Biomedical subjects

Randolph L Geary

Publications and source records attributed to Randolph L Geary.

16 recordsLinked to original sources

PubMed2006

Distal embolic protection during renal artery angioplasty and stenting.

BACKGROUND: Percutaneous renal artery angioplasty and/or stenting (RA-PTAS) is increasingly being used as an alternative to surgery for renal artery revascularization. Unfortunately, renal function responses after RA-PTAS appear to be inferior to those observed after surgical revascularization both in terms of improving and preventing deterioration of renal function postintervention. Atheroembolism during RA-PTAS has been postulated as a potential cause for the disparate results. Strategies to limit the occurrence of atheroembolism, such as the use of distal embolic protection (DEP) systems, may result in improved outcomes after RA-PTAS. METHODS: All RA-PTAS procedures performed with DEP (using a commercially available temporary balloon occlusion and aspiration catheter) between October 2003 and July 2005 were reviewed. Glomerular filtration rate (eGFR) was estimated preintervention and 4 to 6 weeks postintervention using the abbreviated Modification of Diet in Renal Disease formula. Renal function and hypertension response rates as well as procedural data were classified and reported according to American Heart Association guidelines. Renal function improvement and deterioration were defined as a 20% increase and decrease in eGFR, respectively, compared with preoperative values. Continuous and categoric data were analyzed using paired t tests and repeated measures linear models. RESULTS: DEP was used in 32 RA-PTAS procedures in 15 women and 11 men with a mean age of 71 years. All patients were hypertensive, 24 (92%) had renal insufficiency, and the mean preintervention degree of renal artery stenosis was 79%. Immediate technical success was achieved in 100% of RA-PTAS cases. Mean pre- and postintervention serum creatinine and eGFR values were 1.9 vs 1.6 mg/dL (P < .001) and 37 vs 43 mL/min/1.73 m(2) (P < .001), respectively. Renal function was defined as improved after 17 (53%) of 32 procedures and worsened in none (0%). CONCLUSIONS: RA-PTAS using DEP resulted in 4- to 6-week postintervention renal function results approximating those of surgical revascularization. These data suggest that DEP use may prevent renal function harm during RA-PTAS as a result of atheroembolism and warrant further investigation.

Aged↗

PubMed2006

Acute pancreatitis: A complication associated with rheolytic mechanical thrombectomy of deep venous thrombosis.

Percutaneous mechanical rheolytic thrombectomy is increasingly being used for the treatment of arterial, venous, and graft thromboses. We describe three cases of pancreatitis as a complication of mechanical rheolytic thrombectomy used in the treatment of caval and ileofemoral deep venous thrombosis and discuss the possible etiologic factors involved. To our knowledge, this complication has been previously reported in only two cases.

Adult↗

PubMed2005

Expression profiling identifies smooth muscle cell diversity within human intima and plaque fibrous cap: loss of RGS5 distinguishes the cap.

BACKGROUND: The fibrous cap of the atherosclerotic lesion is believed to be critical to stability because disruption of the cap is the final event leading to plaque rupture. We have, therefore, used expression arrays to define the phenotype of the cap and other plaque components. METHODS AND RESULTS: To identify unique expression programs able to distinguish the smooth muscle of the cap from other plaque smooth muscle cells, RNA profiles were determined in human carotid artery media, nonatherosclerotic adjacent intima, fibrous cap of advanced atherosclerotic plaques, and whole advanced plaque with cDNA arrays covering 21,000 or 26,000 Unigene clusters. The molecular signature of each tissue was dominated by a core gene-set with differential expression of <1% of clusters assayed. CONCLUSIONS: Both intima and cap expressed novel genes not previously associated with SMC pathology. If the cap is derived from a unique subpopulation, this pattern is the signature of that particular set of cells. The loss of RGS5 in the fibrous cap is of particular interest because of its role in vessel development and physiology.

Carotid Arteries↗

PubMed2005

Angiotensin II AT1 receptors regulate ACE2 and angiotensin-(1-7) expression in the aorta of spontaneously hypertensive rats.

