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Aortic Balloon Valvuloplasty—Review and Case Series
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Original Article
Aortic Balloon Valvuloplasty—Review and Case Series Richard J. Jabbour, BSc, Ron Dick, FRACP and Anthony S. Walton, FRACP ∗ Epworth Hospital, Level 6, 89 Bridge Road, Richmond 3121, Victoria, Australia
Aortic balloon valvuloplasty (BAV) was initially devised in the 1980s as an alternative procedure to the surgical treatment of aortic stenosis, with the theory behind it being both minimally invasive as well as having a lower complication rate [Hara H, et al. Percutaneous balloon aortic valvuloplasty revisited: time for a renaissance? Circulation 2007 March;115(12):e334–8]. In practice however, the procedure was found to have a higher complication rate with only a modest haemodynamic improvement compared to the surgical approach. Most important of all it had an unacceptably high restenosis rate as a substitute for surgery [Otto CM, et al. 3-year outcome after balloon aortic balloon valvuloplasty: insights into prognosis of valvular aortic stenosis. Circulation 1994;89:642–50]. As a result, the procedure has fallen out of favour and has been abandoned at many health care facilities [Hara H, et al. Percutaneous balloon aortic valvuloplasty revisited: time for a renaissance? Circulation 2007 March;115(12):e334–8]. This article will review the management of patients with severe aortic stenosis that are unsuitable to undergo surgery. (Heart, Lung and Circulation 2008;17S:S73–S81) © 2008 Published by Elsevier Inc on behalf of Australasian Society of Cardiac and Thoracic Surgeons and the Cardiac Society of Australia and New Zealand. Keywords. Aortic balloon valvuloplasty; Aortic stenosis; BAV; Calcific
Aortic Stenosis
Natural History
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The natural history of aortic stenosis is one by which there is a long latent period of decades where the stenosis is mild to moderate. During this phase, the left ventricular outflow obstruction caused by the stenotic valve leads to a gradual increase in the left ventricular systolic pressure. This in turn leads to an increase in left ventricular muscle mass and hypertrophy in order to maintain adequate cardiac output. This subsequent increase in muscle mass leads to an ever increasing myocardial oxygen demand, eventually however, a time is reached when myocardial oxygen demand outweighs the supply leading to ischaemia and then left ventricular failure [3] (Fig. 2). The prognosis of aortic stenosis is excellent as long as the patient remains asymptomatic. However, once symptomatic, survival becomes poor unless the outflow obstruction is relieved [3,5]. Retrospective studies have shown that if the patient suffers from symptoms of angina the median survival is 5 years, syncope 3 years, and heart failure 2 years [3,6,7] (Fig. 3). It is difficult to predict the rate of symptomatic progression in patients with aortic stenosis, therefore a careful clinical follow up is mandatory in each patient [1].
he three main types of aortic stenosis are congenital, rheumatic and calcific (previously known as degenerative). Congenital aortic stenosis can be either unicuspid, which is stenotic from birth, or bicuspid, which is usually fibrotic and calcified by mid adulthood. Additionally congenital aortic stenosis may be tricuspid or have a domeshaped diaphragm [3]. In a recent series of 932 patients undergoing aortic valve replacement (AVR) for aortic stenosis, a congenitally malformed valve was present in 54% [4] (Fig. 1a–d). The next type is rheumatic aortic stenosis in which fibrosis and calcification are present, but there is also fusion of the commisures and cusps leading to a central orifice. Rheumatic fever is declining in frequency in developed nations and this is mirrored by a reduction in the incidence of rheumatic aortic stenosis, but by taking developing nations into account it continues to be a major worldwide problem [3]. The most common of the three types and the one most extensively researched is calcified age associated degeneration, in which there is calcium deposition along flexion lines of the aortic cusps and nodule formation, leading to a restriction of leaflet mobility [3].
Pathogenesis of Aortic Stenosis as a Form of Atherosclerosis ∗
Corresponding author. Tel.: +61 39426693; fax: +61 394214258. E-mail address: [email protected] (A.S. Walton).
Aortic stenosis is considered a form of atherosclerosis with the histological examination of the aortic side of early
© 2008 Published by Elsevier Inc on behalf of Australasian Society of Cardiac and Thoracic Surgeons and the Cardiac Society of Australia and New Zealand.
1443-9506/04/$30.00 doi:10.1016/j.hlc.2008.09.009
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Figure 1. Schematic diagrams of the various types of aortic valve stenosis. (A) Normal tri-leaflet aortic valve, (B) congenital aortic stenosis–bicuspid type, (C) rheumatic aortic stenosis–commissural fusion leading to a central orifice, and (D) calcific aortic stenosis with nodule formation.
valve lesions showing subendothelial cellular and extracellular lipid accumulation, similar to the atherosclerotic disease process. This includes inflammatory cells such as macrophages which take up oxidised LDL and transform into foam cells [3,1,8]. In addition myofibroblasts differentiate into valvular myofibroblasts, an osteoblast-like phenotype that is capable of promoting calcium nodule and bone formation similar to vascular calcification [3]. Also T-lymphocytes infiltrate the endothelium and release cytokines such as matrix metalloproteinases and IL-1B that promote cellular proliferation and extra cellular matrix remodelling along with fibroblasts [8]. These processes represent both inflammatory and proliferative changes and lead to progressive calcification along the flexion lines of the cusps and eventually immobilisation of the leaflets [3] (Fig. 4). Due to similarities between the pathogenesis of aortic stenosis and atherosclerosis, researchers hypothesised that cholesterol lowering drugs would alter the progression of aortic stenosis [9]. Indeed retrospective studies initially demonstrated that the addition of statins did in fact appear to alter the natural history of aortic stenosis [9,10]. However disappointing results from the recent Sim-
vastatin Ezetimibe in Aortic Stenosis trial (SEAS trial), a large prospective, double blind, randomised control trial asking this question concluded that both simvastatin and ezetimibe did not alter this rate [11].
Epidemiology of Calcific Aortic Stenosis The incidence of clinically significant calcific aortic stenosis increases with age, with 2.9% of a the population having critical aortic valve stenosis in the 75–86-year-old range and mild calcification occurring in as much as 40% [12]. As more and more people are living into their 80s and 90s, the incidence of aortic stenosis will also increase.
