The Efficacy and Safety of Antegrade Inoue-Balloon Aortic Valvuloplasty to Treat Calcific Critical Aortic Stenosis

Abstract: Background. Critical aortic stenosis (AS) with severe calcific degeneration often resists conventional retrograde percutaneous balloon aortic valvuloplasty (PBAV). To enhance therapeutic efficacy, a novel PBAV technique has been developed by utilizing a single Inoue balloon via an antegrade approach, performing multiple inflations with step-up increases (M-PBAV) of balloon diameter to the size of the surgical valve ring. Patients and Methods. A total of 405 non-surgical patients with critical AS were treated by M-PBAV and the acute therapeutic response and long-term clinical course were evaluated; some patients underwent the procedure on two or three occasions. Results. In a total of 456 procedures, mean transaortic valve pressure gradient improved from an initial 63.6 ± 17.3 mm Hg to 22.7 ± 8.9 mm Hg post PBAV (P<.01). Mean aortic valve area increased from an initial 0.55 ± 0.15 cm² to 0.98 ± 0.20 cm² immediately after M-PBAV (P<.01). Clinical symptoms (New York Heart Association [NYHA] class) improved over time. Prior to M-PBAV, baseline NYHA class I-II was 9.1%, and NYHA class III-IV was 90.9%. At 12 months post M-PBAV, mortality was 17.1%, with repeat M-PBAV plus surgical AVR at 12.7%, 10.5% NYHA class III-IV, and 59.6% NYHA class I-II. At 24 months post M-PBAV, mortality was 25.8%, with repeat PBAV plus surgical AVR at 19.0%, 8.8% NYHA class III-IV, and 46.2% NYHA class I-II. Adverse events related to the procedure included critical AR (0.5%), cardiac tamponade (1.8%), intraprocedure hemodynamic compromise requiring percutaneous cardiopulmonary support (0.5%), and reversible cerebral ischemia (1.3%). No myocardial infarct or vascular complications occurred. Conclusion. M-PBAV enhanced the therapeutic efficacy and procedural safety of valvuloplasty to treat severely calcified critical AS, and diversified its clinical roles. 

J INVASIVE CARDIOL 2015;27(8):373-380

Key words: balloon aortic valvuloplasty, aortic stenosis

____________________

Symptomatic calcific-sclerotic aortic stenosis (AS) is prevalent in the elderly population and in patients with hemodialysis due to end-stage renal disease. However, the risks of surgical aortic valve replacement (AVR) significantly increase with advanced age and systemic status. Concomitant cardiac disorders often complicate the evaluation of the severity of AS and its symptomatic involvement. Although transcatheter AVR (TAVR) is a useful alternative therapy, it is not always effective for elderly and predominantly female patients with a small body habitus or with miscellaneous comorbid problems – a typical population targeted in the present study. The same situation is apparent in patients with small-caliber iliac-femoral arteries or concomitant peripheral artery disease of the lower extremities, limiting the use of transfemoral TAVR or even retrograde percutaneous balloon aortic valvuloplasty (PBAV). 

It has been noted that severely calcified degenerative valves tend to resist conventional balloon inflation, often responding poorly to a limited number of inflations with a conventional balloon introduced by the retrograde approach.¹ Therefore, the role of retrograde PBAV has been limited to pretreatment TAVR or a transient palliative therapy for patients who have no alternative therapy or who are in hemodynamic compromise.²

In order to perform valvuloplasty on severely calcific AS, improved outcomes are hypothesized by applying multiple inflations in a stable position, repeatedly folding the calcified valve up to the sufficient inflation size (surgical valve diameter), while increasing the inflation diameter stepwise to ensure procedural safety.

