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 particularly common in developing countries (Fig. 21-9).
Aortic stenosis. The aorta has been removed to demonstrate the thickened, fused aortic valve leaflets associated with rheumatic heart disease. (Image courtesy of the Centers for Disease Control and Prevention, Edwin P. Ewing, Jr.)
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.107 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 disease, with a reduced effective valve area without signs of leaflet fusion.
In general, once moderate AS is present, the average rate of progression includes an increase in jet velocity of 0.3 m/s/year, an increase in mean pressure gradient of 7 mm Hg/year, and a decrease in valve area of 0.1 cm2/year (Table 21-12).70 In most adult patients with AS, obstruction develops gradually and includes a long latent period free from symptoms. During this time, the left ventricle typically hypertrophies in response to systolic pressure overload, and normal intracavitary volume is maintained.108 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 increased intracavitary systolic pressures. Patients without a typical hypertrophic response to systolic pressure overload, or with a depressed contractile state of the myocardium, do not follow the common clinical course, but experience an early decrease in ejection fraction due to excessively increased afterload, without a compensatory response.109
Table 21-13Data from ACC/AHA guidelines for AV surgery in specific clinical contexts ||Download (.pdf) Table 21-13 Data from ACC/AHA guidelines for AV surgery in specific clinical contexts
|CLINICAL SETTING ||CLASS OF RECOMMENDATION ||LEVEL OF EVIDENCE |
|Balloon Valvotomy for Aortic Stenosis |
|• Bridge to surgery in hemodynamically unstable patients with AS at high risk for AVR ||IIb ||C |
|• Palliation in adult patients with AS, who are not candidates for AVR ||IIb ||C |
|• Alternative to AVR in adult patients with AS ||III – Harm ||B |
|Surgery for Aortic Stenosis |
|• Symptomatic patients with severe AS ||I ||B |
• Severe AS in the setting of
1) Concomitant CABG
2) Concomitant valvular or aortic surgery
3) LV systolic dysfunction (LVEF <0.50)
|I ||C |
• Moderate AS in the setting of
1) Concomitant CABG
2) Concomitant valvular or aortic surgery
|IIa ||B |
• 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%
|IIb ||C |
|• Mild AS in patients undergoing CABG, when there is high likelihood of rapid progression ||IIb ||C |
|• AVR for prevention of sudden death in asymptomatic patients with AS without any of the findings above ||III – Harm ||B |
|Surgery for Aortic Insufficiency |
|• Symptomatic patients with severe AI ||I ||B |
• Asymptomatic patients with chronic severe AI in the setting of
1) Concomitant CABG
2) Concomitant valvular or aortic surgery
3) LV systolic dysfunction (LVEF ≤0.50)
|I || |
|• 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) ||IIa ||B |
• Moderate AI in the setting of
1) Concomitant CABG
2) Concomitant surgery on the ascending aorta
|IIb ||C |
• 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 of
1) Progressive LV dilatation
2) Declining exercise tolerance
3) Abnormal hemodynamic responses to exercise
|IIb ||C |
|• 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 – Harm ||B |
Concentric left ventricular hypertrophy without chamber dilatation eventually leads to increased end-diastolic pressures and early diastolic dysfunction. Forceful atrial contraction in the face of elevated end-diastolic pressures becomes an important component of ventricular filling, even as mean left atrial and pulmonary venous pressures remain in the normal range. Disorders such as atrial fibrillation that disrupt atrial contraction typically lead to clinical deterioration. Although systolic function is generally 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 mechanism to maintain ejection fraction in the face of high intracavitary pressures, the hypertrophied heart becomes increasingly vulnerable to ischemic injury. Coronary blood flow may become inadequate, despite the absence of epicardial coronary artery disease.110 Coronary vasodilation is mitigated by the hypertrophied myocardium, and the hemodynamic stress of exercise or tachyarrhythmias can lead to subendocardial ischemia and further systolic or diastolic dysfunction. When ischemic injuries occur, patients with ventricular hypertrophy experience larger infarcts and higher mortality rates than those without hypertrophy.111 In some patients, ventricular hypertrophy occurs in excess of what is needed to compensate for increased intracavitary pressures, creating a high-output state that is also associated with increased perioperative morbidity and mortality.112
The characteristic auscultatory findings of AS include a harsh, crescendo-decrescendo systolic murmur at the right second intercostal space, often with radiation to the carotid arteries.1 As the disease progresses, aortic 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 commonly 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.1 Although many patients are diagnosed prior to the onset of symptoms, the most common clinical presentation in patients with a known diagnosis of AS followed prospectively is worsening exertional dyspnea due to a limited capacity to increase cardiac output with exercise, and a progressive rise in end-diastolic pressures leading to pulmonary congestion. 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 ischemic disease, angina occurs without significant epicardial coronary artery disease in half of all patients with AS. Syncope is most common during exertion, 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 findings of AS include atrial fibrillation, pulmonary hypertension, systemic venous hypertension, and rarely sudden death.
