valves demonstrate, once again, the advantage of the versatility of the 'man-made concept' of the pericardial valve. the haemodynamic characteristics of these 3 types of valve are similar to the excellent results found with the original ionescu-shiley valve as described by tandon's group. the minor differences in gradients and in calculated surface area do not show a significant difference at clinical level. the adjacent image portrays the opening characteristics of 4 pericardial valves - hancock (no longer available), mitroflow, edwards and shiley. the cusps of these valves open synchronously up to a very large surface area only minimally different from one valve to another. all 4 valves were manufactured for clinical use and all were 25mm in diameter. the valves were photographed under identical conditions in the mitral side of a 'pulse duplicator' and the flow rates, at peak of diastole were: for each frame, from left to right: 0, 100, 200, 300, and 400 ml/s. regarding infective endocarditis, embolic complications and bleeding due to anticoagulant treatment, there is only scant data in the publications analysed for this article. it is presumed, and not without good reason, that the main emphasis was placed by the authors on structural valve deterioration (svd). it can also be considered logical that these three types of pericardial valves, having a similar structure and dynamic function as the original ionescu pericardial valve, such complications, 'grosso modo', would have occurred at about the same rate as reported by the users of the ionescu valve as already reported in this article. the scientific publications on these three, second generation pericardial valves are not only few in number but they lack some of the necessary, standardised data for a complete, clear and fair evaluation of the results. in order to avoid generalities and averages, the data reporting svd is presented in the form of tables. table iv. mitroflow pericardial valve main author/year no. of patients. valve location patient mean age (range) no. of svd, position actuarial freedom from svd-years revuelta, 1990 130 - all, 90 - a, 27 - m, 10 - d 55.4 (26-74) 1 aortic, 4 mitral at 7 years, all valves 86% loisance, 1993 199 - all, 107 - a, 63 - m, 28 - d, 1 - t 58 at 5 years 94.6%. at 10 years 63.7% sjogren, 2006 152 aortic 79.5 (75-91) at 5 years 99%. at 10 years 82% benhameid, 2008 161 aortic 69.5 (60-94) 19 in group 60-69, 6 in group >70 years at 15 years: 60-70- 62%, >70- 73% yankah, 2008 1513 aortic 72.4 122. stenosis 36.7%, regurgitant 20.4%, both 42.9% at 20 years: >70- 84.8% jamieson, 2009 381 aortic from 3 centres 76.4 (53-91) at 10 years: <60- 85.2%, >60- 85%, 61-70- 95.7%, >70- 83.2% a = aortic; m = mitral; d = mitral and aortic, t = tricuspid, svd = structural valve deterioration. the lack of standardised data presented in the various publications makes interpretation difficult. the discrepancy of the actuarially presented results between the various publications is evident. table v. edwards pericardial valve main author,year no. of patients. valve location patient mean age (range) no. of svd, position actuariel freedom from svd-years pelletier, 1990 284 - all, 222 - a, 77 - m, 2 - t 58 (19-79) 3 valves. 1 - m regurgitation at 26 months, 2 a - thrombus at 20 months, tear at 68 months reoperation for all causes sbe, svd, perivalvular leak. overall 92% at 6 years jamieson,1999. multicentre report 429 all mitral, 318 - m, 101 -d 60.7 calcification 70.4%, leaflet tear 18.5%, both 11.1% at 10 years: age <40 -80%, 41-50 - 91%, 51-60 - 84%, 61-70 - 95% marchand, 2001 435 all mitral, 333 - m, 102 - d 60.7 (8-82) 56 episodes: calcification 73%, tears 20%, both 7%. duration to explant 9.5 years (5-13.6) at 14 years: all patients 66.3%, <65- 62.8%, >65- 85.9% biglioli, 2004 327 all aortic, 298 study group 67.2 (19-83),215 patients aged > 65 considerable increase on the risk of prosthesis replacement after 10 years post op. at 14 years: all patients 52.9%, <65- 35.8%, >65- 83.7% mcclure, 2010 1000 all aortic 74.1 26 valves at 15 years: age <65- 34.7%, 65-75- 89.4%, >75- 99.5% a= aortic; m= mitral; t = tricuspid; svd = structural valve deterioration; sbe = subacute bacterial endocarditis the inverse relationship between the age of the patients and the rate of svd is obvious in most reports. there are very significant differences among the various publications concerning the figures of actuarial freedom from svd. published data from dr. carpentier on structural dysfunction of the valve which carries his name would have been useful, but a search through the relevant medical literature, has not revealed any such publications. table vi. sorin pericarbon pericardial valve main author, year no. of patients.valve location patient mean age (range) no. of svd, position actuarial freedom from svd-years folliguet, 2001 277 all, 224 - a, 39 - m, 10 - d, 3 - p 178 > 75 years (64.3%) 3 aortic, 2 at 7 years, 1 at 2 years at 10 years: all patients - 96.6%, aortic 96.1%, mitral 100% (i) grabenwoger, 1994 144 all, 114 - a, 25 - m, 5 d 69 9 valves - 3 mitral, 6 aortic. 7 stenotic, 2 regurgitant, 9 calcified; valve failure at +/- 55 months post implant (ii) see below caimmi, 1998 78 all mitral 56.9 26 calcified-stenosis at 12 years: 56.8% all. <60- 36.8%; >60- 86.3% seguin, 1998 multicentre report 321 aortic 75.8 6 valves - calcification at 10 years - 83.9% a =aortic; m = mitral; d = mitral and aortic; t = tricuspid; p = pulmonary; svd = structural valve deterioration. (i) this figure should be interpreted with caution because the study was of only 39 patients with mitral replacement and only 2 patients were at risk at 10 years. the patients' ages were not supplied in detail. (ii) this study describes only the pathology of failed valves in 9 patients (out of a series of 144), 51 –79 years old (mean 69) followed-up for 6 – 8 years. the description of clinical use and results of the 144 patients who received sorin pericarbon pericardial valves would have been of great interest, but a search through the relevant medical literature has not found any such publication from the surgical team. the symptoms of valvular stenosis due to