It was previously demonstrated that PBAV by an antegrade approach using an Inoue balloon improved its procedural efficacy and safety over the conventional retrograde method.³ Refinement of the antegrade PBAV technique utilizing the compliant property of the Inoue balloon was therefore pursued. The stenotic valve was initially dilated by an undersized diameter at low pressure as the priming inflations to resolve stenosis. Then, multiple inflations of the same balloon with stepwise increases of dilation size to the surgical valve diameter were performed (M-PBAV). 

This study evaluated the clinical efficacy and safety of M-PBAV in 456 procedures performed in 405 non-surgical patients with critical AS.

Methods

A total of 456 M-PBAV procedures utilizing an Inoue balloon were performed between October 2006 and March 2013 on 405 Japanese patients with critical AS presenting with active cardiovascular symptoms. Each case was thoroughly discussed with the cardiothoracic surgery team concerning the potential risks and possibilities of surgical AVR. The therapeutic and clinical responses of each patient to M-PBAV were analyzed, and procedural efficacy and safety were evaluated. The clinical courses of patients after M-PBAV were followed for a survival period. The clinical status of each case was evaluated at 30 days, 3 months, 6 months, 12 months, and 24 months post procedure. The information related to patients’ medical conditions during the follow-up was obtained from physicians in charge of them during the outpatient period.    

The M-PBAV procedure. The femoral vein (right femoral vein in 450 cases, left femoral vein in 6 cases due to right iliac-femoral venous thrombosis) was accessed and dilated with a 7 Fr dilator. The puncture site was preclosed with a percutaneous suture closure device (Proglide; Terumo Corporation) and a 25 cm, 14 Fr sheath was placed. The suture knot was closed when the sheath was removed at completion of the procedure based on an established method.⁴ An 8.5 Fr Lamp 135° sheath (St. Jude Medical) was inserted into the left atrium (LA) via transseptal approach. A total of 120 U/kg heparin was administered intravenously. Arterial access was obtained at the common femoral artery (n = 446 cases) or upper limb arteries (n = 2 brachial; n = 8 radial) in order to place a 25 cm, 5 Fr sheath for arterial pressure monitoring and for placement of a 10 mm gooseneck snare catheter (ev3). The distal end of the arterial sheath was positioned in the abdominal aorta, and aortic pressure was measured.

A 7 Fr Swan-Ganz catheter was used to measure cardiac output by the thermodilution method. A 7 Fr endhole wedge-balloon catheter (Goodman) was inserted through a Lamp catheter into the LA, across the mitral valve, and into the left ventricle (LV). A simultaneous pressure gradient (ΔP) was measured between the aorta and LV to calculate the mean transaortic valve pressure gradient (mean LV-Ao ΔP). The aortic valve area (AVA) was calculated based on Gorlin’s formula using mean LV-Ao ΔP and cardiac output. Intravenous lidocaine (1 mg/kg) was administered to prevent ventricular arrhythmias caused by catheter manipulation in the LV. The tip of a 0.032˝ spring-tip guidewire (Toray Medical) was manually shaped, creating 4 to 5 coil turns with 5-10 mm radius, and was used as a stylet to facilitate directing the inflated wedge-balloon catheter from the LV apex to the LV outflow. The tip of the wedge catheter was directed in the antegrade direction from the LV to the aorta, crossed by blood flow across the aortic valve, and was further advanced into the aorta. A 0.032˝ extra-stiff wire (Cook Corporation) was inserted through the inner lumen of the wedge catheter, and its distal end was fixed using a gooseneck snare catheter in the descending aorta. Both wedge catheter and Lamp sheath were removed, leaving the extra-stiff wire alone as an intracardiac wire loop. The Inoue balloon (Toray Medical) was inserted from the right femoral venous sheath into the right atrium, and advanced over the wire loop across the aortic valve.⁵ The valvuloplasty was performed by applying multiple manual inflations with stepwise increases of balloon size up to the surgical valve diameter measured by an echocardiogram. A temporary pacemaker was placed in the right ventricle, and the right ventricular burst pacing (200 beats/minute for less than 2 seconds) was applied as needed in order to stabilize the position of the balloon during inflation.⁶ After completion of valvuloplasty, the hemodynamic parameters (mean LV-Ao ΔP and AVA) were reevaluated and compared with the baseline value.

