Degenerative disease of the aortic valve occurs with age. Areas of cusp flexion over time develop fibrosis and calcification, impeding valve excursion and creating obstruction to left ventricular outflow.¹ The most common cause of aortic stenosis (AS) is calcification of a normal trileaflet or congenital bicuspid valve.² Calcific AS is an active disease process characterized by lipid accumulation, inflammation, and calcification, with many similarities to atherosclerosis.^3-5 The degenerative process usually occurs in the sixth decade of life and beyond, but patients with additional valve pathology (bicuspid aortic valves, rheumatic heart valvular disease, radiation valvulopathy) can present much earlier in life with deterioration of valve function and consequent symptoms.^6,7

The 2 most common etiologies of AS amenable to percutaneous treatment are: (1) congenitally bicuspid aortic valves and (2) calcified tricuspid valves. Unicuspid or quadricuspid valves are not normally candidates for a percutaneous approach, with unicuspid disease typically associated with stenosis and quadricuspid valves with regurgitation. Isolated rheumatic AS, rare even in countries with a high prevalence of rheumatic heart disease, is highly amenable to percutaneous intervention because the mechanism of improvement is splitting of the fused commissures.

Bicuspid aortic valves occur in approximately 1.5% of the population, and associated stenosis presents much earlier in life than tricuspid aortic valve disease.⁷ AS in adolescents and young adults is usually noncalcific, is the result of fused bileaflet valves, and is highly amenable to percutaneous balloon intervention. In contrast, AS in bicuspid and tricuspid valves of adults is associated with calcification of the valve that results in thickening, rigidity, and immobility of leaflets, often without commissural fusion.

Balloon aortic valvuloplasty (BAV) has been shown to relieve obstruction of the stenotic valve by 3 mechanisms: (1) fracture of calcium deposits in the leaflets, (2) splitting of fused commissures, and (3) stretching of the aortic annulus.^8,9 Calcium deposits are broken into separate fragments with balloon inflation, facilitating leaflet flexion and allowing better excursion during systole. Splitting of commissures is quite effective by BAV. Stretching of the valve may explain the early gains by BAV, but valve recoil can occur within hours to days, and in this case, results of BAV may be fleeting. Late restenosis (after several months) probably results from progression of the original lesions that produced stenosis.

The development of symptoms can trail the onset of degeneration of the aortic valve by several decades.¹⁰ When present, initial symptoms tend to be dyspnea on exertion and effort angina, although some patients may present with syncope or heart failure.¹¹ Exertional fatigue may be the first manifestation of severe AS in the elderly. Once symptoms are detected, the prognosis is poor without intervention: patients often have mortality within 5 years of angina, 3 years of syncope, and 2 years of heart failure.^12,13 Cohort B of the Placement of Aortic Transcatheter Valves Trial (PARTNER) consisted of inoperable patients randomized to transfemoral transcatheter aortic valve replacement (TF-TAVR) versus medical therapy (including BAV as necessary). The study demonstrated 50% mortality at 1 year with medical therapy including BAV.¹⁴ More recently, 2-year results from the PARTNER trial demonstrated a mortality of 68% with medical therapy and BAV.¹⁵

Surgical aortic valve replacement (SAVR) has been the standard of care for treatment of symptomatic patients with severe AS. SAVR is accepted to alleviate symptoms and prolong survival; however, up to one-third of patients are denied SAVR because of prohibitive surgical risk (eg, advanced age, significant left ventricular dysfunction).¹⁶ Results from the PARTNER trial have shown that transcatheter aortic valve replacement (TAVR; covered in Chapters 42 and 43) is the standard of care for extremely high-risk or “inoperable” patients and is a valid alternative to surgery for high-risk but “operable” patients with symptomatic AS.^14,17 The introduction of TAVR has brought resurgence in the use and utility of BAV.^18,19

Standalone BAV has been reserved for a subset of patients who are too sick to undergo SAVR and are considered inappropriate patients for TAVR. BAV is used in contemporary practice as a bridge to subsequent SAVR or TAVR (class IIb indication).²⁰ In the current era of percutaneous valve replacement, BAV may be used to assess initial clinical improvement and future candidacy for TAVR.²¹

Clinical Subsets

Several important clinical subsets of patients with AS exist with mean aortic valve gradients of less than 40 mm Hg in whom BAV may be used as a diagnostic and therapeutic procedure.

