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S Anidjar

Publications and source records attributed to S Anidjar.

14 recordsLinked to original sources
PubMed1998

Aneurysm of a common celiomesenteric trunk.

Aneurysm of the celiac and/or superior mesenteric arteries are uncommon, accounting for 10% of visceral artery aneurysms. Aneurysms involving a common celiomesenteric trunk are extremely rare. Up to now only two cases have been reported. In this report we describe a saccular aneurysm originating from the bifurcation of a common celiomesenteric trunk. Treatment consisted of resection followed by suture of the aneurysmal neck. This anatomic variation of the visceral arteries probably resulted from a defect in embryonic development suggesting that the aneurysm was congenital in origin. Other etiologies of aneurysms in this location are atherosclerosis, infection, inflammation, and arterial dystrophy. These lesions are almost always surgical indications requiring complete angiographic study of the visceral vasculature.

Aneurysm↗
PubMed1998

Is transcranial Doppler a worthwhile examination for preoperative evaluation of the Circle of Willis? Evaluation of 137 carotid endarterectomies performed under regional anesthesia.

BACKGROUND: Transcranial Doppler is often proposed for evaluation of the Circle of Willis prior to carotid endarterectomy. The purpose of this study was to evaluate preoperative TCD before carotid surgery. METHODS: This is a retrospective report of 137 carotid endarterectomies performed under regional anesthesia operated between January 1992 on June 1996. All patients have a tight stenosis between 70% on 99%, and 49% were symptomatic. Forty-three patients of the 132 had a controlateral hemodynamically significant carotid stenosis with none occlusion. The TCD examinations were all performed with ADMS Doppler Spectradop with 3-MHz and 2-MHz probes. Clinical evaluation during cross-clamping was compared to the preoperative TCD. In 14% of the patients, the TCD could not be performed because there are not temporal bone windows. RESULTS: When the patients could be tested the positive predictive value of the TCD was 18% and the sensitivity was 33%. The negative predictive value was 94%. 8% of the patients were shunted. TCD had numerous difficulties. The most common is the lack of the temporal bone window (40% of the patients). The compression test is often difficult when the lesion is calcareous. Preoperative TCD is not according to our results, a reliable enough examination to modify operative strategy during carotid surgery. When coupled with arteriography it is a good way to study cerebral hemoynamics. CONCLUSIONS: Regional anesthesia with local supplication remains the method of choice to select those patients who require a shunt during carotid surgery. It can be used routinely and it is less complex than the various methods.

Adult↗
PubMed1996

Coronary-coronary bypass graft: an arterial conduit-sparing procedure.

From May 1989 to December 1995, 143 patients underwent myocardial revascularization with one (138 patients) or two (five patients) coronary-coronary bypass grafts in addition to other bypass grafts, for a total of 463 distal anastomoses (mean 3.2 +/- 0.6 per patient). Coronary-coronary bypass grafts were chosen for the following reasons: arterial conduit-sparing procedure, inadequate length for in situ graft, calcified ascending aorta, and stenosed or occluded subclavian arteries. One hundred eleven arterial grafts (75%) were used: 85 right internal thoracic arteries, 18 left internal thoracic arteries, and eight radial arteries. Saphenous vein grafts were used in 37 cases (25%, mostly in our early experience). Coronary-coronary bypass grafts were performed on the right coronary artery in 134 cases (90.5%), on the circumflex artery in five cases (3.3%), on the left anterior descending coronary artery in four cases (2.7%), and between two different coronary arteries in five cases (3.3%). Three patients (2%) died of myocardial infarction. Early postoperative angiography showed a patency rate of 98.6% (72/73). During the mean follow-up of 34.6 +/- 20.8 months, two patients died and two underwent reoperation. Results of exercise testing were normal at 2 months in 97% of patients (90/92), at 1 year in 96% (81/84), and at 3 years in 93% (30/32). In conclusion, the coronary-coronary bypass graft provides good results with a variety of conduits and allows the expanded use of arterial grafts, particularly the internal thoracic artery. This can lead to a sparing of arterial conduit and allow complex myocardial revascularization with a liberal use of internal thoracic arteries.

