Balloon injury to the vessel wall triggers a reaction of thrombosis, inflammation and neointimal proliferation. The inflammatory process is mediated by a complex interaction between blood cells (platelets and leukocytes), coagulation factors (thrombin), and the endothelial/subendothelial layers, and is characterized by a rise in plasma levels of acute-phase reactants,^1–6 chemokines^,7,8 cytokines^3–6,9–11 and circulating cell adhesion molecules.^12,13 Elevated baseline levels of inflammatory markers and their augmentation with vascular injury are individual-specific and correlate with poor procedural and late outcomes.^1,14–19

Drug-eluting stents (DES) have been established as a safe and effective tool in preventing in-stent restenosis and repeat revascularization in selected patients and lesions.^1,2 However, individual and procedure-related factors can reduce their inhibitory effect on neointimal hyperplasia.^3–5 Moreover, it has been shown that plaque morphology can affect not only the immediate stent implantation result,⁶ but even the mid- to long-term outcomes. This can occur by means of plaque prolapse, nonuniform strut and drug distribution,⁷ or exuberant neointimal hyperplasia. Unfortunately, currently available stent platforms may not perform optimally in cases of large plaque burden (such as in-stent restenosis)^8–10 or in vessels rich in elastic media (such as aorto-ostial lesions).¹¹ Thus, in such high-risk lesions, further strategies to limit or avoid restenosis are required.

Peripheral arterial disease (PAD) is a problem of substantial public health importance. The disorder is estimated to affect 27 million people in Europe and North America alone.¹ Recent data have consistently revealed a sharp increase in PAD prevalence with age and generally somewhat higher rates in men than in women.^2,3 In addition, most studies have indicated significant associations between PAD and major cardiovascular disease risk factors. Diabetes and cigarette smoking typically show the strongest risk factor associations with PAD, with hypertension and dyslipidemia correlating as well.^2,3 The generalized systemic process underlying PAD poses a much greater threat to the cardiovascular health of patients than it does to their limbs. Approximately 50% of patients are asymptomatic, which may explain why this disease is often underdiagnosed and thus undertreated.4 However, PAD is associated with significant morbidity and mortality.

This short paper by Moreno et al. claims to show that patients with a chronic total occlusion (CTO) in a non-culprit coronary artery, who also have multivessel disease (MVD) and an acute myocardial infarction (MI) have a worse outcome than those with acute MI and MVD but without a CTO and worse than those with an acute MI but only single vessel disease. This is perhaps a not surprising finding but it is not convincing from this data that the difference is due to the presence of the CTO per se.

Primary percutaneous coronary intervention (PCI) is the best reperfusion strategy in patients with ST-elevation acute myocardial infarction (AMI).¹ This is mainly because it achieves a very high rate of successful recanalization of the infarct vessel in a wide variety of clinical and angiographic situations,² but also by virtually eliminating the risk of intracranial bleeding and reducing the incidence of mechanical complications.³

Drug-eluting stents (DES) significantly decrease the need for a new target vessel revascularization (TVR) after coronary intervention,^1–4 but its widespread use is still limited by cost issues.^5,6 DES are currently used in more than 70% of percutaneous coronary interventions (PCI) performed in the United States,⁷ but in less than 50% of procedures in most other countries. The reasons behind this “selective approach” are not only the high cost of DES when compared to bare metal stents (BMS), but also the belief that restenosis can be reasonably predicted by clinical and angiographic characteristics identified before stent implantation.

Nearly two years after the widespread introduction of drug-eluting stents (DES) on the U.S. market, it is perhaps time to step back and evaluate the impact of this revolutionary technology on the practice of cardiology. Financial modeling has suggested that the introduction of DES has turned PCI procedures from profit generators for hospitals into sources of loss.¹ The penetration of DES within the U.S. is approximately 70%, but varies from region to region.² In many metropolitan areas, adoption is nearly universal. The data for the use of DES are strong and incontrovertible, and the clinical benefit in trial populations is beyond debate. However, the use of DES now extends far beyond the clinical criteria of the randomized trials and includes patients who are at very low baseline risk for restenosis. In this issue of the Journal, Gottschall et al. report a simplified predictive score for target vessel revascularization (TVR) following bare metal stenting.

The development and even progression of coronary atherosclerotic lesions may occur without compromising the lumen in the early phases due to outward growth of the vessel wall; a concept known as “positive” or “outward” arterial remodeling.¹ Remodeling of the arterial wall is an important mechanism in determining luminal narrowing of native atherosclerotic lesions^1–4 and restenosis after percutaneous coronary interventions.^5–7 Moreover, data have suggested that arterial remodeling may be “negative” or “inward”, even in the early stages of plaque development.³ Recently, an association has been identified between the degree of coronary artery remodeling and unstable coronary syndromes. Two recent studies have shown an association between positive arterial remodeling and both unstable angina pectoris and acute myocardial infarction.^8,9

Primary angioplasty has become the preferred therapeutic modality in patients with acute myocardial infarction (AMI). Despite a rapid and sustained restoration of flow through a previously occluded epicardial coronary artery, perfusion at the myocardial level is inadequate in about 25–30% of cases.¹
The exact mechanisms underlying the microvascular dysfunction are not fully understood, but more recent evidence suggests that vasospasm in the myocardial vascular bed, due to platelet-derived vasoconstrictors and/or systemic release of agents such as endothelin, play a central role.²

The pigtail is the preferred catheter for left ventriculography. Because of its end-hole, which allows its manipulation with a guidewire, it can be advanced to the left ventricle both by the femoral and brachial approaches. The design of the catheter with multiple holes virtually eliminates the possibility of myocardial staining and the occurrence of ectopic ventricular beats is small.^1,2 The intramyocardial injection of contrast (myocardial staining) is caused by the improper positioning of the ventriculography catheter and can lead to refractory ventricular tachyarrythmias and occasionally cardiac death.