Biomedical subjects

D Plissonnier

Publications and source records attributed to D Plissonnier.

32 records · Page 2Linked to original sources

PubMed1996

In situ arterial allografting for aortoiliac graft infection: a 6-year experience.

Between October 1988 and May 1994, all aortoiliac graft infections seen in the authors' service were treated by in situ arterial allografting after resection of any infected graft or tissue. Some 83 consecutive cases were treated; there were 68 isolated primary prosthetic infections (82%) and 15 aortoenteric fistulae (18%). Emergency arterial allografting was performed in five cases (6%), elective allografting in 64 cases (77%) and elective allografting after emergency palliative revascularization using a temporary prosthetic graft in 14 cases (17%). Arterial allografts were harvested from cadavers as part of a programme to retrieve multiorgan transplant tissue. Fifteen patients (18%) died either intra- or postoperatively. Three died during the operation, one from septic shock and two from uncontrollable coagulopathy. Twelve patients died in the early postoperative period, from from septic shock, two from myocardial infarction, two from pneumonia, one from a pulmonary embolism, one from an intestinal infarction, one from recurrence of a duodenal fistula and one from disruption of the native aorta at the suture line. Three patients presented with an early complication directly related to the use of the allograft. Eleven early survivors of the series died during follow-up. Among these late deaths, only one could likely be allograft-related. In four patients, the aortic segment of the allograft was mildly dilated on late computed tomography scan; three were reoperated on for disruption of the extra-abdominal segment of their allograft. All four cases were managed with simple suture of the allograft or with the use of a new allograft. Fifteen patients exhibited 19 late occlusive lesions of their allograft; 17 of these lesions had to be treated either with transluminal angioplasty or with surgery using autogenous or allograft material. In all but one case, secondary patency could be achieved through these additional procedures. Late occlusive disease was more prevalent in the femoral segment of the allograft than in the iliac or, moreover, the aortic segment. There were no late amputations in this series.

Adult↗

PubMed1996

[Coronary assessment and surgery for aortic aneurysm: a pragmatic attitude].

High prevalence of coronary artery disease in patients with AAA leads to a high rate of peri-operative cardiac complications. Coronary insufficiency is thus the cause of 40 to 60% of post-operative deaths after aortic surgery. Demonstration of coronary insufficiency depends on the clinical history, electrocardiographic evidence, non-invasive examinations and coronarography. Diagnosis is based on non-invasive tests, and of primary importance exercise tests, which have a high sensitivity. Specificity for predicting post-operative cardiac complications remains low but can be improved by combining with other tests (for example exercise test and Holter recording) or with other clinical parameters. Coronarography provides a precise map of the coronary status but gives little information on functional impairment of encountered lesions. Finally, besides the cost and a certain degree of morbidity, coronarography increases the number of indications for revascularizations with the inconvenience of its intrinsic mortality and also retards the operation increasing the risk of rupture. The evaluation of cardiac risk before surgery must be based on correct use of non-invasive tests, limiting coronarography to cases with frankly positive tests.

Aged↗

PubMed1996

[Treatment of prostheto-digestive using arterial allograft].

From October 1988 to March 1995, we operated 22 patients for fistulization between the prosthesis and the digestive tract to remove the in situ allograft. The delay between the initial operation and treatment for fistulization was 7.3 +/- 4 years. In these patients who had undergone multiple operations (2.5 +/- 1.9 operations per patient), the infected prosthesis was made of Dacron in 21 cases and polytetrafluoroethylene in one. The procedure was planned beforehand in 21 cases who benefited from a complete preoperative work-up and was required in an emergency situation in 6 for digestive bleeding (5 cases) or an abscess of the Scarpa (1 case). Among the patients with an emergency operation, three of the procedures were conducted within a single operative time and three with two separate procedures. The allografts were aorto-aortic tubes (n = 3), aortobifemoral bypasses (n = 14), aorto-iliac bypasses (n = 4) and one aorto-femoral-iliac bypass. Organ revascularization was associated in 8 patients. Seven patients (32%) died post-operatively. Five of them had undergone an emergency procedure. An amputation was required in 2 patients, one at the time the allograft was implanted and the second due to ischaemia despite a permeable allograft. None of the patients had to be amputated due to failure of the allograft. Mean follow-up was 36.6 +/- 20 months. There were 4 deaths post-operatively due to digestive bleeding in 2. The aortic allograft was dilated in 4 patients without re-operation. Thrombosis of the allograft branch occurred in 4 patients, including 3 who had been re-operated successfully. Despite these still perfectable results, treatment of secondary digestive-prosthesis fistulae with an in situ allograft constitutes a real progress in terms of patient survival and preservation of the limb in high-risk patients.