Results

In 46 cases (10%), patients presented with cardiogenic shock and pulmonary edema, and M-PBAV was performed to correct the unstable hemodynamic condition. It was performed as preparation for non-cardiac surgery in 27 cases (6%), and as a bridge for surgical AVR in 14 cases (3%), aiming to optimize the patient’s cardiac and general condition prior to surgery. In the remaining 379 cases (81%), it was electively performed as palliative therapy for symptoms including heart failure, angina, and syncope. A total of 48 cases were performed for a second time and 3 cases were performed for a third time. All patients were diagnosed with severe to critical AS in advance, confirmed either by echocardiogram or cardiac catheterization, demonstrating an AVA of <0.8 cm².

The baseline characteristics of patients are listed in Table 1. Treated patients are generally of advanced age and predominantly female, with small body habitus and high surgical risk. 

Concomitant medical problems, which are shown in Table 2, reveal a high prevalence of hypertension, chronic renal insufficiency, and coronary artery disease (CAD). A total of 26.9% of patients underwent percutaneous coronary intervention (PCI) due to critical CAD after stabilizing their hemodynamic status by M-PBAV, usually treated as elective cases on a separate occasion. A total of 12.1% of patients had active clinical problems related to neoplastic disease, and 9.8% underwent radical treatments including non-cardiac surgery or chemotherapy following M-PBAV. A total of 9.4% of patients had end-stage renal disease treated by chronic hemodialysis. Three patients (0.7%) had a bicuspid aortic valve. 

Procedures. The diameter of the surgical valve ring was obtained by measuring the distance between the sites of attachment of the aortic valve to the aortic base by a parasternal long-axis view of a transthoracic echocardiogram. The size of the Inoue balloon was selected based on the diameter of the surgical valve ring as a targeted maximal inflation diameter.⁵

The Inoue balloon was inflated by manual injection of diluted contrast agent (contrast media to saline ratio = 1:3). It was dilated to the predetermined diameter depending on the injected volume only when there was no constraint on the balloon.   

This established a compliant balloon and created low intraballoon pressures of around 1-3.5 atm. The integral part of the M-PBAV procedure is that a series of priming dilations are initially performed by undersized inflations with low intraballoon pressures, resulting in the resolution of the indentation (Figure 1A). Multiple inflations by the single balloon are performed with an increase of dilation diameter in a stepwise fashion until the target inflation diameter is achieved, as demonstrated in a series of angiograms for a representative case example (Figure 1B).

In this series, the Inoue balloon dilation size was gradually increased from a mean initial diameter of 18.3 mm (estimated intraballoon pressure, 1.3 atm) to a final value of 21.4 mm (intraballoon pressure, 2.5 atm), with an average of 12.3 inflations (Table 3).

In 72.5% of cases, burst right ventricular pacing (200 beats/minute) was applied in order to secure full inflations in the stable position. The mean duration of each rapid ventricular pacing was 1.5 seconds (5 beats of rapid ventricular pacing). It was typically observed that both the mobility of the valve and the AVA were gradually improved over repeated inflations by M-PBAV, as illustrated in case #1 (Figure 2).

In cases of AS with depressed LV function and severely compromised hemodynamic status, M-PBAV was generally well tolerated. Blood pressure was maintained by administering intravenous catecholamine (diluted nor-adrenaline or phenylephrine as needed) and by utilizing intraaortic balloon pump (IABP). Notably, IABP was particularly useful in maintaining vital organ perfusion during the procedure. In the present study, it was used in 8.1% of all cases characterized by unstable hemodynamic status due to cardiogenic shock, concomitant critical mitral regurgitation (MR), or concomitant severe ischemic heart disease.

