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Pharmacological Treatment of Aortic Valve Disease
247
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modulation by atorvastatin (20 mg), Am. J. Cardiol. 102 (6) (2008) 743–748 Epub 2008/09/09.
[44] Rossebo, A. B., T. R. Pedersen, K. Boman, P. Brudi, J. B. Chambers, K. Egstrup, et
al., Intensive lipid lowering with simvastatin and ezetimibe in aortic stenosis, N. Engl. J. Med. 359 (13) (2008) 1343–1356 Epub 2008/09/04.
[45] Cowell, S. J., D. E. Newby, R. J. Prescott, P. Bloomfield, J. Reid, D. B. Northridge, et
al., A randomized trial of intensive lipid-lowering therapy in calcific aortic stenosis, N. Engl. J. Med. 352 (23) (2005) 2389–2397 Epub 2005/06/10.
[46] Chan, K. L., K. Teo, J. G. Dumesnil, A. Ni, J. Tam, Effect of Lipid lowering with
rosuvastatin on progression of aortic stenosis: results of the aortic stenosis pro­gression observation: measuring effects of rosuvastatin (ASTRONOMER) trial, Circulation 121 (2) (2010) 306–314 Epub 2010/01/06.
[47] Gerdts, E., A. B. Rossebo, T. R. Pedersen, K. Boman, P. Brudi, J. B. Chambers, et al.,
Impact of baseline severity of aortic valve stenosis on effect of intensive lipid lowering therapy (from the SEAS study), Am. J. Cardiol. 106 (11) (2010) 1634–1639 Epub 2010/11/26.
[48] Ardehali, R., N. J. Leeper, A. M. Wilson, P. A. Heidenreich, The effect of angiotensin-
converting enzyme inhibitors and statins on the progression of aortic sclerosis and mortality, J. Heart Valve Dis. 21 (3) (2012) 337–343 Epub 2012/07/20.
[49] Otto, C. M., J. Kuusisto, D. D. Reichenbach, A. M. Gown, K. D. O’Brien,
Characterization of the early lesion of’ degenerative’ valvular aortic stenosis. Histological and immunohistochemical studies, Circulation 90 (2) (1994) 844–853 Epub 1994/08/01.
[50] Stewart, B. F., D. Siscovick, B. K. Lind, J. M. Gardin, J. S. Gottdiener, V. E. Smith, et
al., Clinical factors associated with calcific aortic valve disease. Cardiovascular Health Study, J. Am. Coll. Cardiol. 29 (3) (1997) 630–634 Epub 1997/03/01.
[51] Parolari, A., C. Loardi, L. Mussoni, L. Cavallotti, M. Camera, P. Biglioli, et al.,
Nonrheumatic calcific aortic stenosis: an overview from basic science to phar­macological prevention, Eur. J. Cardiothorac. Surg. 35 (3) (2009) 493–504 Epub 2009/01/24.
[52] Novaro, G. M., B. P. Griffin, Calcific aortic stenosis: another face of atherosclerosis?
Cleve. Clin. J. Med. 70 (5) (2003) 471–477 Epub 2003/06/05.
[53] Otto, C. M., K. D. O’Brien, Why is there discordance between calcific aortic stenosis
and coronary artery disease? Heart 85 (6) (2001) 601–602 Epub 2001/05/23.
[54] Nsaibia, M. J., M. C. Boulanger, R. Bouchareb, G. Mkannez, K. Le Quang, F. Hadji, et
al., OxLDL-derived lysophosphatidic acid promotes the progression of aortic valve stenosis through a LPAR1-RhoA-NF-kappaB pathway, Cardiovasc. Res. 113 (11) (2017) 1351–1363 Epub 2017/05/05.
[55] Leopold, J. A., Cellular mechanisms of aortic valve calcification, Circ. Cardiovasc.
Interv. 5 (4) (2012) 605–614 Epub 2012/08/17.
