The field of interventional cardiology has been blossoming for the past 25 years. Since the performance of the first human percutaneous coronary angioplasty in 1977 by Gruentzig,1 angioplasty equipment has never ceased to improve. Miniaturization of the equipment has been one of the most important hallmarks. It has allowed performance of more complex angioplasty procedures and has also helped reduce peri-procedural complications.

There are two principal approaches to achieve femoral artery hemostasis following diagnostic cardiac catheterization or percutaneous coronary intervention (PCI): manual compression or arterial closure devices.1–6 Arterial closure devices are safe and effective in selected patients, with complication rates similar to or lower than manual compression.7 There are two principal types of closure device: suture-based and plugs.8 The Angio-Seal closure device (Daig, Minnetonka, Minnesota) achieves hemostasis by anchoring a collagen plug to the anterior vessel wall through a sheath delivery system.9–11 Recently, a new generation of the Angio-Seal device (Angio-Seal STS Platform™) became available. The Angio-Seal STS simplifies the deployment process for the operator; by eliminating the post-placement spring, the procedure is concluded in the cath lab.

Achieving hemostasis at the arteriotomy site after percutaneous coronary intervention has been discussed in The Journal of Invasive Cardiology previously.1–3 In this month’s Journal, Lasic et al.4 (see pages 356–358) compare the safety and efficacy of the first and new-generation Angio-Seal device in patients undergoing PCI. The first generation Angio-Seal device, while effective, was limited with respect to ease-of-deployment as well as patient comfort (patient immobile while the post-placement spring was intact). Conversely, the new-generation device allows for complete deployment while the patient is still on the catheterization table, reducing the procedure to one step while minimizing patient discomfort. The authors attempted to design and complete a study to demonstrate non-inferiority of the new-generation device compared to its first-generation.

Contrast-induced nephropathy is a frequent cause of hospital-acquired acute or chronic renal insufficiency in patients undergoing cardiac catheterization.1,2 The increasingly frequent use of contrast-enhancing imaging for both diagnosis and intervention in patients undergoing cardiac catheterization has generated concern about the avoidance of contrast-induced nephropathy. Though the precise mechanism (direct tubular injury, tubular obstruction, vasomotor instability or increase glomerular permeability to protein) has not been established, the amount of contrast agent is a predictor of acute renal function deterioration.3,4

Intracoronary radiation, by virtue of its ability to inhibit intimal hyperplasia and constrictive vascular remodeling, reduces restenosis after percutaneous coronary interventions (PCI). Long lesions — longer than the available source length — have been treated by manual multisegmental irradiation or “pullback” method, in which the source is manually pulled back to cover the entire injury length. While the efficacy of manual pullback has been shown in several clinical studies,1–3 doubts have been raised on the precision with which this was achieved, as inaccuracies inadvertently occur in the form of overlaps and gaps.4 A 60 mm transfer device, delivering a 60 mm b-radiation source train in a 5 French catheter, was specially designed to avoid or to minimize the necessity of pullback during brachytherapy of long lesions.

Patients with atherosclerotic renal artery stenosis have higher mortality compared to age and sex-matched controls in the general population.1-4 The risk of all cause death is increased 3.3 fold while the cardiovascular death is increased 5.7 fold.3
Survival following renal artery revascularization has not been systematically evaluated. The observations range from excellent survival following surgical revascularization,5 to adverse outcome following renal artery stenting in patients with abnormal baseline serum creatinine,6 to better survival limited only to patients whose renal function improved following successful renal artery angioplasty.7 However, the available data is retrospective and sample size is small.
The objective of our study was to supplement the existing survival data (and cause of death) in patients undergoing renal artery stenting for atherosclerotic renal artery stenosis and drug refractory hypertension.

Renal artery stenosis (RAS) remains a recognized contributor to hypertension and renal insufficiency. Initially, RAS, an infrequently diagnosed, curable cause of hypertension has become a more frequently diagnosed entity. While many of the younger individuals, particularly females have fibromuscular disease, atherosclerotic renal artery vascular disease is more commonly seen in older individuals. Early repair was surgical and associated with a modest complication rate related to the complexity of intra abdominal vascular surgery. With the advent of percutaneous vascular intervention, currently bolstered by more predictable results achieved with stents, renal revascularization has become much more common.

Case Report. We present the case of a 74-year-old male with a history of hypertension and smoking who was urgently referred for evaluation after he suffered a cardiac arrest after a transurethral prostate resection (TURP) in a community hospital without coronary intervention capabilities. The patient initially presented to the emergency room with progressively worsening abdominal distension and was found to have a distended urinary bladder and bilateral hydronephrosis due to an enlarged prostate. The patient underwent a TURP without complications. While in the recovery room, he was noted to be hypotensive and suddenly had ventricular tachycardia, which progressed to ventricular fibrillation. Advanced cardiac life support measures were immediately implemented, and the patient underwent multiple electrical cardioversions, received several doses of intravenous epinephrine, lidocaine, and atropine, and was intubated.

Endothelial dysfunction. Vascular endothelial cell dysfunction begins well before any morphologic manifestations of atherosclerosis are visible, and continues throughout the entire course, probably waxing and waning along the way. Well in advance of the development of atherosclerotic lesions, endothelial dysfunction exists as an independent predictor of future cardiovascular events.1 We now know that in fact this dysfunction is characterized by several features typical of inflammation, including expression of numerous cellular adhesion molecules, like vascular cell adhesion molecule (VCAM-1), intercellular adhesion molecule (ICAM-1) and E-selectin. The abnormally functioning endothelial cells also release proinflammatory cytokines such as interleukin (IL-1b), tumor necrosis factor (TNF-a) and c-reactive protein (CRP).

Case Report. A 42-year-old Aboriginal man was transferred from a peripheral hospital for coronary angiography. He presented a week earlier with a small anterolateral non-ST elevation myocardial infarction. He was treated with aspirin, clopidogrel, metoprolol, ramipril and a glyceryl trinitrate patch. His previous medical history included chronic renal failure for which he had been having peritoneal dialysis since 1994. His cardiovascular risk factors included continued cigarette smoking and hypertension.
His coronary angiogram, performed with a GE Medical Systems “flat panel” coronary angiographic imaging system, showed a filling defect in the distal left main coronary artery extending into the left circumflex artery (yellow arrow, panels A and B). His other coronary arteries showed evidence of non-critical, but calcified, disease.