Biomedical subjects
R W Frater
Publications and source records attributed to R W Frater.
The Carpentier-Edwards pericardial aortic valve: intermediate results.
The Edwards pericardial aortic valve has unique design features that minimize cusp stress and reduce abrasion wear. Wear tests and in vivo fluid dynamic tests have shown superior performance compared with other bioprostheses. Between August 1981 and July 1985, 719 isolated aortic valves were implanted in 10 US centers. Patients were aged 18 to 90 years (mean, 64 years). Men were 63.3% of the patients. Aortic stenosis was present preoperatively in 63.4% of patients. New York Heart Association functional classes III and IV were assigned to 62% of the patients. Valve sizes were 21 mm or less in 49% of patients. Concomitant procedures (most often coronary artery bypass grafting) were performed in 48% of patients. Hospital mortality was 4.7%. There was one valve-related death due to anticoagulant hemorrhage. Late mortality yielded 23 valve-related deaths: endocarditis (13), anticoagulant hemorrhage (4), thromboembolism (3), structural (2), and pannus overgrowth (1). Freedom from valve-related death at 7 years was 95.5%. Regarding valve survival, cusp tears were not seen. There were 11 calcified valves and eight explants (57 to 107 months). Seven-year freedom from all valve reoperation was 95.5%, with 11% of the patients receiving warfarin sodium, freedom of the total series from hemorrhage at 7 years was 93.3%, and from major thromboembolism, 95.8%. Echocardiographic follow-up of hemodynamics at 7 years yielded the following calculated effective orifice areas: 19 mm, 1 cm2; 21 mm, 1.3 cm2; and 23 mm, 1.4 cm2. Average mean gradient for 19-mm valves was 15 mm Hg. New York Heart Association class improved in 78% of the patients. The Carpentier-Edwards pericardial valve, carefully studied by the Food and Drug Administration guidelines, is easy to use and has excellent hemodynamics.(ABSTRACT TRUNCATED AT 250 WORDS)
Diphenylhydantoin inhibits calcification of bovine pericardial implants and myocardium: a preliminary study.
Calcification is a major cause of glutaraldehyde-fixed bioprosthetic valve failure. Recent studies have shown that dystrophic calcification shares basic features with normal bone mineralization, including crystal initiation through the mediation of cell membranes, usually in the form of extracellular vesicles. In this study, we observed that calcification of the myocardium of DBA/2J mice was inhibited or reversed by diets supplemented with 100 mg/kg diet diphenylhydantoin (dilantin) for 70 days, with a calcification incidence of 25% in the dilantin group versus 58% in control. We further studied the effects of dilantin on bioprosthetic valve calcification. Three groups of young male Sprague-Dawley rats (100 g, 9/group) were implanted subcutaneously with 1-cm2 pieces of glutaraldehyde-fixed bovine pericardium. Controls were fed a ground chow for 45 or 90 days postimplantation; experimentals received the same chow for the first 45 days postimplantation and then were fed the same diet supplemented with 1000 mg dilantin/kg for the succeeding 45 days. Calcium content (microgram/mg dry weight) of the implants in the dilantin group was 137 +/- 18.6 versus 214 +/- 34.3 in 90 days control and 79.9 +/- 41.5 in 45 days control (mean +/- SD, P < 0.01 and P < 0.05 respectively, t test). The tibia calcium content of the dilantin group was not significantly different from 90 days control. We conclude that orally administered dilantin inhibits calcification of glutaraldehyde-fixed bovine pericardial implants preferentially. It does not cause decalcification either of implants that have already calcified or of the bones. The anti-calcification effect of dilantin may be associated with its anti-vitamin D effect.
Improved postfixation treatment of glutaraldehyde fixed porcine aortic valves by monosodium glutamate.
The use of bioprosthetic valves remains limited due to poor long-term durability primarily because of tissue calcification-associated degeneration. Release of locally cytotoxic residual aldehyde after glutaraldehyde fixation is one of the major causes of this degeneration. In this study, monosodium glutamate was used as postfixation treatment to bind residual aldehyde in order to block its toxic effects. Thirty-six pieces of fresh porcine aortic valves were fixed by 0.625% glutaraldehyde for 14 days, and then 18 of them were treated with 1% monosodium glutamate for another 3 days before they were implanted subcutaneously into the backs of two groups of rats (n = 9 in each group) for 45 and 90 days, respectively. Retrieved specimens were examined grossly, and calcium analysis and measurements of tissue collagen and water content were carried out. The results showed that, compared with glutaraldehyde fixed specimens, monosodium glutamate postfixation treated specimens had less calcification (calcium 104.93 + 50.94 versus 141.58 +/- 58.10 at 45 days and 103.07 +/- 76.48 versus 199.33 +/- 53.44 at 90 days, micrograms/mg dry weight, p < 0.01), higher collagen content (hydroxyproline 5.50 +/- 1.29 versus 3.58 +/- 1.48 at 45 days and 5.64 +/- 0.87 versus 4.25 +/- 0.65 at 90 days, micrograms/mg wet weight, p < 0.01), and higher water content (68.00 +/- 6.95% versus 61.33 +/- 8.83% at 90 days, p < 0.05) (mean +/- SD, paired t test). We conclude that monosodium glutamate couples with residual aldehyde, which significantly reduces calcification of glutaraldehyde fixed porcine aortic valves while preserving a higher tissue collagen and water content after implantation. The preserved tissue collagen and water content of the implants is closer to that of unimplanted native valves.