Patients with heavily calcified bicuspid AS (0.74% in this series) favorably responded to M-PBAV. In Figure 3, case #2 illustrates a patient with bicuspid critical AS in cardiogenic shock, which was successfully treated by M-PBAV with IABP support. 

A total of 14 patients (3%) underwent M-PBAV as a bridge procedure, followed by surgical AVR in 1 year. Pathological evaluation of the resected native valve demonstrated a formation of microfracture and tears located between densely calcified segments. Microscopic photographs (Figure 4) revealed that repair by fibrosis occurred, which is a process that repairs valve leaflets treated by PBAV. 

About one-third of patients (32.8%) had concomitant critical CAD, and 26.9% underwent PCI as an elective procedure after hemodynamic stabilization by M-PBAV. A total of 9.8% of patients underwent radical therapies for malignancy, including surgical resection, radiation therapy, or anticancer chemotherapy following hemodynamic stabilization by M-PBAV.

Immediate outcomes. Mean LV-Ao ΔP at the baseline PBAV was 63.6 mm Hg, which improved to 22.7 mm Hg immediately after M-PBAV (P<.05). Mean AVA improved from 0.55 cm² at baseline to 0.98 cm² (P<.01) after M-PBAV (Table 4). The procedural success rate was 99.3%. One case was terminated due to severe spinal deformity, causing significant difficulty in manipulating the catheter via the femoral approach. The mean time to ambulation was 16 hours after the procedure, facilitated by secure hemostasis by venous preclosure technique. This procedure was successful in 95% of cases.

Short-term outcomes (within 30 days). A total of 91% of treated patients were symptomatic due to AS (NYHA class III, 48.1%; NYHA class IV, 42.8%) at baseline prior to M-PBAV (Figure 5). The remaining patients (9%) belonged to NYHA class I or II, and required non-cardiac surgery to treat malignancy or orthopedic disorders. Although significant cardiovascular symptoms were absent in those cases, they were diagnosed with critical AS by echocardiogram and M-PBAV was performed to support stable hemodynamic conditions during non-cardiac surgery. 

Thirty days after the procedure, the rate of all-cause death was 2.8%, while 17.7% remained symptomatic (NYHA class III, 9.7%; NYHA class IV, 8%). Symptomatic patients were noted for frailty and with profoundly poor functional condition prior to M-PBAV, requiring in-hospital rehabilitation even after a successful procedure. A total of 78.4% of patients improved remarkably to a stable clinical condition of NYHA class I (34.7%) or class II (43.7%) and were followed in outpatient care. 

Eleven patients (2.8%) died due to either cardiac or non-cardiac causes within 30 days (Table 5). Out of these cases, 6 deaths (1.5%) were directly due to adverse events related to M-PBAV; namely, case #1 from cardiac tamponade (LA perforation); cases #2 and #3 from critical AR aggravating heart failure; cases #4 and #5 from multiorgan failures associated with cholesterol emboli following IABP placement; and case #6 from intraprocedural cardiogenic shock. 

Intermediate to long-term follow-up. Three months after M-PBAV, a total of 79.6% of patients were maintained at NYHA class I (36.9%) or class II (43%) (Figure 5). The all-cause mortality rate was 6.1%, and 1.3% underwent surgical AVR. Two patients (0.5%) who had a history of chest radiation therapy were treated with repeat M-PBAV due to recurrent symptoms. About 12% of patients remained symptomatic, belonging to either NYHA class III (7.5%) or class IV (4.5%) at this point.

Six months after the procedure, 73.8% of patients were followed and observed to be in a stable condition, with NYHA class I (33.2%) or class II (40.8%). The all-cause mortality rate was 8.9%, and 2.4% were treated with surgical AVR and 1.8% with repeat M-PBAV. A total of 12.6% of patients were symptomatic, with NYHA class III (8.4%) or class IV (4.2%). Poor responders tended to be frail and have poor general condition, severe systemic atherosclerotic disease, and multiorgan disorders.

