Attenuation of rebound ischemia after discontinuation of heparin therapy by glycoprotein IIb/IIIa inhibition with eptifibatide in patients with acute coronary syndromes: observations from the platelet IIb/IIIa in unstable angina: receptor suppression using integrilin therapy (PURSUIT) trial.

Background- A reactivation of ischemia after the discontinuation of intravenous heparin in acute coronary syndromes has been described. The effect of glycoprotein IIb/IIIa blockade on heparin rebound is unknown. Methods and Results- Patients with acute coronary syndromes who received heparin therapy but not initial revascularization in the Platelet IIb/IIIa in Unstable angina: Receptor Suppression Using Integrilin Therapy (PURSUIT) trial were analyzed. Rates of death or myocardial (re)infarction while on heparin therapy and in 12-hour periods in the 2 days after heparin discontinuation were compared between eptifibatide and placebo. There was no difference between study groups in event rates during heparin infusion. In the 12 hours after heparin discontinuation, there was a 2.5-fold increase in all events, an 8-fold increase in death, and a 2-fold increase in myocardial infarction. However, in the 12 hours after heparin discontinuation, there was a significantly lower rate of events (1.68% versus 2.53%, P=0.03) and death (0.77% versus 0.21%, P=0.002) in the eptifibatide group compared with the placebo group. When only considering patients who were on study drug at the time of heparin discontinuation, the reduction in the combined end point was marginally significant, but the difference in the rate of death remained significant (0.68% versus 0.06%, P=0.004). In logistic regression analyses, the multivariate predictors of rebound events were the duration of heparin therapy, age, North American site, and lack of eptifibatide treatment. Conclusions- An increase in death or myocardial infarction occurs in the 12 hours after heparin discontinuation in patients with acute coronary syndromes. This rebound is attenuated by glycoprotein IIb/IIIa inhibition with eptifibatide.

Overestimation of stent delivery balloon diameters by manufacturers' compliance tables: a quantitative coronary analysis of Duet and NIR stent implantation.

Although manufacturers' compliance tables of stent delivery balloons indicate the diameter of the balloon at a given inflation pressure, it is unclear whether these data correlate with in vivo true intracoronary balloon diameters (TBDs). The TBDs of two new-generation balloon-expandable stent delivery systems (Duet and NIR) were measured by quantitative coronary analysis (QCA) in 100 consecutive patients. The manufacturers' stated balloon diameter (BD) of the stent delivery systems overestimated the TBD in 94% +/- 4% of patients receiving both Duet or NIR stent implantations. In only 6% of the patients, the TBD matched the manufacturers' stated balloon diameter. There was no underestimation of TBDs by both manufacturers' compliance tables. The Duet tables overestimated TBDs by 14% +/- 8% (range, 1%-36%), the NIR tables by 18% +/- 8% (range, 1%-41%), P < 0.05, Duet vs. NIR, respectively. When the manufacturers' data were corrected for the differences in reporting data from in vitro tests, i.e., balloon compliance data with or without the stent, the degree of overestimation of diameters was similar for Duet and NIR stent delivery balloons (14% +/- 8% vs. 13% +/- 7%, Duet vs. NIR; P = NS). Manufacturers' compliance tables of both the Duet and NIR stent delivery balloon systems significantly overestimate the true intracoronary balloon diameter. The manufacturers' of stent delivery balloons should clearly state on the box, if balloon compliance data were derived from in vitro bench testing, which phantoms were used for compliance analysis, and that the tables may overestimate the true intracoronary balloon diameter. The findings of the present study have important clinical implications with respect to performing coronary stent implantation with precision.

Is atherosclerosis an infectious disease?

Atherosclerotic coronary artery disease is multifactorial, but several lines of evidence implicate infection as a potential contributing factor. Chlamydia pneumoniae has the most compelling data, with Helicobacter pylori and cytomegalovirus also implicated. Clinical trials of antibiotics to decrease coronary events are underway. Until the results are available, however, we advise against prescribing antibiotics for this purpose.

Assessing the appropriateness of coronary revascularization: the University of Maryland Revascularization Appropriateness Score (RAS) and its comparison to RAND expert panel ratings and American College of Cardiology/American Heart Association guidelines with regard to assigned appropriateness rating and ability to predict outcome.

BACKGROUND: Significant regional variation in procedural frequencies has led to the development of the RAND and American College of Cardiology/American Heart Association (ACC/AHA) guidelines; however, they may be difficult to apply in clinical practice. The University of Maryland Revascularization Appropriateness Score (RAS) was created to address the need for a simplified point scoring system. HYPOTHESIS: The study was undertaken to compare revascularization appropriateness ratings yielded by the RAND Expert Panel Ratings, ACC/AHA guidelines, and the University of Maryland RAS. METHODS: We applied these three revascularization appropriateness scoring systems to 153 catheterization laboratory patients with a variety of cardiac diagnoses and treatments. For each patient, appropriateness scores assigned by each of the three systems were compared with each other and with the actual treatment delivered. Concordance of care with appropriateness score was then correlated with outcome. RESULTS: There were significant differences among all three scoring systems in their ratings and in the concordance of treatment with appropriateness rating. When treatment provided was concordant with RAND ratings, there was a lower occurrence of subsequent coronary artery bypass grafting (CABG), the composite end point of either CABG or percutaneous transluminal coronary angioplasty (PTCA), and the composite end point of death, myocardial infarction (MI), or revascularization. When treatment was concordant with the ACC/AHA guidelines, there was lower occurrence of all-cause mortality, PTCA, the composite end point of either CABG or PTCA, and the composite end point of death, MI, or revascularization. When treatment provided was concordant with the RAS, there was lower occurrence of cardiac death, all-cause death, CABG, the composite end point of either CABG or PTCA, and the composite end point of death, MI, or revascularization. CONCLUSIONS: The RAS is a simple scoring system to assess revascularization appropriateness. When the RAND, ACC/AHA, and RAS systems are compared in a catheterization laboratory population, they rate the same patient differently and vary in their correlation of appropriateness rating with outcome.