Stroke is the third major cause of death in the United States with carotid artery occlusive disease as the underlying etiology in about 20–30% of cases.^1,2 Carotid artery stenting (CAS) is a widely used procedure for carotid artery occlusive disease, especially in patients at high risk for carotid endarterectomy.^3,4 CAS is a less invasive procedure than carotid endarterectomy, but it is not free from risk.

Stent implantation revolutionized interventional cardiology. Stent development required improved antiplatelet therapy and new materials.^1–3 Nonetheless, intimal hyperplasia resulting in in-stent restenosis (ISR) occurs in a significant number of patients. Despite several promising therapeutic approaches using beta-emitting probes or the release of substances from coated stent surfaces, a solution to the ISR problem remains unsatisfactory.^4,5 Recently, polymer-regulated paclitaxel and sirolimus delivery at the site of arterial injury was shown to reduce, but not eliminate, ISR.^6–12 Angiotensin II (Ang II) is an important vasoactive peptide contributing to ISR. Ang II is generated locally in the vessel wall and has a direct trophic influence on vascular smooth muscle cells ( VSMC).¹³ Ang II AT₁ receptors mediate the Ang II-related growth and inflammatory signals.^14,15

Nearly two decades have elapsed since the early percutaneous closure of ventricular septal defects (VSD),^1,2 and controversies surrounding such techniques persist.³ The early types of devices developed for VSD closure were associated with low success rates and high morbidity; this was attributed in part to the design of the devices and the fact that they were not specifically designed for paramembranous VSD (pm- VSD) anatomy.^1,4,5 The pilot devices helped to elucidate the expected efficacy of the procedure, as well as the related complications, such as device embolization, hemolysis, aortic regurgitation and atrioventricular (AV) valve regurgitation. In addition, conduction disturbances and AV block represented a significant concern due to the anatomical proximity of the conduction system.

Rashkind¹ performed catheter closure of ventricular septal defects (VSDs) in animal models in the early 1970s; he initially used hooked, single-disc and double-disc Rashkind devices. Subsequently, other investigators^2–6 attempted transcatheter closure of VSDs using Rashkind’s double-umbrella or clamshell devices. The clamshell device was also used to close muscular VSDs in complex congenital heart defects as a part of overall patient management.⁷ Sideris and his associates^8,9 utilized the buttoned device, Marshall and Perry¹⁰ used the CardioSEAL^® and STARFlex^® devices (NMT Medical, Inc., Boston, Massachusetts), while Le and his colleagues¹¹ applied the Nit-Occlud^® device (pfm - Produkte für die Medizin AG, Köln, Germany) to close VSDs.

The transradial approach to percutaneous coronary intervention (PCI) is established as a safe procedure with improved patient comfort and early ambulation.^1–3 This has translated into early discharge with reduced procedural costs leading to outpatient PCI.^4,5
Increasing numbers of patients are presenting with lesion morphology that requires a debulking strategy. Traditionally, high-speed rotational atherectomy (HSRA) has been performed via the femoral approach using 7 and 8 Fr catheters, and occasionally 9 Fr, to allow the use of a large-sized burr, which limited its use during 6 Fr radial PCI. However, using a smaller burr size would be more than adequate for partial debulking to allow the alteration of plaque compliance and facilitate stenting. Furthermore, operators for whom the radial artery is the default approach have usually scheduled patients for elective HSRA via the femoral route.

Rotational coronary atherectomy can be utilized for maximal plaque debulking or for a less aggressive strategy of lesion modification. The early recommended burr-to-artery ratio of 0.75–8, which was deemed to achieve a delicate balance of maximal debulking without causing undue burr-related vessel trauma, has been challenged. In the CARAT study,¹ a lesion modification strategy (burr-to-artery ratio < 0.7) was compared with a more aggressive lesion debulking strategy (burrto- artery ratio > 0.7) in a prospective multicenter, randomized trial. The findings of the 222 patients from 6 centers showed similar endpoints of final diameter stenosis, inhospital clinical complications and target lesion revascularization at 6 months between the two strategies. The acute angiographic complication rate immediately after atherectomy, however, was higher in the lesion debulking group.

Achieving rapid reperfusion in patients with ST-elevation myocardial infarction (STEM) has been established as an effective and life-saving treatment for these patients. The mortality benefit of primary percutaneous coronary intervention (PCI) is critically dependent on the time required to achieve reperfusion.^1–4 This has been conventionally measured as door-to balloon time with a goal of 90 minutes established as the time within which reperfusion should be achieved.

Acute ST-segment elevation myocardial infarction (STEMI) usually results from atherothrombosis, a disease process involving the rupture of an atherosclerotic plaque with subsequent thrombosis and coronary arterial occlusion at the site of the plaque.¹ Although this condition is associated with significant cardiac morbidity and mortality, the risks of myocardial damage, left ventricular dysfunction and death are reduced if prompt and sustained reperfusion of the infarct-related artery can be achieved.^2,3

Hemophilia A is an inherited X-linked recessive disorder of the intrinsic coagulation pathway which affects 1 in 10,000 males and is characterized by deficiency of factor VIII with resultant bleeding diathesis. Platelet function is normal.

The primary goal of treatment in patients presenting with ST-elevation myocardial infarction (STEMI) is reperfusion of the infarcted myocardium. Percutaneous coronary intervention (PCI) has emerged as preferred reperfusion therapy for STEMI.¹ To protect the microcirculation against distal embolization during primary PCI, various mechanical devices have been developed. Randomized controlled trials have demonstrated that manual thrombus aspiration for STEMI is safe and results in improved myocardial perfusion when compared with conventional angioplasty.^2–4 In some patients, thrombus aspiration itself results in complete restoration of epicardial blood flow, without residual stenosis or angiographic signs of plaque rupture at the culprit lesion. It is currently unclear if additional angioplasty is also necessary in these patients.