107 results on '"Cannon C.P."'
Search Results
2. Ertugliflozin and Incident Obstructive Sleep Apnea: An Analysis from the VERTIS CV Trial
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Wojeck, B.S., primary, Inzucchi, S.E., additional, Neeland, I.J., additional, Mancuso, J.P., additional, Frederich, R., additional, Masiukiewicz, U., additional, Cater, N.B., additional, McGuire, D.K., additional, Cannon, C.P., additional, and Yaggi, H.K., additional
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- 2022
- Full Text
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3. G-protein β3 subunit polymorphism and bleeding in the orbofiban in patients with unstable coronary syndromes–thrombolysis in myocardial infarction 16 trial
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MAREE, A.O., VANGJELI, C., JNEID, H., RYAN, J., COX, D., CANNON, C.P., SHIELDS, D.C., and FITZGERALD, D.J.
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- 2010
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4. POS-354 WORSENING KIDNEY DISEASE INFLUENCES THE EFFICACY OF ERTUGLIFLOZIN ON GLUCOSURIA-MEDIATED ENDPOINTS BUT DOES NOT INFLUENCE THE EFFICACY ON NATRIURESIS-RELATED ENDPOINTS: PRESPECIFIED ANALYSES FROM VERTIS CV
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Cherney, D., primary, Charbonnel, B., additional, Cosentino, F., additional, Pratley, R.E., additional, Dagogo-Jack, S., additional, Shih, W.J., additional, McGuire, D.K., additional, Frederich, R., additional, Maldonado, M., additional, Liu, J., additional, Pong, A., additional, Liu, C., additional, and Cannon, C.P., additional
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- 2021
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5. Independent predictors of heart failure in patients with type 2 diabetes and chronic kidney disease: modeling from the CREDENCE trial
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Mahaffey, K.W, primary, Li, J, additional, Chang, T.I, additional, Sarraju, A, additional, Agarwal, R, additional, Charytan, D.M, additional, Greene, T, additional, Heerspink, H.J.L, additional, Levin, A, additional, Neal, B, additional, Pollock, C, additional, Yavin, Y, additional, Jardine, M, additional, Perkovic, V, additional, and Cannon, C.P, additional
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- 2020
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6. Effects of canagliflozin on cardiovascular death and hospitalization for heart failure by baseline estimated glomerular filtration rate: integrated analyses from the CANVAS Program and CREDENCE
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Mahaffey, K.W, primary, Bakris, G, additional, Blais, J, additional, Cannon, C.P, additional, Cherney, D, additional, Damaraju, C.V, additional, Gogate, J, additional, Greene, T, additional, Heerspink, H.J.L, additional, Januzzi Jr, J.L, additional, Kosiborod, M, additional, Levin, A, additional, Lingvay, I, additional, Weir, M, additional, and Perkovic, V, additional
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- 2020
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7. Identifying high thrombotic risk in atrial fibrillation patients undergoing percutaneous coronary intervention: is there a benefit of triple therapy?
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Bor, W.L, primary, Zwart, B, additional, De Veer, A.J.W.M, additional, Mahmoodi, B.K, additional, Kelder, J.C, additional, Cannon, C.P, additional, and Ten Berg, J.M, additional
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- 2020
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8. Interleukin‐18 in patients with acute coronary syndromes
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Åkerblom, A., James, S.K., Lakic, T.G., Becker, R.C., Cannon, C.P., Steg, P.G., Himmelmann, A., Katus, H.A., Storey, R.F., Wallentin, L., Weaver, W.D., and Siegbahn, A.
