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      The ‘Open-Artery Hypothesis’: New Clinical and Pathophysiologic Insights

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          The open-artery hypothesis states that myocardial reperfusion, even if late for myocardial salvage, provides benefits and prevents adverse cardiac remodeling. While observational data in humans regarding the deleterious impact of a permanent infarct-related artery occlusion and the benefits of spontaneous reperfusion are quite consistent, the reports regarding late revascularization are inconclusive in order to prove such a hypothesis. The observational studies tend to have selection biases, while randomized trials to date are too small to be conclusive. Moreover, the pathophysiological mechanisms underlying presumed benefits of reperfusion are still unclear. However, although the open-artery hypothesis remains unproven, the current evidence suggesting benefits calls for additional studies. Limitations of ischemic left ventricular dilatation and myopathy could markedly reduce cardiovascular morbidity and mortality after acute myocardial infarction.

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          Most cited references 29

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          Platelet glycoprotein IIb/IIIa inhibition with coronary stenting for acute myocardial infarction.

          When administered in conjunction with primary coronary stenting for the treatment of acute myocardial infarction, a platelet glycoprotein IIb/IIIa inhibitor may provide additional clinical benefit, but data on this combination therapy are limited. We randomly assigned 300 patients with acute myocardial infarction in a double-blind fashion either to abciximab plus stenting (149 patients) or placebo plus stenting (151 patients) before they underwent coronary angiography. Clinical outcomes were evaluated 30 days and 6 months after the procedure. The angiographic patency of the infarct-related vessel and the left ventricular ejection fraction were evaluated at 24 hours and 6 months. At 30 days, the primary end point--a composite of death, reinfarction, or urgent revascularization of the target vessel--had occurred in 6.0 percent of the patients in the abciximab group, as compared with 14.6 percent of those in the placebo group (P=0.01); at 6 months, the corresponding figures were 7.4 percent and 15.9 percent (P=0.02). The better clinical outcomes in the abciximab group were related to the greater frequency of grade 3 coronary flow (according to the classification of the Thrombolysis in Myocardial Infarction trial) in this group than in the placebo group before the procedure (16.8 percent vs. 5.4 percent, P=0.01), immediately afterward (95.1 percent vs. 86.7 percent, P=0.04), and six months afterward (94.3 percent vs. 82.8 percent, P=0.04). One major bleeding event occurred in the abciximab group (0.7 percent); none occurred in the placebo group. As compared with placebo, early administration of abciximab in patients with acute myocardial infarction improves coronary patency before stenting, the success rate of the stenting procedure, the rate of coronary patency at six months, left ventricular function, and clinical outcomes.
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            Procedural outcomes and long-term survival among patients undergoing percutaneous coronary intervention of a chronic total occlusion in native coronary arteries: a 20-year experience.

            The study compared procedural outcomes and long-term survival for patients undergoing percutaneous coronary intervention (PCI) of a chronic total coronary artery occlusion (CTO) with a matched non-CTO cohort to determine whether successful PCI of a CTO is associated with improved survival. Percutaneous coronary intervention of a CTO is a common occurrence, and the long-term survival for patients with successful PCI of a CTO has not been clearly defined. Between June 1980 and December 1999, a total of 2,007 consecutive patients underwent PCI for a CTO. Utilizing propensity scoring methods, a matched non-CTO cohort of 2,007 patients was identified and compared to the CTO group. The cohorts were stratified into successful and failed procedures. The in-hospital major adverse cardiac event (MACE) rate was 3.8% in the CTO cohort. Technical success has improved over the last 10 years (overall 74.4%, slope 1.0%/yr, p = 0.02, R2 = 49.9%) as did procedural success (overall 69.9%, slope 1.2%/yr, p = 0.02, R2 = 51.5%) without a concomitant increase in in-hospital MACE rates (slope 0.1%/yr, p = 0.7). There was a distinct 10-year survival advantage for successful CTO treatment compared with failed CTO treatment (73.5% vs. 65.1%, p = 0.001). The CTO versus non-CTO 10-year survival was the same (71.2% vs. 71.4%, p = 0.9). Diabetics in the CTO cohort had a lower 10-year survival compared with nondiabetics (58.3% vs. 74.3%, p < 0.0001). These data represent follow-up of the largest reported series of patients undergoing PCI for a CTO. The 10-year survival rates for matched non-CTO and the CTO cohorts were similar. Success rates have continued to improve without an accompanying increase in MACE rates. A successfully revascularized CTO confers a significant 10-year survival advantage compared with failed revascularization.
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              C-Reactive Protein and Complement Are Important Mediators of Tissue Damage in Acute Myocardial Infarction

              Myocardial infarction in humans provokes an acute phase response, and C-reactive protein (CRP), the classical acute phase plasma protein, is deposited together with complement within the infarct. The peak plasma CRP value is strongly associated with postinfarct morbidity and mortality. Human CRP binds to damaged cells and activates complement, but rat CRP does not activate complement. Here we show that injection of human CRP into rats after ligation of the coronary artery reproducibly enhanced infarct size by ∼40%. In vivo complement depletion, produced by cobra venom factor, completely abrogated this effect. Complement depletion also markedly reduced infarct size, even when initiated up to 2 h after coronary ligation. These observations demonstrate that human CRP and complement activation are major mediators of ischemic myocardial injury and identify them as therapeutic targets in coronary heart disease.

                Author and article information

                S. Karger AG
                December 2003
                16 January 2004
                : 100
                : 4
                : 196-206
                aInstitute of Cardiology, Catholic University, Rome, and bSection of Pathologic Anatomy, Department of Biochemistry, Second University of Naples, Italy; cDepartment of Cardiology, Medical College of Virginia Campus, Virgina Commonwealth University, Richmond, Va., USA
                74813 Cardiology 2003;100:196–206
                © 2003 S. Karger AG, Basel

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                Page count
                Figures: 3, References: 92, Pages: 11


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