Adult↗
PubMed1994

Experimental study of determinants of aneurysmal expansion of the abdominal aorta.

The natural history and the factors determining the expansion of aneurysms have not been elucidated. To study the respective roles of elastolysis, collagenolysis, inflammatory cells, and hypertension in the pathogenesis of aneurysms, two previously described in vivo experimental models were used. An isolated segment of the abdominal aorta was infused with 15 units of pancreatic elastase. The maximal diameter of the aorta was measured before and after infusion and the isolated aorta was excised for classic histologic and immunohistologic studies. Twelve hours after the infusion of elastase the mean diameter of the aorta increased by 30%. The aorta had a cylindric form and only collagen fibers remained. Two and a half days after the infusion the aorta was spherical in shape and the diameter increased by 300% (3.09 +/- 0.08 mm) (p < 0.05). The entire aortic wall was invested by inflammatory cells. Six days after infusion the diameter increased by 421% (4.38 +/- 0.03 mm) (p < 0.05), and immunohistochemical staining showed numerous T lymphocytes and macrophages. Between 6 and 12 days, after perfusion inflammation decreased, the final diameter was 4.23 +/- 0.14 mm (not significant). Sixteen rats had thioglycollate and plasmin infusion, which are nonspecific activators of inflammation. Nine days after infusion the diameter of the aorta had increased by 288%; the elastic fibers of the media were fragmented and rare and the entire aortic wall was invaded by inflammatory cells, predominantly macrophages. The diameter of the aorta increased progressively. Two groups of 17 hypertensive rats (renovascular and spontaneous hypertension) received an aortic infusion of 15 units of pancreatic elastase. Elastolysis overlapped the limits of the infusion and inflammation persisted after 2 weeks. The mean diameter of the aorta (F = 11, p < 0.01) and the mean length of the aneurysms (F = 11.2, p < 0.001) were significantly increased. This study demonstrates that elastolysis and especially collagenolysis are determinants of aneurysmal expansion. Inflammation may be a promoting factor in the degradation of the aortic wall. Hypertension increases the hemodynamic stress to the aorta and activates mural inflammation.

Animals↗
PubMed1992

Pathogenesis of acquired aneurysms of the abdominal aorta.

The incidence of abdominal aortic aneurysm has recently increased. There is still no accurate definition of abdominal aortic aneurysm. The diameter of abdominal aortic aneurysms is the only factor permitting evaluation of the risk of rupture of aneurysms whose growth remains unpredictable. Abdominal aortic aneurysm is a multi-factorial disease associated with aortic aging and atheroma. It differs from stenotic disease by the intensity of degenerative or destructive phenomena in the media. Particular hemodynamic conditions in the infrarenal abdominal aorta seem to enhance the development of aneurysm at this level. While certain constitutional anomalies of the extracellular matrix of proteins seem to enhance the development of abdominal aortic aneurysm, protease activity of as yet undetermined origin also seems to play a prominent role. Family cases of abdominal aortic aneurysms have been reported but the mechanisms responsible remain to be determined. Several genetic markers have been suggested. The most reliable marker of aortic aneurysm is arteriomegaly.

Aorta, Abdominal↗
PubMed1992

Correlation of inflammatory infiltrate with the enlargement of experimental aortic aneurysms.

Inflammatory cells often are seen in the walls of human aortic aneurysms, but their significance is uncertain. To investigate their actions an in vivo model of arterial aneurysms was developed in the rat. Fifteen units of hog pancreatic elastase were infused for 2 hours into the isolated abdominal aorta in 26 rats. The vessels were measured in vivo and were excised for conventional histologic and immunohistologic study at selected intervals. In untreated control rats the diameter of the aorta was 1.04 +/- 0.02 mm. Immediately after infusion with elastase the aorta dilated 26% to 1.31 +/- 0.02 mm (p = NS), with no histologically demonstrable remaining elastic lamellae. Two and one half days after infusion the aorta dilated nearly 300% to 3.09 +/- 0.08 mm (p less than 0.05). These vessels exhibited large numbers of activated macrophages and T cells in the media. Three and 4 days after infusion the vessels dilated 388% to 4.04 +/- 0.09 mm and 367% to 3.82 +/- 0.31 mm, respectively. These vessels also exhibited numerous inflammatory cells in the media. Six days after infusion the vessels enlarged 421% to 4.38 +/- 0.03 mm (p less than 0.05), and the infiltrate persisted staining immunohistologically for macrophages, polymorphic neutrophils, and T lymphocytes. Twelve days after infusion the aneurysms remained enlarged but stable at 4.23 +/- 0.14 mm (p = NS). At this time the number of inflammatory cells regressed to control levels. The temporal correlation between inflammatory infiltrate and aneurysmal enlargement suggests that inflammatory cells may participate in the destruction of the aneurysmal vessel wall thereby promoting progressive enlargement.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1992