- Abstract
Background\ud \ud We aimed to assess associations between circulating IL‐18 concentrations and cardiovascular outcomes in patients with acute coronary syndromes (ACS).\ud \ud \ud \ud Hypothesis and Methods\ud \ud Plasma IL‐18 concentrations were measured at admission, discharge, 1 month, and 6 months in patients with ACS in the PLATelet inhibition and patient Outcomes (PLATO) trial. Associations with outcomes were evaluated with Cox regression models on the composite of CV death, spontaneous myocardial infarction (sMI), or stroke; and on CV death or sMI separately, including adjustment for clinical risk factors and biomarkers (cTnT‐hs, NT‐proBNP, cystatin C, CRP‐hs, and GDF‐15).\ud \ud \ud \ud Results\ud \ud Median IL‐18 concentrations at baseline, discharge, 1 month, and 6 months were 237, 283, 305, and 320 ng/L (n = 16 636). Male sex, obesity, diabetes, and plasma levels of cystatin C, GDF‐15, and CRP‐hs were independently associated with higher IL‐18 levels. Higher baseline IL‐18 levels were associated with the composite endpoint and with CV death (hazard ratio [HR] 1.05, 95% confidence interval [95% CI] 1.02‐1.07 and HR 1.10, 95% CI 1.06‐1.14, respectively, per 25% increase of IL‐18 levels). Associations remained significant after adjustment for clinical variables but became non‐significant after adjustment for all biomarkers (HR 1.01, 95% CI 0.98‐1.04 and HR 1.04, 95% CI 1.00‐1.08, respectively). There were no associations with sMI.\ud \ud \ud \ud Conclusions\ud \ud In ACS patients, IL‐18 concentrations increased after the acute event and remained increased for 6 months. Baseline IL‐18 levels were significantly associated with CV mortality, independent of clinical characteristics and indicators of renal/cardiac dysfunction but this association was attenuated after adjustment for multiple biomarkers.
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- 2019
9. Switching of Oral Anticoagulation Therapy After PCI in Patients With Atrial Fibrillation:The RE-DUAL PCI Trial Subanalysis
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ten Berg, J.M., de Veer, A., Oldgren, J., Steg, P.G., Zateyshchikov, D.A., Jansky, P., Seung, K.-B., Hohnloser, S.H., Lip, G.Y.H., Nordaby, M., Kleine, E., Bhatt, D.L., and Cannon, C.P.
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dabigatran dual therapy ,oral anticoagulant agents ,atrial fibrillation ,cardiovascular diseases ,OAC ,bleeding event ,switching OACs - Abstract
Objectives: The aim of this study was to assess if prior oral anticoagulant agent (OAC) use modifies the lower bleeding risk observed with dabigatran dual therapy (dabigatran twice daily plus a P2Y12 inhibitor) versus warfarin triple therapy (warfarin plus a P2Y12 inhibitor plus aspirin) in patients with atrial fibrillation who underwent percutaneous coronary intervention (PCI). Background: In the RE-DUAL PCI (Randomized Evaluation of Dual Antithrombotic Therapy With Dabigatran Versus Triple Therapy With Warfarin in Patients With Nonvalvular Atrial Fibrillation Undergoing Percutaneous Coronary Intervention) trial, the primary outcome of major bleeding or clinically relevant nonmajor bleeding was lower with dabigatran dual therapy versus warfarin triple therapy in patients with atrial fibrillation who underwent PCI. Methods: A total of 2,725 patients were randomized to dual therapy with dabigatran (110 or 150 mg twice daily) plus clopidogrel or ticagrelor or triple therapy with warfarin plus aspirin and clopidogrel or ticagrelor. Subgroup analysis compared risk for major bleeding or clinically relevant nonmajor bleeding and a composite thromboembolic endpoint in patients with prior OAC use and in those who were OAC treatment naive. Results: Risk for major bleeding or clinically relevant nonmajor bleeding was reduced with both dabigatran dual therapies compared with warfarin triple therapy in both the prior OAC use group (hazard ratios: 0.58 [95% confidence interval (CI): 0.42 to 0.81] and 0.61 [95% CI: 0.41 to 0.92] with 110 and 150 mg dabigatran, respectively) and the OAC-naive group (hazard ratios: 0.49 [95% CI: 0.38 to 0.63] and 0.76 [95% CI: 0.59 to 0.97] with 110 and 150 mg dabigatran) (p for interaction = 0.42 and 0.37, 110 and 150 mg dabigatran, respectively). The risk for thromboembolic events seemed similar with dabigatran dual therapy (both doses) and warfarin triple therapy across subgroups. Conclusions: Bleeding risk was reduced with dabigatran dual therapy versus warfarin triple therapy in patients with atrial fibrillation after PCI, regardless of whether they were prior OAC users or OAC treatment naive. These results suggest that it is also safe to switch patients on OAC pre-PCI to dabigatran dual therapy post-PCI.
