PubMed Health⌕ Search

Biomedical subjects

Atul Aggarwal

Publications and source records attributed to Atul Aggarwal.

At least 19 recordsLinked to original sources
PubMed2006

Optimized scintigraphic evaluation of infection and inflammation: role of single-photon emission computed tomography/computed tomography fusion imaging.

Gallium-67 citrate and radiolabeled white blood cells have become standard inflammation/infection-seeking agents whereas other agents, such as (99m)Tc diphosphonates, commonly are used to infer an infectious process. These radiopharmaceuticals reflect physiologic and pathologic function rather than anatomical abnormality. In the clinical setting, it is often necessary to correlate these functional studies with anatomical imaging. The advent of single-photon emission computed tomography, as well as positron emission tomography, provides tomographic images for direct correlation to anatomic modalities such as computed tomography and magnetic resonance imaging. The methods by which these functional and anatomic imaging modalities are correlated include side-by-side, software, and hardware fusion. Clinically, fusion imaging has been applied primarily to oncologic and neurologic applications. The literature supports the premise that multimodality fusion would increase the specificity of the physiologic modality and increase the sensitivity of the anatomic modality. Our institution uses software fusion to aid in the diagnosis of infection and inflammation. Through case vignettes, we illustrate applications for single-photon emission computed tomography/computed tomography fusion for the diagnosis of infection and inflammation in multiple organ systems.

Equipment Design↗
PubMed2004

Attenuation of platelet reactivity by enoxaparin compared with unfractionated heparin in patients undergoing haemodialysis.

BACKGROUND: Increased platelet reactivity presages adverse cardiac events. Because both haemodialysis and unfractionated heparin (UFH) can increase platelet reactivity, we compared platelet reactivity during haemodialysis when patients were anticoagulated with UFH or enoxaparin. METHODS: Patients (n = 20) underwent consecutive haemodialysis sessions with either UFH or enoxaparin in a random order. Blood was taken from the arterial end of the haemodialysis circuit at the initiation of haemodialysis before anticoagulation. Subsequently, blood was taken during dialysis from the venous end of the circuit 10 min after treatment with UFH or enoxaparin. Platelet reactivity was assessed with the use of flow cytometry by determining the capacity of platelets to bind fibrinogen and the surface expression of P-selectin in response to adenosine diphosphate (ADP, 0 and 0.2 microM). Results were compared with the use of two-way repeated measure ANOVA. RESULTS: Platelet reactivity in arterial blood obtained at the beginning of dialysis prior to patients being treated with either UFH [0.2 microM ADP-induced capacity to bind fibrinogen = 28+/-15% (SD)] or enoxaparin (30+/-18%) was similar (P = 0.15). In contrast, platelet reactivity was less after treatment with enoxaparin compared with UFH (P = 0.006). The 0.2 microM ADP-induced capacity to bind fibrinogen in venous blood obtained 10 min after anticoagulation was 34+/-11% after treatment with UFH and 22+/-11% after treatment with enoxaparin. CONCLUSIONS: Anticoagulation with enoxaparin during haemodialysis is associated with less platelet reactivity compared with UFH. Accordingly, enoxaparin use may contribute to a lesser risk of cardiac events in patients with end-stage renal disease treated with haemodialysis.

Aged↗
PubMed2004

Increased coronary arterial release of interleukin-1 receptor antagonist and soluble CD40 ligand indicative of inflammation associated with culprit coronary plaques.

Blood taken from the coronary artery ostium reflects biochemical changes indicative of thrombosis in the culprit vessel. We sought to determine whether inflammation is manifested by increased concentrations of selected markers in ostial blood sampled from a culprit coronary artery proximal to an atherosclerotic plaque. The concentrations of C-reactive protein (CRP), interleukin (IL)-6, IL-1 receptor antagonist, and soluble CD40 ligand (sCD40L) were measured in blood drawn from 75 patients before percutaneous coronary intervention from the femoral artery and from a guide catheter after engagement of the culprit coronary artery. Results were compared using Student's t tests. An acute coronary syndrome was present in 88% of patients. The concentrations of CRP and IL-6 were similar in coronary ostial and peripheral blood. Concentrations of IL-1 receptor antagonist were consistently greater in coronary arterial compared with peripheral arterial blood (peripheral 545 +/- 378 vs coronary 595 +/- 388 pg/ml, p = 0.003). Concentrations of sCD40L were also greater in the coronary compared with peripheral blood (peripheral 0.80 +/- 0.46 vs coronary 2.12 +/- 2.77 ng/ml, p <0.0001). The increased concentration of IL-1 receptor antagonist and sCD40L in blood drawn from the culprit coronary artery compared with that taken from the peripheral artery suggests that these cytokines contribute directly to inflammation in response to coronary intervention and may potentiate a systemic inflammatory state.

