Coronary artery disease (CAD) is inexorably linked to abnormal cholesterol levels, particularly low-density lipoprotein- C (LDL-C).^1–4 Longstanding hyperlipidemia leads to deposition of oxidized LDL-C in activated macrophages and results, ultimately, in the formation of the atherosclerotic plaque. As it became apparent in the last three decades, most of the plaque resides in the coronary artery wall. The remodeling associated with this process enables patients to have large volumes of plaque without appreciable reduction in the dimensions of the coronary lumen available for blood flow.⁵

Thrombus is highly prevalent in patients with peripheral arterial disease, particularly those with recent symptoms and occluded or subtotally occluded vessels. In a prospective registry of 17 consecutive patients with recent (< 6 months) symptoms and lower-extremity occluded vessels, intravascular ultrasound (IVUS) revealed the presence of a definite thrombus in 16/17 patients (94%). Definite thrombus was present angiographically in only 2/17 patients (11.8%) and therefore was largely underestimated by the angiogram.¹

Percutaneous renal artery stenting is a well-established revascularization modality for the treatment of significant renal artery stenosis (RAS) in selected patients with uncontrolled hypertension, renal insufficiency or heart failure symptoms.^1–3 Despite improving blood pressure control and preserving renal function in some patients,^2–7 in-stent restenosis remains an important problem, as it can occur in up to 39% of patients.^2,8 Optimal stent deployment defined by the poststenting minimal lumen area (MLA) or minimal lumen diameter (MLD) is an important predictor of late stent patency.^9-12 Stent diameter and cross-sectional area post deployment can be determined by visual estimation, quantitative analysis (QA) or by intravascular ultrasound (IVUS). Visual estimation is subjective and has significant inter- and intraobserver variability and inherent limitations.

Renal artery stenosis is mainly a disease of progressive atherosclerosis involving the ostium and proximal third of the main renal artery and the peri-renal aorta. Atherosclerosis accounts for 90% of cases of renal artery stenosis (RAS).¹ The prevalence of atherosclerotic RAS increases with age, particularly in patients with diabetes, hyperlipidemia, diffuse type of peripheral arterial occlusive disease, coronary artery disease or hypertension.^2–6

Nitinol, an alloy composed of 55% nickel and 45% titanium, has been widely used in medical products. With its superelastic and shape-memory properties, nitinol has generated new models of occlusion devices for transcatheter closure of atrial septal defects (ASD) and various other cardiovascular defects. These nitinol devices not only yielded excellent results, but also made for easy and safe device implantation. However, there is a concern about release of nickel after implantation of nitinol devices,^1,2 especially in patients with nickel allergy.^3-5 This is where platinum-activation of nitinol by nanotechnology has a role. By a process called plasma deposition, ultra-thin layers of platinum atoms are deposited on the surface of nitinol wires. The platinum layers prevent nickel release, but do not change the superelastic and shapememory properties of nitinol.

Since the description by King,^1–3 Rashkind^4–6 and their associates of devices to occlude atrial septal defects (ASDs), a number of ASD occluding devices have been designed, investigated and were reviewed elsewhere.^7–12 The devices were initially tested in animal models, followed later by clinical trials in human subjects. These devices include: King and Mill’s device (1976), the hooked Rashkind device (1977); doubledisk Rashkind device (1983); clamshell occluder (1990); first, second- and third-generation buttoned devices (1990); ASDOS (ASD occluding system) (1991); modified Rashkind patent ductus arteriosus umbrella device (1994); inverted buttoned device (1997); Das Angel Wing device (1998); Amplatzer septal occluder (1998); CardioSEAL and STARFlex devices (1998); fourth-generation buttoned device (2000); Helex septal occluder (2000); COD (centering-ondemand) buttoned device (2001); and transcatheter patch (2002).

Stroke is the leading cause of long-term disability and the third leading cause of death after cardiac- and cancer-related deaths. In 2004, the prevalence of stroke was estimated to be 5.7 million (2.4 million males, 3.3 million females). Every year, there are approximately 500,000 new and 200,000 recurrent strokes. Overall, 87% of all strokes are ischemic and 13% are hemorrhagic. Although the stroke-related death rate fell from 20.4% to 6.7% in recent years, it still accounts for 1 in every 16 deaths. The major cause of stroke is large-vessel atherosclerosis (accounting for one-third of all strokes), with the highest risk associated with stenosis of the internal carotid arteries (ICA).

Chronic total occlusion (CTO) represents 10–20% of all angioplasty cases and remains a challenge for interventional cardiologists.^1–3 CTOs are associated with significant angina, impaired left ventricular function and poor long-term outcomes.⁴ Although new devices have been developed and implemented, the success rate for intervention of CTO is still only up to 55–80%.^4,5 Significant limitations to successful recanalization include the failure to cross the wire through the CTO, the age of occlusion, lesion length, lack of presence of a tapered stump, tortuosity and severe calcification.⁶ Previous reports have demonstrated that successful revascularization of CTOs significantly improves angina in symptomatic patients, improves left ventricular function, and reduces mortality.^7–9 Therefore, it is very important to create a useful large animal model of a CTO, which would facilitate the development of nov

Chronic total occlusions (CTOs) present one of the most challenging obstacles to interventional cardiologists in the current era. Technical difficulties associated with percutaneous coronary intervention (PCI) of CTOs are reflected by lower success rates of the procedure (approximately 60–80%) compared to other lesion subsets.^1–3 Furthermore, there are substantial risks associated with this procedure.

During angiography, when the saphenous vein graft (SVG) bypassing a chronic total occlusion (CTO) in a coronary artery is found to be patent without significant obstructive disease, conventional wisdom would suggest adequate distal perfusion supply and negate the need for further intervention. Independent of angiographic appearance, however, SVGs have been shown to exhibit features of endothelial dysfunction.^1,2 Despite the presence of a patent and nonobstructive SVG, regional myocardial perfusion may still be compromised, leading to clinical presentation of ischemia. Recanalization of the native vessel may still be necessary despite a patent SVG.