Aged↗

PubMed1996

[Dissecting aneurysm of the external iliac artery. An unusual course of endofibrosis in an athlete].

A 42-year-old man was consulted because of a pain in his left leg. He was a highly trained biker since 20 years. The echo-Doppler and arteriography evidenced a stenosis, probably due to endofibrosis of the external iliac artery. In addition, it showed an aneurysm and an intimal dissection of this artery. The arteriography confirmed this diagnosis, and normal aspect of the other arteries. Neither conservative nor endovascular treatments were possible because of the anatomic lesions. We resected the external iliac artery and performed a by-pass with the great saphenous. The result at the 5th month was clinically good. The echo-Doppler control did not show any abnormality. The natural course of the endofibrosis of athletes is unknown, although stenosis, revealed by intermittent claudication is usually observed. Only a few cases of dissection and no aneurysmal degeneration have been described before.

Adult↗

PubMed1995

Sequential immunological targeting of chronic experimental arterial allograft.

Arterial wall is the main site involved in the chronic rejection process. The rat aortic allograft model was used here to characterize and describe the sequential evolution of the different targets and effectors of arterial wall immunological injury and response during arterial allograft rejection. Rat abdominal aortae were isografted or allografted from Brown-Norway to Lewis rats. Endothelial and smooth muscle cell injury and humoral and cellular immunological effectors were characterized from 0 to 60 days after transplantation using a battery of specific antibodies. The intimal proliferative response was also characterized over this time. Isografted Brown-Norway aorta adventitia had very few cellular components, which suggests that donor adventitia would be poorly antigenic in allografts. In contrast, allograft adventitia was the site of a major inflammatory cell invasion in which the expression of an adhesion molecule by colonizing capillary endothelial cells could play a main role. This adventitial infiltration continued as long as medial smooth muscle persisted. The luminal endothelial cells disappeared early, probably associated with macrophage margination. In contrast, medial smooth muscle cell disappearance occurred later and was specifically targeted by immunoglobulins. Intimal proliferation was the most delayed phenomenon, involving both inflammatory cell infiltration at an early stage and later myofibroblastic proliferation, and could be related to the specific expression of growth factors in this layer. The rat aortic allograft model appeared useful for characterizing specific targets and effectors of chronic arterial graft rejection, demonstrating an early stage of endothelial injury and the presence of immunoglobulins involved in chronic medial smooth muscle cell injury.

Animals↗

PubMed1994

Cell-free arterial grafts: morphologic characteristics of aortic isografts, allografts, and xenografts in rats.

PURPOSE: Chronic rejection of arterial allografts and xenografts results in arterial wall dilation and rupture, making them unsuitable for long-term arterial replacement in vascular surgery. In the arterial wall, as in other organs, the cells probably carry major antigenic determinants. Arterial wall cellular components can be removed by detergent treatment to produce a graftable matrix tube. METHODS: We compared the patency and macroscopic and microscopic morphologic changes that occurred in sodium dodecyl sulfate (SDS)-treated and untreated arterial isografts, allografts, and xenografts 2 months after implantation in rats. We quantified elastin, collagen, and nuclear density in the three layers of the graft wall (intima, media, and adventitia) by morphometric methods. The SDS treatment removed endothelial and smooth muscle cells and cells in the adventitia but preserved elastin and collagen extracellular matrix. RESULTS: All arterial xenografts, whether SDS treated or untreated, were aneurysmal 2 months after grafting, with loss of the medial cellular and extracellular components. In allografts, SDS treatment prevented dilation, reduced adventitial inflammatory infiltration, and preserved medial elastin. The SDS-treated allografts had an evenly distributed, noninflammatory intimal thickening that was richer in elastin fibers than that in untreated allografts. CONCLUSIONS: These results suggest an interspecies, but not an intraspecies, graft antigenicity of arterial extracellular matrix. The SDS treatment prevented chronic rejection of the arterial allograft and led to the proliferation of an elastin-rich and adapted intima.