Treatment Options In adults, the only effective treatment for a patient with severe, symptomatic calcific aortic stenosis is surgical AVR [13]. However not all patients are suitable for surgery and as a result a low number of operations are carried out compared to the prevalence [14]. Additionally, some patients decline the procedure either due to them being only mildly symptomatic, or the fact that they do not want an operation [14]. It has been found that the surgical mortality of
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AVR increases dramatically with age. In one study looking into this mortality rate it was found to be as high as 17% for the 30 day mortality rate and 40% by 13 months in patients in their 90s. [15,1] Finding a suitable alternative for the typical elderly patient in their 80s and 90s, with multiple co-morbidities, making them unsuitable for surgery is a common problem. They can be either treated expectantly, with aortic valvuloplasty and potentially with the relatively new procedure of percutaneous valve implantation [14].
History of Valvuloplasty The first adult BAV was performed by Alain Cribier in France in 1985 [16]. During this time BAV was shown to be safe, but provided results in aortic valve area and in aortic valve mean pressure gradient that were lower than provided by surgical AVR. The procedure, which has not changed much in 20 years, has been aided by advances in balloon design, guidewires and newer imaging modalities, such as transoesophageal echocardiography and intracardiac echocardiography [14]. Vascular closure devices such as PROSTAR XLTM(Abbott Corp) (Redwood City, CA, USA) have also reduced vascular complications.
Techniques and Advancements
Figure 2. Simplified schematic diagram of the progression of aortic stenosis. Aortic stenosis leads to a progressive left ventricular outflow obstruction, leading in turn to an increased left ventricular systolic pressure. The increase in systolic pressure leads to a compensated hypertrophy, which due to an increase in left ventricular mass subsequently leads to an ever increasing oxygen demand. Eventually the process becomes decompensated leading to ischaemia and then onto left ventricular failure.
Figure 3. Schematic diagram depicting the natural history of aortic stenosis. There is a long latent period of decades, when the gradual narrowing of the valve and increase in left ventricular systolic pressure leads to a compensated hypertrophy. Once symptomatic survival is extremely poor unless outflow obstruction is relieved (6, Permission to reprint has been granted.).
The two main techniques used for BAV are the retrograde and antegrade approach using the femoral artery and vein accordingly. The retrograde approach is the most common, but vascular complications may arise at the site of entry of the femoral artery by using large calibre sheaths and additionally this method may cause the guidewire to have difficulties in crossing a severely stenotic valve [14] (Fig. 5). The antegrade approach was initially developed to reduce the vascular complications associated with the retrograde approach. This process involves an entry site in the femoral vein, with left atrial access obtained by a transseptal puncture. Once in the left atrium the guidewire then crosses the mitral valve into the left ventricle and around the left ventricular apex through to the aortic valve [17]. The antegrade technique also uses the Inoue balloon, which is typically used for mitral valvuloplasty compared to the standard balloon used in the retrograde approach. This has been shown to improve the post aortic valve area compared with the conventional balloon as well as decreasing inflation and deflation times [18]. This is however more complex and may increase the risk of cardiac damage from the catheters. In the retrograde approach, once a guidewire has been positioned through the stenotic valve, an 18–25 mm balloon is advanced over the wire, across the valve into the correct position and then inflated, often multiple times, with dilute contrast material to complete the process [14] (Fig. 5). An addition to these approaches include a new technique called temporary rapid pacing which arrests mechanical systole to preserve balloon stability across the aortic valve during inflation, increasing the success rate of the procedure by decreasing the chance of balloon migration during inflation [18] (Fig. 6).
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Figure 4. Potential mechanistic pathway of aortic valve disease. T lymphocytes migrate through the endothelium and release cytokines including IL-1B and TGF-1B that promote cell proliferation and extracellular matrix remodelling. In addition fibroblasts differentiate into valvular myofibroblasts which possess characteristics of osteoblasts, facilitating calcium nodule and bone formation. LDL that travels through into the subendothelium is oxidised, and then taken up by macrophages to become foam cells (8, Permission to reprint has been granted.).
Mechanisms The mechanism of valvuloplasty has been studied extensively but no single mechanism of action has been
definitively proven. Amongst the hypotheses the commonest is thought to be the fracture of intraleaflet calcific nodules, increasing the flexibility within the calcified aortic valve thereby improving valve opening [1]. Other mechanisms proposed include annular stretching and the separation of fused leaflets, as well as the scattering of leaflet micro-fractures and cleavage planes along collagenised stroma. Since the full understanding of the mechanism of action is not yet known, new strategies of valvular dilation have been difficult to devise [1].
Valvuloplasty Registries
Figure 5. BAV carried out by the retrograde approach. Once the balloon is correctly positioned across the stenotic valve it is inflated with dilute contrast material. Note the temporary pacing wire in the right ventricle and the pigtail shaping of the left ventricular wire (Courtesy of Sharon Waugh).
The two main landmark registries that were carried out were the National Heart Lung and Blood Institute (NHLBI) and the Mansfield Scientific Aortic Valvuloplasty Registry [19,20]. The NHLBI registry contained 674 patients with severe aortic stenosis and the patients had a mean age of 78 ± 9 [2]. In addition 80% of the patients had been deemed inappropriate for surgery by a cardiothoracic surgeon. The Mansfield Scientific contained 492 patients of mean age 79 ± 8.4 with severe aortic stenosis and that were also of high surgical risk. The acute results of the two studies were similar, with the NHLBI study decreasing the aortic mean pressure gradient from 55 ± 21 mmHg to 29 ± 13 mmHg (p < 0.0001), and the Mansfield Scientific from 60 ± 23 mmHg to 30 ± 13 mmHg (p < 0.05). The increase in aortic valve area was found to be nearly identical from 0.5 ± 2 cm2 to 0.8 ± 0.3 cm2 (p < 0.0001) in the NHLBI compared with 0.5 ± 0.18 cm2 to 0.82 ± 0.30 cm2 (p < 0.05) in the Mansfield [19,20]. Although these haemodynamic results are modest at best compared to surgical
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Figure 6. Rapid ventricular pacing stabilises the balloon when it is inflated. A pacing catheter is placed in the right ventricle. Rapid ventricular pacing is initiated at 180 bpm. This temporarily leads to a drop in systemic pressure. The balloon is inflated only after the pacing rate was reached and the blood pressure dropped, and pacing is also continued until the balloon deflated (Courtesy of Sophia Englezon).
