Subsequent Aneurysm Formation Research Articles

Popliteal aneurysm presenting as acute thrombosis and ischemia in a middle-aged man with a history of Kawasaki disease

Kawasaki disease is known to cause a vasculitis of small and medium-sized vessels, with subsequent aneurysm formation. Most of the severe manifestations of the disease occur as a result of coronary aneurysm formation. However, many other arteries have been documented to be involved. A case is presented of a middle-aged man with a history of Kawasaki disease who had an acute ischemic limb from a thrombosed popliteal aneurysm that formed as a result of the disease. This is the first known case report of Kawasaki disease resulting in delayed lower extremity ischemia. Typical findings of patients with Kawasaki disease are presented, along with a case report and review of the literature. A history of Kawasaki disease is an extremely rare but possible cause of peripheral aneurysms, even in middle-aged patients. (J Vasc Surg 1997;26:884-7.)

Symptomatic brachial artery aneurysm in a child

The authors present the case of a 3-year-old boy who had transient ischemic symptoms secondary to thromboembolism from a left brachial artery aneurysm not associated with trauma or an autoimmune or connective tissue disorder. He underwent emergency resection of a brachial artery aneurysm and interposition grafting. Two months later he was found to have a right brachial artery aneurysm and underwent elective aneurysm resection and interposition grafting. He was well at the 3-year follow-up and had no other arterial aneurysms. The risk of limb threat or loss can be avoided by prompt diagnosis and early surgery. The authors advocate brachial artery aneurysm resection when it becomes technically feasible and/or when thrombus is present. Patients with upper extremity aneurysms should have continuous follow-up with serial examinations to detect concomitant or subsequent aneurysm formation.

Technical report: Aneurysm formation after dynamic catheter assisted balloon angioplasty

A male patient underwent recanalisation of a symptomatic popliteal artery occlusion using a dynamic angioplasty catheter, followed by balloon dilatation. A small subintimal dissection lead to an acute reocclusion. Repeat balloon angioplasty reopened the occlusion but was complicated by a distal embolus which was successfully treated by thrombolytic therapy followed by oral anticoagulation. Angiography 9 months later, demonstrated an aneurysm at the site of initial dissection. The artery remained patent and the patient free of claudication. A causal relationship between dynamic angioplasty and subsequent aneurysm formation is suggested and the possible predisposing factors discussed.

Late Results of Preferential Use of Tube Versus Bifurcation Grafts for Abdominal Aortic Aneurysmectomy

The advantages of tube versus bifurcation graft replacement of abdominal aortic aneurysms are well known, yet the risk of future development of iliac occlusive or aneurysmal disease still leads many to use bifurcation grafts routinely. Several studies have reported little risk of this development when patients are followed clinically. They suffer, however, from lack of an objective means of identifying iliac aneurysms. Among 83 patients undergoing abdominal aortic aneurysmectomy during a 53 month period, 36 who had received a tube graft were available for follow-up. After a mean of 54 months from the time of surgery, these patients were evaluated by abdominal and pelvic computed tomography to determine the incidence of subsequent iliac aneurysm formation. No patient had developed symptoms or signs of iliac occlusive disease during this interval. In addition, no residual aortic aneurysms or new iliac aneurysms were noted. In the absence of iliac occlusive or aneurysmal disease, straight graft replacement is the preferred therapy for abdominal aortic aneurysms. The risk of future development of these lesions is minimal.

Influences of laser pulse duration and anastomotic disruption on laser‐assisted microvascular anastomoses (LAMA)

The success rate of laser-assisted microvascular anastomosis (LAMA) can be influenced by many factors, including the parameters of the laser technique used. This study examined the effects of laser pulse duration and the occurrence of anastomotic disruption immediately following first repair attempts on the incidence of aneurysm formation and the patency rate in LAMA. Fifty transected rat femoral arteries in 25 rats were anastomosed with three stay sutures and welded with a CO2 laser at a power of 80 mW. In each rat, the laser was applied in the form of 45 pulses of 0.2 sec duration to one femoral artery (group 1) and in the form of 15 pulses of 0.6 sec duration to the contralateral femoral artery (group 2). Comparison of group 1 with group 2 showed that overall rates of aneurysm formation (30% vs. 17%) and patency rates (92% vs. 96%) did not differ significantly (P less than 0.05) at 3 weeks postoperatively. However, disrupted vessels in both groups had a significantly higher incidence of subsequent aneurysm formation than nondisrupted vessels (54% vs. 0% in group 1, P less than 0.05; 43% vs. 6% in group 2, P less than 0.06; groups 1 and 2 pooled, P less than 0.001). These findings indicate that changes in laser pulse duration such as those tested do not affect the aneurysm and patency rates of LAMA. The results demonstrate, however, that disruption after laser welding plays a significant role in subsequent aneurysm formation.