[56] Abdelbaky, A., E. Corsini, A. L. Figueroa, S. Subramanian, S. Fontanez, H. Emami, et
al., Early aortic valve inflammation precedes calcification: a longitudinal FDG­PET/CT study, Atherosclerosis 238 (2) (2015) 165–172 Epub 2014/12/20.
[57] Mathieu, P., Y. Bosse, G. S. Huggins, A. Della Corte, P. Pibarot, H. I. Michelena, et
al., The pathology and pathobiology of bicuspid aortic valve: state of the art and novel research perspectives, J. Pathol. Clin. Res. 1 (4) (2015) 195–206 Epub 2016/ 08/09.
Giovanni Concistrè
248
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https://t.me/med1917
[58] Otto, C. M., I. G. Burwash, M. E. Legget, B. I. Munt, M. Fujioka, N. L. Healy, et al.,
Prospective study of asymptomatic valvular aortic stenosis. Clinical, echocardio­graphic, and exercise predictors of outcome, Circulation 95 (9) (1997) 2262–2270 Epub 1997/05/06.
[59] Freeman, R. V., C. M. Otto, Spectrum of calcific aortic valve disease: pathogenesis,
disease progression, and treatment strategies, Circulation 111 (24) (2005) 3316–3326 Epub 2005/06/22.
[60] Nkomo, V. T., J. M. Gardin, T.N. Skelton, J. S. Gottdiener, C. G. Scott, M. Enriquez-
Sarano, Burden of valvular heart diseases: a population-based study, Lancet 368 (9540) (2006) 1005–1011 Epub 2006/09/19.
[61] Eveborn, G. W., H. Schirmer, G. Heggelund, P. Lunde, K. Rasmussen, The evolving
epidemiology of valvular aortic stenosis. The Tromso Study, Heart 99 (6) (2013) 396– 400 Epub 2012/09/04.
[62] Hadar, H., D. Meiraz, Thickened renal fascia–asignofretroperitonealpathology, J.
Comput. Tomogr. 5 (2) (1981) 193–198 Epub 1981/06/01.
[63] Lindman, B. R., M. A. Clavel, P. Mathieu, B. Iung, P. Lancellotti, C. M. Otto, et al.,
Calcific aortic stenosis, Nat. Rev. Dis. Primers 2 (2016) 16006 Epub 2016/05/18.
[64] Tsimikas, S., Lipoprotein(a): novel target and emergence of novel therapies to lower
cardiovascular disease risk, Curr. Opin. Endocrinol. Diabetes Obes. 23 (2) (2016) 157–164 Epub 2016/01/31.
[65] Hutcheson, J. D., E. Aikawa, W. D. Merryman, Potential drug targets for calcific aortic
valve disease, Nat. Rev. Cardiol. 11 (4) (2014) 218–231 Epub 2014/01/22.
[66] Smith, J. G., K. Luk, C. A. Schulz, J. C. Engert, R. Do, G. Hindy, et al., Association of
low-density lipoprotein cholesterol-related genetic variants with aortic valve cal- cium and incident aortic stenosis, Jama 312 (17) (2014) 1764–1771 Epub 2014/10/27.
[67] Parolari, A., E. Tremoli, L. Cavallotti, M. Trezzi, S. Kassem, C. Loardi, et al., Do
statins improve outcomes and delay the progression of non-rheumatic calcific aortic stenosis? Heart 97 (7) (2011) 523–529 Epub 2011/01/29.
[68] Rajamannan, N. M., M. Subramaniam, F. Caira, S. R. Stock, T. C. Spelsberg,
Atorvastatin inhibits hypercholesterolemia-induced calcification in the aortic valves via the Lrp5 receptor pathway, Circulation 112 (Suppl. 9) (2005) I229–34 Epub 2005/09/15.
[69] Novaro, G. M., I. Y. Tiong, G. L. Pearce, M. S. Lauer, D. L. Sprecher, B. P. Griffin,
Effect of hydroxymethylglutaryl coenzyme a reductase inhibitors on the progression of calcific aortic stenosis, Circulation 104 (18) (2001) 2205–2209 Epub 2001/10/31.