Long-term follow-up. Twelve months after the procedure, 59.8% of treated patients were maintained at either NYHA class I (23.2%) or class II (36.4%), and were followed on an outpatient basis (Figure 5). The all-cause mortality rate was 17.1%. About 3.9% were treated with surgical AVR, and 8.8% underwent repeat M-PBAV. In total, 10.5% of patients were symptomatic with either NYHA class III (6.2%) or class IV (4.3%).

At 24 months after M-PBAV, 46.2% were controlled at NYHA class I (18.1%) or class II (28.1%), and free of major cardiovascular events. The all-cause mortality rate was 25.8%. Of these, 5.9% had been treated with surgical AVR, and 13.1% were treated with repeat M-PBAV. The repeated procedures provided the same degree of hemodynamic and clinical improvement compared with the initial procedure. A total of 8.8% of patients were symptomatic, with 5.3% at NYHA class III and 3.5% at class IV.

Adverse events related to M-PBAV. The adverse events related to M-PBAV are detailed in Table 6. Clinically significant aggravation of AR was rare, and overall there was no significant aggravation of severity of AR over M-PBAV (Figure 6). 

Critical AR occurred acutely in 2 cases (0.5%) due to persistent dislocation of the single valve leaflet folded in the sinus of Valsalva in 1 case, and due to prolapse of the single valve leaflet in 1 case. Both cases developed refractory hemodynamic compromise, causing fatal acute renal failure and pneumonia associated with pulmonary edema. Two cases of cardiac tamponade from the LA (0.5%) were caused by difficult intracardiac device advancement due to tortuous alignments of major veins and cardiac chambers. In 1 case, it caused rapid hemodynamic compromise unresponsive to resuscitation, resulting in death within 24 hours. Another case was successfully managed by pericardial drainage without consequence. Five cases of cardiac tamponade (1.3%) were caused by temporary pacemaker placement. Four of these were conservatively managed by pericardial drainage, and 1 case required surgical repair of a perforated right ventricle. Six cases (1.5%) developed neurological symptoms (leg weakness or dizziness) consistent with transient cerebral ischemia. They recovered within 7 days without any permanent neurological deficit. 

Discussion 

The observed favorable clinical performance of M-PBAV is speculated to depend on a combination of: (1) the antegrade advancement of devices; (2) the utilization of the Inoue balloon; (3) the application of multiple consecutive inflations of gradually increasing diameter; (4) a minimal requirement of arterial access; and (5) the easy introduction of IABP.

In the initial step of the creation of an intracardiac wire loop, an inflated wedge-balloon catheter was advanced from the LV side of the aortic valve to ascending and eventually to descending aorta. The mechanical stress by device manipulation on the aortic side of the aortic valve and aorta is negligible as compared with a retrograde procedure.⁷

The procedural refinement of M-PBAV is largely dependent on favorable profiles of the Inoue balloon, which was uniquely designed for valvuloplasty by Inoue,⁸ including: (1) durable balloon material maintaining integrity and a smooth surface after multiple inflations; (2) a unique inflation pattern initiating from the distal ends to the middle waist; (3) compliant inflation profiles performed under low pressures (1.5-3 atm) conforming to the lesion; (4) the adjustable diameter of inflation depending on the injected volume of diluted contrast; and (5) a rapid inflation and deflation cycle.⁹ 

Taking advantage of these favorable features, inflation diameters of the single Inoue balloon were increased in a stepwise fashion. Repetitive dilations of calcific-sclerotic valves with multiple inflations were applied in each diameter, gradually increasing the area of microfractures of the diseased valve and retrieving its mobility.