Aneurysm of the rabbit common carotid artery induced by periarterial application of calcium chloride in vivo.

Experimental aneurysmatic dilatation of the rabbit common carotid artery was induced by a single, periarterial application of calcium chloride in vivo. Vessels were fixed in situ after 3 d, 1 wk, 3 wk, 6 wk, and 12 wk by intracardiac perfusion of glutaraldehyde and tissues prepared for light, scanning, and transmission electron microscopy. Progressive focal aneurysmal dilatation was seen limited to the site of calcium application with endothelial damage and thrombus formation in areas of irregular luminal contour. Disruption of the elastic network of the intima and media was seen with varying degrees of intimal fibromuscular hyperplasia and medial disorganization. The calcium-elastic tissue complex was the focus of the inflammatory, arteriosclerotic reaction and subsequent aneurysm formation. The inflammatory cell infiltration initially included primarily neutrophils followed by lymphocytes, plasma cells, monocytes, and multinucleated giant cells. These studies support the hypothesis that disruption of the elastic tissue network of the vascular wall represents an important pathogenetic factor in the initiation of aneurysmal dilatation. In addition, the results of these studies suggest that interaction of calcium with the elastica of the arterial wall may represent an important pathogenetic factor in the initiation of giant cell arteritis.

Differential effects of Nd-YAG laser on collagen and elastin production by chick embryo aortae [formula omitted]: Relevance to laser angioplasty for removal of atherosclerotic plaques

Aortae from 17-day old chick embryos were subjected to irradiation with a Nd:YAG laser at energy densities varying from 1.2 – 4.7 × 10 3 J/cm 2. The aortae were pulse-labeled in vitro with [ 3H]proline or [ 14C]valine, and the synthesis of collagenous polypeptides and soluble elastin was examined by SDS-polyacrylamide gel electrophoresis, followed by fluorography and quantitative scanning densitometry. Irradiation of the aortae with Nd:YAG laser resulted in inhibition of the synthesis of the extracellular matrix proteins. The production of collagen was inhibited to a considerably larger degree than the production of elastin. Thus, the biosynthetic pathway for collagen production appears to be more susceptible to laser inhibition than the corresponding pathway for elastin production. These observations may have relevance to laser angioplasty which has been proposed to be applicable for removal of atherosclerotic plaques in human vessels. Specifically, the results suggest that inhibition of the extracellular matrix production may result in weakening of the vessel wall with subsequent aneurysm formation and rupture.

Anterior uveitis associated with Kawasaki syndrome

Forty-one children with a clinical diagnosis of Kawasaki syndrome had a pediatric ophthalmologic examination performed at a mean time of 8.6 days after onset of fever. Twenty-seven of 41 patients (66%) had evidence of anterior uveitis by slit lamp examination. Bilateral involvement was noted in 25 of 27 patients (97%). Punctate keratitis was evident in 5 of 41 patients (12%). Three of these five had coexisting uveitis. The incidence of anterior uveitis in patients examined during the first week of their illness was 83% (20 of 24 patients), compared to an incidence of 41% (7 of 17) in patients first examined greater than 1 week after onset of disease (P = 0.004). There was no difference in the uveitis, vs. the non-uveitis groups with respect to age, sex, race or subsequent aneurysm formation as a complication of their Kawasaki syndrome. The mean erythrocyte sedimentation rate was not different in the two groups. Anterior uveitis is a common finding early in the course of Kawasaki syndrome. Slit lamp examination may be a helpful clinical tool in identifying patients with Kawasaki syndrome, and uveitis should be considered for inclusion in the Centers for Disease Control case definition of Kawasaki syndrome.

A new serum proteolytic enzyme in aneurysm pathogenesis.

Despite significant progress in elucidating the pathogenesis of aneurysmal disease, the precise etiology of arterial wall degradation remains unclear. Numerous etiologies have been implicated, including stress-strain factors, structural wall abnormalities, and enzyme imbalance. We have previously shown that collagenase and elastase are increased in aortic aneurysm tissue. Herein we report and characterize a newly described serum compound that is able to hydrolyze an artificial elastase substrate but is not elastase. This substance is elevated in patients with atherosclerotic disease and, following aneurysmectomy, its concentration increases by threefold. Examination of the substance reveals that it is bound to lipid and consists of four subunits of molecular weights: 310,000, 62,000, 40,000, and 10,000 daltons. It has characteristics of thiol, carboxyl, and metalloenzymes and is most active at a pH of 7.0 to 8.0. A relationship between this serum compound and aneurysm tissue enzymatic activity is noted. We postulate that this serum compound may be produced by mononuclear cells and released into the serum. Furthermore, monocytes may enter the arterial wall intima and release this substance, resulting in proteolytic arterial wall degradation and subsequent aneurysm formation.

