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Biomedical subjects

Atul Aggarwal

Publications and source records attributed to Atul Aggarwal.

23 records · Page 2Linked to original sources
PubMed2002

Management of Mitral Regurgitation Due to Mitral Prolapse.

Notable advances have been made in the treatment of mitral regurgitation, especially the advances resulting from prolapse of the mitral valve with or without a flail leaflet. Prosthetic mitral valve replacement results in a high incidence of postoperative left ventricular systolic dysfunction. Recognition of the importance of the subvalvular apparatus for preserving contractile function has fostered development of new repair techniques that preserve native valve tissue and reduce or eliminate postoperative systolic dysfunction and the need for anticoagulation. Vasoactive medications have a very limited role in the management of patients with primary mitral regurgitation. Better screening tools enable detection of early ventricular decompensation, and appropriate operative interventions continue to significantly reduce the morbidity and mortality associated with mitral regurgitation. Mortality associated with ischemic mitral regurgitation resulting from annular ring dilatation or structural damage associated with rupture of a papillary muscle continues to be high, and the simplest and most expeditious operative intervention is emphasized.

Journal Article↗
PubMed2002

Decreased platelet reactivity in blood anticoagulated with bivalirudin or enoxaparin compared with unfractionated heparin: implications for coronary intervention.

BACKGROUND: Platelet reactivity predicts complications after percutaneous coronary intervention (PCI). Accordingly, agents that suppress platelet reactivity should decrease adverse events after PCI. This study was designed to determine the effects of therapeutic concentrations of unfractionated heparin (UFH), bivalirudin, or enoxaparin alone or in combination with tirofiban on platelet reactivity. METHODS: Blood taken from 13 patients with coronary artery disease was exposed to each anticoagulant alone or in combination with tirofiban ex vivo. Platelet reactivity was characterized with flow cytometry to quantify the percentage of platelets capable of binding fibrinogen (activation of glycoprotein IIb-IIIa) and expressing P-selectin in response to adenosine diphosphate (ADP, 0, 0.2, and 1 microM). RESULTS: Platelet reactivity was greater in blood treated with UFH than in blood anticoagulated with bivalirudin with respect to both the capacity to bind fibrinogen (by 4 +/- 1.8%, p = 0.01) and P-selectin expression (by 7.7 +/- 0.7%, p, < 0.0001) in response to 1 microM ADP. Platelet reactivity was greater in blood treated with UFH than in blood exposed to enoxaparin with respect to P-selectin expression (by 7 +/- 1.1%, p, < 0.0001) in response to 1 microM ADP. Platelet reactivity was similar in blood treated with bivalirudin or enoxaparin. Addition of tirofiban suppressed the capacity to bind fibrinogen in the presence of each anticoagulant to a similar extent. CONCLUSIONS: As platelet reactivity is greater in blood anticoagulated with UFH in comparison with blood anticoagulated with enoxaparin or bivalirudin, the use of bivalirudin or enoxaparin rather than UFH during PCI should contribute to a reduced incidence of adverse cardiac events after PCI.

Adenosine Diphosphate↗
PubMed2002

Biphasic effects of hemodialysis on platelet reactivity in patients with end-stage renal disease: a potential contributor to cardiovascular risk.

BACKGROUND: Cardiovascular disease is rampant in patients with end-stage renal disease (ESRD), and increased platelet reactivity may contribute. This study is designed to determine effects of hemodialysis in patients with ESRD on platelet reactivity per se. METHODS: Platelet reactivity was determined by flow cytometry in 36 patients with ESRD undergoing hemodialysis. Blood was obtained from arterial and venous ends of the hemodialysis circuit at the beginning and end of the dialysis session. Platelet reactivity was defined with respect to capacity to bind fibrinogen (activation of glycoprotein IIb-IIIa) and expression of P-selectin in response to adenosine diphosphate (ADP; 0, 0.2, and 1.0 micromol/L). Comparison studies were performed with 55 patients with coronary artery disease (CAD) and 38 healthy subjects. RESULTS: Platelet reactivity was increased by exposure to the dialysis circuit (capacity to bind fibrinogen: arterial, 28% +/- 13%; venous, 47% +/- 20%; P < 0.001). Despite this effect, surface expression of P-selectin in response to 1 micromol/L of ADP was lower at the end of the dialysis session (arterial blood at its onset, 40% +/- 16%; arterial blood at its conclusion, 24% +/- 15%; P < 0.05). Confocal microscopy showed increased nonspecific association of fibrinogen with platelets after dialysis, suggesting that increased aggregation after dialysis may be secondary to effects of dialysis on fibrinogen binding, rather than on platelet reactivity. Platelet reactivity was increased similarly in patients with ESRD and those with CAD compared with healthy subjects. CONCLUSION: Although interaction between platelets and the dialysis circuit increases platelet reactivity, continued dialysis decreases platelet reactivity.

Adenosine Diphosphate↗
PubMed2002

Treatment of totally occluded saphenous vein grafts using self-expanding stents.

Patients with saphenous vein graft (SVG) disease represent an increasing proportion of those referred for percutaneous coronary intervention. The success of treatment of occluded SVG with percutaneous intervention has been limited by frequent occurrence of no-reflow phenomenon. Use of self-expanding stents with low pressure pre- and post-dilation may improve success by limiting embolism of atherothrombotic debris. The self-expanding stents provide a meshed design that helps to trap the atherothrombotic debris between the vessel wall and stent struts. Results with two patients are described to illustrate the proposed technique that appears to limit no-reflow during and immediately after the procedure. Adjunctive treatment with a GP IIb-IIIa inhibitor is likely to be of benefit as well. Additional studies are required to demonstrate definitively the potential benefits of this approach.

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