[70] Dichtl, W., H. F. Alber, G. M. Feuchtner, F. Hintringer, M. Reinthaler, T. Bartel, et al.,
Prognosis and risk factors in patients with asymptomatic aortic stenosis and their modulation by atorvastatin (20 mg), Am. J. Cardiol. 102 (6) (2008) 743–748 Epub 2008/09/09.
[71] Rossebo, A. B., T. R. Pedersen, K. Boman, P. Brudi, J. B. Chambers, K. Egstrup, et
al., Intensive lipid lowering with simvastatin and ezetimibe in aortic stenosis, N. Engl. J. Med. 359 (13) (2008) 1343–1356 Epub 2008/09/04.
[72] Cowell, S. J., D. E. Newby, R. J. Prescott, P. Bloomfield, J. Reid, D. B. Northridge, et
al., A randomized trial of intensive lipid-lowering therapy in calcific aortic stenosis, N.
Engl. J. Med. 352 (23) (2005) 2389–2397 Epub 2005/06/10.
Pharmacological Treatment of Aortic Valve Disease
249
Complimentary Contributor Copy
https://t.me/med1917
[73] Chan, K. L., K. Teo, J. G. Dumesnil, A. Ni, J. Tam, Effect of Lipid lowering with
rosuvastatin on progression of aortic stenosis: results of the aortic stenosis pro­gression observation: measuring effects of rosuvastatin (ASTRONOMER) trial, Circulation 121 (2) (2010) 306–314 Epub 2010/01/06.
[74] Gerdts, E., A. B. Rossebo, T. R. Pedersen, K. Boman, P. Brudi, J. B. Chambers, et al.,
Impact of baseline severity of aortic valve stenosis on effect of intensive lipid lowering therapy (from the SEAS study), Am. J. Cardiol. 106 (11) (2010) 1634–1639 Epub 2010/11/26.
[75] Ardehali, R., N. J. Leeper, A. M. Wilson, P. A. Heidenreich, The effect of angiotensin-
converting enzyme inhibitors and statins on the progression of aortic sclerosis and mortality, J. Heart Valve Dis. 21 (3) (2012) 337–343 Epub 2012/07/20.
[76] Otto, C. M., J. Kuusisto, D. D. Reichenbach, A. M. Gown, K. D. O’Brien,
Characterization of the early lesion of’ degenerative’ valvular aortic stenosis. Histological and immunohistochemical studies, Circulation 90 (2) (1994) 844–853 Epub 1994/08/01.
[77] Stewart, B. F., D. Siscovick, B. K. Lind, J. M. Gardin, J. S. Gottdiener, V. E. Smith, et
al., Clinical factors associated with calcific aortic valve disease. Cardiovascular Health Study, J. Am. Coll. Cardiol. 29 (3) (1997) 630–634 Epub 1997/03/01.
[78] Parolari, A., C. Loardi, L. Mussoni, L. Cavallotti, M. Camera, P. Biglioli, et al.,
Nonrheumatic calcific aortic stenosis: an overview from basic science to phar­macological prevention, Eur. J. Cardiothorac. Surg. 35 (3) (2009) 493–504 Epub 2009/01/24.
[79] Novaro, G. M., B. P. Griffin, Calcific aortic stenosis: another face of atherosclerosis?
Cleve. Clin. J. Med. 70 (5) (2003) 471–477 Epub 2003/06/05.
[80] Otto, C. M., K. D. O’Brien, Why is there discordance between calcific aortic stenosis
and coronary artery disease? Heart 85 (6) (2001) 601–602 Epub 2001/05/23.
[81] Nsaibia, M. J., M. C. Boulanger, R. Bouchareb, G. Mkannez, K. Le Quang, F. Hadji, et
al., OxLDL-derived lysophosphatidic acid promotes the progression of aortic valve stenosis through a LPAR1-RhoA-NF-kappaB pathway, Cardiovasc. Res. 113 (11) (2017) 1351–1363 Epub 2017/05/05.