Bovine pericardium versus porcine aortic valve: comparison of tissue biological properties as prosthetic valves.
The choice of a bioprosthetic valve substitute remains controversial with the major concern being primary tissue failure after implantation. We compared biological properties of the two most frequently used bioprosthetic valve materials, bovine pericardium and porcine aortic valve, before and 90 days after subcutaneous implantation in rats. Before implantation, tissue collagen and water content were measured in nine pieces of bovine pericardium and porcine valves, each fixed in 0.625% glutaraldehyde; calcium, tissue collagen, and water content were measured in another nine pieces of the same tissues after 90 days' implantation. Bovine pericardium had higher collagen content than that of porcine valve (hydroxyproline, 7.98 +/- 0.05* vs. 4.56 +/- 0.02 micrograms/mg, dry weight) but lesser water content (72.16 +/- 3.22%* vs. 87.36 +/- 1.62%) before implantation (*p < 0.001, mean +/- SD, t test); after implantation, bovine pericardium still maintained higher collagen content (hydroxyproline, 4.89 +/- 0.04* vs. 2.61 +/- 0.06 micrograms/mg, dry weight) but contained the same amount of water (60.24 +/- 5.08% vs. 61.43 +/- 9.00%) and calcium (214.43 +/- 34.34 vs. 199.33 +/- 53.44 micrograms/mg, dry weight) (*p < 0.001, mean +/- SD, t test). We conclude that bovine pericardium has superior intrinsic biological properties for prosthetic valve manufacture. With proper integration of properties and design it will in some applications be superior to the porcine aortic valve.
Towards understanding the pericardium as valve substitute.
Explore the source record for details and available documents.
Spontaneous host endothelial growth on bioprostheses. Influence of fixation.
BACKGROUND: Neither homografts nor bioprostheses have previously been seen to acquire a host endothelium. We previously reported a direct relation between aldehyde tanning and bioprosthesis calcification and the absence of calcification in the absence of aldehyde. METHODS AND RESULTS: Bovine pericardium was 1) treated with 0.625% glutaraldehyde and stored in 4% formaldehyde, 2) treated with 99.5% glycerol, and 3) treated with 99.5% glycerol and stored in formaldehyde (0.25-4%). The treated pericardium was used to construct stentless mitral valve prostheses (of a single pattern) that were implanted in weanling sheep. After the animals were killed, a strip of anterior cusp from annulus to papillary muscle was processed and examined by scanning electron microscopy for the presence of host endothelial growth. Avoidance of aldehyde allowed host endothelial growth in all cases (six of six), and pure aldehyde treatment inhibited growth in five of six animals. Exposure to aldehyde after glycerol treatment interfered with endothelialization significantly; after longer periods of implantation, however, endothelial growth occurred almost invariably in this group (12 of 13 implanted longer than 200 days). For this group, there was a statistically significant difference for duration of implantation between the valves that grew endothelium and those that did not (218.4 +/- 61.9 versus 128.5 +/- 65.4 days). CONCLUSIONS: Aldehyde treatment inhibits endothelial growth. With glycerol treatment, growth is uniformly present. Limited exposure to aldehydes after glycerol treatment inhibits endothelial growth, but this effect was ameliorated by prolonged implantation. The possibility of host endothelium-covered, noncalcifying bioprostheses is now real.
Early detection of coronary artery graft dysfunction with intraoperative 2-dimensional transesophageal echocardiography.
We report 5 cases in which intraoperative transesophageal echocardiography was instrumental in the early detection of a left ventricular wall-motion abnormality caused by acute dysfunction of a coronary artery bypass graft. The appearance of a wall-motion abnormality on transesophageal echocardiography preceded signs of myocardial ischemia when such signs were detectable with routine monitoring. By facilitating prompt, appropriate correction of technical problems, transesophageal echocardiography enabled the blood flow to be restored and the ischemic insult to be resolved without further complication.
Selection of an artificial heart valve.
Explore the source record for details and available documents.
Aldehyde tanning: the villain in bioprosthetic calcification.
