Restenosis is a major problem for patients undergoing percutaneous transluminal coronary angioplasty (PTCA). Inflammatory processes and genetic factors have been suggested to be involved in the pathogenesis of both atherosclerosis and restenosis. The recently discovered family of Toll-like receptors (TLRs) consists of molecules that initiate signaling after host-pathogen interactions. Recently it has been shown that the TLRs are involved in the development and progression of atherosclerosis by interfering with lipid metabolisms and by mediating inflammation. TLR-2 is a key innate immunity receptor for sensing both endogenous inflammatory mediators and ligands of several microbial pathogens postulated to be involved in atherosclerosis. A frequent single nucleotide polymorphism (SNP) for the TLR-2 gene, resulting in a non-functional receptor, has been described. By genotyping two independent groups of patients receiving PTCA, followed by stent implantation in one group, we found a significantly enhanced frequency of the TLR-2 Arg753Gln SNP in patients with restenosis as compared to those without restenosis (PTCA: 7.21 versus 2.45%, P = 0.014; PTCA/stent: 6.86 versus 1.53%, P = 0.013). In contrast, a common TLR-4 SNP was similarly distributed among the patient groups investigated. We furthermore compared the frequency of both SNPs in the patients with an age-matched group of individuals without atherosclerosis and found a trend towards a lower frequency of the TLR-4 SNP in the atherosclerotic group (PTCA: 5.58; PTCA/stent: 3.85 versus 7.14%). We conclude that in restenosis a functional TLR-2 is protective and potentially involved in a reaction pattern preventing restenosis. Screening for the TLR-2 Arg753Gln SNP may be of importance for stratifying a patient's risk and for preventive and therapeutic measures.

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In patients with coronary artery disease, the possession of the 298Asp and -786C variants of the eNOS gene are a risk factor for coronary in-stent restenosis, demonstrating the importance of the nitric oxide system in restenosis.

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Potassium channel openers or agonists represent a novel new class of compounds in the treatment of a range of cardiovascular disorders, particularly angina pectoris and hypertension. Nicorandil is the only clinically available potassium channel opener with antianginal effects, and with comparable efficacy and tolerability to existing antianginal therapy. It confers benefits through a dual action: opening the mitochondrial KATP channels leading to preconditioning of the myocardium and a nitrate-like effect. Myocardial preconditioning is important in reducing infarct size, severity of stunning and cardiac arrhythmias. These effects make nicorandil a unique antianginal compound that reduces both pre- and after-load and improves coronary blood flow. Comparative and noncomparative studies support the use of nicorandil as monotherapy or in combination with other antianginal therapy for stable angina pectoris. However, large studies are required to confirm its role in the treatment of acute coronary syndromes despite the favourable results from small studies.

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The use of the radial approach in elderly patients undergoing primary and rescue PCI, when successful, is safe and effective as the femoral approach, and leads to fewer vascular complications.