[82] Leopold, J. A., Cellular mechanisms of aortic valve calcification, Circ. Cardiovasc.
Interv. 5 (4) (2012) 605–614 Epub 2012/08/17.
[83] Abdelbaky, A., E. Corsini, A. L. Figueroa, S. Subramanian, S. Fontanez, H. Emami, et
al., Early aortic valve inflammation precedes calcification: a longitudinal FDG­PET/CT study, Atherosclerosis 238 (2) (2015) 165–172 Epub 2014/12/20.
[84] Mathieu, P., Y. Bosse, G. S. Huggins, A. Della Corte, P. Pibarot, H. I. Michelena, et
al., The pathology and pathobiology of bicuspid aortic valve: state of the art and novel research perspectives, J. Pathol. Clin. Res. 1 (4) (2015) 195–206 Epub 2016/ 08/09.
[85] Otto, C. M., I. G. Burwash, M. E. Legget, B. I. Munt, M. Fujioka, N. L. Healy, et al.,
Prospective study of asymptomatic valvular aortic stenosis. Clinical, echocardio­graphic, and exercise predictors of outcome, Circulation 95 (9) (1997) 2262–2270 Epub 1997/05/06.
[86] Freeman, R. V., C. M. Otto, Spectrum of calcific aortic valve disease: pathogenesis,
disease progression, and treatment strategies, Circulation 111 (24) (2005) 3316–3326 Epub 2005/06/22.
Giovanni Concistrè
250
Complimentary Contributor Copy
https://t.me/med1917
[87] Nkomo, V. T., J. M. Gardin, T. N. Skelton, J. S. Gottdiener, C .G. Scott, M. Enriquez-
Sarano, Burden of valvular heart diseases: a population-based study, Lancet 368 (9540) (2006) 1005–1011 Epub 2006/09/19.
[88] Eveborn, G. W., H. Schirmer, G. Heggelund, P. Lunde, K. Rasmussen, The evolving
epidemiology of valvular aortic stenosis. The Tromso Study, Heart 99 (6) (2013) 396– 400 Epub 2012/09/04.
[89] Hadar, H., D. Meiraz, Thickenedr enalfascia–asignofretroperitonealpathology, J.
Comput. Tomogr. 5 (2) (1981) 193–198 Epub 1981/06/01.
[90] Lindman, B. R., M. A. Clavel, P. Mathieu, B. Iung, P. Lancellotti, C. M. Otto, et al.,
Calcific aortic stenosis, Nat. Rev. Dis. Primers 2 (2016) 16006 Epub 2016/05/18.
[91] Tsimikas, S., Lipoprotein(a): novel target and emergence of novel therapies to lower
cardiovascular disease risk, Curr. Opin. Endocrinol. Diabetes Obes. 23 (2) (2016) 157–164 Epub 2016/01/31.
[92] Hutcheso, J. D., E. Aikawa, W. D. Merryman, Potential drug targets for calcific aortic
valve disease, Nat. Rev. Cardiol. 11 (4) (2014) 218–231 Epub 2014/01/22.
[93] Smith, J. G., K. Luk, C. A. Schulz, J. C. Engert, R. Do, G. Hindy, et al., Association of
low-density lipoprotein cholesterol-related genetic variants with aortic valve cal- cium and incident aortic stenosis, Jama 312 (17) (2014) 1764–1771 Epub 2014/10/27.
[94] Parolari, A., E. Tremoli, L. Cavallotti, M. Trezzi, S. Kassem, C. Loardi, et al., Do
statins improve outcomes and delay the progression of non-rheumatic calcific aortic stenosis? Heart 97 (7) (2011) 523–529 Epub 2011/01/29.
[95] Rajamannan, N. M., M. Subramaniam, F. Caira, S. R. Stock, T. C. Spelsberg,
Atorvastatin inhibits hypercholesterolemia-induced calcification in the aortic valves via the Lrp5 receptor pathway, Circulation 112 (Suppl. 9) (2005) I229–34 Epub 2005/09/15.