Animals↗

PubMed1994

[Long occlusion of the superficial femoral artery: revascularization by venous graft].

In long occlusions of the superficial femoral artery, possibilities of revascularization depend on the patency of the above-knee popliteal artery. In case of occlusion of the above-knee popliteal artery, the distal anastomosis is to be performed at the below-knee level or more distally; in this situation, studies demonstrate a clearcut superiority of venous bypasses over prosthetic bypasses. Patency of the above-knee popliteal artery allows to perform a shorter bypass avoiding to cross the knee joint; given comparable results between venous and prosthetic above-knee bypasses in certain series, several authors advocated the preferential, if not systematic use of prosthetic materials at this level; this attitude having the advantage of preserving the saphenous vein for later coronary or distal grafting. A critical analysis of studies advocating this therapeutic option reveals that results of prosthetic and venous above-knee bypasses are equivalent in only very restrictive clinical situations (claudication, good runoff) and for follow up less than 3 years; beyond this follow up, the use of a prosthesis increases the number of secondary procedures necessary for maintaining or restoring patency and for this reason increases slightly the overall mortality owing to the operative mortality associated with each reoperation. Apart from rare cases represented by fragile and high-risk patients, whose lifespan is likely to be short and in whom a quicker operation is advisable, indications of the use of prosthetic grafts depend on the limits of the use of the saphenous vein generated by a poor quality or an insufficient diameter.

Anastomosis, Surgical↗

PubMed1993

Effects of glutaraldehyde on experimental arterial iso- and allografts in rats.

The effects of glutaraldehyde pretreatment and allograft rejection in arterial grafts were assessed, using iso- and allografts in rats. An in situ glutaraldehyde fixation procedure was used to obtain homogeneous cross-linked vascular biografts. Ten Lewis rats were isografted, ten were isografted with a glutaraldehyde-treated aortic segment, ten were allografted with aortic segments from brown Norway (BN) inbred rats, and ten were allografted with glutaraldehyde-treated BN aortas. The macroscopic and microscopic appearances of the grafts were analyzed 3 weeks after the initial surgery. Immunological injury to the media and the intimal response were quantified morphometrically after monochromatic staining of cell nuclei (hematoxylin after periodic acid), elastin (orcein), and calcification (Von Kossa). Untreated isografts were normal. Untreated allografts showed the classical signs of arterial wall rejection: adventitial inflammatory granuloma, reduced medial thickness and smooth muscle cell density, and greatly increased intimal thickness (P < 0.005). Glutaraldehyde treatment significantly decreased the medial thickness in both iso- and allografts (P < 0.001) and prevented the intimal proliferative response (P < 0.005), but did not change adventitial inflammation. It also induced massive calcification mainly in isografts (P < 0.001). Histomorphological modifications of glutaraldehyde-treated grafts are consistent with a partial protective effect of glutaraldehyde against the rejection process, but also with an induction of a nonspecific inflammatory reaction. Glutaraldehyde-induced cross-linking of the extracellular matrix was responsible for ectopic calcification of the arterial grafts which was independent of the rejection process.

Animals↗

PubMed1993

Additive and synergistic effects of a low-molecular-weight, heparin-like molecule and low doses of cyclosporin in preventing arterial graft rejection in rats.

