Biomedical subjects

Anil Hingorani

Publications and source records attributed to Anil Hingorani.

27 records · Page 2Linked to original sources

PubMed2002

Anticoagulation with enoxaparin versus intravenous unfractionated heparin in postoperative vascular surgery patients.

BACKGROUND: The use of postoperative anticoagulation is not uncommon for patients undergoing vascular procedures, whether for adjunctive therapy to the surgical procedure or for resumption of preoperative anticoagulation. We investigated whether low-molecular-weight heparin, specifically enoxaparin, was an effective replacement for intravenous heparin during the postoperative period until achievement of a therapeutic international normalized ratio, together with the impact on postoperative length of stay. METHODS: We retrospectively examined 330 patients who received either traditional intravenous unfractionated heparin with adjusted-dose warfarin daily (n = 169) or subcutaneous low-molecular-weight heparin, specifically enoxaparin 1 mg/kg every 12 hours, with adjusted-dose warfarin daily (n = 161). Safety was defined as incidence of bleeding, hematoma, stroke, expiration, thrombocytopenia, return to surgery for graft thrombosis or hematoma, and readmission within 30 days for hematoma or thrombosis. RESULTS: For all procedures, regardless of type of anticoagulation treatment, there was no difference in the incidence of postoperative complications, except for the increased incidence of return to surgery for graft thrombosis (P =.02), failing graft (P =.0004), and debridement (P =.01) in patients who received unfractionated heparin. For all procedures combined, the average postoperative length of stay was shortened by 2 days with use of low-molecular-weight heparin (P =.0001). CONCLUSIONS: In this series, use of enoxaparin appears to be safe and effective for vascular postoperative anticoagulation. At the same time, its use can significantly reduce the average postoperative length of stay for patients undergoing vascular procedures. Further prospective data are needed before this protocol can be accepted as an alternative for postoperative anticoagulation in this set of patients.

Adult↗

PubMedDate not supplied

Lesser saphenous vein thrombophlebitis: its natural history and implications for management.

Little attention has been given to superficial thrombophlebitis and particularly to lesser saphenous vein thrombophlebitis (LSVT) by vascular surgeons. A prospective nonrandomized study was conducted to assess LSVT's potential association with deep venous thrombosis (DVT) as well as its natural history. Between January 1994 and December 1995, the authors reviewed 33 cases of LSVT detected by duplex scanning in 32 patients at their institution's vascular laboratory. Combined LSVT/DVT was treated with heparin and warfarin. LSVT alone or LSVT plus greater saphenous vein thrombophlebitis (GSVT) were treated with local warm compresses and nonsteroidal antiinflammatory drugs. Follow-up scans were obtained in 23 of the 32 patients and ranged from 2 weeks to 18 months after diagnosis of LSVT. Thirty-one patients had unilateral LSVT and 1 patient had bilateral LSVT. Isolated LSVT was found in 9 patients (28%), LSVT combined with DVT occurred in 21 patients (65.6%), and 2 patients had LSVT/GSVT. LSVT was contiguous with DVT in 15 patients, and in 5 patients it was noncontiguous. Within 3 months, 9 of 16 patients (56%) with LSVT/DVT had complete or partial resolution of their LSVT, and 1 (14%) of the 7 patients with LSVT and LSVT/GSVT had improved. Within 18 months, 13 of 16 patients (81%) with LSVT/DVT had complete resolution of their thrombus while only 3 of 7 patients (43%) with LSVT and LSVT/GSVT had resolved. These data show that LSVT is more often associated with DVT (65.6%) than previously believed. While most LSVT will improve in 18 months, those associated with DVT will resolve sooner. Whether anticoagulation accounted for this difference remains to be proven.

Adult↗

PubMedDate not supplied

Lower extremity deep venous thrombosis: vascular laboratory quality assurance without correlation between ultrasound and venography.