When increased in vascular tissues, angiotensin-converting enzyme 2 (ACE2), a carboxypeptidase that hydrolyzes angiotensin II to angiotensin-(1-7), may augment the growth inhibitory and vasodilatory effects of the heptapeptide. We investigated the regulation of ACE2 and angiotensin-(1-7) expression in aortas and carotid arteries of 12-wk-old male spontaneously hypertensive rats (SHR) by determining the effect of sustained angiotensin type 1 (AT(1)) receptor blockade with olmesartan (10 mg.kg(-1).day(-1), n = 13) compared with those that received atenolol (30 mg.kg(-1).day(-1), n = 13), hydralazine (10 mg.kg(-1).day(-1), n = 13), or vehicle (n = 21). Systolic blood pressures were approximately 30% lower (P < 0.05) in rats treated for 2 wk with olmesartan compared with vehicle-treated rats. Both atenolol and hydralazine produced similar decreases in systolic blood pressure. ACE2 mRNA in the thoracic aorta of olmesartan-treated rats (n = 8) was fivefold greater (P < 0.05) than that in vehicle-treated rats (n = 16), whereas atenolol (n = 8) or hydralazine (n = 8) had no effect. Immunostaining intensities in rats treated with olmesartan (n = 5) were also associated with increased (P < 0.05) ACE2 and angiotensin-(1-7) in thoracic aorta media compared with vehicle-treated rats. In contrast, immunostaining intensities for both ACE2 and angiotensin-(1-7) were not different from vehicle (n = 5) in carotid arteries of SHR medicated with either atenolol (n = 5) or hydralazine (n = 5). A comparison of vessel wall dimensions showed that olmesartan selectively reduced the thoracic aorta media-to-lumen ratio (P < 0.05) and media thickness (P < 0.05) without an effect on carotid artery morphometry. Compared with vehicle-treated SHR, vascular hypertrophy determined from media and lumen measurements was not changed in SHR given either atenolol or hydralazine. These data represent the first report of ACE2 and angiotensin-(1-7) expression in the aorta and carotid arteries of SHR. Increased ACE2 and angiotensin-(1-7) in association with altered dimensions of the thoracic aorta but not carotid arteries in response to olmesartan treatment provides evidence that this pathway is regulated by AT(1) receptors and may be important in mediating the pressure-independent vascular remodeling effects of angiotensin peptides.

Adrenergic beta-Antagonists↗

PubMed2004

The myeloperoxidase product hypochlorous acid oxidizes HDL in the human artery wall and impairs ABCA1-dependent cholesterol transport.

Although oxidatively damaged lipoproteins are implicated in vascular injury, there is little information regarding the role of high-density lipoprotein (HDL) oxidation in atherogenesis. One potential pathway involves hypochlorous acid (HOCl) produced by myeloperoxidase (MPO), a heme protein secreted by phagocytes. We previously showed that 3-chlorotyrosine is a specific product of HOCl. Therefore, to explore the role of oxidized HDL in the pathogenesis of vascular disease, we used MS to quantify 3-chlorotyrosine in HDL isolated from plasma and atherosclerotic tissue. HDL from human aortic atherosclerotic intima had an 8-fold higher level of 3-chlorotyrosine than plasma HDL. Tandem MS analysis identified MPO as a component of lesion HDL, suggesting that the two interact in the artery wall. Moreover, immunohistochemical studies found that specific epitopes derived from HOCl colocalized with apolipoprotein A-I, the major protein of HDL. These observations strongly support the hypothesis that MPO promotes HDL oxidation in the human artery wall. Levels of 3-chlorotyrosine were elevated in HDL isolated from the blood of humans with established coronary artery disease, suggesting that circulating levels of oxidized HDL represent a unique marker for clinically significant atherosclerosis. HDL or lipid-free apolipoprotein A-I exposed to HOCl was less able to remove cholesterol from cultured cells by a pathway requiring the cell membrane transporter ATP-binding cassette transporter A1. The detection of 3-chlorotyrosine in HDL isolated from vascular lesions raises the possibility that MPO, by virtue of its ability to form HOCl, may promote atherogenesis by counteracting the established antiatherogenic effects of HDL and the ATP-binding cassette transporter A1 pathway.

