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Arun Kalyanasundaram

Publications and source records attributed to Arun Kalyanasundaram.

3 recordsLinked to original sources
PubMed2007

Thrombus predicts ischemic complications during percutaneous coronary intervention in saphenous vein grafts: results from TARGET (do Tirofiban and ReoPro give similar efficacy trial?).

BACKGROUND: Saphenous vein graft (SVG) percutaneous coronary intervention (PCI) carries a high risk of ischemic complications. However, there are scant recent data to identify which SVG lesions carry particularly high risk in recent years. We studied demographic and angiographic factors associated with ischemic complications after SVG PCI without distal protection in the TARGET (do tirofiban and reopro give similar efficacy trial?) study. METHODS: TARGET was a multicenter double-dummy, double-blinded study randomizing 4,809 PCI patients to tirofiban or abciximab. Of these, 254 patients underwent PCI involving an SVG lesion. The primary endpoint of this analysis was major adverse cardiac events (MACEs) at 30 days, including death, nonfatal myocardial infarction (MI), and urgent target vessel revascularization. RESULTS: No demographic characteristic was associated with 30-day MACE. Lesion length > 20 mm (odds ratio [OR] = 2.7, P = 0.03), thrombus (OR = 3.9, P = 0.003), eccentricity (P = 0.001), thrombolysis in myocardial infarction flow < 3 post-procedure (OR = 5.6, P = 0.037), and >1 target lesion (OR = 2.5, P = 0.035) were univariate variables associated with 30-day MACE. Multivariate analysis associated only thrombus (OR = 3.8, P = 0.015) with 30-day MACE. No difference in outcomes was noted between patients receiving abciximab and tirofiban. SVG patients had lesser angiographic success (95.6% vs. 98%, P = 0.04) and increased 30-day Q-wave MI (2.5% vs. 0.9%, P = 0.039) compared with non-SVG patients, but a similar incidence of death (0% vs. 0.4%), non-Q-MI (5.9% vs. 4.5%), and target vessel revascularization (0.5% vs. 1%). CONCLUSION: In the era of routine stenting and GpIIb/IIIa inhibitors, thrombus is the angiographic characteristic most closely associated with adverse outcomes of SVG PCI.

Abciximab↗
PubMed2006

Simvastatin suppresses experimental aortic aneurysm expansion.

OBJECTIVE: Abdominal aortic aneurysm (AAA) formation is a result of inflammation and extracellular matrix (ECM) remodeling mediated by matrix metalloproteinases (MMPs). Hydroxymethylglutaryl-coenzyme A inhibitors (statins), although clinically used as lipid-lowering agents, have also been demonstrated to have anti-inflammatory effects. This study was designed to determine whether the hydroxymethylglutaryl-coenzyme A inhibitor simvastatin suppresses aneurysm formation in an elastase-induced rat AAA model. METHODS: Aneurysms were created in adult male Wistar rats by infusion of elastase into isolated infrarenal aortic segments. The rats were randomized to receive either simvastatin (n = 17) or placebo (n = 17) by gastric lavage daily starting the day before surgery. The rats were euthanized and the infrarenal aortas harvested on postoperative day 7. Aortic diameters were measured before infusion, immediately after infusion, and at the time of harvesting. Protein expression was measured by immunoblot analysis. Gene expression profiling using Affymetrix U34A rat genome chips was performed to identify changes in gene expression caused by simvastatin treatment. RESULTS: Mean aneurysm diameter was significantly less in the simvastatin treatment group compared with controls (3.4 +/- 0.08 mm vs 4.3 +/- 0.19 mm; P = .0001). MMP-9 and nuclear factor-kappaB protein levels were decreased in the aortas of simvastatin-treated animals. Gene microarray analysis revealed 315 genes with statistically significant changes in expression (P < .05) in the simvastatin group. Genes related to inflammation, ECM remodeling, and oxidative stress function were downregulated. These included genes for interleukin 1, interleukin 4, inducible nitric oxide synthase, P-selectin, platelet-derived growth factor alpha, tumor necrosis factor, and several chemokines. CONCLUSIONS: Simvastatin significantly suppresses experimental aneurysm expansion and reduces protein levels of MMP-9 and nuclear factor-kappaB. Gene array analysis provides evidence that several mediators of inflammation, matrix remodeling, and oxidative stress are downregulated by simvastatin treatment. This suggests that simvastatin inhibits AAA formation by blocking the expression of certain proinflammatory genes. Simvastatin may be useful as an adjuvant therapy to suppress the growth of small aneurysms.

Animals↗