AVR, with 0.8 cm2 still being viewed as severe aortic stenosis [13], it is the symptomatic benefit that is most important and has lead to its uses today. In the NHLBI study at the 30-day follow-up, 75% of the patients had at least one NYHA class improvement, and only approximately 30% of patients that were alive stayed in class III or IV for 1 year [2]. In the Mansfield registry there was a 20% decrease in the incidence of symptoms of heart failure at 1 year [21]. In both the NHLBI and the Mansfield registries acute complications within 24 h of BAV were high, 25% versus 20.5% respectively. The procedural mortality was 3% in the NHLBI versus 5% in the Mansfield registry. The most common complication in NHLBI was blood loss resulting in transfusion in 23% of cases related predominantly to trauma at the vascular entry site. In the Mansfield registry only 11% of patients had documented vascular trauma at the entry site. Other complications mentioned in both registries with a low frequency included stroke, emboli, myocardial infarctions and ventricular perforation leading to tamponade. The 1-year survival rate of successful balloon valvuloplasties was 64% in the Mansfield registry compared to 55% in the NHLBI registry [2,21]. An interesting study of 50 patients carried out by O’Keefe et al in 1987 demonstrated the 1-year survival of patients with severe aortic stenosis was found to be 57% without any intervention, and therefore compared to the results concluded from the Mansfield and NHLBI registries BAV does not appear to alter the natural history of aortic stenosis, although at present there have been no randomised studies comparing BAV to medical treatment [22]. It has been postulated that the most important pre-
dictor of event free survival after BAV was baseline left ventricular function [23]. To date there have been a number of other studies that have shown reduced complication rates and mortality. For example in a study by Eltchaninoff et al., that involved 86 patients over the age of 80 with severe aortic stenosis, the procedural mortality rate was 2.2%, with no vascular complications occurring periprocedurally [24]. The 1-year survival rate was 73% and 78% of the surviving patients showed a long-term clinical improvement. In another recent study by Shareghi et al. [25], 80 patients of a mean age of 81 ± 10 underwent BAV and there were no periprocedural deaths and only 9% of patients had vascular complications. These two recent studies have significantly better outcomes than the original landmark studies and suggest that the newer imaging modalities, and the use of suture mediated devices such as PROSTAR XLTM(Abbott Corp) (Redwood City, CA, USA) are having a positive effect on the outcome of valvuloplasty.
Current Guidelines Current guidelines from the American College of Cardiologists and American Heart Association for BAV include it to be reasonable as a bridge to surgery in haemodynamically unstable adult patients with AS who are at high risk for surgical AVR. It also suggests that BAV might be a reasonable treatment for palliation in adult patients with aortic stenosis in whom surgical AVR cannot be performed because of serious co-morbid conditions [13]. The guidelines however specifically state that BAV is not to be recommended as an alternative to surgical AVR in adult
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Table 1. Aortic Balloon Valvuloplasty Class IIb 1. Aortic balloon valvotomy might be a reasonable as a bridge to surgery in haemodynamically unstable adult patients with AS who are at a high risk for AVR. 2. Aortic balloon valvotomy might be reasonable for palliation in adult patients with AS in whom AVR cannot be performed because of serious co-morbid conditions. Class III Aortic balloon valvotomy is not recommended as an alternative to AVR in adult patients with AS; certain younger adult without valve calcification may be an exception. Adapted from ACC/AHA 2006. Guidelines for patients with Valvular Heart Disease.
patients with aortic stenosis who are suitable for surgery [13] (Table 1). One of the defining problems in why BAV has fallen out of favour is the fact that there is a high restenosis rate, as high as 80% in 1 year [26,27,1]. The ways of overcoming this problem include repeating the BAV, using anti-restenotic therapy or by percutaneous valve implantation. With respect to repeat BAV in aortic stenosis patients across multiple age groups (59–104), Agarwal et al. [28] showed improved 3-year survival rates over a single valvuloplasty without additional complications with most patients having symptomatic relief for a year or more. Symptomatic palliation in this elderly population with multiple co-morbidities is of extreme importance, reducing the need for repeated often lengthy periods of time in hospital for heart failure and as such dramatically increasing the quality of life for those patients [1]. The radiation following percutaneous balloon aortic valvuloplasty to prevent restenosis (RADAR) pilot study demonstrated that external beam radiation following percutaneous BAV significantly reduced restenosis rates. Restenosis in the RADAR pilot study was 21% at 12 months in a population with an average age of 89 ± 4 years, suggesting utility in elderly patients undergoing BAV [1,27]. Finally percutaneous valves are an exciting development in the field of interventional cardiology. There have been several thousand inserted to date worldwide at various centres. The procedure has been shown to be safe, with more studies ongoing, however due to the excellent safety record of surgery it is likely to be limited to high risk elderly groups at the present time, but with more experience and development may have a greater range of uses [29]. Interestingly BAV is used in percutaneous valve implantation to widen the native aortic valve to enable the percutaneous valve to be positioned correctly [30]. Eventually as more percutaneous valve implantations are performed, more cardiologists will be able to carry out BAV and hopefully this will lead to a revival in its use.
Balloon Aortic Valvuloplasties Carried Out at Three Hospitals in Melbourne 2005–2008 Retrospective data was collected from patients who underwent BAV from 2005 to 2008. There were 18
Figure 7. Catheterisation results of BAV. Of the 21 procedures performed there was an average drop in mean aortic pressure gradient from 47 mmHg to 28 mmHg (p < 0.0001).
patients (male = 10, female = 8) in total, and 21 procedures carried out. The mean age was 79 (range 26–94). Indications for the procedure ranged from severe heart failure symptoms, inappropriate age for surgery, cardiac arrest, sepsis, and metastatic melanoma. The retrograde approach was used in all of the procedures. The balloons used ranged from 16 mm to 25 mm. Haemodynamic data was collected both pre- and post-procedure using both echocardiography and cardiac catheterisation. Changes in mean aortic pressure gradient pre- and post-valvuloplasty as determined by echocardiography were from 52 mmHg to 39 mmHg (p = 0.0027), and from 47 mmHg to 28 mmHg (p < 0.0001) during catheterisation (Fig. 7). The peak-to-peak gradient as determined by catheterisation fell from 53 mmHg to 25 mmHg (p < 0.0001). The aortic valve area also increased from 0.5 cm2 to 0.7 cm2 (p = 0.0418). Although there was a modest haemodynamic improvement, the symptomatic benefit was excellent with 100% of surviving patients in NYHA class I or II post-valvuloplasty at the time of discharge. Three repeat procedures were performed on patients due to the return of symptoms, of an average of 6 months after the first valvuloplasty. The results of the repeat valvuloplasty all showed a significant improvement in gradients and an excellent symptomatic benefit. Procedural mortality was found to be 6% (n = 1). Survival to discharge was 83%. One death was attributable to retroperitoneal bleeding and co-morbidities. The remaining causes of death were unrelated to the procedure and included sepsis, renal failure, intractable heart failure and pneumonia. Non-fatal complications (17%) were related to the site of entry of the femoral sheath. Surgery was required in 2 cases (11%), involving closure of the femoral artery in one and correction of an arterio-venous fistula. No strokes were suffered by any of the patients. These results show a
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Figure 8. Aortic and left ventricular traces pre- and post-valvuloplasty. Both the peak-to-peak gradient and mean aortic pressure gradient are reduced significantly from 35 mmHg to 5 mmHg and 24 mmHg to 4 mmHg respectively (Courtesy of Rohan Wilson).