ATP Binding Cassette Transporter 1↗

PubMed2004

Human atherosclerotic intima and blood of patients with established coronary artery disease contain high density lipoprotein damaged by reactive nitrogen species.

High density lipoprotein (HDL) is the major carrier of lipid hydroperoxides in plasma, but it is not yet established whether HDL proteins are damaged by reactive nitrogen species in the circulation or artery wall. One pathway that generates such species involves myeloperoxidase (MPO), a major constituent of artery wall macrophages. Another pathway involves peroxynitrite, a potent oxidant generated in the reaction of nitric oxide with superoxide. Both MPO and peroxynitrite produce 3-nitrotyrosine in vitro. To investigate the involvement of reactive nitrogen species in atherogenesis, we quantified 3-nitrotyrosine levels in HDL in vivo. The mean level of 3-nitrotyrosine in HDL isolated from human aortic atherosclerotic intima was 6-fold higher (619 +/- 178 micromol/mol Tyr) than that in circulating HDL (104 +/- 11 micromol/mol Tyr; p < 0.01). Immunohistochemical studies demonstrated striking colocalization of MPO with epitopes reactive with an antibody to 3-nitrotyrosine. However, there was no significant correlation between the levels of 3-chlorotyrosine, a specific product of MPO, and those of 3-nitrotyrosine in lesion HDL. We also detected 3-nitrotyrosine in circulating HDL, and linear regression analysis demonstrated a strong correlation between the levels of 3-chlorotyrosine and levels of 3-nitrotyrosine. These observations suggest that MPO promotes the formation of 3-chlorotyrosine and 3-nitrotyrosine in circulating HDL but that other pathways also produce 3-nitrotyrosine in atherosclerotic tissue. Levels of HDL isolated from plasma of patients with established coronary artery disease contained twice as much 3-nitrotyrosine as HDL from plasma of healthy subjects, suggesting that nitrated HDL might be a marker for clinically significant vascular disease. The detection of 3-nitrotyrosine in HDL raises the possibility that reactive nitrogen species derived from nitric oxide might promote atherogenesis. Thus, nitrated HDL might represent a previously unsuspected link between nitrosative stress, atherosclerosis, and inflammation.

Arteries↗

PubMed2004

Surgical management of renal artery aneurysms.

PURPOSE: This retrospective review describes the surgical management and clinical outcome for renal artery aneurysms (RAAs) in 62 consecutive patients. METHODS: From January 1987 through July 2003, 804 patients had operative renal artery (RA) repair involving 1206 kidneys at our center. A subgroup of 62 patients (42 women, 20 men; mean age 46 +/- 18 years) received repair of 72 RAAs. Demographic data, comorbidity, and surgical technique were examined. Blood pressure and renal function response were determined. Patency of repair was evaluated by renal duplex sonography. Primary patency and patient survival were estimated by life-table methods. Tests of association were performed using chi(2) and the Student t tests. RESULTS: Seventy-two RAs were repaired for RAA with a mean diameter of 2.6 cm (range, 1.3 to 5.5 cm). Bilateral RAAs were present in 21 patients. Associated conditions included fibromuscular dysplasia, atherosclerosis, and arteritis in 54%, 35%, and 7%, respectively. Hypertension was present in 89% (mean blood pressure, 171 +/- 35/95 +/- 19 mm Hg; mean medications, 2.2 +/- 1.2 drugs) and renal insufficiency was present in 8% (mean serum creatinine, 1.9 +/- 0.6 mg/dL). RAA repair included bypass (67%), aneurysmorrhaphy (15%), or a combination (17%). One planned nephrectomy (1%) was performed for un-reconstructable disease. Branch RA reconstruction in 78% used ex vivo cold perfusion in 50%, in situ cold perfusion in 29%, and warm in situ repair in 21%. Of 9 bilateral RAA repairs, 7 (78%) were staged and 2 (22%) were simultaneous. Combined aortic reconstruction was required in 6 (10%) patients. Perioperative death occurred in 1 patient (1.6%), and significant morbidity was observed in 8 patients (12%). Hypertension was considered improved in 54%, cured in 21%, and unchanged in 25% at mean follow-up of 48 months (range, 1-156 months). Among patients with renal insufficiency, renal function was improved in 3 (60%), unchanged in 1 (20%), and declined in 1 (20%). Follow-up patency (mean, 33 months; range, 1-118 months) was determined for 64 (91%) RA reconstructions. Product-limit estimate of primary patency at 48 months was 96%. Product-limit estimate of survival was 91% at 120 months. CONCLUSION: RAAs were repaired with low morbidity and mortality. Complex branch RAA repair using cold perfusion preservation and ex vivo techniques resulted in no unplanned nephrectomy, with an estimated primary patency of 96% at 48 months. Beneficial blood pressure response was observed in the majority of hypertensive patients. These results support selective surgical management of RAA.

