The Vehicle, 1968, Vol. 10 no. 2

Vol. 10, No. 2 Table of Contents 1st Prize, ArtCorner of My MindGerry Moreheadpage 4 #1Clyde Simspage 5 Aesthetics for a VagabondByron Nelsonpage 5 1st Prize, Short StorySteam HeatCharles Whitepage 6 a drawingSally Roachpage 6 an untitled themeCatherine Waitepage 8 MoodKevin Sheapage 9 1st Prize, PoetryHome ThoughtsJane Careypage 10 an untitled poemCatherine Waitepage 11 a drawingSally Roachpage 11 GraceJames T. Jonespage 12 LonelinessSally Roachpage 14 Love, JimmyAstaire Pappaspage 14 CapturedJeff Nelsonpage 15 Winnie Davis Neely AwardUnconcernRoger Zulaufpage 17 an untitled poemDavid N. Deckerpage 17 Morality and American Foreign Policy: The Ever-widening GapBruce L. Berrypage 18 La LibertadChris Holavespage 19 1966Roger Zulaufpage 19 SinThomas W. Phippspage 20 a drawingRoger Perkinspage 20 Summer SweatJerry J. Carterpage 20 1st Prize, EssayCuriosityThomas W. Phippspage 21 A Bottle of DreamsMaurice Snivelypage 21 Chalk DustCatherine Waitepage 22 Diffused Existence or, a Meager Attempt at Helping You Over the Rough SpotsJan Gerlachpage 22 To *e.e.Paula Bresnanpage 22 A PoemThomas W. Phippspage 22 Beach PartyJerol Mikeworthpage 22 Wexford\u27s PartyRoy Lueckepage 23 The Four O\u27Clock ClubSally Roachpage 23 Chesterpage 24https://thekeep.eiu.edu/vehicle/1018/thumbnail.jp

Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease

Background: Experimental and clinical data suggest that reducing inflammation without affecting lipid levels may reduce the risk of cardiovascular disease. Yet, the inflammatory hypothesis of atherothrombosis has remained unproved. Methods: We conducted a randomized, double-blind trial of canakinumab, a therapeutic monoclonal antibody targeting interleukin-1β, involving 10,061 patients with previous myocardial infarction and a high-sensitivity C-reactive protein level of 2 mg or more per liter. The trial compared three doses of canakinumab (50 mg, 150 mg, and 300 mg, administered subcutaneously every 3 months) with placebo. The primary efficacy end point was nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. RESULTS: At 48 months, the median reduction from baseline in the high-sensitivity C-reactive protein level was 26 percentage points greater in the group that received the 50-mg dose of canakinumab, 37 percentage points greater in the 150-mg group, and 41 percentage points greater in the 300-mg group than in the placebo group. Canakinumab did not reduce lipid levels from baseline. At a median follow-up of 3.7 years, the incidence rate for the primary end point was 4.50 events per 100 person-years in the placebo group, 4.11 events per 100 person-years in the 50-mg group, 3.86 events per 100 person-years in the 150-mg group, and 3.90 events per 100 person-years in the 300-mg group. The hazard ratios as compared with placebo were as follows: in the 50-mg group, 0.93 (95% confidence interval [CI], 0.80 to 1.07; P = 0.30); in the 150-mg group, 0.85 (95% CI, 0.74 to 0.98; P = 0.021); and in the 300-mg group, 0.86 (95% CI, 0.75 to 0.99; P = 0.031). The 150-mg dose, but not the other doses, met the prespecified multiplicity-adjusted threshold for statistical significance for the primary end point and the secondary end point that additionally included hospitalization for unstable angina that led to urgent revascularization (hazard ratio vs. placebo, 0.83; 95% CI, 0.73 to 0.95; P = 0.005). Canakinumab was associated with a higher incidence of fatal infection than was placebo. There was no significant difference in all-cause mortality (hazard ratio for all canakinumab doses vs. placebo, 0.94; 95% CI, 0.83 to 1.06; P = 0.31). Conclusions: Antiinflammatory therapy targeting the interleukin-1β innate immunity pathway with canakinumab at a dose of 150 mg every 3 months led to a significantly lower rate of recurrent cardiovascular events than placebo, independent of lipid-level lowering. (Funded by Novartis; CANTOS ClinicalTrials.gov number, NCT01327846.