clear haemodynamic improvement in the typical elderly patient with multiple co-morbidities. The more striking benefit is the clear symptomatic benefit and improvement in the quality of life. Our study also showed that if there is restenosis and symptoms return, a repeat valvuloplasty is a viable option to overcome the problem. With careful case selection and improving vascular access techniques BAV can be a useful technique in high risk patients.
Case Presentations from Epworth Hospital Case 1 An 83-year-old GP, with known severe aortic stenosis on maximal medical therapy however was still classified as NYHA class IV heart failure. He underwent an angiogram that showed severe stenosis of the circumflex marginal branch. Prior to planned surgical AVR he developed heart block and cardiogenic shock requiring temporary pacing. Emergency BAV was carried out, which was successful with marked symptomatic improvement and change in mean aortic pressure gradient from
46 mmHg to 22 mmHg. He subsequently had a pacemaker inserted, and 3 months later had an elective AVR and a single bypass graft. 8 months following his surgery he continued to remain very well and his aortic valve mean gradient was only 8 mmHg.
Case 2 A 94-year-old lady, with severe aortic stenosis with known left ventricular heart failure NYHA class IV. The patient lived in a care home and wanted more mobility but did not want to undergo an operation. Her mean pressure gradient was 24 mmHg and aortic valve area 0.5 cm2 . Her left ventricular ejection fraction was 30%. She was offered an elective BAV and she accepted. A retrograde approach with a 20 mm balloon was taken and she had temporary pacing wire at 190 bpm inserted into the right ventricle. Post-valvuloplasty the mean pressure gradient was 4 mmHg and aortic valve area 0.7 cm2 (Fig. 8). She had marked symptomatic improvement and now is NYHA class II. To date, she remains happy with
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her lifestyle and the increase in the activities of daily living.
Conclusion Balloon aortic valvuloplasty may be an old procedure that has fallen out of favour with most health care centres, but it has a role in the elderly patient with multiple comorbidities and a high risk for surgery. The advent of the temporary rapid pacing, and vascular closure devices all reduce complication rates. The restenosis rate is still a problem, but a repeat valvuloplasty is a valid option with low risk. The importance of symptomatic palliation in an elderly patient who is not suitable for surgery must never be forgotten.
References [1] Hara H, Pedersen WR, Ladich E, Mooney M, Virmani R, Nakamura M, Feldman T, Schwartz RS. Percutaneous balloon aortic valvuloplasty revisited: time for a renaissance? Circulation 2007 March;115(12):e334–8. [2] Otto CM, Mickel MC, Kennedy JW, Alderman EL, Bashore TM, Block PC, Brinker JA, Diver D, Ferguson J, Homes Jr DR. Three year outcome after balloon aortic balloon valvuloplasty: insights into prognosis of valvular aortic stenosis. Circulation 1994;89:642–50. [3] Otto CM, Bonow RO. Valvular heart disease. In: Zipes DP, Libby P, Bonow RO, Braunwald E, editors. Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine. 8th ed. St. Louis, Mo: WB Saunders; 2007, chap. 62, pp. 1625–34. [4] Roberts WC, Ko JM. Frequency by decades of unicuspid, bicuspid and tricuspid aortic valves in adults having isolated aortic valve replacement for aortic stenosis, with or without associated aortic regurgitation. Circulation 2005;111: 920. [5] Varadarajan P, Kapoor N, Bansal RC, Pair RG. Clinical profile and natural history of 453 nonsurgically managed patients with severe aortic stenosis. Ann Thoracic Surg 2006;82: 2111–5. [6] Ross Jr J, Braunwald E. Aortic stenosis. Circulation 1968;38(Suppl. 5):V-61. [7] Rosenhek R, Binder T, Porenta G, Lang I, Christ G, Schemper M, Maurer G, Baumgartner H. Predictors of outcome in severe, asymptomatic aortic stenosis. N Engl J Med 2000;343:611–7. [8] Freeman RV, Otto CM. Spectrum of calcific aortic valve disease: pathogenesis, disease progression and treatment strategies. Circulation 2005;111:3316–26. [9] Rosenhek R. Statins for aortic stenosis. N Eng J Med 2005 June;352(23):2441–3. [10] Rosenhek R, Rader F, Loho N, Gabirel H, Heger M, Klaar U, Schemper M, Binder T, Maurer G, Baumgartner H. Statins but not angiotensin converting enzyme inhibitors delay progression of aortic stenosis. Circulation 2004;110:1291–5. [11] Rossebo AB, Pedersen TR, Boman K, Brudi P, Chambers JB, Egstrup K, Gerdts E, Gohlke-Barwolf C, Holme I, Kesaniemi YA, Malbecq W, Nienaber CA, Ray S, Skjaerpe T, Wachtell K, Willenheimer R. Intensive lipid lowering with Simvastatin and Ezetimibe in Aortic Stenosis. N Engl J Med; 2008 September [Epub ahead of print]. [12] Lindroos M, Kupari M, Heikkala J, Tilvis R. Prevalence of aortic valve abnormalities in the elderly: an echocardiographic study of a random population sample. J Am Coll Cardiol 1993;21:1220–5.