Adult↗

PubMed2004

Regulator of G protein signaling 5 marks peripheral arterial smooth muscle cells and is downregulated in atherosclerotic plaque.

OBJECTIVE: Regulator of G protein signaling 5 (RGS5), an inhibitor of Galpha(q) and Galpha(i) activation, was recently identified among genes highly expressed in smooth muscle cells (SMCs) of aorta but not vena cava. This finding prompted the hypothesis that RGS5 provides long-term G protein inhibition specific to normal arterial SMC populations and that loss of expression may in turn contribute to arterial disease. METHODS: To test this hypothesis we characterized RGS5 gene expression throughout the vasculature of nonhuman primates to determine whether RGS5 was restricted to arteries in other vascular beds and whether expression was altered in arterial disease. RESULTS: In situ hybridization localized RGS5 message to medial SMCs of peripheral arteries, including carotid, iliac, mammary, and renal arteries, but not accompanying veins. SMCs of many small arteries and arterioles also expressed RGS5, including glomerular afferent arterioles critical to blood pressure regulation. Differential expression persisted in culture, inasmuch as RGS5 message was significantly higher in SMCs derived from arteries than from veins at real-time polymerase chain reaction. It was remarkable that the only major arterial bed lacking RGS5 was the coronary circulation. In atherosclerotic peripheral arteries RGS5 was expressed in medial SMCs, but was sharply downregulated in plaque SMCs. CONCLUSION: These data identify RGS5 as a new member of a short list of genes uniquely expressed in peripheral arteries but not coronary arteries. Persistence of an arterial pattern of RGS5 expression in culture and lack of expression in coronary arteries support a unique SMC phenotype fixed by distinct lineage or differentiation pathways. The association between loss of expression and arterial wall disease has prompted the new hypothesis that prolonged inhibition by RGS5 of vasoactive or trophic G protein signaling is critical to normal peripheral artery function.

Animals↗

PubMed2004

Differential effects of Rho-kinase inhibition on artery wall mass and remodeling.

PURPOSE: Constrictive remodeling and new artery wall mass contribute to lumen narrowing in atherosclerosis and following injury. Rho-kinase, an important regulator of myosin phosphorylation and cytoskeletal reorganization, is critical to smooth muscle cell (SMC) growth and vasoconstriction, but its role in artery wall remodeling is poorly defined. We hypothesized that constrictive artery wall remodeling is dependent on Rho signaling so that blocking Rho-kinase would promote outward artery wall remodeling in response to intimal hyperplasia and thus limit lumen narrowing. METHODS: To test this hypothesis, we first studied the effects of the Rho-kinase inhibitor fasudil on SMC remodeling of collagen matrix in vitro. Mouse aortic SMCs were seeded into three-dimensional collagen gels with and without fasudil, and extent of contraction was measured at 24 hours. We then used the mouse carotid ligation model to study the effects of Rho-kinase inhibition on remodeling and intimal hyperplasia in vivo. C57B6/J mice were randomly assigned to fasudil (100 mg/kg per day) or vehicle and underwent unilateral carotid artery ligation or sham ligation. Remodeling and wall mass were measured after 28 days. RESULTS: Fasudil blocked SMC contraction of collagen gels in a dose-dependent manner. Complete inhibition of collagen gel remodeling was achieved between 10 and 30 micromol/L fasudil. In control mice, carotid ligation caused significant thickening of the adventitia, media, and intima (P <.01) and outward remodeling of the carotid wall. The external elastic lamina (EEL) area increased by 14% versus sham (P <.05), but this increase was insufficient to prevent lumen narrowing (-42% vs sham, P <.05). Fasudil treatment had favorable effects on wall mass, inhibiting neointimal (P =.04), medial (P =.03), and adventitial thickening (P =.07) versus controls. Opposite our hypothesis, however, fasudil did not enhance outward artery wall remodeling or improve lumen caliber. Rather, inhibiting Rho-kinase blocked outward remodeling in response to ligation. EEL area was significantly smaller in treated versus control animals (P =.04) and slightly smaller versus shams (P = NS). These data suggest that Rho activation contributes significantly to both hyperplasia and outward remodeling of the injured artery wall. Rho-kinase may prove an important target to limit intimal hyperplasia and prevent restenosis when remodeling is improved by other means (eg, stents).