An important group of patients are those with severe AS and secondary depression of left ventricular function. In this subset of patients, the aortic valve gradient is low due to the inability of the left ventricle to sufficiently open the stenotic valve. In this group, pharmacologic agents, such as dobutamine, that increase flow across the valve will result in a dramatic rise in gradient.²² These patients typically benefit from relief of aortic valve obstruction.²³ In contrast, patients with moderate AS and left ventricular dysfunction do not have an increase in gradient with dobutamine and do not benefit from SAVR. In cases where there remains an uncertainty after dobutamine challenge, we have performed BAV to evaluate whether increasing the valve area correlates with improved clinical symptoms and ventricular recovery.

Another complicated group of patients has only been distinctly identified in the past several years. These patients have small hypertrophied ventricles, preserved ejection fraction, and low aortic valve gradients. This group sometimes has high valvuloarterial impedance AS and has low gradient because of decreased stroke volume. In these patients, when an uncertainty exists about the degree of AS, we have performed BAV as a diagnostic procedure and have been aggressive with blood pressure control (afterload reduction). Those with an excellent clinical response can be sent for SAVR or TAVR with mortality benefit.²⁴ BAV can be used to assess clinical response in patients with severe lung disease as well.

BAV was originally performed in 1985 and was initially proposed as an alternative to SAVR in patients who were considered too elderly or high risk with severe AS.^25-27 Initial enthusiasm in the late 1980s was subsequently tempered by studies demonstrating high rates of complications, lack of durability, and little or no impact on long-term survival, particularly in centers with low experience.^28-30 Until recently, the use of BAV had significantly waned; it was restricted to very-high-risk patients with severe heart failure or cardiogenic shock and was often used as a bridge to SAVR.

The introduction of TAVR in 2002 and technical improvements with reduction of sheath diameter, rapid pacing, and vascular closure devices have brought the nearly dormant BAV technique back into the mainstream. The problem of restenosis has been addressed by the advent of TAVR.^18,31 Several very busy structural heart centers such as ours perform more than 200 BAVs a year, a volume that has been sufficient to train multiple attending physicians and fellows. For these trainees, BAV has been a gateway procedure for learning the essentials of TAVR.

The evaluation of AS begins with the patient history and physical examination. Often, only transthoracic echocardiography (TTE) is used to quantify the degree of stenosis as retrograde catheterization has been associated with an increased risk of stroke, particularly if prolonged attempts are needed to cross the aortic valve.³² If there is any discrepancy between the patient’s presentation and echocardiographic results, retrograde catheterization should be performed to measure the simultaneous gradient across the aortic valve (class I indication), as described below.³³ In patients with low transvalvular gradient and low cardiac output, dobutamine infusion can aid in diagnosing patients with true AS from those with “flow-dependent” stenosis.²² Assessment of concomitant coronary artery disease is important prior to BAV and can often be accomplished in the same session. Venous and arterial access sites should also be evaluated prior to the procedure.

After assessing candidacy for BAV, it is important to obtain and review multimodality imaging for optimal procedural planning. TTE is the initial, and often only, imaging modality of choice due to its ease and safety. TTE establishes the diagnosis of AS and allows assessment of valve morphology (ie, bicuspid, functionally bicuspid, or trileaflet valve), left ventricular outflow tract size, and baseline left ventricular function. Understanding valve morphology prior to BAV is critical as balloon dilatation of a bicuspid or functionally bicuspid valve with an oversized balloon may result in acute severe aortic regurgitation.