Evidence of left ventricular hypertrophy is found in approximately 85% of patients with AS on routine EKG, though the correlation between the absolute electrocardiographic voltages in precordial leads and the severity of AS is poor.1 EKG also may demonstrate signs of left atrial enlargement, and various forms and degrees of atrioventricular or intraventricular block due to calcific infiltration of the conduction system. Routine chest X-ray usually demonstrates a normal heart size, with rounding of the left ventricular border and apex. Cardiac enlargement on chest X-ray is a sign of left ventricular failure and cardiomegaly, and is a late finding.
Transthoracic echocardiography is indicated in all patients with a systolic murmur graded ≥2/6, a single second heart sound, or symptoms characteristic of AS.70 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 presence of other associated valvular disease. Doppler evaluation should be performed to define the maximum jet velocity, which is the most useful measure for following disease severity and predicting clinical outcome.1Additionally, color flow Doppler assesses the severity of the stenotic lesion by allowing calculations of the mean transvalvular pressure gradient, and effective valve orifice area (Table 21-12).70 Follow-up TTE is variably 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 fluoroscopy may be indicated to assess the degree of valve calcification and effective valve orifice area. As in other patients with valvular heart disease, coronary angiography should be performed prior to aortic valve surgery in most patients.70 Since the symptoms of AS oftentimes mimic those of ischemic disease, cardiac catheterization and coronary angiography may be necessary at the initial evaluation in patients with AS. Stress-echocardiography may also be useful in the asymptomatic patient with AS in order to elicit exercise-induced symptoms, or abnormal blood pressure responses during exertion. It is also useful in the evaluation of low-gradient AS in patients with depressed LV function.70 However, exercise stress-echocardiography is contraindicated in patients with ischemic heart disease.70 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.1
Indications for Operation
Based on the severity of AS and the overall physical condition of the patient (Table 21-12), AVR may be recommended for the treatment of AS (Table 21-13).70 In patients with severe calcific AS, AVR is the only effective treatment, though controversy exists as to the timing of intervention in asymptomatic patients. Balloon valvotomy creates a modest hemodynamic effect and temporary symptom improvement in patients with calcific AS. However, the procedure has not been shown to affect long-term outcomes, and is often used in high-risk patients in which the contribution of the AS to the patients’ symptoms is a matter of debate.113
Table 21-14Data from ACC/AHA guidelines for TV surgery in specific clinical contexts ||Download (.pdf) Table 21-14 Data from ACC/AHA guidelines for TV surgery in specific clinical contexts
|CLINICAL SETTING ||CLASS OF RECOMMENDATION ||LEVEL OF EVIDENCE |
|Surgery for Tricuspid Valve Disease |
|• TVr for severe TI in patients with MV disease requiring MV surgery ||I ||B |
|• TVR or annuloplasty for severe symptomatic primary TI ||IIa ||C |
|• TVR for severe TI secondary to diseased/abnormal TV leaflets not amenable to annuloplasty or TVr ||IIa ||C |
• Annuloplasty for less than severe TI in patients undergoing MV surgery in the setting of
1) Pulmonary hypertension
2) Tricuspid annular dilatation
|IIb ||C |
|• TVR or annuloplasty is not indicated in asymptomatic patients with TI, a normal MV, and a PASP <60 mm Hg ||III – Harm ||C |
|• TVR or annuloplasty is not indicated in patients with mild primary TI ||III – Harm ||C |
|MV = mitral valve; PASP = pulmonary artery systolic pressure; TI = tricuspid insufficiency; TV = tricuspid valve; TVr = tricuspid valve repair; TVR = tricuspid valve replacement. |
The most common cause of isolated aortic insufficiency (AI) in patients undergoing AVR is aortic root disease, and represents over 50% of such patients in some studies.1 Other common causes of AI include congenital abnormalities of the aortic valve such as bicuspid aortic valve, calcific degeneration, rheumatic disease, infective endocarditis, systemic hypertension, 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.70 Although most of these lesions produce chronic aortic insufficiency, rarely acute severe aortic regurgitation can result, often with devastating consequences.