[96] Novaro, G. M., I. Y. Tiong, G. L. Pearce, M. S. Lauer, D. L. Sprecher, B. P. Griffin,
Effect of hydroxymethylglutaryl coenzyme a reductase inhibitors on the progression of calcific aortic stenosis, Circulation 104 (18) (2001) 2205–2209 Epub 2001/10/31.
[97] Dichtl, W., H. F. Alber, G. M. Feuchtner, F. Hintringer, M. Reinthaler, T. Bartel, et al.,
Prognosis and risk factors in patients with asymptomatic aortic stenosis and their modulation by atorvastatin (20 mg), Am. J. Cardiol. 102 (6) (2008) 743–748 Epub 2008/09/09.
[98] Rossebo, A. B., T. R. Pedersen, K. Boman, P. Brudi, J. B. Chambers, K. Egstrup, et
al., Intensive lipid lowering with simvastatin and ezetimibe in aortic stenosis, N. Engl. J. Med. 359 (13) (2008) 1343–1356 Epub 2008/09/04.
[99] Cowell, S. J., D. E. Newby, R. J. Prescott, P. Bloomfield, J. Reid, D. B. Northridge, et
al., A randomized trial of intensive lipid-lowering therapy in calcific aortic stenosis, N. Engl. J. Med. 352 (23) (2005) 2389–2397 Epub 2005/06/10.
[100] Chan, K. L., K. Teo, J. G. Dumesnil, A. Ni, J. Tam, Effect of Lipid lowering with
rosuvastatin on progression of aortic stenosis: results of the aortic stenosis pro­gression observation: measuring effects of rosuvastatin (ASTRONOMER) trial, Circulation 121 (2) (2010) 306–314 Epub 2010/01/06.
[101] Gerdts, E., A. B. Rossebo, T. R. Pedersen, K. Boman, P. Brudi, J. B. Chambers, et al.,
Impact of baseline severity of aortic valve stenosis on effect of intensive lipid lowering therapy (from the SEAS study), Am. J. Cardiol. 106 (11) (2010) 1634–1639 Epub 2010/11/26.
Pharmacological Treatment of Aortic Valve Disease
251
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[102] Ardehali, R., N. J. Leeper, A. M. Wilson, P. A. Heidenreich, The effect of angiotensin-
converting enzyme inhibitors and statins on the progression of aortic sclerosis and mortality, J. Heart Valve Dis. 21 (3) (2012) 337–343 Epub 2012/07/20.
[103] Otto, C. M., J. Kuusisto, D. D. Reichenbach, A. M. Gown, K. D. O’Brien,
Characterization of the early lesion of’ degenerative’ valvular aortic stenosis. Histological and immunohistochemical studies, Circulation 90 (2) (1994) 844–853 Epub 1994/08/01.
[104] Stewart, B. F., D. Siscovick, B. K. Lind, J. M. Gardin, J. S. Gottdiener, V. E. Smith, et
al., Clinical factors associated with calcific aortic valve disease. Cardiovascular Health Study, J. Am. Coll. Cardiol. 29 (3) (1997) 630–634 Epub 1997/03/01.
[105] Parolari, A., C. Loardi, L. Mussoni, L. Cavallotti, M. Camera, P. Biglioli, et al.,
Nonrheumatic calcific aortic stenosis: an overview from basic science to phar­macological prevention, Eur. J. Cardiothorac. Surg. 35 (3) (2009) 493–504 Epub 2009/01/24.
[106] Novaro, G. M., B. P. Griffin, Calcific aortic stenosis: another face of atherosclerosis?
Cleve. Clin. J. Med. 70 (5) (2003) 471–477 Epub 2003/06/05.
[107] Otto, C. M., K. D. O’Brien, Why is there discordance between calcific aortic stenosis
and coronary artery disease? Heart 85 (6) (2001) 601–602 Epub 2001/05/23.