The Inoue balloon is compliant and inflations are performed under relatively low pressures (1.5-3 atm), initially conforming to the configuration of aortic stenosis as priming dilations. The repetitive dilations (even with the same diameter) gradually increase both valvular area and mobility. This gradual process plays an integral part in achieving full dilation securely and in avoiding unfavorable mechanical stress on aortic valve or aorta. After the priming inflations, balloon dilations are repeated with stepwise increased diameter until reaching the targeted surgical valve diameter.  

When the balloon is inflated, it bends the calcific-sclerotic valvular leaflet upward to the sinus of Valsalva and obstructs the valve orifice, causing a transient reduction of blood flow across aortic valve. The closure of the aortic valve is dependent on diastolic Ao-LV pressure gradient and transaortic valvular flow. Prolonged inflations could cause a profound reduction in transaortic valvular flow and a failure of valvular closure, resulting in development of acute aortic insufficiency. Completing each stroke of inflation in the shortest duration is critically important in order to prevent intraprocedural hemodynamic compromise. The Inoue balloon has a remarkably short inflation-deflation cycle and its interference on hemodynamic status during the valvuloplasty is substantially reduced compared with the conventional balloon used for the retrograde procedure. Furthermore, in cases with marked reductions of transvalvular flow at baseline due to decompensated heart failure, intraprocedural IABP is useful in supporting hemodynamic status and in preventing acute aortic insufficiency.¹⁰ The simultaneous use of IABP is readily available during antegrade PBAV due to its minimal requirement of arterial access.

The Inoue balloon is able to self-position and enables operators to perform PBAV without the burst right ventricular pacing.⁵ In PBAV with multiple step-up inflations, the initial to early stages of inflations are performed without burst right ventricular pacing. In the subsequent mid to late stages of serial inflations, the Inoue balloon could slip due to unstable positioning as a result of the increased transvalvular flow and the improved mobility of the aortic valve. The burst right ventricular pacing is then utilized in those situations in order to prevent slipping of the balloon and to avoid inadvertent or ineffective inflations at the plaque-rich proximal ascending aorta. The use of Inoue balloon limits the duration of pacing to 1.5 seconds due to its rapid inflation-deflation cycle, which causes negligible interference with the patient’s hemodynamic conditions.

In order to enhance the safety and efficacy of M-PBAV in future cases, phased-array intracardiac echocardiogram (ICE) could play a critical role in monitoring therapeutic effects of balloon inflations or in diagnosing potential complications in their early stages. 

Our cases represent typical clinical pictures of elderly patients with symptomatic AS in a real-world cardiology practice in Japan. Their profiles are noted for advanced age, miscellaneous cardiac or non-cardiac comorbidities, and small body habitus, and thus were potentially difficult candidates for TAVR. 

M-PBAV was effectively utilized as a part of comprehensive management, combined with radical therapies of concomitant cardiac or non-cardiac disease. Concomitant critical CAD is easily treatable by subsequent PCI once a patient’s hemodynamic condition is stabilized by M-PBAV.

Of note, patients had concomitant active neoplastic disease in 12% of cases. Such patients were difficult to treat, because of the inability to pursue either therapy for malignancy or AS, as each was mutually inhibiting. M-PBAV stabilizes a clinical condition, supporting surgical therapy or aggressive chemotherapy as radical therapies for malignancy. 

Due to a significant time lag in introducing TAVR as compared with the European Union nations and the United States, most of our cases were referred to M-PBAV in the period while TAVR was still under clinical trials and had not been practically available in Japan. 

In the TAVR era, M-PBAV is expected to play a unique role based upon its robust therapeutic effect and enhanced safety. Pretreatment with M-PBAV prepares the patient for TAVR or surgical AVR to be performed under the most favorable clinical and hemodynamic conditions. In cases where there is any ambiguity regarding the severity of AS or the need for valve replacement, M-PBAV could be performed as a diagnostic therapy to offset the hemodynamic and clinical impacts of AS, without replacing the valve. 