Venography is rarely available for comparison with ultrasonography (US) as a means for quality assurance (QA) in the detection of lower extremity venous thrombosis. New QA methods must be implemented. We compared results of multiple serial studies performed in the same extremity as a QA indicator. From a 3-year sample of close to 9,000 venous tests, we obtained a subset of 44 patients who had 331 tests in 71 lower extremities throughout the years. A positive or negative study preceded or followed by another positive or negative study was considered as a confirmed study. A negative or positive study not preceded or followed by a negative or positive study was considered as unconfirmed. Explanations were then sought to explain unconfirmed results. There were 169 (51%) and 124 (37%) confirmed positive and negative studies, respectively, and 13 (4%) and 25 (8%) unconfirmed positive and negative studies, respectively. Of the 13 unconfirmed positive tests, 2 were preceded by negative tests, 3 were preceded and followed by negative tests, and 8 were followed by negative tests. Of these 13 tests, 4 documented extensive venous thrombosis. Of the 25 unconfirmed negative tests, 11 followed treatment for venous thrombosis, 6 had recurrent thrombosis with intermittent lysis, and 8 were followed by positive tests. Considering the low probability of extensive thrombosis being a false-positive test, positive predictive value was 95% (173/182). Excluding 11 negative tests following treatment for venous thrombosis, negative predictive value was 90% (124/138) and accuracy was 93% (297/320). US versus US and literature US versus venography comparisons of these statistics were similar.

Female↗

PubMedDate not supplied

The effect of von hippel-lindau gene transfer on human vascular smooth muscle cell proliferation and apoptosis.

Von Hippel-Lindau (VHL) gene is a tumor suppressor gene that plays a genome "gatekeeper'' role and controls several downstream effector genes. We have previously demonstrated that both in vivo and in vitro adenovirus-mediated gene transfer of tumor suppressor genes into the vascular endothelium is effective in decreasing neointimal hyperplasia and abnormal cell proliferation. The degree of apoptosis induced by these genes is critical in mediating the in vivo responses to gene therapy and the maintenance of the crucial balance between cell death and viability. Since VHL gene is known to regulate vascular endothelial growth factor (VEGF) as well as other angiogenic factors, it may exhibit a greater potential in the attenuation of vascular disorders in comparison to other tumor suppressor genes. This study focused on whether adenovirus-mediated VHL gene transfer into human vascular smooth muscle cells has an effect on cell proliferation and induction of apoptosis. Human aortic smooth muscle cells (HASMC) were grown as monolayers and transfected with varying titers of adenovirus containing the VHL cDNA (AdVHL). The negative controls were adenovirus containing green fluorescent protein (AdGFP), vector alone (AdNull), and virus-free infection medium. Adenovirus encoding wild-type p53 (Adp53) was used as positive control. Cell viability and proliferation were determined by using trypan blue exclusion and MTS-based CellTiter 96 AQ Proliferation Assay. Apoptosis was evaluated by TUNEL assay, morphologic changes, and nucleosomal DNA degradation. Following AdVHL transfection HASMCs demonstrated a dose-dependent decrease in viability as compared to negative controls (p < 0.05). AdVHL-transfected cells exhibited a decrease in their proliferative ability by 40.21 +/-1.66 (SEM)%. In cultures transfected with the positive control, Adp53, the cell viability as well as proliferation was highly reduced (p < 0.001). AdGFP and AdNull did not increase HASMC apoptosis above baseline levels. The cells exposed to adenoviruses expressing tumor suppressor genes underwent apoptosis, with Adp53 demonstrating a very high magnitude of cell death (75.27 +/-3.52 [SEM]%). AdVHL expression caused 45.36 +/-2.55 (SEM)% apoptosis in HASMC. Recombinant adenovirus-mediated VHL expression is efficacious in limiting vascular smooth muscle cell growth in vitro. Overexpression of VHL suppresses HASMC proliferation and regulates apoptosis. Further experiments are indicated to examine whether VHL may be a useful adjunct in limiting myointimal hyperplasia.

Adenoviridae↗

PubMedDate not supplied

Early transposition of the sartorius muscle for exposed patent infrainguinal bypass grafts.

The traditional approach for patent and exposed and infected infrainguinal bypass grafts in the groin has included wide operative debridement and secondary or delayed primary closure. However, this has been associated with significant risk of further contamination and length of stay. The authors reviewed their experience using the wide debridement, sartorius muscle flap transposition, and primary wound closure as an alternative. During the past 5 years, they have had 50 patients with major wound necrosis or infection in the groin or thigh with the graft or native artery being exposed after debridement. This group included 28 men; 74% of the patients had hypertension, 58% had diabetes, and 20% had renal failure. The grafts were split evenly between native vein and prosthetic material. After wide debridement, closure was performed by the vascular surgeon using the sartorius muscle flap. Postoperatively, there was an 8% major amputation rate and a 12% mortality rate in the first 30 days. One patient developed a pseudoaneurysm 5 weeks after placement of the flap. This patient underwent removal of the infected polytetrafluoroethylene graft with ligation of the common femoral artery. None of the procedures have resulted in further systemic or graft sepsis. None have resulted in arterial or graft blowout. Follow-up was for an average of 18 months. Closure of groin and thigh wounds with exposed bypass graft or native artery can be safely performed with the sartorius muscle flap with excellent results. The length of stay of these patients compared to historical controls is acceptable. Furthermore, the chance of infection of the native artery or bypass may be reduced. Familiarity with this simple technique can be a valuable tool for the vascular surgeon.

