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Pharmacological Treatment of Aortic Valve Disease
247
Complimentary Contributor Copy
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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
Complimentary Contributor Copy
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
Complimentary Contributor Copy
https://t.me/med1917
[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
Complimentary Contributor Copy
https://t.me/med1917
[116] Hadar, H., D. Meiraz, Thickened renalfascia–asignofretroperitonealpathology, 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.

Surgical Treatment of Aortic Valve Disease
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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,
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