Finally, M-PBAV could potentially function as the last resort to treat symptomatic patients with critical AS who have no alternative therapeutic options, providing years of sufficient symptomatic relief. Those groups include patients who are treated by chronic hemodialysis due to end-stage renal disease, which has been excluded from the therapeutic indication of TAVR. The utilization of M-PBAV for symptomatic AS in patients under chronic dialysis has been a growing indication to treat complex cases whose therapeutic options tend to be limited due to comorbid conditions. Perhaps the most appealing benefit of M-PBAV is that it provides a durable symptomatic palliation for a few years in nearly one-half of treated cases. The procedure is also repeatable, reproducing a similar degree of symptomatic alleviation in each individual procedure, as needed. 

Conclusion

The integration of an antegrade approach, utilization of Inoue balloon, and multiple dilations with a stepwise increase of the inflation diameter enhance therapeutic efficacy and procedural safety of aortic valvuloplasty to treat non-surgical critical AS patients. It can improve the mobility of a diseased valve and its area of opening in cases with severe calcification. 

M-PBAV has the potential for multiple roles, functioning as a bridge therapy for TAVR, emergent reestablishment of hemodynamic condition in cardiogenic shock due to critical AS, a hemodynamic preparation for non-cardiac surgery, and palliative therapy providing durable symptomatic relief. 

References

1. Isner JM, Samuels DA, Slovenkai GA, et al. Mechanism of aortic balloon valvuloplasty: fracture of valvular calcific deposits. Ann Intern Med. 1988;108:377-380.
2. Kuntz RE, Tosteson AN, Berman AD, et al. Predictors of event-free survival after balloon aortic valvuloplasty. N Engl J Med. 1991;325:17-23.
3. Sakata Y, Syed Z, Salinger M, et al. Percutaneous balloon aortic valvuloplasty: antegrade transseptal vs. conventional retrograde transarterial approach. Catheter Cardiovasc Interv. 2005;64:314-321.
4. Mylonas I, Sakata Y, Salinger M, et al. The use of percutaneous suture-mediated closure for the management of 14 French femoral venous access. J Invasive Cardiol. 2006;18:299-302.
5. Abdou SM, Chen YL, Wu CJ, Lau KW, Hung JS. Concurrent antegrade transseptal Inoue-balloon mitral and aortic valvuloplasty. Catheter Cardiovasc Interv. 2013;82:E712-E717.
6. Witzke C, Don CW, Cubeddu RJ, et al. Impact of rapid ventricular pacing during percutaneous balloon aortic valvuloplasty in patients with critical aortic stenosis: should we be using it? Catheter Cardiovasc Interv. 2011;75:444-452.
7. Feldman T. Transseptal antegrade access for aortic valvuloplasty. Catheter Cardiovasc Interv. 2000;50:492-494.
8. Inoue K, Owaki T, Nakamura T, Kitamura F, Miyamoto N. Clinical application of transvenous mitral commissurotomy by a new balloon catheter. J Thoracic Cardiovasc Surg. 1984;87:394-402.
9. Eisenhauer AC, Hadjipetrou P, Piemonte TC. Balloon aortic valvuloplasty revisited: the role of the Inoue balloon and transseptal antegrade approach. Catheter Cardiovasc Interv. 2000;50:484-491.
10. Aksoy O, Yousefzai R, Singh D, et al. Cardiogenic shock in the setting of severe aortic stenosis: role of intra-aortic balloon pump support. Heart. 2011;97:838-843.

___________________________

From the Department of Cardiology, Ikegami General Hospital, Tokyo, Japan.

Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. The authors report no conflicts of interest regarding the content herein.

Manuscript submitted January 6, 2014, provisional acceptance given March 31, 2014, final version accepted December 4, 2014.

Address for correspondence: Yoshihito Sakata, MD, FACC, FSCAI, Department of Cardiology, Ikegami General Hospital, Ikegami 6-1-19, Ota, Tokyo 146-0082, Japan. Email: sakatachicago@yahoo.co.jp