Arteriosclerotic intimal proliferation is one of the main long-term complications of organ transplantation. Low-molecular-weight, heparin-like molecules prevent myointimal proliferation in arterial wall injury and limit rejection in skin allografts. Cyclosporin limits rejection but has no major effect on intimal proliferation. Therefore, an experimental protocol was designed to test whether heparin-like molecules interacted with low doses of cyclosporin to prevent arterial wall immune system injury and response in a model of arterial graft rejection in normotensive and hypertensive rats. Aortic allografts were performed in spontaneously hypertensive rats (SHRs) and Wistar-Kyoto (WKY) normotensive control rats. Four groups of 10 allografted (SHR and WKY) rats were used: one group was treated with placebo, one with low doses of cyclosporin (2 mg/kg body wt per day), one with low-molecular-weight, heparin-like molecule (1 mg/kg body wt per hour), and one with low doses of cyclosporin plus low-molecular-weight, heparin-like molecule. Ten SHRs and 10 WKYs were isografted and served as the control groups. All rats were killed 8 weeks after aortic grafting. Structural parameters of the grafted segment were measured by morphometric analysis on formalin-fixed sections with specific stains. The classical signs of immune system injury and response were present in the untreated allografts in SHRs and WKYs: inflammatory infiltration of the adventitia, medial injury, and intimal proliferative response. Low doses of cyclosporin had a significant beneficial effect on immune medial injury by increasing medial thickness and the number of remaining smooth muscle cells and decreasing the extracellular matrix injury. Cyclosporin had no protective effect on intimal proliferation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1993

In situ allograft replacement of infected infrarenal aortic prosthetic grafts: results in forty-three patients.

PURPOSE: Dissatisfaction with conventional methods of treatment of infected infrarenal aortic prosthetic grafts and excellent long-term results reported by heart surgeons after allograft replacement for management of infections involving the ascending aorta have prompted us to investigate allograft replacement in the management of arterial infections. METHODS: From October 1988 to April 1992, 43 consecutive patients with infected infrarenal aortic prosthetic grafts underwent in situ replacement with preserved allografts obtained from cadavers as part of a program to retrieve multiorgan transplant tissue. Thirty-four patients had isolated prosthetic infections, whereas nine had aortoenteric fistulas. One patient had a concomitant below-knee amputation for septic arthritis of the ankle as a result of septic emboli. Nineteen patients had nonvascular-associated procedures, including 17 intestinal procedures. RESULTS: Five patients (12%) died after operation: four of general causes and one of rupture of the native aorta as a result of persistent infection. Three patients successfully underwent repeat operation for allograft-related complications (one case each of occlusion, septic rupture, and graft-enteric fistula). All surviving patients were discharged after control angiography showed patent allografts. Two patients were unavailable for follow-up. The other 36 patients have been monitored with serial duplex and computed tomography scanning for a mean follow-up of 13.8 months (range 1 to 42 months). There were four late deaths: three were unrelated to the vascular operation, and one may have been caused by late persistent or recurrent infection. Nine patients (26%) have had pathologic changes in the allograft, with three (9%) requiring repeat operation. There were no early or late postoperative amputations in the entire series. CONCLUSIONS: Although complete protection against persistent or recurrent infection has not been achieved and late deterioration may be expected, in situ allograft replacement seems to be a major advance in the management of infected infrarenal aortic prosthetic grafts.

Adult↗

PubMed1992

Effect of perindopril on the immune arterial wall remodeling in the rat model of arterial graft rejection.

A model of arterial graft arteriosclerosis is described in which arterial wall immune injury was induced by grafting segments of abdominal aorta between two histologically incompatible strains of rats. The effect of hypertension and its treatment with the angiotensin-converting enzyme (ACE) inhibitor perindopril was tested using inbred spontaneously hypertensive rats (SHR) and their normotensive controls (Wistar-Kyoto [WKY]). Each of the grafted hypertensive and normotensive rats was randomly allocated to placebo treatment (10 SHR, 10 WKY) and perindopril treatment (2 mg/kg/day) (10 SHR, 10 WKY). The immune injury and the arterial wall response were quantified morphometrically 2 months after the grafting using specific stains for collagen, elastin, and nuclei. Hypertension was associated with a significant increase in intimal thickness. Treatment with perindopril greatly reduced intimal proliferation, decreasing the intimal thickness and the collagen content within the intimal layer. In contrast, hypertension and ACE inhibition had little effect on the arterial wall injury. We conclude that hypertension and its treatment with perindopril significantly affect graft arteriosclerosis. These effects seem to be independent of their effects on arterial wall injury, but not independent of blood pressure.

Analysis of Variance↗

PubMed1991

Effect of converting enzyme inhibition on allograft-induced arterial wall injury and response.