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- 2019
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10. Total Cardiovascular Events Analysis of the EXAMINE Trial in Patients with Type 2 Diabetes and Recent Acute Coronary Syndrome
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Cavender, M.A., White, W.B., Liu, Y., Massaro, J.M., Bergenstal, R.M., Mehta, C.R., Zannad, F., Heller, S., Cushman, W.C., and Cannon, C.P.
- Abstract
BACKGROUND: Alogliptin, a dipeptidyl-peptidase 4 inhibitor, is approved for the treatment of patients with type 2 diabetes. EXAMINE was a randomized-controlled clinical trial designed to demonstrate the cardiovascular safety of alogliptin. In the trial, 5380 patients with established T2DM who had a recent ACS event (between 15-90 days) were randomized to treatment with either alogliptin or placebo. HYPOTHESIS: To better understand and describe the cardiovascular (CV) safety of alogliptin, we analyzed data from the EXAMINE randomized clinical trial to determine whether treatment with alogliptin affected recurrent and total CV events. METHODS: Poisson regression analysis was performed to compare the total number of occurrences of CV death, MI, stroke, unstable angina, and coronary revascularization between all patients randomized to alogliptin versus placebo groups. RESULTS: Patients with recurrent CV events were older and more likely to have renal disease and history of heart failure. There were 1100 first CV events and an additional 666 recurrent events over a median of 18 months of follow-up. There were no significant differences with regard to the total number of events in patients treated with alogliptin (n=873) or placebo (n=893; p=0.52). Furthermore, there were no differences in the types of events seen in patients treated with alogliptin or placebo. CONCLUSION: Alogliptin did not increase the risk of either first or recurrent CV events when compared to placebo in patients with type 2 diabetes and recent ACS. These data support the CV safety of alogliptin in patients who are at increased risk of future CV events.
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- 2018
11. High-sensitivity C-reactive Protein, Low-Density Lipoprotein Cholesterol, and Cardiovascular Outcomes in Patients with Type 2 Diabetes in the EXAMINE (Examination of Cardiovascular Outcomes With Alogliptin Versus Standard of Care) Trial
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Hwang, Y.-C., Morrow, D.A., Cannon, C.P., Liu, Y., Bergenstal, R., Heller, S., Mehta, C., Cushman, W., Bakris, G.L., Zannad, F., and White, W.B.
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nutritional and metabolic diseases ,cardiovascular diseases - Abstract
OBJECTIVE: We sought to assess the risk of major adverse cardiovascular events (MACE) by utilizing high-sensitivity C-reactive protein (hsCRP) level and low-density lipoprotein cholesterol (LDL-C) in patients with type 2 diabetes and recent acute coronary syndrome. RESEARCH DESIGN AND METHODS: Study participants enrolled in the EXAMINE trial, were stratified by baseline hsCRP levels (3 mg/l) and were also sub-divided into 4 groups according to baseline hsCRP (≤3 or >3 mg/l) and achieved LDL-C (3 mg/l, respectively (P3 mg/l, the adjusted hazard ratio (95% confidence interval) was 1.42 (1.13, 1.78; P=0.002) for MACE compared with patients with hsCRP
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- 2017
12. Platelet-related biomarkers and their response to inhibition with aspirin and p2y12-receptor antagonists in patients with acute coronary syndrome
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Lowenstern, A., Storey, R.F., Neely, M., Sun, J.-L., Angiolillo, D.J., Cannon, C.P., Himmelmann, A., Huber, K., James, S.K., Katus, H.A., Morais, J., Siegbahn, A., Steg, P.G., Wallentin, L., and Becker, R.C.
