Over the past decade there have been tremendous advancements in the technique and procedural success rates in the field of interventional cardiology.

Percutaneous coronary intervention (PCI) in patients with depressed left ventricular function requires patience, technical skills and, at times, even a counterintuitive approach. In this high-risk group, standard PCI methods, mainly balloon angioplasty and stenting, are incapable of adequate reduction of target plaque burden, frequently resulting in suboptimal outcomes. The extent of atherosclerotic disease, complex plaque morphology, diminished myocardial reserve for tolerance of ischemia during intervention and associated comorbidities, render PCI a considerable challenge.

Several large randomized clinical trials and meta-analyses have shown that inhibition of platelet aggregation with platelet glycoprotein IIb/IIIa inhibitors (GPI) improves outcomes in patients presenting with acute coronary syndromes and in those undergoing percutaneous coronary intervention (PCI).^1–5 Platelet GPI inhibits the thrombotic cascade directly by blocking the final common pathway of platelet aggregation, and indirectly, by inhibiting the generation of thrombin.^6,7 Traditionally, GPI are administered as an intravenous (IV) bolus, followed by a prolonged infusion (12–18 hours). Many patients undergoing PCI (both in the United States and worldwide) do not receive a GPI, in part owing to concerns about bleeding and cost.

This paper has prospectively examined the efficacy of the use of bolus glycoprotein IIb/IIIa inhibitor (GPI) during percutaneous coronary intervention (PCI) in a single-arm registry. Both in-hospital outcomes and bleeding complications as defined in the REPLACE-2 trial¹ were examined. Oral antiplatelet therapy consisted of aspirin and preloading with clopidogrel 300 p.o. q.d. (immediately prior to PCI), followed up with 75 mg p.o. daily.

The underlying pathobiology in most patients with acute coronary syndromes (ACS) is culprit lesion disruption with associated thrombosis.¹ There is an increasing body of evidence showing that these culprit lesions, the so-called “vulnerable” plaques, have an increase in local temperature when compared with the temperature of a more normal region of the coronary wall.

A patent foramen ovale (PFO) can be identified in as many as 25% of the adult population.¹ Though in the vast majority of cases the PFO is clinically silent, its presence is associated with serious and well-recognized complications. The association between a PFO and paradoxical embolization resulting in cerebrovascular and other systemic events has been recognized for many years. The combination of a PFO and atrial septal aneurysm (ASA) has been shown to increase the risk for cryptogenic stroke nearly five-fold in patients younger than 55 years of age.⁴ Furthermore, the presence of a PFO has been associated with platypnea orthodeoxia syndrome, and lately has been implicated in migraine headaches as well.^2,3

Why do residual shunts exist after patent foramen ovale (PFO) closure devices are placed? Possible explanations include the use of a device too small for the defect, inability of the placed device to adequately conform to the defect, leakage through the device, septal mobility limiting adequate fusion of the device to the tissue, presence of septal perforations and remodeling or trauma to the septal tissue. In this issue of the Journal of Invasive Cardiology, Zajarias et al¹ identify septal mobility as being predictive of a residual shunt after placing an Amplatzer PFO occluder device. Although this relationship may concur with many interventionalists’ empiric observations, several questions seem to be hiding in the shadows of this study. Probably the most important is a fundamental one: Is residual shunting after PFO closure clinically relevant?

Early restoration of normal coronary perfusion after myocardial infarction (MI) limits infarct size, preserves left ventricular (LV) function and reduces mortality. The primary objective of reperfusion therapy is not only to restore epicardial vessel patency, but also to reperfuse tissue in order to maintain myocyte viability and, thus, LV function.

Myocardial fractional flow reserve (FFR) is an invasive index of the physiologic significance of a coronary stenosis. FFR is simply measured as the mean intracoronary pressure distal to a lesion divided by the mean aortic pressure during maximal hyperemia. An FFR value of < 0.75 has been shown to be highly predictive of ischemia on noninvasive testing in patients with coronary artery disease.^1–5 As there has been much debate regarding the possible effects of microvascular disease on the pressure measurements used to calculate FFR, this initial work was performed in patients with normal left ventricular mass (LVM) and no evidence of ventricular hypertrophy.

The concept of fractional flow reserve (FFR) was introduced by Pijls et al in his publication in 1993.¹ This concept uses pressure measurement as a surrogate for flow, in a state where resistance is minimal and constant, a state of maximal hyperemia. This is usually achieved using intracoronary or intravenous adenosine administration. The ratio of the mean pressure distal to an epicardial coronary stenosis as measured by the pressure-monitoring wire, to the mean proximal pressure, measured as the aortic pressure from the tip of the guiding catheter, is the fractional flow reserve.