causes a sudden volume overload of the left ventricle.54 Although an acute increase in preload provides a small increase in overall Brunicardi_Ch21_p0801-p0852.indd 82601/03/19 5:32 PM 827ACQUIRED HEART DISEASECHAPTER 21stroke volume due to the Starling mechanism, the left ventricle often is unable to accommodate the large regurgitant volume and maintain forward stroke volume in the acute setting due to a lack of remodeling. Left ventricular end-diastolic and left atrial pressures increase dramatically as the LV is unable to develop compensatory chamber dilation. Although tachycardia develops as a compensatory mechanism to maintain forward flow, this attempt is often inadequate, and patients frequently present in heart failure and even cardiogenic shock. Moreover, subendo-cardial myocardial ischemia frequently develops as a result of decreased coronary diastolic perfusion pressures and increased LV


Surgery_Schwartz

Surgery_Schwartz. present in heart failure and even cardiogenic shock. Moreover, subendo-cardial myocardial ischemia frequently develops as a result of decreased coronary diastolic perfusion pressures and increased LV end-diastolic pressure, as well as increased myocardial oxy-gen demand due to acute dilation. In the setting of a chronic ventricular hypertrophy and preexisting diastolic dysfunction, the pressure-volume relationship is even more extreme, exacer-bating the hemodynamic derangements seen in acute AI.Chronic AI generally has a more indolent course, with vol-ume overload of the LV causing compensatory increases in left ventricular end-diastolic volume and chamber compliance as well as a combination of eccentric and concentric hypertrophy.155 Compensatory remodeling of the LV allows for accommodation of the regurgitant volume without a significant increase in fill-ing pressures and maintains the preload reserve of the cham-ber. Eccentric left ventricular hypertrophy develops, permitting


Surgery_Schwartz

Surgery_Schwartz. of the regurgitant volume without a significant increase in fill-ing pressures and maintains the preload reserve of the cham-ber. Eccentric left ventricular hypertrophy develops, permitting normal contractile performance across the enlarged chamber circumference and subsequent ejection of a larger total stroke volume in order to maintain forward flow, despite the regurgi-tant fraction.155,156 However, the enlarged chamber size results in an increase in systolic myocardial wall stress and causes further ventricular hypertrophy. As the disease progresses, recruitment of preload reserve and compensatory hypertrophy maintains ejection fraction within the normal range despite elevated after-load, causing many patients to remain asymptomatic throughout the compensatory phase.155,157Eventually, left ventricular compensatory mechanisms fail, and systolic dysfunction ensues. As the disease progresses, preload reserve may become exhausted, the hypertrophic response may become inadequate, and


Surgery_Schwartz

Surgery_Schwartz. left ventricular compensatory mechanisms fail, and systolic dysfunction ensues. As the disease progresses, preload reserve may become exhausted, the hypertrophic response may become inadequate, and impaired myocardial contractility may develop so that ejection fraction begins to decline.158 Although left ventricular systolic dysfunction related to excessive afterload is reversible early in the course, irrevers-ible damage occurs once chamber enlargement predominates as the primary cause of diminished myocardial contractility.Clinical Manifestations. In cases of acute severe AI, patients are symptomatic and invariably present with compensatory tachycardia, often associated with acute pulmonary congestion and cardiogenic shock.2 Because the left ventricular and aortic pressures often equalize before the end of diastole, the diastolic murmur of AI may be short and/or soft. The reduced systolic pressure may attenuate the increase in peripheral pulse pressure seen in chronic AI, and early


Surgery_Schwartz

Surgery_Schwartz. before the end of diastole, the diastolic murmur of AI may be short and/or soft. The reduced systolic pressure may attenuate the increase in peripheral pulse pressure seen in chronic AI, and early closing of the mitral valve due to elevated left ventricular end-diastolic pressures may diminish the intensity of the first heart sound in the acute setting.In patients with chronic AI, symptoms of heart fail-ure and myocardial ischemia develop after the compensatory phase.2 Patients gradually begin to complain of exertional dys-pnea, fatigue, orthopnea, and paroxysmal nocturnal dyspnea, often after significant myocardial dysfunction has developed. Angina is a common complaint late in the course, especially during sleep when heart rate slows and arterial diastolic pres-sure falls. Patients also may experience exertional angina secondary to diminished coronary perfusion in the setting of myocardial hypertrophy. Occasionally, the compensatory tachy-cardia that develops with chronic AI will


Surgery_Schwartz

Surgery_Schwartz. may experience exertional angina secondary to diminished coronary perfusion in the setting of myocardial hypertrophy. Occasionally, the compensatory tachy-cardia that develops with chronic AI will cause palpitations, and the increased pulse pressure will cause a sensation of pound-ing in the patient’s head. Peripherally, the widened pulse pres-sure causes a forceful, bounding, and quickly collapsing pulse known as Corrigan’s water-hammer pulse. Premature ventricu-lar contractions have been reported to cause particularly trou-bling symptoms, owing to the heave of the volume-loaded left ventricle during the postextrasystolic beat. The classic ausculta-tory finding associated with AI is a high-pitched decrescendo diastolic murmur heard best in the left third intercostal space; an associated S3 gallop is often indicative of late disease. The Austin Flint murmur has also been described, and it is heard as a middiastolic rumble at the apex that simulates mitral stenosis and occurs in severe