Adult↗
PubMed2004

Bleeding complications after contemporary pharmacoinvasive therapy for ST elevation myocardial infarction.

BACKGROUND: Pharmacoinvasive therapy for the treatment of ST elevation myocardial infarction (STEMI) is a strategy that combines early restoration of coronary flow via pharmacologically induced thrombolysis with subsequent, prompt percutaneous coronary intervention (PCI). Prior studies suggesting a heightened bleeding risk of PCI performed early after fibrinolysis predated contemporary pharmacoinvasive practice including use of femoral closure devices (CD), fibrin specific thrombolytics, lower doses of heparin and stents. METHODS: Consecutive patients were included in this retrospective registry study if they underwent emergent PCI for ST elevation myocardial infarction (STEMI) followed by immediate use of a groin closure device. Between Oct 1, 2002 and Jan 1, 2003, 27 patients were treated with immediate use of CD after post-thrombolytic PCI, performed within 12 hours of thrombolysis (pharmacoinvasive group). 58 patients were treated with immediate use of CD after primary PCI for STEMI. The two groups were compared with respect to the incidence of successful groin closure, bleeding complications, and clinical outcomes. Bleeding events were categorized according to the TIMI criteria. All baseline clinical and treatment variables were compared between the two groups to determine and the association of these variables (including use of thromblytic therapy) with TIMI major and TIMI minor bleeding was determined. RESULTS: Pharmacoinvasive recanalization with PCI occurred 348 +/- 183 minutes after initiation of fibrinolytic therapy. Glycoprotein IIb/IIIa inhibitors were used less frequently in the patients treated with a thrombolytic agent (59% vs. 90%, p < 0.01). Successful immediate hemostasis was obtained with CD in greater than 85% of patients in both groups (89% for pharmacoinvasive group vs. 86% for primary PCI group, p = 0.89). No patient required vascular surgical intervention. TIMI major bleeding and transfusion requirements were less than 5% in both groups. Antecedent thrombolytic therapy was not a predictor of bleeding complications after PCI. CONCLUSIONS: Use of CD as part of a contemporary pharmacoinvasive strategy is associated with a low rate of major bleeding complications.

Adult↗
PubMed2004

Soluble CD40 ligand is an early initiator of inflammation after coronary intervention.

BACKGROUND: This prospective study evaluated the early increase in markers of inflammation after coronary stenting, and the predictors of early rise. Elevation of markers of inflammation after percutaneous coronary intervention correlates with an increased risk of adverse events. The role of soluble CD40 ligand (sCD40L) as a potential initiator of inflammation after stenting has not been described. METHODS: Seventy-five patients were treated with heparin alone (n=25), or randomized to adjuvant treatment with eptifibatide (n=26) or abciximab (n=24) during stenting. Systemic blood was obtained before coronary stenting and at 10 min after stenting. C-reactive protein (CRP), interleukin (IL)-6, IL-1 receptor antagonist and sCD40L were determined by enzyme liberated immunosorbent assay. RESULTS: sCD40L exhibited the greatest relative rise (35%, P=0.01 compared to concentrations before intervention) in the first 10 min after stenting. In a logistic regression model, an early increase in the concentration of sCD40L was predicted by baseline laboratory values (white blood count and sCD40L level before stenting) and procedural characteristics (number of stents and glycoprotein IIb-IIIa inhibitor assignment). CONCLUSIONS: In conclusion, a systemic inflammatory response is detectable 10 min after coronary stent placement. The early increase in sCD40L suggests a possible role for this marker in the initiation of inflammation after coronary stenting.

Abciximab↗
PubMed2004

Development of glycoprotein IIb-IIIa antagonists: translation of pharmacodynamic effects into clinical benefit.