A new serum proteolytic enzyme in aneurysm pathogenesis

Despite significant progress in elucidating the pathogenesis of aneurysmal disease, the precise etiology of arterial wall degradation remains unclear. Numerous etiologies have been implicated, including stress-strain factors, structural wall abnormalities, and enzyme imbalance. We have previously shown that collagenase and elastase are increased in aortic aneurysm tissue. Herein we report and characterize a newly described serum compound that is able to hydrolyze an artificial elastase substrate but is not elastase. This substance is elevated in patients with atherosclerotic disease and, following aneurysmectomy, its concentration increases by threefold. Examination of the substance reveals that it is bound to lipid and consists of four subunits of molecular weights: 310,000, 62,000, 40,000, and 10,000 daltons. It has characteristics of thiol, carboxyl, and metalloenzymes and is most active at a pH of 7.0 to 8.0. A relationship between this serum compound and aneurysm tissue enzymatic activity is noted. We postulate that this serum compound may be produced by mononuclear cells and released into the serum. Furthermore, monocytes may enter the arterial wall intima and release this substance, resulting in proteolytic arterial wall degradation and subsequent aneurysm formation.

Aortic laceration due to rapid deceleration.

Progressively increasing numbers of motor vehicles on the high-ways are resulting in an ever-enlarging number of accident victims with a wide variety of injuries. As these vehicles have become faster and faster, the rapid deceleration type of accident is occurring with increasing frequency. A similar type of injury often accompanies aircraft crashes. Of particular importance in many such accidents is the possibility of potentially fatal damage to the thoracic aorta. 1-5 These rapid deceleration injuries to the thoracic aorta vary from intimal tears, which may progress to dissection and occlusion of the lumen or subsequent aneurysm formation, all the way to partial or complete transection of the aorta. Although the majority of patients with partial to complete transection of aorta die immediately, some 10% to 20% survive long enough to reach the hospital and can be salvaged if the true extent of the injury is recognized rapidly and repaired expeditiously. 2,4

MULTIPLE INTRAPARENCHYMAL RENAL ANEURYSMS IN POLYARTERITIS NODOSA.

Polyarteritis nodosa is a widespread disease, characterized by a focal necrotizing inflammation of the vessel walls. It primarily affects arteries of medium and small size. Renal involvement is reported in roughly 80 per cent of the cases (1), and the kidney is the most frequent organ affected. It is the purpose of this paper to document for the first time the in vivo demonstration of multiple intraparenchymal renal aneurysms occurring in this disease. Pathology The microscopic pathological changes of polyarteritis nodosa can be divided into stages, one or all of which can be observed at necropsy (9). Initially, mucoid degeneration and acute fibrinoid necrosis begin in the media, subsequently extending into the other layers. Infiltration of neutrophils and later by eosinophils then occurs, associated with destruction of the elastic lamina and subsequent aneurysm formation. The acute cellular infiltration subsides with the appearance of chronic inflammatory cells, but the prominent part of the next phase is marked proliferation of connective tissue which replaces areas of destroyed intima and media. This can lead to the characteristic nodularity. If thrombosis hasn't already occurred it does so at this time, leaving a vessel that now resembles a fibrous cord. Any of the vessels of the kidney may be involved, but the arcuate and interlobular arteries and arterioles are affected the most frequently. Thus, multiple small infarcts of the kidney are a prominent feature. The scarring which results is responsible for the irregular renal contour so frequently noted on gross examination. The glomeruli are also abnormal in most patients. The healed glomerulitis and vasculitis seem to be prominent features associated with the production of hypertension in polyarteritis nodosa (10). Aneurysm formation in the parenchymal vessels, although virtually pathognomonic of polyarteritis, is a rather uncommon pathologic finding. Ralston and Kvale (7) in reviewing 30 cases from the Mayo Clinic did not find a single instance of renal artery or arteriolar aneurysm. Davson (1), however, discovered at autopsy 4 cases of intrarenal aneurysms, in a series of 14 of polyarteritis. A review of the renal pathology in 32 autopsied cases of polyarteritis at the Columbia-Presbyterian Medical Center disclosed that in only 1 were gross or microscopic intrarenal artery aneurysms found. Death in this instance was precipitated by rupture of one of the aneurysms, renal rupture, and retroperitoneal hemorrhage. This complication of polyarteritis is well recognized, and over 30 cases describing this morbid sequence of events have appeared in the literature (4, 6, 11). Patients in this group are invariably males in the third or fourth decade, often hypertensive, who present with flank pain and a palpable mass. Most will die of retroperitoneal hemorrhage, with polyarteritis diagnosed at autopsy.