Computed tomography (CT) provides a wealth of cardiac, thoracic, and peripheral information in assessing a patient’s feasibility for TAVR and procedural planning.³⁴ A CT scan will show in detail the aortic root anatomy (including annular, sinotubular, and sinus of Valsalva dimensions as well as coronary heights above the annulus), aortobifemoral anatomy, and details of arterial diameters and calcification. A gated, contrast CT with less than 1-mm slices will allow detailed 3-dimensional reconstruction, which can be invaluable for evaluation of the aortic annulus and peripheral arteries. Review of the CT scan prior to BAV aids in procedural planning. The lower extremity with larger diameter iliofemoral caliber is reserved for potential future TF-TAVR. Additionally, accurate assessment of the femoral bifurcation and areas of calcification will guide arterial access for BAV and successful percutaneous arteriotomy closure.

Factors contributing to limited reserve (ie, depressed left ventricular ejection fraction, last remaining coronary vessel/graft, biventricular failure, or hemodynamic shock) should be identified prior to BAV to assist with procedural planning. These patients tend to not tolerate pacing runs, and it may be more beneficial to perform BAV without rapid ventricular pacing. Additionally, in patients with hemodynamic shock or in those who cannot lay supine, hemodynamic support devices (intra-aortic balloon counterpulsation) and a wedge may be used.

Patients are prepared from the upper thigh to the subxiphoid area in case emergent pericardiocentesis is required. Defibrillator pads are placed in the anterior-posterior position to facilitate treatment of ventricular arrhythmias during the procedure. Patients with difficulty in breathing are positioned semi-recumbent with the assistance of a wedge cushion. The procedure begins with the administration of minimal conscious sedation and local anesthesia.

Special Instruments and Pharmacologic Agents

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  “Micropuncture” access kits that use a 21-gauge needle and 0.018-inch wire for arterial entry are best for fluoroscopic or ultrasound-guided access.

  
  
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  Percutaneous arteriotomy closure devices such as the Perclose ProGlide (Abbott Vascular, Abbott Park, IL), ProStar XL (Abbott Vascular), and Angio-Seal (St. Jude Medical, St. Paul, MN).

  
  
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  For patients with depressed ejection fraction, low coronary reserve, or hemodynamic compromise, 10-mL syringes of norepinephrine (16 μg/mL) and epinephrine (0.1 mg/mL) are helpful when treating acute hypotension. Background low doses of norepinephrine continuous infusion may also be helpful to maintain blood pressure, particularly with escalating doses of sedation.

Antithrombotic Therapy

Unfractionated heparin (dose of 5000 IU) should be used after arterial access to maintain an activated clotting time (ACT) of 250 to 300 seconds. Direct thrombin inhibitors have been used in patients with heparin allergies. Cases can be performed without any anticoagulation, although stroke risk is higher. In those cases, frequent catheter exchanges are performed to minimize clotting on the wire used during BAV, and procedure time is minimized.

Vascular Access, Right Heart Catheterization, and Supra-aortic Angiography

Right common femoral arterial access is obtained with a micropuncture access kit and cannulated with a 6- or 7-Fr sheath. If the right femoral artery is unavailable for access, the left femoral artery, the brachial artery, the axillary artery, or an antegrade transseptal approach via the femoral vein can be used. To limit vascular complications in the arm, we recommend a cut down and maximum sheath size of 10-Fr. Common femoral venous access is obtained and cannulated with a 7-Fr sheath. A 7-Fr Swan-Ganz catheter is advanced from the femoral vein, and baseline right-sided pressures are recorded. Cardiac output measurements using either thermodilution or the Fick principle should wait until the aortic valve has been crossed to reduce error if calculation of the aortic valve area is performed during catheterization. After a right heart catheterization is performed, a temporary pacing wire is advanced to a stable position in the right ventricular apex. Placement of the lead in the base of the right ventricular free wall can increase the risk of perforation or loss of capture. A 6-Fr pigtail catheter is then advanced from the femoral artery and placed superior to the aortic valve. Aortic angiography in the left anterior oblique projection is not mandatory but can be helpful to define the details of the valve anatomy and assess the degree of insufficiency (Fig. 41A-1). Patients with more than moderate aortic regurgitation are in general not considered for BAV. Patients with moderate aortic insufficiency or less are reasonable candidates for BAV, particularly if the valve is trileaflet.