This article will review the development of glycoprotein IIb-IIIa antagonists, with particular emphasis on the characteristics and pharmacodynamic studies of each agent that is available for clinical use. Abciximab is a Fab fragment of the 7E3 antibody that has high affinity and a slow rate of dissociation from glycoprotein IIb-IIIa. In contrast, the small molecules eptifibatide and tirofiban, have a much more rapid rate of dissociation, with an off time of 10 to 15 s. Accordingly, the circulating pool of abciximab is predominantly associated with platelets, whereas maintenance of a consistent concentration of tirofiban and eptifibatide in the blood is critical in order to achieve and sustain their inhibitory effects. The affinity of abciximab and tirofiban for glycoprotein IIb-IIIa are substantially greater than that of eptifibatide, necessitating maintenance of greater molar concentrations of eptifibatide in blood in order to achieve effective inhibition of the binding of fibrinogen to the activated conformer of glycoprotein IIb-IIIa.

Binding Sites↗
PubMed2003

Comparison of inflammatory markers in patients with diabetes mellitus versus those without before and after coronary arterial stenting.

Patients with diabetes are at increased risk for adverse events after coronary stenting, perhaps reflecting a pro-inflammatory state. To characterize the inflammatory response to coronary stenting in patients with and without diabetes, blood samples were obtained from 75 patients before stenting and 10 minutes, 1 hour, and 24 hours later. C-reactive protein (CRP, microg/ml), interleukin (IL)-6 (pg/ml), IL-1 receptor antagonist (pg/ml), and soluble CD40 ligand (ng/ml) were assayed in each sample by enzyme-linked immunosorbent assay. Concentration changes after stenting were identified by repeated-measures analysis of variance. Multivariate analysis was performed to delineate independent predictors of increased concentrations of inflammation markers. Overall, 88% of patients had acute coronary syndromes; 36% had elevated markers of cardiac injury. The preprocedural concentrations of CRP in those with diabetes were more than twice as high as those in patients without diabetes. Two independent predictors of elevated preprocedural CRP concentrations were diabetes (odds ratio 3.95, 95% confidence interval 1.17 to 13.4) and a cardiac marker-positive acute coronary syndrome (odds ratio 3.70, 95% confidence interval 1.22 to 11.2). Preprocedural concentrations of IL-6, IL-1 receptor antagonist, and soluble CD40 ligand tended to be greater in patients with diabetes. The increase in CRP after stenting was much greater for patients without diabetes compared with that in patients with diabetes such that the apparent intensity of inflammation after 24 hours was similar in those with and without diabetes. Thus, patients with and without diabetes exhibit different inflammatory responses to stenting, reflecting the lower preprocedural inflammation in those without diabetes versus those with diabetes.

Acute Disease↗
PubMed2003

Increase in interleukin-6 in the first hour after coronary stenting: an early marker of the inflammatory response.

BACKGROUND: Inflammation after coronary stenting presages adverse outcomes after percutaneous coronary intervention (PCI). While changes in inflammatory markers have been defined 24-72 hours after PCI, potential changes during the first few hours have not. This study was designed to determine if a systemic inflammatory response could be measured within the first hour after stenting. METHODS: Patients (n = 25) undergoing coronary stenting, with predominantly (n = 23) acute coronary syndromes were enrolled prospectively in this registry. Blood samples were collected before PCI, and 10 minutes, 1 hour and 18-24 hours later. No patient received a glycoprotein IIb-IIIa inhibitor. Concentrations of C-reactive protein (CRP), interleukin-6 (IL-6), and interleukin-1 receptor antagonist (IL-1Ra) and soluble CD40 ligand (sCD40L) were measured using ELISA. RESULTS: CRP and sCD40L did not change in the first hour after stenting. By contrast, IL-6 increased in the first hour (before = 7.6 +/- 7.7 pg/ml, 1 hour = 12 +/- 12 pg/ml; p < 0.001). The concentration of IL-1Ra tended to be greater after 1 hour (before = 426 +/- 261 pg/ml, 1 hour = 511 +/- 406 pg/ml; p = 0.11). Increase in IL-1Ra was apparent only in female subjects (p = 0.004 for the difference in trend between the two genders). A correlation was not observed between the increase in IL-6 at 1 hour and the increase in CRP at 24 hours (r = -0.21). CONCLUSIONS: In patients undergoing coronary stenting, increase in IL-6 can be detected 1 hour after PCI, and thus IL-6 may be an early initiator of the systemic inflammatory response to stenting.

Aged↗