- Abstract
The PLATelet inhibition and patient Outcomes (PLATO) trial showed that treatment with ticagrelor reduced the rate of death due to vascular causes, myocardial infarction and stroke when compared to clopidogrel in patients with ST-elevation or non-ST-elevation acute coronary syndrome (ACS). While the comparative benefit of ticagrelor over clopidogrel increased over time, event rates accrued in both groups during the study period. The purpose of our biomarker-based exploratory analysis was to determine whether long-term platelet inhibition may be associated with platelet adaptation. A sample of 4000 participants from the PLATO trial also consented to participate in a prospectively designed biomarker substudy. Blood samples were procured at baseline, immediately prior to hospital discharge and at 1 and 6 months. Markers of platelet activity, including platelet count, serum CD40-ligand and soluble P-selectin were analyzed. Mean levels were compared at discharge, 1 and 6 months following study drug initiation—first for all patients and subsequently stratified by treatment group. A linear mixed model was used to estimate the short-term change rate (baseline to 1 month) and long-term change rate (1–6 months) for each biomarker. A Cox proportional hazards model was used to calculate hazard ratios for each change in biomarker over the two time periods examined: baseline to 1 month and 1 to 6 months. Prior to randomized treatment (baseline), sCD40 ligand and sP-selectin levels were elevated above the normal range of the assay (0.39 and 33.5 µg/L, respectively). The mean level of each biomarker was significantly different at 1 month compared to baseline (p
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- 2017
13. Growth Differentiation Factor 15 at 1 Month After an Acute Coronary Syndrome Is Associated With Increased Risk of Major Bleeding
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Lindholm, D., Hagström, E., James, S.K., Becker, R.C., Cannon, C.P., Himmelmann, A., Katus, H.A., Maurer, G., López-Sendón, J.L., Steg, P.G., Storey, R.F., Siegbahn, A., and Wallentin, L.
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embryonic structures - Abstract
BACKGROUND: Growth differentiation factor-15 (GDF-15) is related to major bleeding when measured at initial presentation in patients with acute coronary syndromes (ACSs) treated with dual antiplatelet therapy. It is unknown whether follow-up measurements provide additional information. The objective of this study was to investigate whether GDF-15 measured 1 month after an ACS provides additional information beyond the baseline levels with regard to the risk of major bleeding. METHODS AND RESULTS: GDF-15 was measured at baseline and at 1 month after an ACS in 4049 patients included in the PLATelet inhibition and patient Outcomes (PLATO) trial. The association between 1-month GDF-15 level and non-coronary artery bypass grafting surgery-related major bleeding was assessed by a multivariable Cox model, adjusting for baseline GDF-15, age, anemia, impaired renal function, history of gastrointestinal bleeding, and sex. Elevated GDF-15 (>1800 ng/L) at 1 month was associated with an increased risk of non-coronary artery bypass grafting-related major bleeding (3.9% versus 1.2%; hazard ratio, 3.38; 95% CI, 1.89-6.06), independent of baseline GDF-15. Patients who had elevated GDF-15 levels at baseline and subsequent nonelevated GDF-15 at 1 month had a similar risk as patients who had nonelevated levels at both measurements. CONCLUSIONS: GDF-15 at 1 month after an ACS is related to the risk of bleeding during DAPT and provides additional information on the bleeding risk beyond baseline GDF-15 levels. GDF-15 levels may therefore be useful as part of decision support concerning long-term antithrombotic treatment in patients post-ACS. CLINICAL TRIAL REGISTRATION: URL: http://www.clinicaltrials.gov. Unique identifier: NCT00391872.