Surgery_Schwartz

Surgery_Schwartz. gallop is often indicative of late disease. The Austin Flint murmur has also been described, and it is heard as a middiastolic rumble at the apex that simulates mitral stenosis and occurs in severe AI when the regurgitant jet impedes mitral valve leaflet opening.Diagnostic Studies. In the acute setting, TTE should be per-formed to confirm the presence and severity of aortic regurgita-tion, the degree of pulmonary hypertension, and the cause of valvular dysfunction.98 When aortic dissection is suspected as the cause of acute AI, TEE or chest CT angiography may be substituted if more readily available.159,160 In these patients with confirmed aortic dissection, cardiac catheterization and coro-nary angiography are rarely indicated and can delay life-saving urgent surgical intervention.In cases of chronic AI, the ECG frequently demonstrates left axis deviation and, late in the course, intraventricular con-duction defects associated with left ventricular dysfunction. On chest X-ray, the


Surgery_Schwartz

Surgery_Schwartz. of chronic AI, the ECG frequently demonstrates left axis deviation and, late in the course, intraventricular con-duction defects associated with left ventricular dysfunction. On chest X-ray, the left ventricle enlarges predominantly in an infe-rior and leftward direction, causing marked increase in the long axis diameter of the heart, frequently with little or no change in the transverse diameter. The chest X-ray should be examined for aneurysmal dilation of the aorta.2 An initial TTE should be performed to confirm the diagnosis and severity of AI, assess the cause of AI (including valve morphology and aortic root size and morphology), and assess the degree of left ventricular hypertrophy, volume, and systolic function.98 Follow-up TTE is indicated on an annual or semiannual basis in patients with asymptomatic moderate to severe AI in order to assess changes from baseline parameters and direct the timing of surgery. Any abrupt change in signs or symptoms in a patient with chronic AI


Surgery_Schwartz

Surgery_Schwartz. with asymptomatic moderate to severe AI in order to assess changes from baseline parameters and direct the timing of surgery. Any abrupt change in signs or symptoms in a patient with chronic AI is an indication for TTE examination.Additional preoperative studies are indicated in certain patient populations.98 In patients with poor windows on TTE, TEE or MRI is indicated for initial and serial assessment of AI severity and left ventricular volume and function at rest. In symptomatic patients with chronic AI, it is reasonable to pro-ceed directly to TEE or cardiac catheterization if TTE examina-tions are inadequate. Exercise stress testing may be helpful for an assessment of functional capacity and symptomatic responses in patients with equivocal symptoms. Coronary angiography should be performed prior to valve surgery in most patients.98Indications for Operation. Based on the morphology and severity of valve dysfunction (see Table 21-10), AV repair or replacement may be performed for


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Surgery_Schwartz. prior to valve surgery in most patients.98Indications for Operation. Based on the morphology and severity of valve dysfunction (see Table 21-10), AV repair or replacement may be performed for the treatment of AI (see Table 21-11).96 Although the indications for AV repair and AV replacement do not differ, it is recommended that AV repair be performed only in those surgical centers that have developed the appropriate technical expertise, gained experience in patient selection, and which have demonstrated outcomes equivalent to those of valve replacement.Brunicardi_Ch21_p0801-p0852.indd 82701/03/19 5:32 PM 828SPECIFIC CONSIDERATIONSPART IIAortic Valve Operative Techniques and ResultsAortic valve surgery has traditionally been performed through a median sternotomy with the assistance of cardiopulmonary bypass. However, minimally invasive incisions for aortic valve surgery have been introduced, including mini-sternotomy and mini-thoracotomy approaches. After the aorta is cross-clamped,


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Surgery_Schwartz. bypass. However, minimally invasive incisions for aortic valve surgery have been introduced, including mini-sternotomy and mini-thoracotomy approaches. After the aorta is cross-clamped, cold blood cardioplegia is delivered antegrade through the aortic root and/or retrograde through the coronary sinus.Aortic Valve Replacement. During aortic valve replacement, an aortotomy is performed, extending medially from approxi-mately 1 to 2 cm above the right coronary artery and inferiorly into the noncoronary sinus. The valve is completely excised. The annulus is thoroughly debrided of calcium deposits. At this point, the annulus is sized and an appropriate prosthesis is selected. Pledgeted horizontal mattress sutures are then placed into the aortic valve annulus and subsequently through the sew-ing ring of the prosthetic valve, taking care to avoid damage to the coronary ostia, the conduction system, and the MV appara-tus. The annular sutures may be placed from below the annulus, seating the