Regardless of its cause, AI produces volume overload with dilation and hypertrophy of the left ventricle, and subsequent 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 include disorders such as age-related (degenerative) 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.114 In these disorders, 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 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 valves 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.1 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 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.
The basic pathophysiologic abnormality of AI is the retrograde flow of a portion of the LV stroke volume into the left ventricle during diastole, producing left ventricular volume overload.
Acute severe AI results most commonly from infective endocarditis, acute aortic dissection, or trauma, and causes a sudden volume overload on the left ventricle.31 Although an acute increase in preload provides a small increase in overall stroke volume due to the Starling mechanism, the left ventricle 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 left ventricle 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, subendocardial myocardial ischemia frequently develops as a result of decreased coronary diastolic perfusion pressures and increased left ventricular end-diastolic pressure, as well as increased myocardial oxygen 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, exacerbating the hemodynamic derangements seen in acute AI.
Chronic AI generally has a more indolent course, with volume overload of the left ventricle causing compensatory increases in left ventricular end-diastolic volume and chamber compliance, and a combination of eccentric and concentric hypertrophy.115 Compensatory remodeling of the left ventricle allows for accommodation of the regurgitant volume without a significant increase in filling pressures, and maintains the preload reserve of the chamber. 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 regurgitant fraction.115,116 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 afterload, causing many patients to remain asymptomatic throughout the compensatory phase. 115,117
Eventually, 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/or impaired myocardial contractility may develop so that ejection fraction begins to decline. 118Although left ventricular systolic dysfunction related to excessive afterload is reversible early in the course, irreversible damage occurs once chamber enlargement predominates as the primary cause of diminished myocardial contractility.
In cases of acute severe AI, patients are symptomatic and invariably present with compensatory tachycardia, often associated with acute pulmonary congestion and cardiogenic shock.1 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 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 failure and myocardial ischemia develop after the compensatory phase.1 Patients gradually begin to complain of exertional dyspnea, 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 pressure falls. Patients may also experience exertional angina secondary to diminished coronary perfusion in the setting of myocardial hypertrophy. Occasionally, the compensatory tachycardia that develops with chronic AI will cause palpitations, and the increased pulse pressure will cause a sensation of pounding in the patient’s head. Peripherally, the widened pulse pressure causes a forceful, bounding, and quickly collapsing pulse known as Corrigan’s or water-hammer pulses. Premature ventricular contractions have been reported to cause particularly troubling symptoms, owing to the heave of the volume-loaded left ventricle during the postextrasystolic beat. The classic auscultatory 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 is heard as a middiastolic rumble at the apex that simulates mitral stenosis, and occurs in severe AI when the regurgitant jet impedes mitral opening.
In the acute setting, TTE should be performed to confirm the presence and severity of aortic regurgitation, the degree of pulmonary hypertension, and the cause of valvular dysfunction.70 When aortic dissection is suspected as the cause of acute AI, TEE should be performed for diagnosis, though chest computed tomography may be substituted if more readily available.119,120 Cardiac catheterization, aortography, and coronary angiography are rarely indicated, and often delay necessary urgent surgical intervention.
In cases of chronic AI, the EKG frequently demonstrates signs consistent with left axis deviation and, late in the course, intraventricular conduction defects associated with left ventricular dysfunction. On chest X-ray, the left ventricle enlarges predominantly in an inferior 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.1 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.70 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 is also an indication for TTE examination.
Additional preoperative studies are variably indicated in certain patient populations.70 In patients with poor windows on TTE, TEE, or magnetic resonance imaging 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 proceed directly to TEE or cardiac catheterization if TTE examinations are inadequate. Exercise stress testing may be helpful for an assessment of functional capacity and symptomatic responses in patients with a history of equivocal symptoms. Coronary angiography should be performed prior to valve surgery in most patients.70
Indications for Operation
Based on the morphology and severity of valve dysfunction (Table 21-12), AV repair or replacement may be performed for the treatment of AI (Table 21-13).70 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 demonstrated outcomes equivalent to those of valve replacement.
Aortic Valve Operative Techniques and Results
Aortic valve surgery has traditionally been performed through a median sternotomy incision with the assistance of cardiopulmonary bypass and moderate systemic hypothermia. 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. A left ventricular vent may be inserted through the right superior pulmonary vein to help maintain a bloodless field during the procedure, and to aid in de-airing at the conclusion of the operation.