Amputation, Surgical↗

PubMedDate not supplied

Decreased production of nitric oxide by peripheral blood mononuclear cells of patients with peripheral vascular disease.

Although prior studies have implicated nitric oxide (NO), a molecular messenger, in the development and progression of atherosclerosis, most of these studies have centered on atherosclerotic plaques. The current investigation determines whether a correlation exists between the presence of altered levels of NO production by peripheral blood mononuclear cells (PBMCs) and atherosclerotic disease. Venous blood was collected from 8 surgical patients having severe peripheral vascular disease and 8 healthy controls. PBMCs were separated by gradient centrifugation, diluted to 10(5) cells per mL, and cultured. Lipopolysaccharide (LPS), at doses of 10, 25, and 50 ng/mL, was used to stimulate NO production. Total nitric oxide assay was performed to determine the levels of NO produced by PBMCs at 24 and 48 hours. When stimulated by LPS there was an increase in NO production in the PBMCs cultured from control as well as patient samples, as compared to basal NO levels. However, the data demonstrate a significant decrease in the nitric oxide production in the patients with atherosclerosis as compared to that in the control group (p < 0.05). The differential production of nitric oxide by PBMCs of patients with atherosclerotic disease and healthy controls not only suggests that it has a role in the pathogenesis of this disease but also underlines its systemic nature. Blood cells circulating in the body with altered levels of NO production could have profound effects in the microvascular environment mediating molecular pathways and signaling cascades that activate and augment atherosclerosis.

Aged↗

PubMedDate not supplied

Morbidity and mortality associated with internal jugular vein thromboses.

The authors have noted a significant incidence of pulmonary embolism and mortality associated with upper extremity deep venous thrombosis (UEDVT). Since there is an association between the site of lower extremity DVT (LEDVT) and pulmonary embolism, they hypothesized that there might also be a correlation between the site of UEDVT and the incidence of pulmonary embolism (PE) and associated mortality. To further elucidate this hypothesis, they analyzed the mortality rate and incidence of PE diagnosed with subclavian/axillary or internal jugular vein thrombosis during a 5-year period at their institution. Two hundred and ten patients were diagnosed with acute internal jugular and/or subclavian/axillary DVT during a 5-year period by duplex scanning. The indications for the duplex examination were upper extremity swelling in 187 (89%) or as part of the work-up for pulmonary embolism in 23 (11%). There were 126 women (60%) and 84, men (40%). The mean age was 67 +/-18 years (range 1-101 years). The patients were divided into 3 groups based on the location of the thrombus: Group I-UEDVT involving the subclavian and/or axillary veins (n = 128); Group II-internal jugular vein thrombosis alone (n = 21); and Group III-concomitant subclavian/axillary and internal jugular vein DVT (n = 61). Risk factors were presence of central venous catheter or pacemaker in 127 patients (60%), malignancy in 78 patients (37%), concomitant lower extremity deep venous thrombosis (LEDVT) in 40 patients (19%), and history of LEDVT in 6 patients (3%). Eighty (38%) patients had more than 1 risk factor. The mean follow-up period was 13 +/-1 months (range 0-49 months). Mortality rates at 1, 3, and 12 months were 13%, 31%, and 40% for Group I; 14%, 33%, and 42% for Group II; and 23%, 44%, and 59% for Group III. The mortality rate in Group I was statistically significantly higher for patients >/=75 years old, patients not treated with anticoagulation, and patients who underwent placement of a central venous line. The same risk factors did not achieve statistical significance in the 2 other groups. The number of patients diagnosed with pulmonary embolism by ventilation/perfusion scans in Groups I, II, and III that could be attributed to the UEDVT solely was 8 (4%), 1 (0.5%), and 3 (2.4%), respectively. Contrary to the initial hypothesis of a relationship between the site of thrombosis and the incidence of pulmonary embolism and mortality, these data showed no statistical differences in mortality rate or incidence of pulmonary embolism among the 3 groups studied. These data also suggest that internal jugular vein thrombosis is a disease process associated with mortality and morbidity rates comparable to those of subclavian/axillary vein thrombosis.

