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Subodh Arora

Publications and source records attributed to Subodh Arora.

16 recordsLinked to original sources
PubMed2006

The effects of the type of anesthesia on outcomes of lower extremity infrainguinal bypass.

OBJECTIVE: Three main types of anesthesia are used for infrainguinal bypass: general endotracheal anesthesia (GETA), spinal anesthesia (SA), and epidural anesthesia (EA). We analyzed a large clinical database to determine whether the type of anesthesia had any effect on clinical outcomes in lower extremity bypass. METHODS: This study is an analysis of a prospectively collected database by the National Surgical Quality Improvement Program (NSQIP) of the Veterans Affairs Medical Centers. All patients from 1995 to 2003 in the NSQIP database who underwent infrainguinal arterial bypass were identified via Current Procedural Terminology codes. The 30-day morbidity and mortality outcomes for various types of anesthesia were compared by using univariate analysis and multivariate logistic regression to control for confounders. RESULTS: The NSQIP database identified 14,788 patients (GETA, 9757 patients; SA, 2848 patients; EA, 2183 patients) who underwent a lower extremity infrainguinal arterial bypass during the study period. Almost all patients (99%) were men, and the mean age was 65.8 years. The type of anesthesia significantly affected graft failure at 30 days. Compared with SA, the odds of graft failure were higher for GETA (odds ratio, 1.43; 95% confidence interval [CI], 1.16-1.77; P = .001). There was no statistically significant difference in 30-day graft failure between EA and SA. Regarding cardiac events, defined as postoperative myocardial infarction or cardiac arrest, patients with normal functional status (activities of daily living independence) and no history of congestive heart failure or stroke did worse with GETA than with SA (odds ratio, 1.8; 95% CI, 1.32-2.48; P < .0001). There was no statistically significant difference between EA and SA in the incidence of cardiac events. GETA, when compared with SA and EA, was associated with more cases of postoperative pneumonia (odds ratio: 2.2 [95% CI, 1.1-4.4; P = .034]. There was no significant difference between EA and SA with regard to postoperative pneumonia. Compared with SA, GETA was associated with an increased odds of returning to the operating room (odds ratio, 1.40; 95% CI, 1.20-1.64; P < .001), as was EA (odds ratio, 1.17; 95% CI, 1.05-1.31; P = .005). GETA was associated with a longer surgical length of stay on univariate analysis, but not after controlling for confounders. There was no significant difference in 30-day mortality among the three groups with univariate or multivariate analyses. CONCLUSIONS: Although GETA is the most common type of anesthesia used in infrainguinal bypasses, our results suggest that it is not the best strategy, because it is associated with significantly worse morbidity than regional techniques.

Aged↗
PubMed2006

Thiamine (vitamin B1) improves endothelium-dependent vasodilatation in the presence of hyperglycemia.