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

PubMed2003

Loss of expression of tropomyosin-1, a novel class II tumor suppressor that induces anoikis, in primary breast tumors.

Suppression of tropomyosins (TMs), a family of actin-binding, microfilament-associated proteins, is a prominent feature of many transformed cells. Yet it is unclear whether downregulation of TMs occur in human tumors. We have investigated the expression of tropomyosin-1 (TM1) in human breast carcinoma tissues by in situ hybridization and immunofluorescence. TM1 mRNA and protein are readily detectable in normal mammary tissue. In contrast, TM1 expression is abolished in the primary human breast tumors. Expression of other TM isoforms, however, is variable among the tumors. The consistent and profound downregulation of TM1 suggests that TM1 may be a novel and useful biomarker of mammary neoplasms. These data also support the hypothesis that suppression of TM1 expression during the malignant conversion of mammary epithelium as a contributing factor of breast cancer. In support of this hypothesis, we show that the ability to suppress malignant growth properties of breast cancer cells is specific to TM1 isoform. Investigations into the mechanisms of TM1-induced tumor suppression reveal that TM1 induces anoikis (detachment induced apoptosis) in breast cancer cells. Downregulation of TM1 in breast tumors may destabilize microfilament architecture and confer resistance to anoikis, which facilitates survival of neoplastic cells outside the normal microenvironment and promote malignant growth.

Anoikis↗

PubMed2003

Acute occlusive mesenteric ischemia: surgical management and outcomes.

Acute mesenteric ischemia secondary to arterial occlusion (AMI) remains a highly lethal condition. To examine recent trends in management and associated outcomes, we examined our institutional experience over a recent 10-year period. All patients treated for AMI between January 1990 and January 2000 were identified (76 patients, 77 cases) and their medical records examined. At presentation, 64% demonstrated peritonitis and 30% exhibited hypotension. The interval from symptom onset to treatment exceeded 24 h in 63% of cases. Etiology was mesenteric thrombosis in 44 patients (58%) and embolism in 32 patients (42%). Thirty-five patients (46%) had prior conditions placing them at high risk for the development of AMI including chronic mesenteric ischemia (n = 26) and inadequately anticoagulated chronic atrial fibrillation (n = 9). Surgical management consisted of exploration alone in 16 patients, bowel resection alone in 18 patients, and revascularization in 43 patients, including 28 who required concomitant bowel resection. Overall, intestinal necrosis was present in 81% of cases. Perioperative mortality was 62% and long-term parenteral nutrition (TPN) was required in 31% of survivors. Peritonitis (odds ratio [OR] 9.4, 95% confidence interval [CI] 1.6, 54.0; p = 0.012 and bowel necrosis (OR 10.4, CI 1.9, 56.3; p = 0.007) at presentation were independent predictors of death or survival dependent upon TPN. We conclude that AMI remains a highly lethal condition due in large part to advanced presentation and inadequate recognition and treatment of patients at high risk.

Adult↗

PubMed2003

Vascular failure: a hypothesis.