During aortic valve replacement, an aortotomy is performed, extending medially from approximately 1to 2cm above the right coronary artery and inferiorly into the noncoronary sinus, and the valve is completely excised. The annulus is thoroughly debrided of calcium deposits. After the calcium has been removed, the ventricle is copiously irrigated with saline. 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 sewing ring of the prosthetic valve, taking care to avoid damage to the coronary ostia, the conduction system, and the MV apparatus. The annular sutures may be placed from below the annulus, seating the valve supra-annularly, or from above the annulus for intra-annular placement (Fig. 21-10).
Aortic valve replacement. The stented porcine bioprosthesis as viewed through an aortotomy.
The major components to increased operative risk associated with surgical AVR include age, body surface area, diabetes, renal failure, hypertension, chronic lung disease, peripheral vascular disease, neurologic events, infectious endocarditis, previous cardiac surgery, myocardial infarction, cardiogenic shock, NYHA functional status, and pulmonary hypertension. For most patients, the risk associated with AVR is 1% to 5%, and 5-year survival has been reported to be >80%, even in patients >70 years of age.69,121 The choice of valve is dependent on many patient-related factors, and is accompanied by the attendant postoperative risks of decreased durability, and thromboembolic vs. hemorrhagic complications for biological and mechanical valves, respectively.
Although aortic valve replacement is performed more commonly, AV repair may be recommended at surgical centers with extensive experience, technical expertise, and outcomes equivalent to valve replacement. 70
For patients with aortoannular ectasia, AI is due to annular dilatation and distortion of the sinotubular junction. For these patients, competence of the aortic valve can be achieved by functionally repairing the annulus in a method analogous to homograft implantation. The aneurysmal portion of the aortic root is excised, and the aortic valve is reimplanted inside a tubular Dacron graft, with concomitant reimplantation of the coronary arteries. Alternatively, the aneurysmal tissue and supravalvular tissue can be excised in their entirety, with subsequent implantation of the Dacron graft onto the superior aspect of the annulus and reimplantation of the coronary arteries.
Valve-sparing root replacement for root and annular stabilization in patients with AI due to aortoannular ectasia has led to a more durable outcome than is seen with subcommissural annuloplasty or leaflet-related procedures alone. One study demonstrated equivalent overall survival between patients undergoing subcommissural annuloplasty or aortic valve repair without annuloplasty, and patients undergoing valve-sparing root replacement at 6 years. 122 However, patients that underwent valve-sparing root replacement had higher freedoms from reoperation and aortic insufficiency >2+ (100% vs. 90%, P=0.03; and 100% vs. 77%, P=0.002, respectively) at midterm follow-up.
For patients with AI associated with redundant leaflet tissue, aortic valve repair may be accomplished with free margin plication or resuspension of the valve cusps, with or without triangular resection of the redundant segment. Excision of the diseased portion of the involved valve cusp improves symmetry of the valve leaflets, and annular plication of one or both commissures helps to ensure adequate coaptation. Generally, the free margins of the excised leaflets are reapproximated primarily, but in the absence of adequate cusp tissue, a triangular autologous or bovine pericardial patch may be used for cusp restoration.
AV cusp repair with a free margin plication or resuspension technique has demonstrated encouraging results, both in patients with tricuspid and bicuspid aortic valves. Freedom from AV reoperation in patients with a tricuspid AV has been reported to be 89% to 92% at 10 years, with a freedom from recurrent AI >2+ of 80% to 86% at the same time point. In patients with bicuspid aortic valves, who generally represent a younger cohort of patients, 10-year survival has been reported at 94% following AV repair, with a freedom from AV reoperation of 81% at the same time point. 123
As mentioned previously, the Ross procedure involves replacing the diseased AV with the patient’s native pulmonary valve as an autograft, which is in turn replaced with a homograft in the pulmonic position.80 The autograft may be implanted in the aortic position directly with resuspension of the valve commissures, or in association with a root replacement, which requires reimplantation of the coronary ostia.
The cylinder root replacement technique is most reproducible, and involves transecting the native aorta approximately 5mm above the sinotubular ridge, with subsequent excision of the aortic valve leaflets and supra-annular tissue. The main pulmonary artery is transected at the bifurcation and the right ventricular outflow tract is incised, allowing the pulmonary valve and artery to be removed en bloc from the outflow tract. The annulus of the pulmonary autograft is sewn to the native aortic annulus with continuous or interrupted sutures, and the coronary ostia are reimplanted into the pulmonary artery graft. The pulmonary valve and right ventricular outflow tract are subsequently reconstructed using homograft tissue.