Arterial hypertension and aneurysmal dilatation.

Hemodynamic parameters and especially systemic hypertension are considered to be significant factors in the progression of aortic aneurysmal dilatation. We have recently described an original experimental model of aortic aneurysm induced by transparietal infusion of elastase in the rat abdominal aorta. In order to evaluate the effect of hypertension on the aneurysmal remodeling of the arterial wall induced by perfusion of elastase activity, this experimental model was applied to renovascular hypertensive (N = 17), spontaneously hypertensive (N = 18) and normotensive rats (N = 17). The aneurysms were induced by infusion of 15 units of hog pancreatic elastase of a one centimeter isolated aortic segment in anesthetized rats which were sacrificed two weeks later. The aneurysmal length and diameter were measured in vivo using a micrometer in a surgical microscope. The aortas were then fixed in formalin and embedded in paraffin for standard histological study. The animals which died during the experimental period were examined. All rats presented a macroscopic aneurysm two weeks after the infusion of elastase. Histologically, the aneurysmal area was characterized by the disappearance of the normal elastic network and by the presence of a collagenic wall. The dimensions of the aneurysms (transversal diameter and length) were greater in hypertensive than in normotensive animals (F = 11, P less than 0.001) and aneurysmal dimensions were positively correlated with the level of blood pressure (r = 0.56, P less than 0.001). Moreover, the frequency of aortic rupture was greater in renovascular hypertensive (4/17) than in spontaneously hypertensive (1/18) and normotensive (0/17) rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

[Acquired aneurysms of the infrarenal abdominal aorta].

Abdominal aortic aneurysms (AAA) are the result of a degenerative process of the aortic wall. The incidence of AAA has increased during the last three decades. Computerized axial tomography is the best method for investigating AAA. For aneurysms of 4-5 cm or more in antero-posterior diameter, the risk of rupture is definitely high and justifies a preventive surgery. Precise evaluation of myocardial function and of coronary circulation may limit the operative risk and may improve the life expectancy. Screening of AAA in populations at risk will allow to survey the natural history of aneurysmal disease and limit the incidence of rupture which keeps a high mortality rate.

Age Factors↗
PubMed1991

[Pathogenesis of acquired abdominal aortic aneurysms].

Abdominal aortic aneurysms are the result of a destructive process of the aortic media. The incidence of abdominal aortic aneurysms is increasing but the reasons remain unknown. The mechanical and structural characteristics of the abdominal aorta explain the frequency of acquired aneurysms at this location. Classically, atherosclerosis is the main etiologic factor, but the abdominal aortic aneurysm is distinguishable from the aged aorta and occlusive atherosclerotic disease by the apparent absence of a reparative process. Some authors have tried to differentiate aneurysmal disease from occlusive atherosclerotic disease. Atherosclerosis could lead to plaque and stenosis or, in some unknown circumstances, to atrophy of the media and aneurysmal dilation. Proteolytic enzymes within the aortic wall play an important role in the destruction of the extracellular matrix of the aortic wall. Plasmin could locally worsen the proteolysis. Inflammatory cells might be responsible for these proteolytic activities. Calcium could play a role in the activation of inflammatory cells. Genetic markers and familial grouping have been reported by several authors. The discovery of constitutional or acquired factors that could lead to activation of degradative phenomena within the aortic wall will facilitate the identification of patients at risk, and improve screening of asymptomatic aneurysms.

Aneurysm↗
PubMed1991

Pathophysiology of arterial aneurysms.