Although cardiac failure has been studied extensively, vascular failure is not a recognizable term. We suggest that it is reasonable to argue that failure of the vessel to control its mass, contractile capacity, and lumen will involve pathways similar to cardiac failure. Vascular failure, or perhaps more accurately arterial failure, has very different consequences. Failure to control mass and external diameter will result in hypertension or loss of lumen in atherosclerosis. We review what is known about this normal remodeling response and its failure, and propose directions for research.

Humans↗

PubMed2002

Expression profiling identifies 147 genes contributing to a unique primate neointimal smooth muscle cell phenotype.

OBJECTIVE: This study represents the first in an effort to systematically characterize different intimas by using expression array analysis. METHODS AND RESULTS: We compared smooth muscle cells (SMCs) of the neointima formed 4 weeks after aortic grafting with those from normal aorta and vena cava from cynomolgus monkeys. Hybridization to cDNA arrays identified subsets of 147 and 45 genes differentially expressed in the neointima versus the aorta and vena cava, respectively. The expression pattern differentiating neointima from aortic SMCs was characterized largely by suppression. Only 13 genes were induced in the neointima: 7 encoded matrix proteins (6 collagens and 1 versican) and 2 encoded inducers of matrix synthesis (osteoblast-specific factor-2/Cbfa1 and connective tissue growth factor). The genes suppressed most in the neointima included the regulator of G-protein signaling-5, SPARClike-1/hevin, and nonmuscle myosin heavy chain-B. A smaller gene set differentiated the neointima from the vena cava. Most were induced (39 of 45 genes), and overlap with the neointima-aorta set was significant (10 of 13 genes). Array results were validated with Northern analysis, in situ hybridization, or immunohistochemistry. CONCLUSIONS: These data underscore the importance of matrix synthesis in neointimal maturation, and novel genes, newly associated with neointimal SMCs (regulator of G-protein signaling-5 and osteoblast-specific factor-2/Cbfa1), have raised new hypotheses regarding the pathogenesis of intimal hyperplasia.

Animals↗

PubMed2002

Metalloproteinase inhibition and the response to angioplasty and stenting in atherosclerotic primates.

Determinants of restenosis after angioplasty include constrictive remodeling and intimal hyperplasia. Both processes require extensive matrix turnover, so matrix metalloproteinases (MMPs) have become potential targets of antirestenosis therapies. We studied the effects of RO113-2908, a broad-spectrum MMP inhibitor (MMPI), on the response to iliac artery angioplasty and stenting in atherosclerotic cynomolgus monkeys. Lumen diameter (LD) was measured angiographically, and artery wall geometry was assessed after perfusion-fixation at 4 weeks. Angiogenesis was measured in subcutaneous polyvinyl alcohol disks. Treatment provided significant, systemic MMP inhibitory activity (97+/-2.2% inhibition of 25 nmol/L MMP-12 by serum) and inhibited angiogenesis (P=0.007). In contrast, loss of gain in LD (P=0.73) and constrictive remodeling (external elastic lamina area ratio [injured/uninjured x 100]: MMPI, 106.3+/-9.6% vs control, 119.9+/-7.2%; P=0.27) were not substantially improved 4 weeks after angioplasty. Treatment also failed to reduce intimal hyperplasia after angioplasty (intimal area [mm(2)]: 1.4+/-0.3 vs 1.6+/-0.2, P=0.65) or stenting (2.4+/-0.2 vs 2.8+/-0.2, P=0.12). In summary, inhibition of MMP activity reduced angiogenesis but failed to prevent constrictive remodeling or intimal hyperplasia after angioplasty and stenting in atherosclerotic primates. Additional research is needed to define the spectrum of matrix-degrading proteases critical in healing atherosclerotic arteries after angioplasty.

Animals↗

PubMed2002

Survival of young patients after abdominal aortic aneurysm repair.