Adolescent↗

PubMedDate not supplied

Impact of duplex arteriography in the evaluation of acute lower limb ischemia from thrombosed popliteal aneurysms.

Acute limb-threatening ischemia from thrombosis may be the initial presentation of popliteal artery aneurysms (PAA) and is associated with amputation rates of 20-30%. Since contrast angiography may miss the diagnosis, the authors suspect that thrombosis of PAA may be an underappreciated cause of acute ischemia. Routine use of duplex arteriography (DA) may aid in the diagnosis and may help identify the outflow vessels with improved results. One hundred and nine patients (group 1) from 1994 to 1997 and 201 patients from 1998 to 2001 (group 2) presenting with acute limb-threatening ischemia were studied. None of the group 1 patients underwent preoperative DA and no diagnosis of acute popliteal artery aneurysm thrombosis was made. Ten patients with acute ischemia due to thrombosed popliteal artery aneurysms were identified in group 2 when preoperative DA was routinely performed. Urgent revascularization based on the results from DA was performed with use of autogenous saphenous vein in all patients. Six patients had functioning bypasses with a mean follow-up of 15.6 months. There were 3 deaths, 2 within 30 days and 1 after 2(1/2) years with functioning grafts. One patient was lost to follow-up. No major amputations were performed. Incidence of thrombosed popliteal artery aneurysms as the cause of acute limb-threatening ischemia is probably underestimated. Routine use of DA may provide the diagnosis and identifies the available outflow vessels. Contrary to previously published reports, urgent revascularization of an acutely ischemic extremity from thrombosed popliteal aneurysm can provide excellent rates of limb salvage.

Acute Disease↗

PubMedDate not supplied

Role of apoptosis and proteolysis in the pathogenesis of iliac artery aneurysms.

The objective of this study was to investigate the role of inflammation, programmed cell death, its molecular modulators, and proteolysis in the pathogenesis of iliac artery aneurysms (IAAs). Nineteen IAA specimens were obtained from patients undergoing elective surgical repair. All were males with ages ranging from 55 to 85 years (mean 73 years). Controls were iliac arteries (n=6) retrieved from surgical patients without aneurysmal disease. Standard histochemical techniques were used to assess elastic lamellae fragmentation and inflammatory infiltrate in aneurysmal and normal tissues Identification of different types of cells in the aneurysm wall and detection of death-pro molecules, Fas, p53, perforin, apoptosis-mediating bcl-2 family proteins, apoptotic death substrate, and poly(adenosine diphosphate-ribose) polymerase were performed immunohistochemically. Apoptosis was detected by terminal deoxynucleotidyl transferase-mediated digoxigenin-deoxyuridine triphosphate nick end-labeling (TUNEL) assay and caspase activity. Proteolytic activity was determined by 10% gelatin gel zymography. There is a conspicuous disruption and fragmentation of elastic lamellae in IAAs compared with normal arteries. Increased gelatinolytic activity was observed at 92, 72, and 67 kDa in the aneurysmal tissues. There was a significant loss of vascular smooth muscle cells (VSMCs) in the IAA walls compared with normal arteries (p < .02). Large numbers of inflammatory cells were observed in the IAA specimens (p = .01). Only aneurysmal arteries showed CD8+ T cells expressing death-promoting molecules. CD3+, CD8+, CD20+, CD30+, and CD68+ immunoreactive cells were significantly more prominent in the aneurysmal tissues than in the control arteries. There was a significant increase in the number of cells undergoing apoptosis in aneurysmal tissue than in the normal vessels (p < .02), as well as in the expression of bax, p53, CPP-32, and Fas. Apoptotic cells and proapoptotic molecules predominantly localized to the inflammatory infiltrate. VSMC apoptosis was significant in IAAs. The data confirm the architectural disruption of the IAA wall and illustrate an apparent biologic response involving inflammatory infiltrate, apoptosis, and signaling molecules capable of initiating cell death. In addition to compromising the mechanical integrity of the vessel wall, VSMC loss may contribute to imbalance in the protein profile, accelerating extracellular matrix degradation that could favor IAA development.

Aged↗