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[13] Bonow RO, Carabello BA, Chatterjee K, Bonow RO, Carabello BA, Chatterjee K, de Leon AC Jr, Faxon DP, Freed MD, Gaasch WH, Lytle BW, Nishimura RA, O’Gara PT, O’Rourke RA, Otto CM, Shah PM, Shanewise JS, Smith SC Jr, Jacobs AK, Adams CD, Anderson JL, Antman EM, Fuster V, Halperin JL, Hiratzka LF, Hunt SA, Lytle BW, Nishimura R, Page RL, Riegel B. ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (writing committee to revise the 1998 guidelines for the Management of Patients with Valvular Heart Disease): Developed in collaboration with the Society of Cardiovascular Anesthesiologists: endorsed by the Society for CardiovascularAngiography and Interventions and the Society of Thoracic Surgeons/Circ 114:e84, 2006. [14] Ji DM, Si BD. Percutaneous aortic valve interventions. In: Cohn Lh, editor. Cardiac surgery in the adult. New York: McGraw-Hill; 2008. pp. 963–71. [15] Edwards MB, Taylor KM. Outcomes in nonagenerians after heart valve replacement operation. Ann Thorac Surg 2003;75:830–4. [16] Cribier A, Savin T, Saoudi N, Rocha P, Berland J, Letac B. Percutaneous transluminal valvuloplasty of acquired aortic stenosis in elderly patients: an alternative to valve replacement? Lancet 1986;1:63–7. [17] Feldman T. Transseptal antegrade access for aortic valvuloplasty. Catheter Cardiovasc Inter 2000;50:492–4. [18] Eisenhauer AC, Hadjipetrou P, Piemonte TC. Balloon aortic valvuloplasty revisted: the role of the Inoue balloon and transseptal antegradeapproach. Catheter Cardiovasc Inter 2000;50:492–4. [19] McKay RG. The Mansfield Scientific Aortic Valvuloplasty Registry: overview of acute haemodynamic results and procedural complications. J Am Coll Cardiol 1991 February;17(2): 485–91. [20] Registry NHLBI. Percutaneous balloon aortic valvuloplasty. Acute and 30-day follow up results in 674 patients from the NHLBI Balloon Valvuloplasty Registry. Circulation 1991;84:2383–97. [21] O’Neill WW. Predictors of long-term survival after percutaneous aortic valvuloplasty: report of the Mansfield Scientific Balloon Aortic Valvuloplasty Registry. J Am Coll Cardiol 1991;17:193–8. [22] O’Keefe Jr JH, Vlietstra RE, Bailey KR, Holmes Jr DR. Natural history of candidates for balloon aortic valvuloplasty. Mayo Clin Proc 1987 November;62(11):986–91. [23] Kuntz RE, Tosteson AN, Berman AD, Goldman L, Gordon PC, Leonard BM, McKay RG, Diver DJ, Safian RD. Predictors of event free survival after balloon aortic valvuloplasty. N Engl J Med 1991;325:17–23. [24] Eltchaninoff H, Cribier A, Tron C, Anselme F, Koning R, Soyer R, Letac B. Balloon aortic valvuloplasty in elderly patients at high risk of surgery, or inoperable: immediate and mid-term results. Eur Heart J 1995;16(8):1079–84. [25] Shareghi S, Rasouli L, Shavelle D, Burstein S, Matthews R. Current results of balloon aortic valvuloplasty in high risk patients. J Invasive Cardiol 2007;19(1):1–5. [26] Feldman T, Glagov S, Carroll JD. Restenosis following successful balloon valvuloplasty: bone formation in aortic valve leaflets. Cathet Cardiovasc Diag 1993;29:1–7. [27] Pedersen WR, Van Tassel RA, Pierce TA, Pence DM, Monyak DJ, Kim TH, Harris KM, Knicklelbine T, Lesser JR, Madison JD, Mooney MR, Goldenberg IF, Longe TF, Poulose AK, Graham KJ, Nelson RR, Pritzker MR, Pagan-Carlo LA, Boisjolie CR, Zenovich AG, Schwartz RS. Radiation following percu-
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Original Article
Aortic Balloon Valvuloplasty—Review and Case Series Richard J. Jabbour, BSc, Ron Dick, FRACP and Anthony S. Walton, FRACP ∗ Epworth Hospital, Level 6, 89 Bridge Road, Richmond 3121, Victoria, Australia
Aortic balloon valvuloplasty (BAV) was initially devised in the 1980s as an alternative procedure to the surgical treatment of aortic stenosis, with the theory behind it being both minimally invasive as well as having a lower complication rate [Hara H, et al. Percutaneous balloon aortic valvuloplasty revisited: time for a renaissance? Circulation 2007 March;115(12):e334–8]. In practice however, the procedure was found to have a higher complication rate with only a modest haemodynamic improvement compared to the surgical approach. Most important of all it had an unacceptably high restenosis rate as a substitute for surgery [Otto CM, et al. 3-year outcome after balloon aortic balloon valvuloplasty: insights into prognosis of valvular aortic stenosis. Circulation 1994;89:642–50]. As a result, the procedure has fallen out of favour and has been abandoned at many health care facilities [Hara H, et al. Percutaneous balloon aortic valvuloplasty revisited: time for a renaissance? Circulation 2007 March;115(12):e334–8]. This article will review the management of patients with severe aortic stenosis that are unsuitable to undergo surgery. (Heart, Lung and Circulation 2008;17S:S73–S81) © 2008 Published by Elsevier Inc on behalf of Australasian Society of Cardiac and Thoracic Surgeons and the Cardiac Society of Australia and New Zealand. Keywords. Aortic balloon valvuloplasty; Aortic stenosis; BAV; Calcific
Aortic Stenosis
Natural History
T
The natural history of aortic stenosis is one by which there is a long latent period of decades where the stenosis is mild to moderate. During this phase, the left ventricular outflow obstruction caused by the stenotic valve leads to a gradual increase in the left ventricular systolic pressure. This in turn leads to an increase in left ventricular muscle mass and hypertrophy in order to maintain adequate cardiac output. This subsequent increase in muscle mass leads to an ever increasing myocardial oxygen demand, eventually however, a time is reached when myocardial oxygen demand outweighs the supply leading to ischaemia and then left ventricular failure [3] (Fig. 2). The prognosis of aortic stenosis is excellent as long as the patient remains asymptomatic. However, once symptomatic, survival becomes poor unless the outflow obstruction is relieved [3,5]. Retrospective studies have shown that if the patient suffers from symptoms of angina the median survival is 5 years, syncope 3 years, and heart failure 2 years [3,6,7] (Fig. 3). It is difficult to predict the rate of symptomatic progression in patients with aortic stenosis, therefore a careful clinical follow up is mandatory in each patient [1].
he three main types of aortic stenosis are congenital, rheumatic and calcific (previously known as degenerative). Congenital aortic stenosis can be either unicuspid, which is stenotic from birth, or bicuspid, which is usually fibrotic and calcified by mid adulthood. Additionally congenital aortic stenosis may be tricuspid or have a domeshaped diaphragm [3]. In a recent series of 932 patients undergoing aortic valve replacement (AVR) for aortic stenosis, a congenitally malformed valve was present in 54% [4] (Fig. 1a–d). The next type is rheumatic aortic stenosis in which fibrosis and calcification are present, but there is also fusion of the commisures and cusps leading to a central orifice. Rheumatic fever is declining in frequency in developed nations and this is mirrored by a reduction in the incidence of rheumatic aortic stenosis, but by taking developing nations into account it continues to be a major worldwide problem [3]. The most common of the three types and the one most extensively researched is calcified age associated degeneration, in which there is calcium deposition along flexion lines of the aortic cusps and nodule formation, leading to a restriction of leaflet mobility [3].