PURPOSE: This study assessed the cardiovascular disease, perioperative results, and survival after surgical abdominal aortic aneurysm repair in young patients (< or = 50 years) compared with randomly selected older patients who also underwent abdominal aortic aneurysm repair. METHODS: We reviewed hospital records to identify young and randomly selected control patients (3 for each young patient, > or = 65 years, matched for year of operation) with degenerative (atherosclerotic) abdominal aortic aneurysms undergoing repair between Jan 1, 1988, and Mar 31, 2000. Patients with congenital aneurysms, pseudoaneurysms, aortic dissections, post-coarctation dilations, aortic infection, arteritis, or aneurysms isolated to the thoracic aorta were excluded. Mortality data and cause of death were obtained from medical records and the National Death Index RESULTS: Among 1168 patients who underwent abdominal aortic aneurysm repairs, 19 young patients (1.6%) and 57 control patients were identified. The mean age was 48.4 years in the young group and 72.2 years in the control group. There were no differences in sex or race between the two groups. When comparing existing cardiovascular disease between the groups, there were no differences in the incidence of earlier coronary revascularization (26% vs 16%) or non-cardiac vascular surgery (5% vs 9%), but aneurysms were more commonly symptomatic in young patients (53% vs 21%; P <.01). Aneurysmal disease was limited to the infrarenal aorta in similar proportions of patients (89% vs 88%). No statistically significant differences were seen in the incidence of perioperative deaths (16% young vs 9% control; P =.40) or postoperative complications (37% young vs 26% control; P =.38). The estimated survival rate of the young group was not different from that of the control group (3-year survival rate, 73% vs 69%; P =.32) or the entire cohort of patients (older than 50 years; n = 1101) who underwent repair of abdominal aortic aneurysms during the study period (3-year survival 73% vs 75%; P =.63) CONCLUSION: After abdominal aortic aneurysm repair, young patients had perioperative results and follow-up mortality rates similar to those of control patients. Cardiovascular disease was the predominant cause of death after abdominal aortic aneurysm repair in the young patients. When compared with an age older than 50 years at the time of abdominal aortic aneurysm repair, young age alone was not associated with increased survival.

Adult↗

PubMedDate not supplied

Chronic visceral ischemia: symptom-free survival after open surgical repair.

A retrospective review of patients treated with a history of chronic visceral ischemia (CVI) was made to determine primary patency of open surgical repair and estimated symptom-free survival. Patients with CVI between 1990 and 2003 were reviewed. Included were those with chronic symptoms alone (C-CVI) and acute-on-chronic symptoms (A-CVI). Data were obtained from a vascular database. Symptom-free survival and graft patency were estimated by using product limit estimates. Fifty-eight patients (13 men, 45 women; mean age: 63 years) were treated surgically for C-CVI (34 patients) and A-CVI (24 patients). All patients had postprandial abdominal pain and weight loss (mean: 17 kg). One fourth reported food fear. Preoperative imaging demonstrated disease of the superior mesenteric artery (SMA) (100%; 64% occluded), celiac axis (89%; 37% occluded), and inferior mesenteric artery (IMA) (54%; 60% occluded). Multiple vessels were involved in 95% of patients (mean: 2.3 vessels/patient). Operative management included antegrade revascularization of 80 vessels. Combined aortic and/or renal procedures were performed in 7 patients. Patient demographics and visceral disease did not differ for C-CVI and A-CVI; however, perioperative mortality differed significantly (10% for C-CVI vs 54% for A-CVI [p < 0.001]). Intestinal gangrene at presentation was associated with perioperative (hazard ratio [HR]: 7.6; 95% CI: 2.7-21.6; p=0.0002) and follow-up death (HR: 7.8; CI 2.8-21.9; p <0.0001). Follow-up (mean: 34 months) was complete for 54/68 vessels (79%). Estimated primary and primary assisted patency at 5 years were 81% and 89% respectively. Estimated symptom-free survival for hospital survivors was 57% at 70 months. Open antegrade methods of visceral artery repair for CVI were durable and associated with 57% symptom-free survival at 70 months. Patient demographics and distribution of visceral artery anatomy were similar; however, perioperative mortality for C-CVI and A-CVI differed dramatically. Improved outcomes for A-CVI require recognition and treatment of CVI before onset of intestinal gangrene.

Aged↗