Prognostic value of changes in arterial stiffness in men with coronary artery disease

Iana A Orlova, Eradzh Yu Nuraliev, Elena B Yarovaya, Fail T AgeevOutpatient department, Russian Cardiology Research Center, Moscow, Russian Federation Background: Men with coronary artery disease (CAD) have been shown to have enhanced arterial stiffness. Arterial function may change over time according to treatment, but the prognostic value of these changes has not been investigated.Objectives: The aim of the present study was to assess whether an improvement in large artery rigidity in response to treatment, could predict a more favorable prognosis in a population of men with CAD.Methods: A total of 161 men with CAD (mean age 56.8 ± 10.9 years) being treated with conventional therapy underwent brachial-ankle pulse wave velocity (PWVba) measurements at baseline and after six months. Follow-up period was 3.5 years. End-points were major adverse cardiac events (MACE): acute myocardial infarction, unstable angina, coronary intervention, or cardiac death.Results: During the three-year follow-up period (since initial six-month follow-up), 30 patients experienced MACE. After six-month follow-up, PWVba had not improved (∆PWVba ≥ 0%, relative to baseline) in 85 (52.8%) of 161 men (Group 1), whereas it had improved (∆PWVba < 0%) in the remaining 76 men (47.2%) (Group 2). During follow-up, we noticed 24 cardiovascular events in Group 1 and six events in Group 2 (P < 0.001). Cox proportional hazards analyses demonstrated that independent of conventional risk factor changes, absence of PWVba decrease was a predictor of MACE (RR 3.99; 95% CI:1.81–8.78; P = 0.004). The sensitivity of ∆PWVba was 80% and its specificity was 54%.Conclusions: This study demonstrates that an improvement in arterial stiffness may be obtained after six months of conventional therapy and clearly identifies patients who have a more favorable prognosis.Keywords: arterial stiffness, coronary artery disease, prognosi

A Plagionotus arcuatus ssp. arcuatus darázscincér (Coleoptera: Cerambycidae) fajon belüli kommunikációjának a vizsgálata két, földrajzilag távoli, európai populáción

A bársonyos darázscincér, Plagionotus arcuatus ssp. arcuatus (L.) Európa nagyobb részén gyako- rinak számító szaproxilofág cincér faj, melyet a nyári hónapokban a szabadban tárolt, frissen kivágott tölgyfa alkalmi kártevőjeként tartunk számon. Annak érdekében, hogy azonosítsuk azokat a csalo- gató illatanyagokat, amelyek felhasználhatók a faj rajzáskövetésére, illatanyag gyűjtést végeztünk az imágókból, majd szabadföldi viselkedésvizsgálatokat végeztünk az azonosított illatanyagokkal, melyek a faj lehetséges aggregációs feromon komponensei. Három vegyület, az (R)-3-hidroxihexán- 2-on, az (R)-3-hidroxioktán-2-on, és az (R)-3-hidroxidekán-2-on viszonylag nagy mennyiségben volt jelen a hím kivonatokban Magyarországon és Svédországban egyaránt, függetlenül a filter típusától (aktív szén vagy PorapakTM Q, ezeket a bogarak által kibocsátott illatanyagok megkötésére hasz- náljuk), illetve függetlenül a kivonat készítésére használt oldószer típusától (hexán, dietil éter, vagy diklórmetán). A hidroxi-keton és annak rokon vegyületeinek egyike sem volt kimutatható a nőstények- ből származó kivonatokban. A szabadföldi vizsgálatokban mindkét országban a C6 és a C10 illatanya- gok keveréke, illetve a háromkomponensű keverék csalogatta a legtöbb bogarat. A kontroll csapdák, más kombinációk illetve az önmagukban alkalmazott illatanyagok csalogató hatása nem volt jelen- tős. A hímek és nőstények hasonlóan reagáltak a kezelésekre. Eredményeink azt mutatják, hogy a (R)-3-hidroxihexán-2-on és a (R)-3-hidroxidekán-2-on a bársonyos darázscincér hímek által termelt aggregációs feromon komponensei, míg a (R)-3-hidroxioktán-2-on szerepe nem tisztázott. Az azo- nosított feromonkomponensek a bársonyos darázscincér populáció megfigyelésére alkalmazhatóak

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.