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- 2017
14. Mortality following cardiovascular and bleeding events occurring beyond 1 year after coronary stenting: A secondary analysis of the Dual Antiplatelet Therapy (DAPT) Study.
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Hopkins J., McGarry T., Nygaard T., Pow T., Larkin T., Caulfield T., Stys T., Lee T., Mansouri V., Srinivas V., Gupta V., Marquardt W., Ballard W., Bachinsky W., Colyer W., Dillon W., Felten W., French W., Kuehl W., Nicholas W., Nicholson W., Phillips W., Khatib Y., Al-Saghir Y., Hawa Z., Masud Z., Jafar Z., Muller D., Meredith I., Rankin J., Worthley M., Jepson N., Thompson P., Hendriks R., Whitbourn R., Duffy S., Stasek J., Novobilsky K., Naplava R., Coufal Z., Vaquette B., Bressollette E., Teiger E., Coste P., Rihani R., Darius H., Bergmann M.W., Radke P., Sebastian P., Strasser R., Hoffmann S., Behrens S., Moebius-Winkler S., Rutsch W., Lupkovics G., Horvath I., Kancz S., Forster T., Koszegi Z., Devlin G., Hart H., Elliott J., Ormiston J., Abernathy M., Fisher N., Kay P., Harding S., Jaffe W., Hoffmann A., Sosnowski C., Trebacz J., Buszman P., Dobrzycki S., Kornacewicz-Jach Z., Iancu A.C., Ginghina C.D., Matei C., Dobreanu D., Bolohan F.R., Dorobantu M., Jacques A., Jain A., Bakhai A., Gershlick A., Adamson D., Newby D., Felmeden D., Purcell I., Edmond J., Irving J., De Belder M., Pitt M., Kelly P., O'Kane P., Clifford P., Suresh V., Secemsky E.A., Yeh R.W., Kereiakes D.J., Cutlip D.E., Cohen D.J., Steg P.G., Cannon C.P., Apruzzese P.K., D'Agostino R.B., Massaro J.M., Mauri L., Kaplan A., Ahmed A., Ahmed A.-H., Albirini A., Moreyra A., Rabinowitz A., Shroff A., Moak A., Jacobs A., Kabour A., Gupta A., Irimpen A., Rosenthal A., Taussig A., Ferraro A., Chhabra A., Pucillo A., Spaedy A., White A., Pratsos A., Shakir A., Ghitis A., Agarwal A., Chawla A., Tang A., Barker B., Bertolet B., Uretsky B., Erickson B., Rama B., McLaurin B., Dearing B., Negus B., Price B., Brott B., Bhambi B., Bowers B., Watt B., Donohue B., Hassel C.D., Croft C., Lambert C., O'Shaughnessy C., Shoultz C., Kim C., Caputo C., Nielson C., Scott C., Wolfe C., McKenzie C., Brachfeld C., Thieling C., Fisher D., Simon D., Churchill D., Dobies D., Eich D., Goldberg D., Griffin D., Henderson D., Kandzari D., Lee D., Lewis D., Mego D., Paniagua D., Rizik D., Roberts D., Safley D., Abbott D., Shaw D., Temizer D., Canaday D., Myears D., Westerhausen D., Ebersole D., Netz D., Baldwin D., Letts D., Harlamert E., Kosinski E., Portnay E., Mahmud E., Korban E., Hockstad E., Rivera E., Shawl F., Shamoon F., Kiernan F., Aycock G.R., Schaer G., Kunz G., Kichura G., Myers G., Pilcher G., Tadros G., Kaddissi G.I., Ramadurai G., Eaton G., Elsner G., Mishkel G., Simonian G., Piegari G., Chen H., Liberman H., Aronow H., Tamboli H.P., Dotani I., Marin J., Fleischhauer J.F., Leggett J., Mills J., Phillips J., Revenaugh J., Mann J.T., Wilson J., Pattanayak J., Aji J., Strain J., Patel J., Carr J., Moses J., Chen J.-C., Williams J., Greenberg J., Cohn J., Douglas J., Gordon J., Griffin J., Hawkins J., Katopodis J., Lopez J., Marshall J., Wang J., Waltman J., Saucedo J., Galichia J., McClure M., Kozina J., Stella J., Tuma J., Kieval J., Giri K., Ramanathan K., Allen K., Atassi K., Baran K., Khaw K., Clayton K., Croce K., Skelding K., Patel K., Garratt K., Harjai K., Chandrasekhar K., Kalapatapu K., Lin L., Dean L., Barr L., MacDonald L., Cannon L., Satler L., Gruberg L., Tami L., Bikkina M., Shah M., Atieh M., Chauhan M., Litt M., Unterman M., Lechin M., Zughaib M., Fisch M., Grabarczyk M., Greenberg M., Lurie M., Rothenberg M., Stewart M., Purvis M., Hook M., Leesar M., Buchbinder M., Weiss M., Guerrero M., Abu-Fadel M., Ball M., Chang