Current controversies in PCI pharmacotherapy.

Coronary artery disease and atherothrombosis are complex pathologic entities. The intricate interplay between anatomical, cellular and molecular factors characterizes their pathogenesis and determines their clinical manifestations. Coronary artery revascularization strategies, by restoring myocardial blood perfusion, only partially treat ischemic heart disease in its complexity. Pharmacological therapies targeting molecular and cellular components involved in the pathophysiology of atherothrombosis are mandatory in order to prevent cardiovascular complications during and after revascularization and therefore improve clinical outcomes. The developments of antithrombotic pharmacotherapies occurred as a result of an improved understanding of the mechanisms underlying atherothrombotic disease. Unfortunately, the optimal antithrombotic therapy, in both acute and chronic settings, often set significant challenges in daily practice. The main objective of optimal antithrombotic therapies, targeting coagulation factors or the platelet system, is to maximize the anti-thrombotic efficacy while minimizing the bleeding risk. The subtle balance between ischemic and bleeding risk is a complex clinical conundrum that involves pharmacologic factors, the clinical phenotype of coronary artery disease and patient's clinical comorbidities. In a contemporary era, in which a broad armamentarium of pharmacologic agents and diagnostic tools are available, physician practice should shift toward a progressively more customized patient care. For this purpose, selection of the optimal acute and chronic percutaneous coronary intervention (PCI) pharmacotherapy, in terms of potency, duration and adherence, cannot disregard an individualized and careful evaluation of the patient's ischemic and hemorrhagic risk. It is within this context that in the present review article we sought to expose the current topics of debate and controversies in acute and chronic anticoagulant and antiplatelet therapies in patients undergoing PCI.

Targeting transradial approach.

Radial access for percutaneous coronary interventions (PCI) emerged as a valid alternative to the standard femoral access with the aim of reduce the incidence of access-site bleeding and consequently improve clinical outcomes. Access-site bleeding is still one of the most common complications after PCI and is associated with increased short- and long-term morbidity and mortality. Benefits in access-site bleeding have been consistently observed in high-risk patients undergoing PCI and in particular in STEMI patients where the antithrombotic regimen is more aggressive. Moreover, other advantages with TR access have been reported including better cost-effectiveness, patient preference, reduced in-hospital length-of-stay, earlier patient ambulation, increased safety in patients on oral anticoagulant and the potential for same-day hospital discharge. The benefits of transradial access in PCI led the interventional community to expand its use to endovascular interventions and more recently, to cardiac structural interventions such as transcatheter aortic valve implantation. The aim of this review is to try to give to the reader a wide view of the state-of-the-art of transradial access in PCI and its current use in endovascular and structural interventions.

Role of new sirolimus self-apposing stent in coronary interventions.

Device technology in interventional cardiology is continuously evolving. Self-expandable (SE) coronary artery stents were the first device to be implanted within a human coronary artery. However, because of their initial limitations, balloon-expandable (BE) stents were predominantly developed and used in the last 30 years. Unfortunately, in challenging anatomical settings such as bifurcation lesions, large, ectatic or aneurysmal vessels, tapered vessels or vasoconstricted arteries, outcomes with BE stents are not always optimal. The Stentys (Stentys SA, Paris, France) SE nitinol stents were initially developed for the treatment of coronary bifurcation lesions. The understanding of the underlying mechanism involved in incomplete stent apposition and subsequent stent thrombosis led to the introduction of self-apposing stents in the treatment of acute coronary syndrome in order to overcome the limitations of drug-eluting stents in presence of high thrombus burden. In this regard, Stentys allows a progressive stent expansion which could reduce the rates of incomplete stent apposition by conforming to vascular remodeling. Enhancing the advantages of this technology by adding the release of an antiproliferative drug to prevent restenosis is even more attractive and potentially effective. Recently, the results of the new Stentys sirolimus-eluting stent have been reported. This article provides an overview of the pathobiological rational, device characteristics and results of the new Stentys self-expandable sirolimus-eluting stent.

Severe exertional dyspnea in a patient with localized emphysema.

The case of a middle-aged, male smoker who presented with progressive severe dyspnea is described. The cause of the progressive severe dyspnea remained unexplained after a comprehensive history, physical examination, chest radiograph, electrocardiogram and spirometry. Subsequent investigations resulted in a diagnosis of localized pulmonary emphysema. Detailed exercise testing helped uncover the physiological basis of the patient's extreme dyspnea.

Influence of left ventricular asynchrony on filling in coronary artery disease.

To evaluate whether the extent of left ventricular (LV) asynchrony plays a role in the impairment of LV rapid filling in patients with coronary artery disease (CAD), 48 patients underwent both radionuclide angiography and cardiac catheterization. Patients were divided into group I (n = 33), with normal LV kinesis or only mild hypokinesia, and group II (n = 15), with LV dyskinesia or akinesia. Radionuclide ejection fraction was higher in group I than in group II (62 +/- 12 vs 44 +/- 20%; p less than 0.001). Peak filling rate was significantly lower in group II (1.9 +/- 0.8 vs 2.6 +/- 0.9 end-diastolic counts/s; p less than 0.01). Time to end-systole coefficient of variation, an index of the extent of LV asynchrony, was significantly higher in group II than in group I (43 +/- 10 vs 35 +/- 6; p less than 0.0002). In group I, a highly significant inverse relation was found between this index of asynchrony and peak filling rate (r = 0.71; p less than 0.0001). This correlation was found even when time to end-systole coefficient of variation was normalized to the RR interval (r = 0.49; p less than 0.01) and when peak filling rate was expressed in stroke counts (r = 0.57; p less than 0.001). The correlation between peak filling rate and index of asynchrony was maintained up to an end-systole coefficient of variation value of approximately 35. In group II patients (most with an asynchrony value greater than or equal to 35) no relation was found between time to end-systole coefficient of variation and peak filling rate.