[108] Nsaibia, M. J., M. C. Boulanger, R. Bouchareb, G. Mkannez, K. Le Quang, F. Hadji, et
al., OxLDL-derived lysophosphatidic acid promotes the progression of aortic valve stenosis through a LPAR1-RhoA-NF-kappaB pathway, Cardiovasc. Res. 113 (11) (2017) 1351–1363 Epub 2017/05/05.
[109] Leopold, J. A., Cellular mechanisms of aortic valve calcification, Circ. Cardiovasc.
Interv. 5 (4) (2012) 605–614 Epub 2012/08/17.
[110] Abdelbaky, A., E. Corsini, A. L. Figueroa, S. Subramanian, S. Fontanez, H. Emami, et
al., Early aortic valve inflammation precedes calcification: a longitudinal FDG­PET/CT study, Atherosclerosis 238 (2) (2015) 165–172 Epub 2014/12/20.
[111] Mathieu, P., Y. Bosse, G. S. Huggins, A. Della Corte, P. Pibarot, H. I. Michelena, et
al., The pathology and pathobiology of bicuspid aortic valve: state of the art and novel research perspectives, J. Pathol. Clin. Res. 1 (4) (2015) 195–206 Epub 2016/ 08/09.
[112] Otto, C. M., I. G. Burwash, M. E. Legget, B. I. Munt, M. Fujioka, N. L. Healy, et al.,
Prospective study of asymptomatic valvular aortic stenosis. Clinical, echocardio­graphic, and exercise predictors of outcome, Circulation 95 (9) (1997) 2262–2270 Epub 1997/05/06.
[113] Freeman, R. V., C. M. Otto, Spectrum of calcific aortic valve disease: pathogenesis,
disease progression, and treatment strategies, Circulation 111 (24) (2005) 3316–3326 Epub 2005/06/22.
[114] Nkomo, V. T., J. M. Gardin, T. N. Skelton, J. S. Gottdiener, C. G. Scott, M. Enriquez-
Sarano, Burden of valvular heart diseases: a population-based study, Lancet 368 (9540) (2006) 1005–1011 Epub 2006/09/19.
[115] Eveborn, G. W., H. Schirmer, G. Heggelund, P. Lunde, K. Rasmussen, The evolving
epidemiology of valvular aortic stenosis. The Tromso Study, Heart 99 (6) (2013) 396– 400 Epub 2012/09/04.
Giovanni Concistrè
252
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[116] Hadar, H., D. Meiraz, Thickened renalfasciaasignofretroperitonealpathology, J.
Comput. Tomogr. 5 (2) (1981) 193–198 Epub 1981/06/01.
[117] Lindman, B. R., M. A. Clavel, P. Mathieu, B. Iung, P. Lancellotti, C. M. Otto, et al.,
Calcific aortic stenosis, Nat. Rev. Dis. Primers 2 (2016) 16006 Epub 2016/05/18.
In: Perspectives in Aortic Valve Disease ISBN: 978-1-53618-769-4
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Editor: Giovanni Concistrè © 2020 Nova Science Publishers, Inc.
Chapter 13
SURGICAL TREATMENT OF AORTIC VALVE DISEASE:
INDICATIONS, RISK STRATIFICATION
AND OUTCOMES
Rafik Margaryan
Ospedale del Cuore “G. Pasquinucci,”
Fondazione Toscana Gabriele Monasterio, Massa, Italy
ABSTRACT
Aortic stenosis (AS) is the most common valve disease requiring surgical intervention in high income countries [1]. Calcification of the aortic cusps is the most common cause of aortic stenosis [1]. Valve replacement is the only durable treatment for this lesion and, unlike aortic insufficiency, which can be managed by means of valve repair in selected patients(see chapter 19, 20), aortic stenosis resulting from calcification of the cusps almost always requires valve replacement, and in recent years also sutureless trans-cathter valve implantation. A comprehensive review of transcatheter aortic valve implantation is well coverd [2], and this technique will be reviewed and discussed deeply in chapter 21. In this chapter we will mainly focus on aortic valve replacement (aortic valve repair will be discussed in chapters 19 and 20).
