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As our understanding of the pathophysiology of adverse cardiovascular events evolves, the central role of platelets has become increasingly recognized. Plaque rupture, platelet activation, aggregation, and thrombus formation occur as a result of complex interactions between platelets, vascular endothelium, inflammatory cells, and circulating proteins and red blood cells. These processes can lead to vascular occlusion, ischaemia, and infarction in the native circulation consequent on plaque erosion or disruption. Similarly, during percutaneous coronary intervention and stent implantation, coronary vessel trauma and inflammation, as well as delayed stent endothelialization with ongoing exposure of the platelet-atttrative metal stent struts, combine to make some patients susceptible to adverse thrombotic events, including the potentially fatal stent thrombosis. This chapter will review key components of the processes and determine how therapeutic strategies can attenuate potential adverse cardiovascular events.

Congestive heart failure (CHF) is a major source of morbidity, mortality, and health-care resource consumption. However, the incidence of symptomatic CHF after primary percutaneous coronary intervention (PCI) for ST-segment elevation myocardial infarction (STEMI) has rarely been fully reported. We therefore examined the early and late incidence, predictors, and implications of CHF in the large-scale, prospective, randomized HORIZONS-AMI trial.New York Heart Association (NYHA) functional classification was prospectively collected from patient-level data at baseline, 30 days, 6 months, and at 1 and 2 years from 3,343 patients with STEMI undergoing PCI at 123 centers in 11 countries. The baseline incidence of CHF (before the index STEMI) was 2.6%, increasing to 4.6% 1 month after primary PCI (P.0001), 4.7% at 1 year, and 5.1% at 2 years. The incidence of NYHA class III/IV symptoms was 0.4% at baseline and 0.8% at 2 years (P = .03). CHF at 1 year was associated with diabetes (P.0001), dyslipidemia (P = .009), previous MI (P.0001), previous revascularization (P = .01), anterior STEMI (P = .02), and baseline TIMI grade 0 flow (P = .01) but not procedural anticoagulation with bivalirudin versus heparin + GPIIb/IIIa inhibitors (P = .93) or use of drug-eluting versus bare metal stents (P = .66). Among patients in whom CHF was not present at baseline but developed after PCI, the rate of all-cause mortality was significantly higher during 2-year follow-up (7.3% vs 2.0%, P.0001), as was cardiac mortality (2.4% vs 0.8%, P = .004), reinfarction (9.4% vs 5.2%, P = .0009), stent thrombosis (7.0% vs 3.8%, P = .007), and ischemic target vessel revascularization (19.4% vs 11.8%, P.0001).In the HORIZONS-AMI trial, the development of new-onset CHF within 2 years after contemporary PCI, although infrequent, was associated with significantly increased rates of mortality and major adverse ischemic events.

Major changes in the management of symptomatic obstructive coronary artery disease have been seen in the past 10 years with a substantial shift towards percutaneous coronary intervention (PCI). In the UK in 2005, for example, 73 000 PCIs were performed compared with 22 000 isolated coronary artery bypass grafting (CABG) procedures.1 Recently, there has been much debate about which of these two revascularisation options is “better” as measured by clinical outcome and overall cost effectiveness. This editorial will attempt to redress the balance on the use of PCI versus medical treatment in stable angina and its use in multivessel disease. Some have interpreted the recently published COURAGE trial,2 which randomised ( after coronary angiography) 2287 patients with positive non-invasive tests to either optimal medical treatment (OMT) or PCI, as indicating that OMT is equivalent to PCI for stable coronary artery disease and suggested that PCI is an overcostly, overused procedure. The 4.6-year composite of death/non-fatal myocardial infarction was 19.0% for PCI with OMT and 18.5% for OMT alone (p = 0.62). The relevance of this study to UK practice is doubtful since angioplasty in the UK is generally reserved for patients who have continuing symptoms despite OMT, although clearly there are patients who undergo PCI where there is clear evidence on objective non-invasive testing of silent ischaemia and a significant lesion in the same territory. It has never been the interventionist’s claim that PCI has an impact on mortality. Given that patients with left main stem disease and important left ventricular dysfunction (the very patients who may benefit prognostically from revascularisation) were excluded from this trial it seems highly likely that a similar trial comparing CABG with OMT would also show no difference. It is important to note that >40% of patients had little or no angina at trial entry. At follow-up 32.6% …

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