Percutaneous coronary intervention is associated with mechanical endovascular injury and endothelial denudation. Re-endothelialization is essential for restoration of normal vascular homeostasis and regulation of neointimal hyperplasia. The endothelial progenitor cell recently emerged as an important component of the response to vascular injury, having the potential to accelerate vascular repair through rapid re-endothelialization. There remains considerable uncertainty over the precise identity and function of endothelial progenitor cells, and harnessing their therapeutic potential remains a challenge. A better understanding of the role of circulating progenitors in the response to vascular injury is necessary if we are to develop effective strategies to enhance vascular repair after percutaneous coronary intervention. In this review, we examine the preclinical and clinical evidence of a role for bone marrow-derived putative endothelial progenitor cells after iatrogenic vascular injury associated with balloon angioplasty and stent deployment. Therapies designed to mobilize endothelial progenitors or to increase their ability to home to the site of stent implantation may have a role in the future management of patients undergoing percutaneous coronary intervention.

No abstract

This multicenter registry indicates a high rate of Linox lead failure, particularly in female patients. Ongoing surveillance of the Linox ICD lead performance is recommended.

ObjectiveThe inflammatory cytokine, tumour necrosis factor α (TNF-α), exerts deleterious cardiovascular effects. We wished to determine the effects of TNF-α antagonism on endothelial function and platelet activation in patients with acute myocardial infarction.Design and setting and patientsA double-blind, parallel group, randomised controlled trial performed in a tertiary referral cardiac centre. 26 patients presenting with acute myocardial infarction randomised to receive an intravenous infusion of etanercept (10 mg) or saline placebo.Main outcome measuresLeucocyte count, plasma cytokine concentrations, flow cytometric measures of platelet activation and peripheral vasomotor and fibrinolytic function were determined before and 24 h after study intervention.ResultsConsistent with effective conjugation of circulating TNF-α, plasma TNF-α concentrations increased in all patients following etanercept (254±15 vs 0.12±0.02 pg/ml; p<0.0001), but not saline infusion. Etanercept treatment reduced neutrophil (7.4±0.6 vs 8.8±0.6×109 cells/l; p=0.03) and plasma interleukin-6 concentrations (5.8±2.0 vs 10.6±4.0 pg/ml; p=0.012) at 24 h but increased platelet–monocyte aggregation (30±5 vs 20±3%; p=0.02). Vasodilatation in response to substance P, acetylcholine and sodium nitroprusside, and acute tissue plasminogen activator release were unaffected by either treatment (p>0.1 for all).ConclusionsFollowing acute myocardial infarction, etanercept reduces systemic inflammation but increases platelet activation without affecting peripheral vasomotor or fibrinolytic function. We conclude that TNF-α antagonism is unlikely to be a beneficial therapeutic strategy in patients with acute myocardial infarction.