Preservation of bioprosthetic valves may play a role in valvular calcification. Subcutaneous implants in rats were used to test the effect of different preservation solutions. Fifty male Sprague-Dawley rats were divided into five groups. Fresh bovine pericardium was treated in one of five ways: group A: 99.5% glycerol for 1 week; group B: as group A, then normal saline wash and 0.25% formaldehyde storage for 24 h; group C: as group A, then normal saline wash and 4% formaldehyde storage for 24 h; group D: as group A, then normal saline wash and 0.625% glutaraldehyde storage for 24 h; group E: 0.625% glutaraldehyde and 4% buffered formaldehyde storage. Treated bovine pericardium was cut into 1-cm2 pieces and washed for 30 min with normal saline before implantation. In each animal, three pieces were implanted in the subcutaneous tissue of the back. After 70 days, retrieved specimens were examined grossly, and X-ray densitometry, calcium analysis, and histological examinations were carried out. The results showed that glycerol-treated tissue (group A) had less calcification (calcium 6.92 +/- 4.46 micrograms/mg dry weight) than other groups: group B (calcium 323.12 + 63.56 micrograms/mg dry weight); group C (calcium 240.65 + 13.47 micrograms/mg dry weight); group D (calcium 232.29 + 13.01 micrograms/mg dry weight). These differences were markedly significant (p less than 0.0001). It appears that aldehydes play an important role in the calcification of bioprosthetic valves. Experience with glutaraldehyde- and glycerol-treated pericardium in valvular applications in sheep support these observations.
Surgical technique for artificial mitral chordae implantation.
Failure of reconstructive procedures of the mitral valve is often ascribed to diffuse alteration of the subvalvular apparatus, which prevents the utilization of well-established techniques such as chordal transposition or shortening. For this reason, in 1986 after 2 years of animal experiments, we started the clinical use of expanded-polytetrafluoroethylene mitral chordae. Details of the surgical procedure are presented. Our experience is based on 51 patients with a mean follow-up of about 20 months (range 3-57). Four patients had the valve replaced during the same operation: one patient died later of cardiac failure and two underwent reoperation, 8 and 18 months after operation. Forty-one patients are in New York Heart Association Functional Class I and three in Class II. We suggest this technique in association with other traditional procedures to increase the number of mitral valves repaired, mostly because of degenerative etiology.
Atrial contribution to ventricular filling in mitral stenosis.
BACKGROUND: The importance of the contribution of atrial systole to ventricular filling in mitral stenosis is controversial. The cause of reduced cardiac output following the onset of atrial fibrillation may be due to an increased heart rate, a loss of booster pump function, or both. METHODS AND RESULTS: We studied the atrial contribution to filling under a variety of conditions by combining noninvasive studies of patients with computer modeling. Thirty patients in sinus rhythm with mild-to-severe stenosis were studied with two-dimensional and Doppler echocardiography for measurement of mitral flow velocity and mitral valve area (MVA). The mean +/- SD atrial contribution to left ventricular filling volume was 18 +/- 10% and varied inversely with mitral resistance. Patients with mild mitral stenosis (MVA, 1.8 +/- 0.7 cm2) and severe mitral stenosis (MVA, 0.9 +/- 0.2 cm2) had atrial contributions of 29 +/- 4% and 9 +/- 5%, respectively. The pathophysiological mechanisms responsible for these trends were further investigated by the computer model. In modeled severe mitral stenosis, increasing heart rate from 75 to 150 beats/min caused an increase of 5.2 mm Hg in mean left atrial pressure, whereas loss of atrial contraction at a heart rate of 150 beats/min caused only a 1.3 mm Hg increase. CONCLUSIONS: The atrial booster pump contributes less to ventricular filling in mitral stenosis than in the normal heart, and the loss of atrial pump function is less important than the effect of increasing heart rate as the cause of decompensation during atrial fibrillation.
Aprotinin and open heart operations.
Explore the source record for details and available documents.
Artificial mitral valve chordae: experimental and clinical experience.
Failure of mitral valve reconstructive procedures often may be ascribed to severe or progressive alterations of subvalvar apparatus. Expanded polytetrafluoroethylene sutures were used to replace anterior leaflet mitral valve chordae in 8 animals (hypertensive dogs and growing sheep). After the positive results obtained during a 13-month follow-up, 5-0 sutures of the same material were introduced in clinical practice to replace mitral valve chordae. Twelve patients had two to six anterior leaflet chordae replaced for degenerative or rheumatic disease. In 3 patients, the intraoperative result was not acceptable and a prosthetic valve was inserted during the same operation. One case of late failure has been recorded so far (18 months after the procedure), owing to rupture of a natural chorda shortened at operation. Since that event, we have implanted supportive artificial chordae in case of diffuse alteration of natural chordae. The remaining patients show satisfactory hemodynamic results, and no valve-related events have been recognized up to 30 months after operation. We suggest use of 5-0 polytetrafluoroethylene sutures in replacing anterior leaflet chordae in degenerative, rheumatic, and congenital mitral valve diseases.