Brachial artery vasoactivity (BAVA) is a reliable, noninvasive method of assessing endothelium-dependent vasodilatation (EDV) in vivo. Acute hyperglycemia, impaired glucose tolerance (IGT), and diabetes mellitus impair EDV, a precursor to atherosclerosis. Thiamine is a coenzyme important in intracellular glucose metabolism. The purpose of this study was to evaluate the effect of thiamine on BAVA in the presence of hyperglycemia. Ten healthy subjects (group H, mean age 27 years), 10 patients with impaired glucose tolerance by World Health Organization criteria (group IGT, mean age 65 years), and 10 patients with non-insulin-dependent diabetes mellitus (group NIDDM, mean age 50 years) were studied. Duplex ultrasound was used to measure brachial artery flow changes in response to reactive hyperemia following brachial artery tourniquet occlusion for 5 min. This test was performed after a 10 hr fast and at 30, 60, and 120 min after a 75 g oral glucose challenge along with measurements of blood glucose level (BGL). A week later, BAVA evaluation was repeated after administration of 100 mg of intravenous thiamine. BAVA (% increased blood flow) at peak and trough BGL was compared with and without thiamine. BAVA at peak glucose improved from 69.0 +/- 6.4% to 152.8 +/- 22.9% in group H (p < 0.005), from 57.6 +/- 12.6% to 139.7 +/- 12.4% in group IGT (p < 0.005), and from 57.8 +/- 8.3% to 167.8 +/- 11.6% in group NIDDM (p < 0.005) following administration of thiamine. On the other hand, at trough glucose levels, BAVA remained essentially unchanged in group H (prethiamine 83.8 +/- 6.5% vs. post-thiamine 83.8 +/- 17.0%, p > 0.05) as well as group IGT (prethiamine 96.7 +/- 8.5% vs. post-thiamine 104.0 +/- 17.4%, p > 0.05). BAVA at trough glucose was not measured in group NIDDM secondary to trough BGL > 140 mg/dL. EDV was improved by thiamine in the presence of hyperglycemia in healthy subjects and in patients with IGT and NIDDM. The mechanism by which thiamine improves EDV is not due to a glucose-lowering effect as thiamine had no effect on EDV under normoglycemic conditions. Routine administration of thiamine might improve endothelial function and therefore slow the development and progression of atherosclerosis, especially in patients with IGT and NIDDM who are prone to develop accelerated atherosclerosis.

Adult↗
PubMed2006

Hypoxia attenuates insulin-induced proliferation and migration of human diabetic infrapopliteal vascular smooth muscle cells.

The proliferative effects of insulin on infrapopliteal vascular smooth muscle cells (VSMCs) have been established. We examined the effect of hypoxia in the presence and absence of insulin on the proliferation and migration of human diabetic infrapopliteal VSMCs in vitro. VSMCs isolated from the infrapopliteal arteries of male diabetic patients of identical disease and clinical patterns undergoing below-knee amputation were harvested and grown to subconfluence. Cells were then exposed to control medium (M199/1% fetal bovine serum/2% antibiotic-antimycotic) or control medium with 100 ng/mL insulin in oxygen concentrations of 17% (normoxia), 5%, and 1%. Cellular proliferation was assayed using [methyl-3H]-thymidine incorporation. Migration assays were performed using the Corning Costar Transwell system. Lactate dehydrogenase was assayed and compared among groups as a marker for cytotoxicity. VSMCs in normoxic conditions (17%) had a significant increase in both proliferation (100 +/- 6.5% vs. 124 +/- 4.7%, p = 0.007) and migration [73.2 +/- 9.3 vs. 118.1 +/- 14.9 cells/4 high-power fields (HPF), p = 0.03] when exposed to insulin. Of cells exposed to insulin, those at both 5% (75.9 +/- 7.9%, p = 0.0001) and 1% (73.6 +/- 4%, p < 0.0001) hypoxia proliferated at a significantly decreased rate compared with cells at normoxia (124 +/- 4.7%). Migration of these insulin-exposed cells was significantly decreased at 1% hypoxia (63.1 +/- 9.0 cells/4HPF) compared to those at normoxia (118.1 +/- 14.9 cells/4HPF, p = 0.006) and 5% hypoxia (101.2 +/- 10.0 cells/4HPF, p = 0.01). There were no significant differences in migration between cells at normoxia and 5% hypoxia. Finally, hypoxia and insulin exerted no significant effect on cytotoxicity. The proliferative and promigratory effects of insulin on diabetic VSMCs are attenuated in hypoxic conditions in a manner unrelated to cytotoxicity.

Cell Hypoxia↗
PubMed2006

Carotid plaque morphologic characteristics.

Carotid artery atherosclerosis is predominantly believed to mirror atherosclerosis elsewhere in the body. Endothelial injury results in expression of cell surface adhesion molecules with expression of sequence of genes involved in the inflammatory pathway and expression of proinflammatory cytokines. The combination of the inflammatory mediators and contribution by monocytes infiltrating the intima and vascular smooth muscle cell proliferation result in the development of atheromatous plaque with a lipid-rich necrotic core. Complications of these atheromatous plaques can lead to plaque instability, rupture, and subsequent hemorrhage or ulceration. The significant risk factors, characteristics associated with symptoms, and available diagnostic imaging modalities are also discussed with review of the relevant literature.