Interes in severe aortic stenosis treatment still remainsof many researchers and clinicians (see Figure 2). Since the replacement of aortic valve is only known treatment, nowadays different approaches are applied to it: surgical (radical, real replacement) and catheter bases techniques(implantation, not replacement). However when to do it is important. For a note there is a recent randomized trial [3] who has addressed that question beautifully.
Keywords: aortic stenosis, surgical aortic valve replacement, transfemoral aortic valve
implantation, outcomes
Corresponding Author’s Email: margaryan@ftgm.it.
, MD, PhD
Rafik Margaryan
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INTRODUCTION
In 1947, Smithy and Parker at the University of South Carolina in Charleston first
reported an experimental study of aortic valvotomy [4]. During the early 1950s, Bailey and coauthors in Philadelphia used closed methods either a dilator introduced transventricularly or a digital approach through a ‘poncho’ sewn onto the ascending aorta in clinical attempts to relieve severe aortic stenosis [5, 6]. Success in some patients was obtained by them and by Ellis and Kirklin. [7] In 1951 developed a ball valve prosthesis for rapid insertion into the descending thoracic aorta [8].
An effective approach to surgical treatment of aortic valve disease in adults began with
the advent of clinical cardiopulmonary bypass in 1954 and 1955. At first, aortic valvotomy and removal of calcific deposits were all that could be acchieved [9, 10]. Then Bahnson and colleagues and, independently, Hufnagel and Conrad developed a single-leaflet prosthesis that was commercialized [11, 12]. Generally, the leaflets were used to partially replace the aortic valve, but three leaflets could be used together for total aortic valve replacement. Probably the first single-unit prosthesis for total aortic valve replacement was the polytetrafluroethylene (PTFE) sleeve prosthesis developed and first used by McGoon at the Mayo Clinic in 1961. Introduction of the ball valve prosthesis by Harken and colleagues and Starr and colleagues in 1960 and reported in 1963 established aortic valve surgery on a firm basis [13, 14]. Many types of prosthetic valves have subsequently developed. In 1956, Murray demonstrated that the aortic valve could be used as an allograft valve transplant in the descending thoracic aorta in patients with aortic regurgitation, [15] and Kerwin and colleagues reported 6-year follow­up [16]. The first orthotopic insertions of an allograft valve using the double-suture-line technique were performed in 1962 by Barratt-Boyes and separately by Ross using a single­sutureline technique described by Duran and Gunning [17, 18]. In 1967, Ross and colleagues introduced the pulmonary autograft for aortic valve replacement [19]. In 1965, Binet and colleagues in Paris implanted porcine xenograft aortic valves, sterilized and preserved in a special formaldehyde solution, directly into the aortic root [20]. Stent-mounted bioprostheses are manufactured to provide a standard device that is easily implanted and provides reproducible results in the aortic position. Glutaraldehyde preserved stent-mounted porcine valves were introduced by Carpentier and colleagues in Paris in 1967 [21]. David and colleagues revived the concept of direct insertion of nonstented porcine xenografts into the aortic root [22]. This valve was manufactured on a limited trial basis by Hancock Laboratory and by St. Jude Medical as the Toronto SPV (stentless porcine valve). In April 2002, Professor Alan Cribier at the University of Rouen, France, performed the first percutaneous aortic valve implantation for aortic stenosis in a 62-year-old man who was not a candidate for surgery [23]. Cribier used the antegrade transseptal approach through the femoral vein. Frirst transapical approach was used by Lange et al. [24] in 2007 with successful implantation of suturles Corevalve (Medtronic Inc). First suturless aortic valve Shrestha et al. [25] have describe first implantation of Perceval suturless valve implatation in human. All the timeline related to surgical treatment of aortic valve is designed in Figure 1.
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Figure 1. Timeline related to Aortic Valve Procedures.
Figure 2. Hits percentage of ‘Surgical Treatment of Aortic Valve Disease’ term in European PUBMED.