Pathogenesis of Aortic Stenosis as a Form of Atherosclerosis ∗
Corresponding author. Tel.: +61 39426693; fax: +61 394214258. E-mail address: [email protected] (A.S. Walton).
Aortic stenosis is considered a form of atherosclerosis with the histological examination of the aortic side of early
© 2008 Published by Elsevier Inc on behalf of Australasian Society of Cardiac and Thoracic Surgeons and the Cardiac Society of Australia and New Zealand.
1443-9506/04/$30.00 doi:10.1016/j.hlc.2008.09.009
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Figure 1. Schematic diagrams of the various types of aortic valve stenosis. (A) Normal tri-leaflet aortic valve, (B) congenital aortic stenosis–bicuspid type, (C) rheumatic aortic stenosis–commissural fusion leading to a central orifice, and (D) calcific aortic stenosis with nodule formation.
valve lesions showing subendothelial cellular and extracellular lipid accumulation, similar to the atherosclerotic disease process. This includes inflammatory cells such as macrophages which take up oxidised LDL and transform into foam cells [3,1,8]. In addition myofibroblasts differentiate into valvular myofibroblasts, an osteoblast-like phenotype that is capable of promoting calcium nodule and bone formation similar to vascular calcification [3]. Also T-lymphocytes infiltrate the endothelium and release cytokines such as matrix metalloproteinases and IL-1B that promote cellular proliferation and extra cellular matrix remodelling along with fibroblasts [8]. These processes represent both inflammatory and proliferative changes and lead to progressive calcification along the flexion lines of the cusps and eventually immobilisation of the leaflets [3] (Fig. 4). Due to similarities between the pathogenesis of aortic stenosis and atherosclerosis, researchers hypothesised that cholesterol lowering drugs would alter the progression of aortic stenosis [9]. Indeed retrospective studies initially demonstrated that the addition of statins did in fact appear to alter the natural history of aortic stenosis [9,10]. However disappointing results from the recent Sim-
vastatin Ezetimibe in Aortic Stenosis trial (SEAS trial), a large prospective, double blind, randomised control trial asking this question concluded that both simvastatin and ezetimibe did not alter this rate [11].
Epidemiology of Calcific Aortic Stenosis The incidence of clinically significant calcific aortic stenosis increases with age, with 2.9% of a the population having critical aortic valve stenosis in the 75–86-year-old range and mild calcification occurring in as much as 40% [12]. As more and more people are living into their 80s and 90s, the incidence of aortic stenosis will also increase.
Treatment Options In adults, the only effective treatment for a patient with severe, symptomatic calcific aortic stenosis is surgical AVR [13]. However not all patients are suitable for surgery and as a result a low number of operations are carried out compared to the prevalence [14]. Additionally, some patients decline the procedure either due to them being only mildly symptomatic, or the fact that they do not want an operation [14]. It has been found that the surgical mortality of
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AVR increases dramatically with age. In one study looking into this mortality rate it was found to be as high as 17% for the 30 day mortality rate and 40% by 13 months in patients in their 90s. [15,1] Finding a suitable alternative for the typical elderly patient in their 80s and 90s, with multiple co-morbidities, making them unsuitable for surgery is a common problem. They can be either treated expectantly, with aortic valvuloplasty and potentially with the relatively new procedure of percutaneous valve implantation [14].
History of Valvuloplasty The first adult BAV was performed by Alain Cribier in France in 1985 [16]. During this time BAV was shown to be safe, but provided results in aortic valve area and in aortic valve mean pressure gradient that were lower than provided by surgical AVR. The procedure, which has not changed much in 20 years, has been aided by advances in balloon design, guidewires and newer imaging modalities, such as transoesophageal echocardiography and intracardiac echocardiography [14]. Vascular closure devices such as PROSTAR XLTM(Abbott Corp) (Redwood City, CA, USA) have also reduced vascular complications.
Techniques and Advancements
Figure 2. Simplified schematic diagram of the progression of aortic stenosis. Aortic stenosis leads to a progressive left ventricular outflow obstruction, leading in turn to an increased left ventricular systolic pressure. The increase in systolic pressure leads to a compensated hypertrophy, which due to an increase in left ventricular mass subsequently leads to an ever increasing oxygen demand. Eventually the process becomes decompensated leading to ischaemia and then onto left ventricular failure.
Figure 3. Schematic diagram depicting the natural history of aortic stenosis. There is a long latent period of decades, when the gradual narrowing of the valve and increase in left ventricular systolic pressure leads to a compensated hypertrophy. Once symptomatic survival is extremely poor unless outflow obstruction is relieved (6, Permission to reprint has been granted.).
The two main techniques used for BAV are the retrograde and antegrade approach using the femoral artery and vein accordingly. The retrograde approach is the most common, but vascular complications may arise at the site of entry of the femoral artery by using large calibre sheaths and additionally this method may cause the guidewire to have difficulties in crossing a severely stenotic valve [14] (Fig. 5). The antegrade approach was initially developed to reduce the vascular complications associated with the retrograde approach. This process involves an entry site in the femoral vein, with left atrial access obtained by a transseptal puncture. Once in the left atrium the guidewire then crosses the mitral valve into the left ventricle and around the left ventricular apex through to the aortic valve [17]. The antegrade technique also uses the Inoue balloon, which is typically used for mitral valvuloplasty compared to the standard balloon used in the retrograde approach. This has been shown to improve the post aortic valve area compared with the conventional balloon as well as decreasing inflation and deflation times [18]. This is however more complex and may increase the risk of cardiac damage from the catheters. In the retrograde approach, once a guidewire has been positioned through the stenotic valve, an 18–25 mm balloon is advanced over the wire, across the valve into the correct position and then inflated, often multiple times, with dilute contrast material to complete the process [14] (Fig. 5). An addition to these approaches include a new technique called temporary rapid pacing which arrests mechanical systole to preserve balloon stability across the aortic valve during inflation, increasing the success rate of the procedure by decreasing the chance of balloon migration during inflation [18] (Fig. 6).
