in the mitral position where the risk remained constant during the whole period of follow-up in spite of different schemes of long-term anticoagulation. the favourable embolic rate and virtual lack of valve thrombosis of the pericardial valve appears to be due to the quality of the tissue, and especially to the design of the valve with a smooth and synchronous movement of the three cusps and the streamlined structure conferring the valve optimal hydrodynamic characteristics even at low flow rates. infective endocarditis infective endocarditis is a severe condition which occurs on native as well as on artificial valves. both mechanical prosthetic devices and tissue heart valves are affected. the incidence of endocarditis, in western countries, ranges from 1.5 to 6.2 cases per 100,000 people per annum. the cumulative rate of prosthetic valve endocarditis is 1.5 to 3.0% at one year following valve replacement and 3 to 6% at five years, the risk being the greatest during the first six months after valve replacement. prosthetic valve endocarditis arising within two months of valve surgery is generally the result of intra-operative contamination of the prosthesis or a bacteraemic post-operative complication. the nosocomial nature of these infections is reflected in their primary microbial causes: coagulase-negative staphylococci, s. aureus, facultative gram negative bacilli, diphtheroids and fungi. epidemiologic evidence suggests that prosthetic valve endocarditis due to coagulase negative staphylococci that presents between 2 and 12 months after surgery is often nosocomial in origin but with a delayed onset. this short introduction may help to reflect on the various and sometimes opposing view-points concerning the 'origin' of prosthetic valve endocarditis. as in most recent scientific reports, some descriptions of tissue valve endocarditis suffer from the same lack of clarity and standardization in the presentation of facts and do not give all relevant details for a better understanding of events and their causes. from eight published articles of large series of patients with ionescu-shiley pericardial valves, only one report presents a higher than average number of valvular bacterial infections. the other seven publications describe the rate of infection with figures of similar magnitude. table ii. freedom from infective endocarditis main author no. of patients duration of follow-up years linearized rate of infection actuarial freedom from infective endocarditis pavie 675 5 98.2% for all patients, 97.8% for aortic, 99% for mitral, 100% for multiple valve replacements duncan (a) 2720 6 97.3% for all patients, 97.4% for aortic valves, 97.6% for mitral valves, 96.3% for multiple valve replacement ionescu (b) 1171 10 93.7% for all patients, 94.7% for aortic valves, 97.1% for mitral valves, 89.3% for multiple valve replacement zhu 520 10 98% for all patients revuelta 239 8 0.67% per patient year garcia-bengochea 248 8 0.78% per patient year holden (c) 290 6 1.1% per patient year bachet (d) 224 6 1.6% per patient year footnotes to the table: (a): the authors make a remark: prior to heart valve replacement 86 patients suffered from infective endocarditis but only 9 of these patients developed recurrent infection following pericardial valve replacement. (b): of the 17 cases of infection, 15 occurred between 1976 and 1981 and only 2 cases between 1981 and 1985. ionescu's group took draconian measures in trying to jugulate post-operative infections which they considered to be, in great part, nosocomial in origin. those measures were directed at systematic pre-operative dental examination and treatment, search for any hidden, potential foci of infection - urological, upper and lower respiratory tract, judicious selection of antibiotic cover of the patient before, during and following heart valve replacement operations and strict monitoring of all signs of infection in the post-operative period. it appears that these measures had borne fruit. (c): on two occasions, holden successfully implanted pericardial valves in patients with infective endocarditis and he advocates the use of such valves in similar situations because the pericardial valves are considered to be more resistant to infection than other devices. (d): this group considers that in its hands the pericardial valves were more prone to infection than the porcine valves, and also when compared to the results with pericardial valves published by other surgeons. in conclusion, it is obvious that the risk of infective endocarditis in pericardial valves is not dissimilar from that encountered in porcine valves at least up to ten years after valve insertion. it can also be considered that the minor variations occurring in the published reports are due to local hospital differences, surgical technique, general handling of the valves and other factors. one rarely finds a patient who was treated medically for proven endocarditis on his own valve who does not require valve replacement sooner or later. there is no fundamental reason why any pericardial valve should become infected more frequently than another one except if the patient becomes septicaemic and the infecting organisms will reach the valve area. it appears illogical to claim that because one surgeon reported a higher incidence of infective endocarditis with one type of valve, that there could be any significant differences between 'his' valves and those implanted by other surgeons. the difference is in the number of patients with circulating infecting micro-organisms capable of infecting the valve area. most authors do not consider infective endocarditis as a valve-related failure and do not include cases of infection in such statistics. the pericardial valve does not behave in a different way from other tissue valves as far as infection is concerned, with probably one exception. in the impression of some surgeons, the pericardium itself seems to be more resistant to infection than the porcine valve. primary tissue failure the durability of the pericardial valve, like that of all other artificial heart valves, depends on multiple factors, one of the most important being the environment in which the artificial valves function. primary or intrinsic tissue failure occurred with pericardial valves and it has been reported in several publications. unfortunately, many reports do not contain some of the essential data and details necessary for building a clear image of this crucial aspect of valve performance. table iii tabulates some of the available data on primary tissue failure. table iii. primary tissue failure main author no. of patients follow-up years no. of valve failures free from failure. actuarial pavie (a) 675 5 2 aortic. calcified and fibrosed 99.1% all patients revuelta 90 aortic 8 2 valves calcified (0.71% per patient year) 89.9% gonzales-lavin 240 aortic 8 12 valves, 11 calcified 88.4% aortics only garcia-bengochea 248 8 2 valves (0.22% per patient year) duncan (b) 2720 6 77 valves. 