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To determine whether data available to physicians in the emergency room can accurately identify which patients with acute chest pain are having myocardial infarctions, we analyzed 482 patients at one hospital. Using recursive partitioning analysis, we constructed a decision protocol in the format of a simple flow chart to identify infarction on the basis of nine clinical factors. In prospective testing on 468 other patients at a second hospital, the protocol performed as well as the physicians. Moreover, an integration of the protocol with the physicians' judgments resulted in a classification system that preserved sensitivity for detecting infarctions, significantly improved the specificity (from 67 per cent to 77 per cent, P less than 0.01) and positive predictive value (from 34 per cent to 42 per cent, P = 0.016) of admission to an intensive-care area. The protocol identified a subgroup of 107 patients among whom only 5 per cent had infarctions and for whom admission to non-intensive-care areas might be appropriate. This decision protocol warrants further wide-scale prospective testing but is not ready for routine clinical use.

Background-Previous investigators have shown that systemic markers of inflammation may be increased in patients withacute ischemic syndromes or after percutaneous coronary revascularization and that persistent elevation in these markers is predictive of excess risk of subsequent adverse cardiac events. By virtue of its cross-reactivity with the glycoprotein IIb/IIIa, av␤3, and ␣M␤2 receptors, abciximab may reduce inflammatory processes. Methods and Results-Assays for the inflammatory markers C-reactive protein, interleukin-6, and tumor necrosis factor-␣ were performed on serum samples obtained from 160 patients in a placebo-controlled, randomized trial of abciximab during angioplasty. Eighty patients each had received a placebo or abciximab bolus plus a 12-hour infusion. Serum samples were drawn at baseline (before revascularization), 24 to 48 hours after study drug administration, and 4 weeks after study drug administration. Between baseline and 24 to 48 hours, the increase in C-reactive protein was 32% less in patients receiving abciximab than placebo (Pϭ0.025); the rise in interleukin-6 levels was 76% less in the abciximab group (PϽ0.001); and the rise in tumor necrosis factor-␣ levels was 100% less with abciximab therapy (Pϭ0.112). By 4 weeks, most marker levels had returned to baseline, with no significant differences between placebo and abciximab groups. Conclusions-Systemic markers of inflammation increase in the first 24 to 48 hours after angioplasty, but the magnitude of that rise is diminished by periprocedural abciximab. Some of the long-term clinical benefit derived from this agent may be related to an anti-inflammatory effect.

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The observation that laser-induced fluorescence (LIF) spectra of atherosclerotic and normal artery are different has been proposed as the basis for guiding a "smart" laser angioplasty system. The purpose of this study was to investigate the causes of this difference in LIF. Helium-cadmium laser-induced (325 nm) fluorescence was recorded from pure samples of known constituents of normal and atherosclerotic artery including collagen, elastin, calcium, cholesterol, and glycosaminoglycans. Similarities between the LIF spectra of atherosclerotic plaque and collagen and normal aorta and elastin were noted. LIF spectroscopy was then performed on specimens of atherosclerotic aortic plaque (n=9) and normal aorta (n=13) and on their extracted lipid, collagen, and elastin. Lipid extraction did not significantly alter atherosclerotic plaque or normal aortic LIF, suggesting a minor contribution of lipid to arterial LIF. The LIF spectra of normal aorta wall was similar to the spectra of the extracted elastin, whereas the LIF spectra of atherosclerotic aortic plaque was similar to the spectra of the extracted collagen. These observations are consistent with the reported relative collagen-to-elastin content ratio of 0.5 for normal arterial wall and 7.3 for atherosclerotic plaque. A classification algorithm was developed to discriminate normal and atherosclerotic aortic spectra based on an elastin and collagen spectral decomposition. A discriminant score was formed by the difference of elastin and collagen (E-C) coefficients and used to classify 182 aortic fluorescence spectra. The mean E-C value was +0.83±0.04 for normal and -0.48±0.07 for atherosclerotic aorta (p<0.001). Classification accuracy was 92%. With 325-nm excitation, collagen and elastin are therefore the major fluorophores of aortic atherosclerotic plaque and normal aortic wall, respectively, and the difference between normal and atherosclerotic arterial fluorescence appears to be due to differences in relative collagen and elastin content. Consistent with this observation, a classification algorithm based on a collagen and elastin spectral decomposition can accurately classify normal and atherosclerotic aortic fluorescence spectra. Other laser lines may excite different chromophores. These findings will require validation for muscular arteries. (Circulation 1989;80:1893-1901 The difference between the laser-induced fluorescence spectra of atherosclerotic plaque and normal arterial wall has been well established1-5 and has been proposed as the basis

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Intracoronary saline infusion should be incorporated into all excimer laser coronary angioplasty procedures.