Carotid Artery Diseases↗
PubMed2005

Aortic angiosarcoma presenting as distal arterial embolization.

Aortic angiosarcoma is a rare, malignant neoplasm of the vasculature, with 24 case reports in the literature. Patients usually present with either aneurysmal or occlusive disease. Treatment consists of en bloc resection of the vessel and contiguous structures with postoperative chemoradiation therapy. Despite surgery and adjunctive measures, prognosis remains dismal as a result of early metastasis and late diagnosis. We report a case of aortic angiosarcoma that presented with distal thromboembolic phenomenon.

Aged↗
PubMed2005

Evaluation of the microcirculation in vascular disease.

Insufficient blood flow through end-resistance arteries leads to symptoms associated with peripheral vascular disease. This may be caused in part by poor macrocirculatory inflow or impaired microcirculatory function. Dysfunction of the microcirculation occurs in a similar fashion in multiple tissue beds long before the onset of atherosclerotic symptoms. Impaired microcirculatory vasodilatation has been shown to occur in certain disease states including peripheral vascular disease, diabetes mellitus, hypercholesterolemia, hypertension, chronic renal failure, abdominal aortic aneurysmal disease, and venous insufficiency, as well as in menopause, advanced age, and obesity. Microcirculatory structure and function can be evaluated with transcutaneous oxygen, pulp skin flow, iontophoresis, and capillaroscopy. We discuss the importance of the microcirculation, investigative methods for evaluating its function, and clinical applications and review the literature of the microcirculation in these different states.

Humans↗
PubMed2005

Evaluation of macrocirculatory endothelium-dependent and endothelium-independent vasoreactivity in vascular disease.

Macrocirculatory endothelium-dependent and independent vasodilatation is integral to tissue-bed oxygen delivery and homeostasis. Dysfunction of macrocirculatory vasoreactivity is a precursor to atherosclerosis and occurs in a similar fashion in multiple tissue beds long before the onset of symptoms. Impaired macrocirculatory vasodilatation has been shown to occur in certain disease states including diabetes mellitus, hypercholesterolemia, chronic renal failure, peripheral arterial atherosclerosis, and abdominal aortic aneurysms, as well as secondary to smoking, advanced age, menopause, high-fat diet, and sedentary lifestyle. Brachial artery vasoreactivity is a noninvasive means of assessing macrocirculatory vasodilatory capacity that may help identify patients at increased risk for peripheral and cardiovascular disease and allow for objective assessment and monitoring of treatment. Endothelium-dependent vasoreactivity, or flow-mediated dilatation, is measured after brachial artery occlusion with a pneumatic blood pressure cuff, and endothelium-independent vasoreactivity is measured after the administration of sublingual nitroglycerin. The accuracy of brachial artery vasoreactivity is dependent on hematologic variables, as well as diurnal, day-to-day, ultrasound operator, and reader variations; however, the overall coefficient of variation is only 1.8%. We discuss the importance of the macrocirculation, investigative methods for evaluating macrocirculatory vasoreactivity, and review the literature of vasoreactivity in these different states.

Atherosclerosis↗
PubMed2004

Medical factors affecting patency of arteriovenous access.

