Backsliding and Reversal: The J Curve Revisited

In this article we argue that democratic transitions can reverse, oscillate, or simply stall. These transitions are exemplified in the different types of states we categorize. We construct a model of stability vs openness using three dimensions of stateness, namely authority, legitimacy, and capacity. With the additional application of a six-fold typology of states, we offer a robust analytical framework with which to identify and explain changes in state status. Our construct of stability and openness leads to a novel development of a global conflict damage index, which is built upon conflict risk, but considers a state’s capacity to deal with conflict. The paper concludes with implications for policy and the application of the model to conflict prediction when states under go transition

Design of a clinical trial for the assessment cardioversion using Transesophageal Echocardiography (The ACUTE Multicenter Study)

Patients with atrial fibrillation (AF) undergoing cardioversion are at an increased risk of cardioembolic stroke and require anticoagulation, The Assessment of Cardioversion Using Transesophageal Echocardiography (ACUTE) Multicenter Study is a randomized clinical trial of patients undergoing electrical cardioversion of AF of >2 days' duration comparing a transesophageal-guided strategy (TEE) with brief anticoagulation to the conventional anticoagulation strategy. patients randomly assigned to the TEE-guided strategy receive therapeutic anticoagulation before TEE and cardioversion, followed by 4 weeks of anticoagulation, Patients with thrombus imaged by TEE have postponement of cardioversion, continue anticoagulation for 3 weeks, and undergo a repeat TEE, Conventional strategy patients receive 3 weeks of anticoagulation before cardioversion, followed by 4 weeks of anticoagulation after cardioversion, The primary end point events are ischemic stroke, transient ischemic attack, and systemic embolization for an 8-week period from enrollment, Secondary end points are major and minor bleeding, all-cause mortality, successful return to and maintenance of sinus rhythm, and cost effectiveness, Analysis is based on the intention-to-treat principle. The anticipated rates of embolism of 2.9% for conventional strategy and 1.2% for the TEE-guided strategy are based on published research and the completed pilot study, The ACUTE Multicenter Study will randomize therapy and follow an estimated 3,000 patients from 65 study sites to determine the relative efficacy of the TEE-guided and conventional approaches to electrical cardioversion for patients in AF, The results of this investigation will have important clinical implications for the management of patients with AF undergoing electrical cardioversion. (C) 1998 by Excerpta Medica, Inc.Cleveland Clin Fdn, Dept Cardiol, Sect Cardiovasc Imaging, Cleveland, OH 44195 USAUniv Louisville, Louisville, KY 40292 USAUniv Nebraska, Omaha, NE 68182 USAWinthrop Univ Hosp, Mineola, NY 11501 USAEscorts Heart Inst & Res Ctr, New Delhi, IndiaCtr Med Caracas, Caracas, VenezuelaUniv Fed Sao Paulo, Sao Paulo, BrazilLancaster Heart Fdn, Lancaster, PA USAUniv Essen Gesamthsch, Essen, GermanyEl Azhar Univ, Cairo, EgyptSt Elisabeth Hosp, Tilburg, NetherlandsUniv Pittsburgh, Med Ctr, Pittsburgh, PA USARiverside Methodist Hosp, Columbus, OH 43214 USAUniv Rochester, Strong Mem Hosp, Rochester, NY 14642 USAUniv Calif San Francisco, San Francisco, CA 94143 USAUniv Massachusetts, Worcester, MA 01605 USAHosp Vera Cruz, Belo Horizonte, MG, BrazilHosp Socor, Belo Horizonte, MG, BrazilSaginaw Heart Grp, Saginaw, MI USAUniv Calif San Diego, San Diego, CA 92103 USANew England Med Ctr, Boston, MA 02111 USAWhite River Junction VA Med Ctr, White River Junction, VT USAUniv Cincinnati, Cincinnati, OH USAVet Affairs Med Ctr, Bronx, NY USAVirginia Commonwealth Univ, Med Coll Virginia, Richmond, VA 23298 USAHarbor UCLA Med Ctr, Torrance, CA 90509 USAOsped Civile, Cento, ItalyUniv Chicago, Med Ctr, Chicago, IL 60637 USAUniv Texas, SW Med Ctr, Dallas, TX USAManly Hosp, Manly, NSW, AustraliaPrince Henry Hosp, Sydney, NSW, AustraliaN Shore Univ Hosp, Manhasset, NY USABaylor Coll Med, Methodist Hosp, Houston, TX 77030 USATexas Heart Inst, Houston, TX 77025 USAUniv New Mexico, Albuquerque, NM 87131 USARoyal Victoria Hosp, Montreal, PQ H3A 1A1, CanadaColumbia Cardiovasc Clin, Columbia, SC USAAustin Heart, Austin, TX USAOhio State Univ, Columbus, OH 43210 USAMed Coll Wisconsin, Froedtert Mem Lutheran Hosp, Milwaukee, WI 53226 USASt Nicholas Hosp, Milwaukee Cardiovasc Res, Milwaukee, WI USABlodgett Mem Med Ctr, Grand Rapids, MI USAClearwater Cardiovasc Consultants, Largo, FL USAN Cent Heart Fdn, Sioux Falls, SD USASentara Norfolk Gen Hosp, Norfolk, VA USALoma Linda VA Med Ctr, Loma Linda, CA USAMacNeal Ctr Clin Res, Berwyn, IL USATemple Univ Hosp, Philadelphia, PA 19140 USAHungarian Inst Cardiol, Budapest, HungaryBoston Univ, Boston, MA 02215 USABeth Israel Hosp, Boston, MA 02215 USAHosp Servidores Estado, Logoa, BrazilE Carolina Univ, Greenville, NC USAHartford Hosp, Hartford, CT 06115 USAGrad Hosp Philadelphia, Philadelphia, PA 19146 USASt Lukes Roosevelt Hosp, New York, NY 10025 USAAlton Ochsner Med Fdn & Ochsner Clin, New Orleans, LA 70121 USAEaston Hosp, Easton, PA USASt Johns Mercy Med Ctr, St Louis, MO 63141 USAMichigan Capital Med Ctr, Lansing, MI USAAlbany Med Coll, Albany, NY 12208 USAMontefiore Med Ctr, Bronx, NY 10467 USAUniv Kansas, Med Ctr, Kansas City, KS 66103 USAAndroscoggin Cardiol Associates, Auburn, ME USACleveland Clin Fdn, Dept Biostat & Epidemiol, Cleveland, OH 44195 USAEmory Univ, Sch Publ Hlth, Atlanta, GA USACleveland Clin Fdn, Dept Biostat, Cleveland, OH 44195 USACleveland Clin Fdn, Dept Vasc Med, Cleveland, OH 44195 USACleveland Clin Fdn, Dept Neurol, Cleveland, OH 44195 USAUniv Fed Sao Paulo, Sao Paulo, BrazilWeb of Scienc