calcification are insidious and often well tolerated by the patient. the reported svd rate may be lower than would have been, if the valves were assessed by echocardiography. this pertains to the figures in tables iv, v and vi. there are very few published reports containing sufficient data in order to be useful. one can only note, without much comment, the gross difference between the svd shown in these three tables. a scientific comparison among these 3 second generation valves, and between them and the ionescu-shiley valves is practically impossible. the number of patients in the published series varies considerably. for the shiley valves there had been an almost equal distribution of mitral and aortic replacements. for the new generation valves, the ratio was about 5:1 in favour of the aortic valve. the much smaller number of mitral valve replacements is due in part to the reduction of mitral valve disease in the general population and, at the same time, because of the increase in the number of patients with degenerative aortic valve disease in a progressively aging population. another reason appears to be the perception of some surgeons that pericardial valves in the mitral position are more susceptible to svd, than in the aortic position. the time-frame of their usage also varies. surgical techniques and experience in general have evolved over the past 40 years. the lessons from the past might have borne fruit. the experience with the shiley valves shows that 75-80% of valve failure was due to calcification and only 20-25% failed because of abrasion and possibly because of design flaws. the knowledge about the type of valve failure - abrasion and, especially, calcification - have placed tissue valves in a new perspective and gave the surgeons a different outlook. the greatest achievement after the first 10–15 years of usage of the first pericardial valves, was the realisation of the inverse relationship between patient age and valve calcification. this was known before, from the porcine valve experience, but it has not received sufficient emphasis until the use of pericardial valves. the data presented in the above three tables allow one to draw some conclusions based on existing factual results but also on overall general impressions. the second generation of pericardial valves have only occasionally failed due to tissue abrasion, although tears have still occurred. calcification of the tissue occurred later in elderly patients because mineralisation develops later and advances slower in old age. these modified valves have been used preferentially, if not exclusively, in older patients and in a considerably larger proportion for aortic valve replacement rather than in the mitral position where the risk of svd was, and remains, higher. these elements distort significantly all chance of a comparison with the series of shiley valves. during the 1970s and 80s, shiley pericardial valves had been used in patients of all ages, and particularly in patients under the age of 65 years. during the 1990s and into the following decade, the mean age of patients receiving the second generation of pericardial valves varied between 67.2 and 72 years, a very significant difference in age. the technical improvements made in the second generation of valves has apparently reduced the risk of cusp abrasion. this advantage was not fully exploited because these valves were used only in a small proportion in young patients who would have benefited more from this technical advancement. despite claims that all 3 types of second generation valves were treated with 'so-called' anticalcification processes, the clinical results have not shown any benefit from such chemical treatment. the only reason for the reduced rate of calcification - and therefore of structural valve deterioration - in patients receiving these second generation valves was the advanced age of the patients who received them. the age of the patients was shifted from a mean of around 50 years with shiley valves, to a mean of between 67 and 72 years with the second generation valves. it is regretable that pericardial valves, which are known to carry a very low risk of embolisation, were not used more often in the mitral position where the need and benefit would have been greater. however, in general, the second generation pericardial valves represent a progress in the armoury of devices for the treatment of heart valve disease. if the process of valve calcification could be controlled, these pericardial valves would become the panacea for patients in need of heart valve replacement. in general, it is known that success depends on knowing how long it will take to succeed. for the time being, one has to accept that most of the aspects of the present are accessible only to prophesy, about the future, the understanding of the phenomenon 'calcification' and its prevention, may lay somewhere beyond the horizon. a short history of the introduction in clinical use of valves made of animal tissue for heart valve replacement in humans allows us to appreciate the evolution of this chapter of cardiac surgery and to imagine future potential developments in this field. 1965 duran and gunning in oxford, england, published their experimental work of implanting porcine aortic valves in dogs and the previous year they had already performed the first successful porcine aortic valve replacement in one human patient. 1965 binet and associates in paris, france, began the use of porcine aortic valves for aortic valve replacement in humans. 1967 ionescu and associates in leeds, england, used for the first time porcine aortic valves mounted on an original valve support for mitral valve replacement in humans. 1969 hancock laboratory in irvine, california introduces the first commercially available porcine aortic valve for use in patients. 1969 carpentier and associates in paris, france, advocate the use of glutaraldehyde for chemical treatment of porcine aortic valves. 1971 ionescu and others in leeds, england, creates the first bovine pericardial heart valve and begins its implantation in humans. 1980 since the early 1980s several modified pericardial valves have