INDICATIONS
Early therapy should be strongly recommended in all symptomatic patients with severe
aortic stenosis because of their bad prognosis [26, 27]. Watchfull waiting for asyntomatic patients seem to harm more the one has expected, early surgical aortic valve replacement resulted in a significantly lower risk of operative mortality or death from cardiovascular causes during the follow-up period than conservative care among asymptomatic patients with very severe aortic stenosis [3]. Patients with severe comorbidities indicating a survival of < 1 year and patients in whom severe comorbidities or their general condition at an advanced age make it unlikely that the intervention will improve quality of life or survival [27]. In all other patients surgery should be recommended in particular circumstances, such as impaired left ventricular function, abnormal exercise test, or the presence of left ventricular hypertrophy in the absence of systemic hypertension [26, 27]. Aortic valve surgery is recommended in
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asymptomatic patients with aortic insufficiency and left ventricular ejection fraction ≤50%, and in patients with normal systolic function, but an enlarged left ventricle (end-diastolic
diameter ≥35 mm/m2, end‐systolic diameter ≥25 mm/m2 [26, 27]). Patients with ascending
aortic aneurysm and aortic insufficiency should undergo surgery when the diameter of the aorta is ≥55 mm, and at an earlier stage when associated with particular conditions, such as BAV or genetic aneurysms. Patients with low-flow, low-gradient aortic stenosis and reduced ejection fraction in whom the depressed ejection fraction is predominantly caused by excessive afterload, LV function usually improves after intervention [28, 29]. Intervention is definitely advised when severe aortic stenosis is confirmed at increasing flow, 10 while patients who are classified as having pseudosevere aortic stenosis at increasing flow should receive conventional treatment for heart failure [28, 30]. Although the outcome of patients without flow reserve is compromised by a higher operative mortality, SAVR (as well as TAVI) has also been shown to improve ejection fraction and clinical status in such patients [31, 32]. Patients with low-flow, low-gradient aortic stenosis and preserved ejection fraction are the most challenging subgroup. Data on their natural history and outcome after surgical or catheter intervention remain controversial [33–35]. In concomitatn aneruismatic dilatation of thoracic aorta surgery is recommended when the aortic root reaches 45 mm as measured by CT scanning or MRI in patients with Loeys–Dietz syndrome, at a diameter of 50 mm in patients with Marfan syndrome or familial aneurysms, or at a smaller diameter in patients with a family history of aortic dissection [26, 27]. There are no specific guidelines for choosing thype of prosthesis. However, in our istitution there is patient/case based method
and generally meccanical valve is recommended for patients ≤ 60 years old, above that
boundery the biological vavlves are preffered. Stutureless vlaves, sience these are fairly new to our practice is preffered ≥ 75 years old [36].
RISK STRATIFICATION
Risk stratification applies to any sort of intervention and is required for weighing the risk
of intervention against the expected natural history of aortic valve desease as a basis for decision making. Most experience relates to surgery and TAVI. The EuroSCORE I (http://www.euroscore.org/calc.html) overestimates operative mortality and its calibration of risk is poor and it is was mainly build for conventional surgery. Consequently, it should no longer be used to guide decision making not for conventiona nor for minimally invasive surgery. The EuroSCORE II and the Society of Thoracic Surgeons (STS) score (http://riskcalc.sts.org/stswebriskcalc/#/) more accurately discriminate high- and low-risk surgical patients and show better calibration to predict postoperative outcome after valvular surgery in conventional [37, 38] and minimally invasive surgery [39]. Scores have major limitations for practical use by insufficiently considering disease severity and not including major risk factors such as frailty, porcelain aorta, chest radiation etc. While EuroSCORE I markedly overestimates 30-day mortality and should therefore be replaced by the better performing EuroSCORE II in this regard as it has been used in many TAVI studies/registries and may still be useful to identify the subgroups of patients for decision between intervention modalities and to predict 1-year mortality. However, it seems that there is necessity to update some scores (EuroSCORE II) as STS is updated continously. A very simple score (age,