Surgical management of endocarditis in drug addicts and long-term results.
From 1977 to May 1989, 57 successive patients who were known drug addicts with endocarditis were operated on at the Weiler Division of Montefiore Medical Center and the Albert Einstein College of Medicine. The most common lesion was aortic endocarditis. Thirty day in hospital mortality was 9%. Recurrent infection did not occur in the preAIDS era. Since the advent of HIV positive patients, failure of antibiotics to control the infection preoperatively has been seen and carries with it a severe risk of recurrent and fatal postoperative sepsis. The long-term survival was, at about 10% over 5-10 years, just good enough to warrant continued efforts in this very difficult group of patients.
Use of extruded polytetrafluoroethylene sutures as chordal substitutes.
Explore the source record for details and available documents.
Relationship between diastolic shape (eccentricity) and passive elastic properties in canine left ventricle.
This study was designed to investigate the relationship between left ventricular (LV) eccentricity, volume, and passive elastic properties. Eight open-chest fentanyl-anesthetized dogs were instrumented with an LV micromanometer, a remote-controlled mitral valve occluder, and two pairs of ultrasonic crystals to measure anterior-posterior and base-apex dimensions. We identified the presence of elastic recoil forces with negative LV diastolic pressure in nonfilling diastoles (end-systolic volume clamp). Using linear regression analysis we related midwall eccentricity to volume in nonfilling diastoles at the time of LVPmin and at end diastole, and in normal beats at end systole at LVPmin and at end-diastole. Intersection of the end-systolic and end-diastolic lines (transitional volume, Vt = 38.0 + 6.4 ml) divides cycles with and without the presence of elastic recoil forces. Vt is analogous to the equilibrium volume (V0), determined as the volume intercept of the logarithmic passive pressure-volume (P-V) relationship using LV volume estimated from LV weights (V0 nl = 37.6 + 4.4 ml), or the volume intercept of the linearized P-V relationship calculated from a prolate spheroidal model using measured minor and major diameters (V0 l = 44.5 + 3.5 ml). Linear regression analysis was also used to relate the square of peak mitral flow (MF2) with the corresponding atrioventricular pressure gradient (delta P); the slope represents a dissipative constant for the cycles without, P = 0.00058(MF)2 + 0.35 (n = 48, r = 0.73), and with elastic recoil P = 0.00035(MF)2 + 0.21 (n = 24, r = 0.81).(ABSTRACT TRUNCATED AT 250 WORDS)
Effect of early diastolic loading on myocardial relaxation in the intact canine left ventricle.
Early transmitral flow (MiF) patterns depend strongly on the rate of fall of measured left ventricular pressure (Pm) determined by both the active decay of pressure (Pa) due to myocardial relaxation and the increase in pressure due to stretch of passive elements during filling (Pp). This study was designed to uncouple passive forces from deactivation in order to reveal the instantaneous rate and duration of myocardial relaxation. We assumed a parallel combination of passive and active elements: Pm(t,V) = Pa(t) + Pp(V), with no constraints on the form of Pa(t), where t is time and V is ventricular volume. Pp(V) was determined by a retrospective analysis of data obtained in 11 anesthetized dogs instrumented for volume clamping with a remote-controlled mitral valve, with left atrial and left ventricular micromanometers, and with an electromagnetic probe to measure MiF. The passive pressure-volume relation (both positive and negative portions) was determined by clamping at end-systolic volume or after various filling volumes, and fit to logarithmic functions. Pp(t) was then calculated from Pp(V) and V(t) (integral of MiF). Time to end relaxation (Ter) was defined as time when Pa = 0. During isovolumic relaxation, when dPp/dt = 0, dPm/dt is equal to the relaxation rate, dPa/dt. In completely isovolumic relaxations, asymptote P infinity = -7 +/- 6 mm Hg (thus, Pa is 7 mm Hg greater than Pm) and Ter = 40 +/- 15 msec, compared with 175 +/- 53 msec during normal filling. In high versus low inotropic state, Pa at the beginning of filling was greater (18.1 +/- 6.1 vs. 12.2 +/- 3.9 mm Hg), and Ter was shorter (170 +/- 42 vs. 228 +/- 43 msec). Active pressure Pa(t) during filling is not an exponential function, and at any time, it was always greater after filling than in nonfilling beats, which indicates an increase in the relaxation duration. We conclude that myocardial relaxation is modulated by filling, which slows its rate and increases its duration, and is therefore a function of both ventricular volume and time. Such a mechanism may have an important role in regulating the diastolic pressure-volume relation.