Arteriovenous access failure is multifactorial in nature with contributions from both medical and surgical etiologies. Medical causes of arteriovenous access failure are rare, and therefore infrequently identified as a major contributing source of malfunction. Although they account for only 10-15% of all cases of access failure, their importance should not be underestimated, especially in cases where a surgical source cannot be identified. Most medical causes are derived from Virchow's triad of endothelial cell injury, stasis, and hypercoaguability. Endothelial cell injury occurs through oxidative stress, activated platelets, increased levels of circulating tumor necrosis factor-alpha, and preexisting intimal hyperplasia. Stasis can occur through prolonged access compression, hypotension, or hypoalbuminemia. Finally, patients with renal failure requiring hemodialysis are frequently at increased risk for hypercoaguable states, except for situations of platelet dysfunction, and therefore access failure. Potential treatments include identifying and removing the offending source, as well as innovative, new medications to prevent their reoccurrence. Treatment is aimed at improving quality of life, as well as decreasing morbidity and hospital admissions in this difficult patient population.

Anticoagulants↗
PubMed2004

Strategies of arteriovenous dialysis access.

Surgical management of the patient who requires hemodialysis access, while continuing to demand more attention from the vascular surgeon, suffers from discrepancies of approach and strategy. With the increase in incidence of dialysis dependent renal failure among our population, many have attempted to present a uniform, logical strategy with which the vascular surgeon can most effectively treat the hemodialysis patient in the long term. Most notably, the multidisciplinary Dialysis Outcomes Quality Initiative (DOQI) guidelines present the surgeon with a rough outline of hemodialysis access insertion strategy, and it has become nationally recognized as an acceptable summary of treatment strategy and goals. The decision as to the most appropriate surgical access to offer a patient depends on immediate need for hemodialysis, history and physical examination findings, and suitability of available veins in the extremity. While percutaneous, catheter based access affords the luxury of immediate access, these devices suffer from several complicating factors, such as infection, and damage to large, proximal veins. For long-term access, the autogenous access, while perhaps less successful in the immediate short term, is always the preferred access type given its favorable longevity. The surgeons should focus on sites distally on the extremity, reserving proximal sites for potential future access insertions should the primary access fail. In the absence of suitable vein, prosthetic access may be considered. When both the upper and lower aspects of both upper extremities have been exhausted, the surgeon should consider access insertion elsewhere, such as the lower extremity.

Arteriovenous Shunt, Surgical↗
PubMed2002

Syndrome X and diabetes: what is the mystery?

Syndrome X describes a combination of clinical phenomena that have been statistically linked to hyperinsulinema in the absence of frank diabetes. Since its original description, Syndrome X has come to represent several phenotypes that have hemodynamic and metabolic effects on the individual, as well as major effects on the development of vascular disease. Further, this syndrome is reaching epidemic proportions, As such, a thorough understanding of this condition is becoming increasingly important for the modern vascular surgeon. The mainstay of therapy revolves around early diagnosis and management with diet changes, exercise, and reduction of cardiovascular risk factors.

Blood Glucose↗
PubMed2002

Cutaneous microcirculation in the neuropathic diabetic foot improves significantly but not completely after successful lower extremity revascularization.