Ezetimibe added to statin therapy after acute coronary syndromes

BACKGROUND: Statin therapy reduces low-density lipoprotein (LDL) cholesterol levels and the risk of cardiovascular events, but whether the addition of ezetimibe, a nonstatin drug that reduces intestinal cholesterol absorption, can reduce the rate of cardiovascular events further is not known. METHODS: We conducted a double-blind, randomized trial involving 18,144 patients who had been hospitalized for an acute coronary syndrome within the preceding 10 days and had LDL cholesterol levels of 50 to 100 mg per deciliter (1.3 to 2.6 mmol per liter) if they were receiving lipid-lowering therapy or 50 to 125 mg per deciliter (1.3 to 3.2 mmol per liter) if they were not receiving lipid-lowering therapy. The combination of simvastatin (40 mg) and ezetimibe (10 mg) (simvastatin-ezetimibe) was compared with simvastatin (40 mg) and placebo (simvastatin monotherapy). The primary end point was a composite of cardiovascular death, nonfatal myocardial infarction, unstable angina requiring rehospitalization, coronary revascularization ( 6530 days after randomization), or nonfatal stroke. The median follow-up was 6 years. RESULTS: The median time-weighted average LDL cholesterol level during the study was 53.7 mg per deciliter (1.4 mmol per liter) in the simvastatin-ezetimibe group, as compared with 69.5 mg per deciliter (1.8 mmol per liter) in the simvastatin-monotherapy group (P<0.001). The Kaplan-Meier event rate for the primary end point at 7 years was 32.7% in the simvastatin-ezetimibe group, as compared with 34.7% in the simvastatin-monotherapy group (absolute risk difference, 2.0 percentage points; hazard ratio, 0.936; 95% confidence interval, 0.89 to 0.99; P = 0.016). Rates of pre-specified muscle, gallbladder, and hepatic adverse effects and cancer were similar in the two groups. CONCLUSIONS: When added to statin therapy, ezetimibe resulted in incremental lowering of LDL cholesterol levels and improved cardiovascular outcomes. Moreover, lowering LDL cholesterol to levels below previous targets provided additional benefit

Vorapaxar in the secondary prevention of atherothrombotic events

Item does not contain fulltextBACKGROUND: Thrombin potently activates platelets through the protease-activated receptor PAR-1. Vorapaxar is a novel antiplatelet agent that selectively inhibits the cellular actions of thrombin through antagonism of PAR-1. METHODS: We randomly assigned 26,449 patients who had a history of myocardial infarction, ischemic stroke, or peripheral arterial disease to receive vorapaxar (2.5 mg daily) or matching placebo and followed them for a median of 30 months. The primary efficacy end point was the composite of death from cardiovascular causes, myocardial infarction, or stroke. After 2 years, the data and safety monitoring board recommended discontinuation of the study treatment in patients with a history of stroke owing to the risk of intracranial hemorrhage. RESULTS: At 3 years, the primary end point had occurred in 1028 patients (9.3%) in the vorapaxar group and in 1176 patients (10.5%) in the placebo group (hazard ratio for the vorapaxar group, 0.87; 95% confidence interval [CI], 0.80 to 0.94; P<0.001). Cardiovascular death, myocardial infarction, stroke, or recurrent ischemia leading to revascularization occurred in 1259 patients (11.2%) in the vorapaxar group and 1417 patients (12.4%) in the placebo group (hazard ratio, 0.88; 95% CI, 0.82 to 0.95; P=0.001). Moderate or severe bleeding occurred in 4.2% of patients who received vorapaxar and 2.5% of those who received placebo (hazard ratio, 1.66; 95% CI, 1.43 to 1.93; P<0.001). There was an increase in the rate of intracranial hemorrhage in the vorapaxar group (1.0%, vs. 0.5% in the placebo group; P<0.001). CONCLUSIONS: Inhibition of PAR-1 with vorapaxar reduced the risk of cardiovascular death or ischemic events in patients with stable atherosclerosis who were receiving standard therapy. However, it increased the risk of moderate or severe bleeding, including intracranial hemorrhage. (Funded by Merck; TRA 2P-TIMI 50 ClinicalTrials.gov number, NCT00526474.)