Current interventional cardiology reports最新文献

Late responses to nonstent coronary interventions are determined less by intimal hyperplasia than by the direction and magnitude of arterial remodeling, except in diabetic patients. Negative arterial remodeling is a late event, is often preceded by an early (nonsustained) positive remodeling, and is distinct from passive elastic recoil. Diabetic patients have an exaggerated intimal hyperplastic response. Plaque burden may play an important role in the restenosis process by amplifying the negative remodeling. Stents reduce restenosis by opposing the late negative remodeling to offset a stent-related increase in neointimal hyperplasia. Both probucol and radiation appear to reduce late lumen loss after balloon angioplasty by promoting positive remodeling.

Atherosclerotic cardiovascular disease, the major cause of death in the Western world, is a multi-factorial process with a large number of interacting variables. Despite a significant understanding of many of these variables, the underlying causes of atherosclerosis are still not clearly defined. Recent studies have documented a possible association between chronic inflammation and a variety of chronic bacterial infections (including Chlamydia pneumoniae, Helicobacter pylori, and a variety of periodontal infectious agents) and the development or progression of atherosclerosis. Because these bacterial agents are sensitive to a variety of antibiotic agents, it has been proposed that antimicrobial therapy might be useful in the primary or secondary prevention of atherosclerosis. This article reviews the evidence supporting an association between chronic bacterial infection and atherosclerosis, describes the results of preliminary secondary prevention antibiotic treatment trials, and discusses a variety of ongoing and planned large multicenter clinical trials of antibiotics in patients with atherosclerotic heart disease. Potential pitfalls associated with the broad use of antibiotics to treat heart disease are also discussed.

Coronary balloon angioplasty was first used in 1977; since then, indications for percutaneous coronary intervention have expanded. However, despite significant advances in reducing the incidence of acute complications, chronic restenosis of dilated lesions remains a serious and frequent problem. The mechanisms of restenosis can be described as a combination of effects involving three main components: vessel recoil and remodeling, hemostatic activation and thrombus formation, and neointimal hyperplasia. Thrombosis is associated with vascular and plaque injury. In animal models thrombus at the injury site is a major determinant of intimal hyperplasia and restenosis. Although the introduction of coronary stenting has limited the effect of vessel recoil and remodeling, no effective therapy is yet available to prevent restenosis. This article reviews the potential role of the hemostatic system in restenosis and those drugs and techniques that may inhibit its effect on the restenotic process.

The high frequency of restenosis after percutaneous coronary angioplasty is still a major clinical problem. It occurs in 30% to 60% of patients and limits the long-term success of angioplasty. Many clinical trials have been conducted to resolve this problem, using a wide range of pharmacologic agents such as antiplatelet agents, anticoagulation drugs, lipid-lowering drugs, angiotensin-converting enzyme inhibitors, anti-inflammatory drugs, and antiproliferative drugs. Thus far, no effective drug has been reported, with the exception of probucol, which unfortunately is not approved by the US Food and Drug Administration because it prolongs the QT time, and possibly trapidil and cilostazol, two agents that are currently being tested in larger trials. Stent implantation has significantly reduced the frequency of restenosis in patients with 1) short lesions in large coronary arteries, (> 3.0 mm), 2) native coronary restenosis lesions, 3) venous bypass graft obstructions, 4) chronic total occlusions, and 5) acute myocardial infarction in patients referred for primary percutaneous intervention. A significant problem is the occurrence of in-stent restenosis because it is associated with a high recurrence of restenosis, after repeat coronary intervention irrespective of the technique or device used. Brachytherapy may limit this problem. The high restenosis rate occurring in long lesions and in small vessels still remains an unresolved issue.

The risk of developing radiocontrast nephropathy (RCN) is high in patients who are at risk, particularly those patients with diabetes and renal insufficiency. The development of RCN is associated with a significant increase in in-hospital mortality. RCN seems to develop as a result of dye-induced hypoperfusion of the renal medullary tubules. A variety of measures have been assessed to prevent the development of RCN, none more effective than saline hydration. Clinical evidence is now accumulating showing the potential to prevent RCN through the use of selective dopamine receptor agonists.

A large number of atrial septal defect (ASD) closure devices have been investigated in an attempt to develop a nonsurgical, transvenous method of occlusion of ASD. Some of the devices have been discontinued and several are in clinical trials at this time, but none are approved for general clinical use. There are no prospective, randomized clinical trials to compare the available devices. Based on separate clinical trials, the feasibility, safety, and effectiveness of all devices appear similar. Considerations pertaining to the size of the device delivery sheath, ease of implantation, cost and availability are different with each of the devices; some devices have advantages in some aspects, and others with another. Approval by the regulatory authorities and larger clinical use with longer follow-up results may eventually determine the most appropriate device for a given clinical use.

Coronary restenosis after percutaneous interventions remains a major clinical problem even in the days of coronary stents. Understanding the pathophysiologic mechanisms and the assessment of therapies for the prevention of restenosis relies on experimental animal models. This article describes the most frequently used animal models of coronary artery restenosis and the differences among them. The variable response to injury in the different models should be considered in the interpretation of the effective therapies before they are transferred into clinical trials. The rat carotid model played an important role as a pioneer in animal models for restenosis but has failed to predict results of clinical restenosis. This lack of predictability highlights a fundamental lack of understanding of the basic molecular mechanisms that control vascular healing after injury.

The patent ductus arteriosus was the first congenital cardiac lesion to undergo successful closure in the cardiac catheterization laboratory. Porstmann in 1966 reported the successful closure of the ductus with an Ivalon foam plug. Since then numerous devices have been used to close the ductus. For the smaller ductus (< 4 mm in diameter), the Gianturco coil is now routinely used. For a ductus more than 4 mm in diameter, the devices used are currently undergoing clinical trials.

Intracoronary radiation therapy has been developed in an attempt to decrease restenosis after balloon angioplasty and stent implantation. Two parallel technologies, one employing radioactive stents, the other catheter-based radiation (using either beta- or gamma-emitters), have been the subject of both animal and human studies. In vivo intravascular ultrasound imaging studies have helped us to determine the morphologic effect of brachytherapy on the vessel wall. This article is aimed at revising the potential and limitations of this new technique and summarizing the results of the currently reported clinical trials.