Converting enzyme inhibition (CEI) can prevent myointimal proliferation after arterial wall balloon injury. Because intimal proliferation is the main long-term complication of chronic vascular rejection, we tested the effect of CEI (perindopril, 1 mg/kg twice a day) on arterial rejection-induced intimal proliferation, using a model of aortic allograft in normotensive Wistar-Kyoto and spontaneously hypertensive rats. Eight-week-old rats were grafted and studied 2 months later. The structural parameters of the transplanted aortic wall were measured by morphometric analysis of specifically stained, formol-fixed sections. CEI did not prevent adventitial inflammatory infiltration but significantly increased the number of living cells and prevented the partial destruction of elastic laminae in the media, thereby increasing medial thickness to close to that of sham-operated controls. CEI significantly decreased intimal thickness and intimal collagen density, without changing the absolute number of intimal smooth muscle cells. The intimal thickness and the intimal collagen density were significantly correlated with the effect of CEI on blood pressure. CEI partially prevented the consequences of immune injury to the media within the arterial wall, probably by suppressing the proinflammatory activity of angiotensin II. It also decreased the recipient arterial wall response by acting more on the trophicity of intimal cells and on their ability to produce collagen rather than by directly inhibiting smooth muscle cell proliferation in our model of arterial allograft.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1990

Pathophysiological role of the vascular smooth muscle cell.

The vascular smooth muscle cell of the arterial media plays a predominant role in functional and structural alterations of the arterial wall in pathophysiological processes such as arterial hypertension, atheroma, or normal aging. The observed alterations are related to the three activities of the vascular smooth muscle cell, namely contractility, secretion of proteins from the extracellular matrix, and proliferation and migration. In arterial hypertension, vascular smooth muscle cells are functionally more contracted and structurally hypertrophic, and more collagen is secreted than under normal conditions. Similar structural changes are observed in the normal aging process. With respect to vascular smooth muscle cells, atheroma is characterized by their subintimal migration and proliferation, and by excessive excretion of collagen associated with other phenotypic modifications that are expressed in their regression to a myofibroblastic state. Regardless of the pathophysiological context, these phenotypic modifications of the vascular smooth muscle cell are always linked to an activation of the phosphoinositol pathways and to calcium accumulation. The activation of the phosphoinositol pathways seems to be a common feature of the different types of arterial hypertension. This activation can be associated with an increase in vasoactive peptides such as angiotensin II, vasopressin, or endothelin as in the secondary types of hypertension or directly related to an increase in vasoconstriction; or, as an exception, it can be spontaneously active in vivo and in vitro, as in the model of cultured vascular smooth muscle cells of the spontaneously hypertensive rat (SHR).(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗

PubMedDate not supplied

Allograft-induced arterial wall injury and response in normotensive and spontaneously hypertensive rats.

The role of genetically determined immune attack and blood pressure in graft rejection-induced arterial wall injury and response was assessed by studying the compliance and changes in wall structure of aortic isografts and allografts in normotensive (Wistar-Kyoto [WKY]) and hypertensive (spontaneously hypertensive [SHR]) rats. Six groups of 8-week-old rats were compared: sham-operated in both strains, isografts, and allografts between the two strains (SHR aortas grafted in WKYs, designated SWs; WKY aortas grafted in SHRs, designated WSs; isografts in SHRs, designated SSs; and isografts in WKYs, designated WWs). Each arterial graft was studied 8 weeks after transplantation for volume and compliance (pressures of 75-175 mm Hg) under basal conditions. The amounts of collagen, elastin, and nuclei in the media and intima of the walls of control and grafted aortas were quantified morphometrically. Isografts and controls had the same mechanical characteristics under basal conditions: the arterial volume and arterial compliance of hypertensive rats were lower than those of normotensive rats (p less than 0.001). Allografts had a greater initial volume (p less than 0.001) and a lower compliance (p less than 0.001) than did isografts. Allografts in SHRs (SSs) were initially dilated, whereas allografted WKYs (WWs) were not. There was intimal proliferation in hypertensive isografts (14 +/- 0.77 microns) and in both types of allografts (WS, 69 +/- 1.55 microns; SW, 44 +/- 1.81 microns); nucleus density was higher in hypertensive allografts (WS) than in normotensive allografts (SW); and collagen density was also higher in SW than in WS allografts. Allografts had decreased medial thickness and decreased smooth muscle cell density.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