OBJECTIVE: The purpose of this study was the examination of the effect of successful large vessel revascularization on the microcirculation of the neuroischemic diabetic foot. RESEARCH DESIGN AND METHODS: We measured the cutaneous microvascular reactivity in the foot in 13 patients with diabetes with peripheral arterial disease and neuropathy (group DI) before and 4 to 6 weeks after successful lower extremity arterial revascularization. We also compared them with age-matched and sex-matched groups of 15 patients with diabetes and neuropathy, seven patients without neuropathy, and 12 healthy patients for control. We used single-point and laser Doppler scan imaging for the measurement of the foot skin vasodilatation in response to heating to 44 degrees C and to iontophoresis of 1% acetylcholine (endothelial-dependent response) and 1% sodium nitroprusside (endothelial-independent response). RESULTS: The group DI response to heat increased from 289% +/- 90% before surgery (percent increase over baseline measured in volts) to 427% +/- 61% (P <.05) after surgery but was still comparable with the response of the patients with diabetes and neuropathy (318% +/- 51%) and lower than the responses of the patients without neuropathy (766% +/- 220%) and the healthy patients for control (891% +/- 121%; P <.0001). The group DI acetylcholine response also improved from 6% +/- 4% before surgery to 26% +/- 8% after surgery (P <.05) and was similar to the responses of patients with diabetes and neuropathy (18% +/- 3%) and patients without neuropathy (38% +/- 8%) but still lower when compared with the response of the patients for control (48% +/- 9%; P <.001). The sodium nitroprusside response for group DI improved from 10% +/- 4% to 29% +/- 9% (P <.05) and was similar to the responses of the neuropathic (25% +/- 9%), nonneuropathic (32% plus minus 6%), and control (40% +/- 5%) groups. The group DI neurovascular response, which depends on the healthy function of the C-fiber nociceptors, was similar at baseline (5% +/- 9%) and after surgery (14% +/- %10) and in the neuropathic group (33% +/- 21%), but it was dramatically reduced when compared with the nonneuropathic (110% +/- 40%) and control (198% +/- 54%) groups (P <.001). CONCLUSION: Impaired vasodilation in the diabetic neuropathic lower extremity leads to functional ischemia, which improves considerably but is not completely corrected with successful bypass grafting surgery. Therefore, patients with diabetes and neuropathy may still be at high risk for the development of foot ulceration or the failure to have an existing ulcer heal despite adequate correction of large vessel blood flow.

Acetylcholine↗
PubMed2002

Progesterone inhibits human infragenicular arterial smooth muscle cell proliferation induced by high glucose and insulin concentrations.

INTRODUCTION: Diabetes mellitus is a significant risk factor for atherosclerotic peripheral vascular disease. Hyperglycemia and hyperinsulinemia, as encountered in patients with type II diabetes, have been shown to stimulate vascular smooth muscle cell (VSMC) proliferation, a paramount feature in atherosclerosis. Female sex hormones, such as estrogen, have been suggested to inhibit VSMC proliferation. However, the role of progesterone, particularly in patients with diabetes mellitus, has not been examined. Therefore, we studied the effect of progesterone on VSMCs exposed to various concentrations of glucose and insulin. METHODS: Human infragenicular VSMCs isolated from the tibial arteries of five male patients with diabetes undergoing lower extremity amputation were used. Immunocytochemical studies with confocal microscopy were performed for progesterone receptor identification in these VSMCs. Cells were grown to subconfluence, followed by exposure to deprived media with various glucose (100 and 200 mg/dL) and insulin (no insulin and 100 ng/mL) concentrations. Cells were then additionally exposed to physiologic progesterone (10 ng/mL, progesterone group) and compared with a no-progesterone group. Cell count and methyl-(3)H-thymidine incorporation were used to determine cellular proliferation. Cell count with hemocytometry was performed on day 6. DNA synthesis as reflected through methyl-(3)H-thymidine incorporation was measured at 24 hours. RESULTS: Immunocytochemical studies with confocal microscopy showed cytosolic progesterone receptors. The no-progesterone group showed a significant rise in cell count (P <.05) at all concentrations of glucose or insulin compared with the control group containing 100 mg/dL glucose concentration. The no-progesterone group also showed a significant rise in thymidine incorporation (P <.05) in the 100 mg/dL glucose-100 ng/mL insulin group and the 200 mg/dL glucose-100 ng/mL insulin group compared with the 100 mg/dL glucose group. In the cell count studies, progesterone significantly inhibited cellular proliferation in several settings. All cell groups cultured with insulin or an elevated glucose concentration showed a significant (P <.05) antiproliferative effect when exposed to progesterone. With thymidine incorporation, progesterone showed a similar antiproliferative effect in cells stimulated with glucose or insulin. CONCLUSION: Significant reductions in cell proliferation as determined with both cell count and thymidine incorporation suggest that progesterone is an inhibitor of VSMC proliferation induced by our in vitro models of hyperglycemia and hyperinsulinemia. Therefore, progesterone may have a protective role against the atherosclerotic changes associated with type II diabetes.

Aged↗