52 calcified, 25 tears 91.5% mitral, 86.2% mitral and aortic, 84.5% aortic bachet 224 6 5 valves. 4 tears, 1 calcified (0.80% per patient year) van swieten 444 6 2 valves, tears (0.20% per patient year) zhu (c) 520 9 5 valves 92.1% mitral, 89.9% aortic ionescu 1171 9-10 25 valves. 15 tears, 9 calcified, 1 fibrosed. (mitral 0.72%, aortic 0.94% per patient year) 88.7% mitral, 86.9% aortic keon 637 8 19 valves. 15 tears, 4 calcified 89% mitral, 87% aortic kawazoe 319 7 4 valves. 3 mitral, 1 mitral and aortic (all cusp tears) 93.4% mitral, 90.5% aortic nistal (d) 133 aortic 7 8 valves. all calcified, 2 with additional tears 80% all valves moran 400 5 9 valves (8 mitral, 1 aortic) 4 calcified - mean age 37.5, 5 tears - mean age 50.2. (0.87% per patient year) remarks for primary tissue failure (a): the ages of the patients range from 8 to 90 years (mean 57). 74% were over 70 years of age. the age of the two patients with valve failure (calcification) was not mentioned. (b): the most important element in this large series is the demonstration that one of the most important factors in valve calcification is the age of the patient at the time of valve implantation. (c): in this series, the authors mention, in addition, 4 cases of entanglement of sutures around the struts. these 4 patients were re-operated upon at between one week and 50 months following the first valve operation. (d): the authors stated that all 8 failures were due to valve calcification and that 2 of them had additional tears. they find that their results with 'calcification' in all failed valves are contrary to gabbay's results where failures occurred mainly through cusp tears. this table is only an attempt to give a general impression and to provide a basis for a more detailed interpretation of results. however, several conclusions can be formulated on the complex, varied, and in some cases controversial results published. as very often, a good amount of significant data is missing and this complicates the task of being precise and fair in interpreting the results. it appears that the great majority of pericardial valves function correctly until about 6 to 7 years post implantation. beyond seven years of follow-up, the actuarial figures for freedom from valve failure start to decrease. in the table, the risk of valve failure seems to be greater in the aortic position as reported by some authors. in reality, the general consensus among surgeons, in various presentations and formal discussions, shows the contrary. at 10 years, and beyond, the pericardial valve did function well in the aortic position, as reported by various authors., several pericardial valves were explanted from the aortic position at 16, 17 and 18 years following implantation, and a few valves between 21 and 23 years. pericardial valves in the mitral position fared less well beyond 5 – 6 years, as reported in some series, but not in others. ravichandran reported a series of 34 patients (with 41 valves) who were re-operated upon for removal of failed ionescu-shiley pericardial valves. the failures occurred at a mean duration since 'implantation' of 11.3 years (mean range 3–17 years). there were 30 mitral and 11 aortic valves involved, and the majority were moderately or heavily calcified. watanabe describes a case of an ionescu-shiley bioprosthesis which functioned 24years in the mitral position of a patient. the known modes of tissue valve failure are: tearing of the pericardium, calcification of the valve and, exceptionally, fibrosis of the cusps. tears represent approximately 25% and calcification 75% of primary failure. in some cases both pathologies could be encountered in the same valve. this proportion varies considerably and could be seen reversed in some series of patients. the causes for pericardial tears were described in detail and can be summarised as an abrasive mechanism produced by the rubbing of the pericardium over the dacron-covered margin of the supporting stent. such tears progress slowly until a part of one of the cusps becomes flail and the amount of regurgitation increases. this explains the fact that there is no sudden catastrophic failure with the pericardial valve, except when the initial, obvious clinical signs and symptoms of incipient malfunction have been missed or disregarded by the treating physician or the patient. there may be, in a minority of cases, some slightly different mechanisms of pericardial damage at points of three-dimensional flexure or perforation caused by the excessively long ends of sutures used in aortic valve replacement. several techniques have been used in order to reduce or abolish 'abrasion', as will be described later. within the limitation of the intrinsic durability of the chemically treated bovine pericardium, various modifications, physical and chemical, could be employed to eliminate this type of failure and considerably extend the functioning life of this valve. valve calcification is a local representation of a general biologic phenomenon which occurs under specific conditions in various parts of the body, especially in younger individuals. valve calcification is known to have taken place in all types of tissue valves. because some important details are not given in the reported series (age of patients, timing of occurrence, position of the valve, etc.) it is difficult to form a clear-cut conclusion in all situations. one report on a large series of patients followed for six years, presented at a symposium in 1985, gave clear and complete information regarding the relationship between valve calcification and the age of the patients at the time of valve implantation. the authors showed that in the groups of patients aged between 10 and 59 years, the incidence of valve calcification ranged from 31.8% (in the age group of 10 to 20 years) to 1.8% (in the group aged 50 to 59 years) to reach zero calcification in