The primary benefit of the Ross procedure compared to traditional AV surgery is a low risk of thromboembolism without the need for systemic anticoagulation. Although patients undergoing the Ross procedure are generally younger, perioperative mortality has been reported to be as low as 2.5% in this group, with an overall survival of 90% at 18-year follow-up.124 However, the long-term durability of the procedure is somewhat questionable. Although Ross reported a freedom from autograft replacement of 75% at 20 years, other groups have reported freedom from autograft reoperation and allograft reintervention of 51% and 82%, respectively, at 18-year follow-up.124,125 Progressive aortic insufficiency has been described as a cause of late failure in these patients, as well as calcification of the pulmonary homograft and pulmonary stenosis.
Transcatheter Aortic Valve Replacement
Transcatheter aortic valve replacement (TAVR) is relatively new technology that has proven beneficial for the treatment of AS in seriously ill patients who are not candidates for conventional surgery. The procedure remains the focus of ongoing clinical trials, and thus there are no published indications for operation endorsed by the American College of Cardiology or the American Heart Association. However, the Edwards SAPIEN heart-valve system that has been used thus far in the TAVR experience has been recently approved by the Food and Drug Administration for labeled-indications associated with published early results.
The Edwards SAPIEN heart-valve system consists of a trileaflet bovine pericardial valve with a balloon-expandable stainless steel support frame, and can be inserted by either the transfemoral, transaortic, or transapical route. The transfemoral route involves performing a standard balloon aortic valvuloplasty, followed by transfemoral insertion of either a 22- or 24-French sheath, depending on the size of the valve selected for implantation. The balloon catheter and overlying collapsed bioprosthetic heart valve is then advanced across the native aortic valve under fluoroscopy, and deployed during rapid right ventricular pacing. If the patient’s peripheral vascular system is not amenable to femoral arterial cannulation, the transapical or transaortic route is chosen. In the transapical approach, a small intercostal incision is performed over the left ventricular apex, and a dedicated delivery catheter is inserted through the left ventricular apex and across the native aortic valve as described above. The transaortic approach is usually done through a ministernotomy. Other approaches that have been described include transaxillary, transsubclavian, and transcarotid. The particular role of each approach in a specific patient still remains to be defined, and continues to change as the technology improves.
A large multicenter clinical trial has been performed on patients that were judged to be too high risk or inoperable for traditional AVR, based on assumed risks of ≥10% to 15% and ≥50% 30-day mortality, respectively. In patients that had previously been deemed inoperable, TAVR markedly reduced the rate of death from any cause (49.7% vs. 30.7%, P = <0.001), the rate of death from cardiovascular causes (41.9% vs. 19.6%, p = <.001), and the rate of repeat hospitalization (44.1% vs. 22.3%, p = <.001) at one year compared with standard medical therapy.126 Although the rates of neurological events (10.6% vs. 4.5%, P = 0.04), major vascular complications (16.8% vs. 2.2%, P = <.001), and major bleeding events (22.3% vs. 11.2%, P = 0.007) were higher in the TAVR group, these patients also experienced a significant reduction in symptoms and increased functional capacity compared with patients receiving standard medical therapy. In patients at high risk for traditional AVR, the rate of death from any cause, and from cardiovascular causes, was found to be noninferior in the TAVR group, compared with the surgical group.127 The rate of major bleeding events was higher in the surgical group (19.5% vs. 9.3%, P= <0.001) at 30 days, and patients in the TAVR group had a significantly shorter length of stay in the intensive care unit (3 vs. 5 days, P = <0.001), and a shorter index hospitalization (8 vs. 12 days, P = <.001). Although more patients in the TAVR group experienced a reduction in symptoms to NYHA class II or lower (P = <0.001), they also experienced more neurological events (8.3% vs. 4.3%, P = 0.04), and major vascular complications (11.3% vs. 3.5%, P = <.001) at one year.
Although it is clear that TAVR represents a distinct set of periprocedural risks, it has demonstrated benefits in morbidity and mortality, especially in patients deemed inoperable for surgical AVR. Ongoing trials are examining the potential role of TAVR in patients with AS at moderate risk for traditional AVR.