Studies were performed to evaluate the contributions of elastin and collagen to the formation of arterial aneurysms. Dog carotid arteries and human external and internal iliac arteries were excised, mounted horizontally in a tissue bath, and were pressurized. Vessel diameter and longitudinal force were measured. the vessels were treated with elastase or collagenase. Those treated with elastase dilated, but never ruptured. Those treated with collagenase dilated still more and, in every case, ruptured. Circumferential stability resulted from recruitment of previously non-loaded collagen fibers, and from a change in geometry from a cylinder to a sphere. The laminated thrombus lining the lumen has little intrinsic strength and therefore does not confer strength to the aneurysmal wall. Treatment with elastase also reduces the retractive force exerted by the vessel in the longitudinal direction. Therefore loss of elastin permits the vessel to elongate and to become tortuous. In aged human arteries collagen also contributes a small portion of the retractive force. Progressive enlargement of aneurysms results from continued failure of wall connective tissues reflecting a) genetically defective collagen and or b) activity of the immune system.

Aneurysm↗
PubMed1990

Elastase-induced experimental aneurysms in rats.

An experimental in vivo model of aortic aneurysm was established by perfusing an isolated segment of rat abdominal aorta with pancreatic elastase. Ten rats were used in each protocol. Saline-perfused aortas developed no aneurysmal dilations. Elastase-perfused aortas contained aneurysms in the perfused area and a total loss of elastic tissue. Control aortas contained no elastic tissue lesions. There was a quantitative relation between the amount of elastase perfused and aneurysm formation: 1-2 units induced neither macroscopic nor microscopic lesions; 3-6 units induced microscopic elastic tissue damage without macroscopic aneurysm; and more than 6 units produced aneurysmal dilation in all cases. In situ elastase secretion by macrophages was induced by perfusing rat aortas with thioglycollate-activated macrophages or with thioglycollate alone. There was aortitis without true aneurysm and a total loss of elastic tissue in the vicinity of activated macrophages within the aortic media. Perfusion of infra-aneurysmal amount of elastase (1 or 2 units) or thioglycollate plus plasmin (2 units) always induced a large aneurysm, whereas plasmin alone induced neither macroscopic nor microscopic lesions. These morphological results were supported by the significantly elevated elastolytic activity within the aortic wall of animals perfused with thioglycollate plus plasmin 9 days, after perfusion (207.6 +/- 54.8 micrograms elastin-rhodamine lysed/18 hr; control rats, 25.43 +/- 11.13). The results suggest that the presence of elastase within the aortic media leads to aneurysm formation. Activated macrophages within the aortic media may be responsible for elastase secretion and elastic tissue destruction. Plasmin may enhance elastase activity and aggravate the aneurysmal lesion.

Animals↗
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

Endovascular grafting in elastase-induced experimental aortic aneurysms in dogs: feasibility and preliminary results.

PURPOSE: A new model of aortic aneurysm was developed in 12 beagles to study the feasibility of endoluminal exclusion of aortic aneurysms. MATERIALS AND METHODS: After preliminary experiments in four dogs, aneurysms were induced by infusing elastase into an isolated segment of the abdominal aorta in eight dogs. To create aortic endoprostheses, a Palmaz stent was sutured onto each end of an ultrathin Dacron tube. Endoprosthesis placement was performed under fluoroscopic and intravascular ultrasonographic (US) guidance. The endoprostheses were introduced via a femoral arteriotomy, through a 12-F sheath positioned in the aorta, and then were expanded on an angioplasty catheter. RESULTS: Intravascular US and aortography showed aneurysms in the elastase-perfused area in the eight animals and demonstrated the exclusion of the aneurysm by the endoprostheses in six cases. Intravascular US was more accurate than aortography in demonstrating two cases of endoprosthesis dysfunction. Aneurysm formation was proportional to the loss of elastic tissue observed at histologic examination of the elastase-infused area. Macro- and microscopic examinations confirmed thrombosis of the excluded part of the aneurysm and patency of all grafts. CONCLUSION: This model and intravascular US appear helpful in exploring the feasibility of endovascular treatment of abdominal aortic aneurysm.

Animals↗