Georges Badaoui

Effect of High Bolus Dose Tirofiban on the Inflammatory Response Following Percutaneous Coronary Intervention

Tirofiban at the bolus dose of 10 µg/kg does not suppress the inflammatory response following percutaneous coronary intervention (PCI). This may be due to less than optimal inhibition of platelet aggregation. High bolus dose tirofiban (25 µg/kg) allows better inhibition of platelet aggregation but its anti‐inflammatory effect remains unknown.

Percutaneous coronary intervention increases leptin and decreases adiponectin levels

Objective  The study was designed to examine the effect of percutaneous coronary intervention (PCI) on adiponectin and leptin levels. We have previously demonstrated that PCI triggers a systemic inflammatory response. We hypothesized that inflammation participates in the pathogenesis of diabetes mellitus and the metabolic syndrome by modulating levels of adiponectin and leptin.

Substernal goitre: a rare cause of pulmonary hypertension and heart failure.

Benign substernal goitres usually extend into the upper anterior mediastinum and are easily extractable through a cervical approach. Very infrequently these tumours extend into the thoracic cavity causing compression of mediastinal structures. The authors report a case of pulmonary hypertension and severe cardiac failure secondary to a long-standing substernal goitre, and support the surgical management of this disease.

BEYOND LDL-CHOLESTEROL REDUCTION: EFFECT OF EZETIMIBE IN COMBINATION WITH ATORVASTATIN ON OXIDIZED LDL-CHOLESTEROL IN PATIENTS WITH CORONARY ARTERY DISEASE OR CORONARY ARTERY DISEASE EQUIVALENT

Methods: This is a prospective, randomized, double-blind, placebo controlled trial. Inclusion criteria were stable coronary artery disease (CAD) or CAD equivalent. All patients were placed on atorvastatin (atorva) 40 mg/day and were then randomized to eze 10 mg/day vs. placebo. Patients who were on statin therapy prior to inclusion, were allowed to enter the study as long as the potency of their statin was < atorva 20 mg/day. LDL levels were not entry criteria. Total LDL, LDL particle size, large buoyant LDL, small dense LDL, HDL, VLDL, and ox-LDL, were measured at baseline and following 8 weeks of therapy.

Tirofiban does not attenuate the acute inflammatory response triggered by percutaneous coronary interventions

Background: Percutaneous coronary intewention (PCI) triggers an inflammatory response which is incriminated in the pathogenesis of future adverse cardiac events. Tirofiban improves the outcome of PCI by inhibiting platelets aggregation, but its effect on the inflammatory response remains unknown. Methods: Patients with stable coronaty artery disease and no known inflammatory conditions who were undergoing PCI, were randomized to receive a bolus and a 24-hour infusion of tirofiban vs. saline. High sensitivity C-reactive protein (hs-CRP). interleukin-6 (IL-6), tumor necrosis factor alpha (TNF), and soluble intracellular adhesion molecules @ICAM) were measured at baseline and 46 hours after the procedure. Fleeufts: Forty patients were enmlled, 21 in the tirofiban group and 19 in the saline group. Stenting was performed in all but 1 patient who had balloon angioplasty. Troponin T was undetectable in all patients at baseline and 24 hours later. Levels of hs-CRP, IL-6, and TNF increased following PCI (h&RF? 9.li13.6 mg/dL vs. 16.5il5.5 mg/dL, p<O.OOl; IL-6: 4.4g.4 pg/mL vs. 6.324.5 pg/mL, p=O.Ol; TNF: 4.722 pg/mL vs. 7.3i10.4 pg/mL. p=O.O9). Levels of slCAM did not change (214110 ng/mL vs. 221 fl0 ng/mL, p=NS). None of the changes in the 4 markers was significantly affected by the use of tirofiban (table). Conclusion: hs-CRP, IL-6 (and probably TNF) but not slCAM are increased 46 hours after PCI. This acute inflammatory response however, is not attenuated by the use of tirofiban.