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Figure 4. Potential mechanistic pathway of aortic valve disease. T lymphocytes migrate through the endothelium and release cytokines including IL-1B and TGF-1B that promote cell proliferation and extracellular matrix remodelling. In addition fibroblasts differentiate into valvular myofibroblasts which possess characteristics of osteoblasts, facilitating calcium nodule and bone formation. LDL that travels through into the subendothelium is oxidised, and then taken up by macrophages to become foam cells (8, Permission to reprint has been granted.).
Mechanisms The mechanism of valvuloplasty has been studied extensively but no single mechanism of action has been
definitively proven. Amongst the hypotheses the commonest is thought to be the fracture of intraleaflet calcific nodules, increasing the flexibility within the calcified aortic valve thereby improving valve opening [1]. Other mechanisms proposed include annular stretching and the separation of fused leaflets, as well as the scattering of leaflet micro-fractures and cleavage planes along collagenised stroma. Since the full understanding of the mechanism of action is not yet known, new strategies of valvular dilation have been difficult to devise [1].
Valvuloplasty Registries
Figure 5. BAV carried out by the retrograde approach. Once the balloon is correctly positioned across the stenotic valve it is inflated with dilute contrast material. Note the temporary pacing wire in the right ventricle and the pigtail shaping of the left ventricular wire (Courtesy of Sharon Waugh).
The two main landmark registries that were carried out were the National Heart Lung and Blood Institute (NHLBI) and the Mansfield Scientific Aortic Valvuloplasty Registry [19,20]. The NHLBI registry contained 674 patients with severe aortic stenosis and the patients had a mean age of 78 ± 9 [2]. In addition 80% of the patients had been deemed inappropriate for surgery by a cardiothoracic surgeon. The Mansfield Scientific contained 492 patients of mean age 79 ± 8.4 with severe aortic stenosis and that were also of high surgical risk. The acute results of the two studies were similar, with the NHLBI study decreasing the aortic mean pressure gradient from 55 ± 21 mmHg to 29 ± 13 mmHg (p < 0.0001), and the Mansfield Scientific from 60 ± 23 mmHg to 30 ± 13 mmHg (p < 0.05). The increase in aortic valve area was found to be nearly identical from 0.5 ± 2 cm2 to 0.8 ± 0.3 cm2 (p < 0.0001) in the NHLBI compared with 0.5 ± 0.18 cm2 to 0.82 ± 0.30 cm2 (p < 0.05) in the Mansfield [19,20]. Although these haemodynamic results are modest at best compared to surgical
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Figure 6. Rapid ventricular pacing stabilises the balloon when it is inflated. A pacing catheter is placed in the right ventricle. Rapid ventricular pacing is initiated at 180 bpm. This temporarily leads to a drop in systemic pressure. The balloon is inflated only after the pacing rate was reached and the blood pressure dropped, and pacing is also continued until the balloon deflated (Courtesy of Sophia Englezon).
AVR, with 0.8 cm2 still being viewed as severe aortic stenosis [13], it is the symptomatic benefit that is most important and has lead to its uses today. In the NHLBI study at the 30-day follow-up, 75% of the patients had at least one NYHA class improvement, and only approximately 30% of patients that were alive stayed in class III or IV for 1 year [2]. In the Mansfield registry there was a 20% decrease in the incidence of symptoms of heart failure at 1 year [21]. In both the NHLBI and the Mansfield registries acute complications within 24 h of BAV were high, 25% versus 20.5% respectively. The procedural mortality was 3% in the NHLBI versus 5% in the Mansfield registry. The most common complication in NHLBI was blood loss resulting in transfusion in 23% of cases related predominantly to trauma at the vascular entry site. In the Mansfield registry only 11% of patients had documented vascular trauma at the entry site. Other complications mentioned in both registries with a low frequency included stroke, emboli, myocardial infarctions and ventricular perforation leading to tamponade. The 1-year survival rate of successful balloon valvuloplasties was 64% in the Mansfield registry compared to 55% in the NHLBI registry [2,21]. An interesting study of 50 patients carried out by O’Keefe et al in 1987 demonstrated the 1-year survival of patients with severe aortic stenosis was found to be 57% without any intervention, and therefore compared to the results concluded from the Mansfield and NHLBI registries BAV does not appear to alter the natural history of aortic stenosis, although at present there have been no randomised studies comparing BAV to medical treatment [22]. It has been postulated that the most important pre-
dictor of event free survival after BAV was baseline left ventricular function [23]. To date there have been a number of other studies that have shown reduced complication rates and mortality. For example in a study by Eltchaninoff et al., that involved 86 patients over the age of 80 with severe aortic stenosis, the procedural mortality rate was 2.2%, with no vascular complications occurring periprocedurally [24]. The 1-year survival rate was 73% and 78% of the surviving patients showed a long-term clinical improvement. In another recent study by Shareghi et al. [25], 80 patients of a mean age of 81 ± 10 underwent BAV and there were no periprocedural deaths and only 9% of patients had vascular complications. These two recent studies have significantly better outcomes than the original landmark studies and suggest that the newer imaging modalities, and the use of suture mediated devices such as PROSTAR XLTM(Abbott Corp) (Redwood City, CA, USA) are having a positive effect on the outcome of valvuloplasty.
