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494 Abstracts

nd other variables that differ from swine. Furthermore, theonclusions of the study may not apply to bystander CPRerformed by two rescuers without interruptions in compres-ions when two ventilations are delivered.

DARK CHOCOLATE IMPROVES CORONARY VA-OMOTION AND REDUCES PLATELET REACTIV-TY. Lammer AJ, Hermann F, Sudano I, et al. Circulation007;116:2376–82.

This randomized, double-blinded, case-control trial evalu-ted the effect on coronary vascular and platelet function byavonoid-rich dark chocolate, a substance with known antiox-

dant properties. Twenty-two heart transplant patients sched-led for routine coronary angiography were randomized to tworoups; one receiving 40 g dark chocolate (70% cocoa) and theontrol group receiving 40 g of cocoa-free chocolate. Twoours after ingestion of dark chocolate, control subjects werevaluated for serum levels of flavonoids catechin and epicatechin,oronary artery diameter, coronary vasomotion (% change ofiameter) after cold pressor test, shear stress-dependent plateletunction, and three different biomarkers of oxidative stress.erum epicatechin concentration increased significantly afterark chocolate ingestion, although no change was noted inatechin concentrations. Coronary artery diameter increasedignificantly (2.36 ¡ 2.51 mm) after dark chocolate ingestion,lthough no change was noted after control ingestion. Endo-helium-dependent coronary vasomotion (percent change ofrtery diameter induced by cold pressor test) improved signif-cantly after dark chocolate ingestion (4.5% vs. �4.6%). Noignificant change was noted between groups for two of thexidative stress biomarkers (TRAP assay—total radical-reducingntioxidant potential and FRAP assay—ferric-reducing an-ioxidant potential), although 8-isoprostanes were reducedignificantly after dark chocolate consumption and their levelsere not altered after control consumption. Shear stress-ependent platelet adhesion decreased from 4.9% to 3.8% inhe dark chocolate group and was not significantly altered in theontrol group. The authors conclude that a short-term effect ofavonoid-rich dark chocolate results in improved coronaryasodilatation, improved coronary vasomotion and shear stress-ependent platelet adhesion.

[Zachary D. Tebb, MD,

Denver Health Medical Center, Denver, CO]

Comment: Although this study is limited by the small sam-le size, the physiologic effects of dark chocolate are impres-ive, although prospective, long-term randomized studies withortality and morbidity outcomes are needed to determine the

otential of dark chocolate to beneficially affect atherothrom-osis in a clinical setting. It should be noted that industryollaboration occurred in this study.

GLUCOSE-INSULIN-POTASSIUM THERAPY IN PA-IENTS WITH ST-SEGMENT ELEVATION MYOCAR-IAL INFARCTION. Diaz R, Goyal A, Mehta, SR, et al.

AMA 2007;298:2399–405. r

This study reviewed the data from both the Clinical Trial ofeviparin and Metabolic Modulation in Acute Myocardial In-

arction Treatment and Evaluation - Estudios Clinicos Latinomerica (CREATE-ECLA) and the Organization for the As-

essment of Strategies for Ischemic Syndromes-6 (OASIS-6)rial. The primary intervention of both trials was a glucose-nsulin-potassium (GIK) infusion for 24 h after the diagnosis ofT-segment elevation MI (STEMI). The objective was to ex-mine the clinical outcomes at 30 days and 6 months in theASIS-6 trial and 30-day outcomes in the combined trialopulation. The primary outcomes were death, heart failure,nd composite of death or heart failure. Subgroup analysis waslso performed for the timing of initiation of GIK infusion. Theombined trials had a total population of 22,943 patients withcute STEMI. Time to clinical events between intervention andontrols were compared using the log-rank statistic with theox proportional hazards model used to estimate hazards ra-

ios. The analysis of the OASIS-6 trial showed no differenceetween GIK and control groups at 30 days or 6 months forajor outcomes. The combination of the trials also showed no

ifference in intervention vs. control in the categories of deathp � 0.33), heart failure (p � 0.82), or for the composite ofeath or heart failure (p � 0.99). Additionally, no furtherenefit was found in the subgroup analysis of symptom onset toime of randomization to therapy. The authors conclude thatIK infusion provides no further benefit in STEMI, and the

voidance of infusion-related hyperglycemia, hyperkalemia,nd net fluid gain may be advisable.

[Andrew French, MD,

Denver Health Medical Center, Denver, CO]

Comment: This study is limited by the fact that it is retro-pective and combines the data from two heterogeneous studyopulations. Nevertheless, it adds further evidence as to theack of efficacy of GIK therapy in patients with STEMI.

PERSISTENCE OF CONTRADICTED CLAIMS INHE LITERATURE. Tatsioni A, Bonitsis NG, Ioannidis

PA. JAMA 2007;298:2517–26.The objectives of this study were to examine what happens

o the scientific literature when a highly prominent claim isefuted, and to understand how these benefits continue to beefended in the literature. To this effect, the highly disputedeneficial claims of the use of vitamin E for cardiovascularisease were analyzed via retrospective review of citationounts as well as characteristics of the citing articles. Articlesrom 1997, 2001, and 2005 were sampled that referenced twoighly cited epidemiologic studies that proposed major cardio-ascular benefits associated with vitamin E in 1993. Theseears were chosen as representative of before, early, and latefter publication of refuting evidence, respectively. Articlesrom 2005 were also separately sampled that referenced theost cited contradicting randomized trial (HOPE trial, pub-

ished in 2000). When the context of the citation was pertinento the association between vitamin E and cardiovascular dis-ase prevention, the overall stance of the article was catego-

ized as favorable, equivocal, or unfavorable. The main hypoth-