Current Guidelines Current guidelines from the American College of Cardiologists and American Heart Association for BAV include it to be reasonable as a bridge to surgery in haemodynamically unstable adult patients with AS who are at high risk for surgical AVR. It also suggests that BAV might be a reasonable treatment for palliation in adult patients with aortic stenosis in whom surgical AVR cannot be performed because of serious co-morbid conditions [13]. The guidelines however specifically state that BAV is not to be recommended as an alternative to surgical AVR in adult
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Table 1. Aortic Balloon Valvuloplasty Class IIb 1. Aortic balloon valvotomy might be a reasonable as a bridge to surgery in haemodynamically unstable adult patients with AS who are at a high risk for AVR. 2. Aortic balloon valvotomy might be reasonable for palliation in adult patients with AS in whom AVR cannot be performed because of serious co-morbid conditions. Class III Aortic balloon valvotomy is not recommended as an alternative to AVR in adult patients with AS; certain younger adult without valve calcification may be an exception. Adapted from ACC/AHA 2006. Guidelines for patients with Valvular Heart Disease.
patients with aortic stenosis who are suitable for surgery [13] (Table 1). One of the defining problems in why BAV has fallen out of favour is the fact that there is a high restenosis rate, as high as 80% in 1 year [26,27,1]. The ways of overcoming this problem include repeating the BAV, using anti-restenotic therapy or by percutaneous valve implantation. With respect to repeat BAV in aortic stenosis patients across multiple age groups (59–104), Agarwal et al. [28] showed improved 3-year survival rates over a single valvuloplasty without additional complications with most patients having symptomatic relief for a year or more. Symptomatic palliation in this elderly population with multiple co-morbidities is of extreme importance, reducing the need for repeated often lengthy periods of time in hospital for heart failure and as such dramatically increasing the quality of life for those patients [1]. The radiation following percutaneous balloon aortic valvuloplasty to prevent restenosis (RADAR) pilot study demonstrated that external beam radiation following percutaneous BAV significantly reduced restenosis rates. Restenosis in the RADAR pilot study was 21% at 12 months in a population with an average age of 89 ± 4 years, suggesting utility in elderly patients undergoing BAV [1,27]. Finally percutaneous valves are an exciting development in the field of interventional cardiology. There have been several thousand inserted to date worldwide at various centres. The procedure has been shown to be safe, with more studies ongoing, however due to the excellent safety record of surgery it is likely to be limited to high risk elderly groups at the present time, but with more experience and development may have a greater range of uses [29]. Interestingly BAV is used in percutaneous valve implantation to widen the native aortic valve to enable the percutaneous valve to be positioned correctly [30]. Eventually as more percutaneous valve implantations are performed, more cardiologists will be able to carry out BAV and hopefully this will lead to a revival in its use.
Balloon Aortic Valvuloplasties Carried Out at Three Hospitals in Melbourne 2005–2008 Retrospective data was collected from patients who underwent BAV from 2005 to 2008. There were 18
Figure 7. Catheterisation results of BAV. Of the 21 procedures performed there was an average drop in mean aortic pressure gradient from 47 mmHg to 28 mmHg (p < 0.0001).
patients (male = 10, female = 8) in total, and 21 procedures carried out. The mean age was 79 (range 26–94). Indications for the procedure ranged from severe heart failure symptoms, inappropriate age for surgery, cardiac arrest, sepsis, and metastatic melanoma. The retrograde approach was used in all of the procedures. The balloons used ranged from 16 mm to 25 mm. Haemodynamic data was collected both pre- and post-procedure using both echocardiography and cardiac catheterisation. Changes in mean aortic pressure gradient pre- and post-valvuloplasty as determined by echocardiography were from 52 mmHg to 39 mmHg (p = 0.0027), and from 47 mmHg to 28 mmHg (p < 0.0001) during catheterisation (Fig. 7). The peak-to-peak gradient as determined by catheterisation fell from 53 mmHg to 25 mmHg (p < 0.0001). The aortic valve area also increased from 0.5 cm2 to 0.7 cm2 (p = 0.0418). Although there was a modest haemodynamic improvement, the symptomatic benefit was excellent with 100% of surviving patients in NYHA class I or II post-valvuloplasty at the time of discharge. Three repeat procedures were performed on patients due to the return of symptoms, of an average of 6 months after the first valvuloplasty. The results of the repeat valvuloplasty all showed a significant improvement in gradients and an excellent symptomatic benefit. Procedural mortality was found to be 6% (n = 1). Survival to discharge was 83%. One death was attributable to retroperitoneal bleeding and co-morbidities. The remaining causes of death were unrelated to the procedure and included sepsis, renal failure, intractable heart failure and pneumonia. Non-fatal complications (17%) were related to the site of entry of the femoral sheath. Surgery was required in 2 cases (11%), involving closure of the femoral artery in one and correction of an arterio-venous fistula. No strokes were suffered by any of the patients. These results show a
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Figure 8. Aortic and left ventricular traces pre- and post-valvuloplasty. Both the peak-to-peak gradient and mean aortic pressure gradient are reduced significantly from 35 mmHg to 5 mmHg and 24 mmHg to 4 mmHg respectively (Courtesy of Rohan Wilson).
clear haemodynamic improvement in the typical elderly patient with multiple co-morbidities. The more striking benefit is the clear symptomatic benefit and improvement in the quality of life. Our study also showed that if there is restenosis and symptoms return, a repeat valvuloplasty is a viable option to overcome the problem. With careful case selection and improving vascular access techniques BAV can be a useful technique in high risk patients.
Case Presentations from Epworth Hospital Case 1 An 83-year-old GP, with known severe aortic stenosis on maximal medical therapy however was still classified as NYHA class IV heart failure. He underwent an angiogram that showed severe stenosis of the circumflex marginal branch. Prior to planned surgical AVR he developed heart block and cardiogenic shock requiring temporary pacing. Emergency BAV was carried out, which was successful with marked symptomatic improvement and change in mean aortic pressure gradient from
46 mmHg to 22 mmHg. He subsequently had a pacemaker inserted, and 3 months later had an elective AVR and a single bypass graft. 8 months following his surgery he continued to remain very well and his aortic valve mean gradient was only 8 mmHg.
Case 2 A 94-year-old lady, with severe aortic stenosis with known left ventricular heart failure NYHA class IV. The patient lived in a care home and wanted more mobility but did not want to undergo an operation. Her mean pressure gradient was 24 mmHg and aortic valve area 0.5 cm2 . Her left ventricular ejection fraction was 30%. She was offered an elective BAV and she accepted. A retrograde approach with a 20 mm balloon was taken and she had temporary pacing wire at 190 bpm inserted into the right ventricle. Post-valvuloplasty the mean pressure gradient was 4 mmHg and aortic valve area 0.7 cm2 (Fig. 8). She had marked symptomatic improvement and now is NYHA class II. To date, she remains happy with
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her lifestyle and the increase in the activities of daily living.
Conclusion Balloon aortic valvuloplasty may be an old procedure that has fallen out of favour with most health care centres, but it has a role in the elderly patient with multiple comorbidities and a high risk for surgery. The advent of the temporary rapid pacing, and vascular closure devices all reduce complication rates. The restenosis rate is still a problem, but a repeat valvuloplasty is a valid option with low risk. The importance of symptomatic palliation in an elderly patient who is not suitable for surgery must never be forgotten.
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