M., Cunningham M., Del Core M., Jones M., Kelberman M., Lim M., Ragosta M., Rinaldi M., Rosenberg M., Savage M., Tamberella M., Kellett M., Vidovich M., Effat M., Mirza M.A., Khan M., Dib N., Laufer N., Kleiman N., Farhat N., Amjadi N., Schechtmann N., Bladuell N., Quintana O., Gigliotti O., Best P., Flaherty P., Hall P., Gordon P., Gurbel P., Ho P., Luetmer P., Mahoney P., Mullen P., Teirstein P., Tolerico P., Ramanathan P., Kerwin P., Lee P.V., Kraft P., Wyman R.M., Gonzalez R., Kamineni R., Dave R., Sharma R., Prashad R., Aycock R., Quesada R., Goodroe R., Magorien R., Randolph R., Bach R., Kettelkamp R., Paulus R., Waters R., Zelman R., Ganim R., Bashir R., Applegate R., Feldman R., Frankel R., Hibbard R., Jobe R., Jumper R., Maholic R., Siegel R., Smith R., Stoler R., Watson R., Wheatley R., Gammon R., Hill R., Sundrani R., Caputo R., Jenkins R., Stella R., Germanwala S., Hadeed S., Ledford S., Dube S., Gupta S., Davis S., Martin S., Waxman S., Dixon S., Naidu S., Potluri S., Cook S., Crowley S., Kirkland S., McIntyre S., Thew S., Lin S., Marshalko S., Guidera S., Hearne S., Karas S., Manoukian S., Rowe S., Yakubov S., Pollock S., Banerjee S., Allaqaband S., Choi S., Mulukutla S., Papadakos S., Bajwa T., Addo T., Schreiber T., Haldis T., Mathew T., Hopkins J., McGarry T., Nygaard T., Pow T., Larkin T., Caulfield T., Stys T., Lee T., Mansouri V., Srinivas V., Gupta V., Marquardt W., Ballard W., Bachinsky W., Colyer W., Dillon W., Felten W., French W., Kuehl W., Nicholas W., Nicholson W., Phillips W., Khatib Y., Al-Saghir Y., Hawa Z., Masud Z., Jafar Z., Muller D., Meredith I., Rankin J., Worthley M., Jepson N., Thompson P., Hendriks R., Whitbourn R., Duffy S., Stasek J., Novobilsky K., Naplava R., Coufal Z., Vaquette B., Bressollette E., Teiger E., Coste P., Rihani R., Darius H., Bergmann M.W., Radke P., Sebastian P., Strasser R., Hoffmann S., Behrens S., Moebius-Winkler S., Rutsch W., Lupkovics G., Horvath I., Kancz S., Forster T., Koszegi Z., Devlin G., Hart H., Elliott J., Ormiston J., Abernathy M., Fisher N., Kay P., Harding S., Jaffe W., Hoffmann A., Sosnowski C., Trebacz J., Buszman P., Dobrzycki S., Kornacewicz-Jach Z., Iancu A.C., Ginghina C.D., Matei C., Dobreanu D., Bolohan F.R., Dorobantu M., Jacques A., Jain A., Bakhai A., Gershlick A., Adamson D., Newby D., Felmeden D., Purcell I., Edmond J., Irving J., De Belder M., Pitt M., Kelly P., O'Kane P., Clifford P., Suresh V., Secemsky E.A., Yeh R.W., Kereiakes D.J., Cutlip D.E., Cohen D.J., Steg P.G., Cannon C.P., Apruzzese P.K., D'Agostino R.B., Massaro J.M., Mauri L., Kaplan A., Ahmed A., Ahmed A.-H., Albirini A., Moreyra A., Rabinowitz A., Shroff A., Moak A., Jacobs A., Kabour A., Gupta A., Irimpen A., Rosenthal A., Taussig A., Ferraro A., Chhabra A., Pucillo A., Spaedy A., White A., Pratsos A., Shakir A., Ghitis A., Agarwal A., Chawla A., Tang A., Barker B., Bertolet B., Uretsky B., Erickson B., Rama B., McLaurin B., Dearing B., Negus B., Price B., Brott B., Bhambi B., Bowers B., Watt B., Donohue B., Hassel C.D., Croft C., Lambert C., O'Shaughnessy C., Shoultz C., Kim C., Caputo C., Nielson C., Scott C., Wolfe C., McKenzie C., Brachfeld C., Thieling C., Fisher D., Simon D., Churchill D., Dobies D., Eich D., Goldberg D., Griffin D., Henderson D., Kandzari D., Lee D., Lewis D., Mego D., Paniagua D., Rizik D., Roberts D., Safley D., Abbott D., Shaw D., Temizer D., Canaday D., Myears D., Westerhausen D., Ebersole D., Netz D., Baldwin D., Letts D., Harlamert E., Kosinski E., Portnay E., Mahmud E., Korban E., Hockstad E., Rivera E., Shawl F., Shamoon F., Kiernan F., Aycock G.R., Schaer G., Kunz G., Kichura G., Myers G., Pilcher G., Tadros G., Kaddissi G.I., Ramadurai G., Eaton G., Elsner G., Mishkel G., Simonian G., Piegari G., Chen H., Liberman H., Aronow H., Tamboli H.P., Dotani I., Marin J., Fleischhauer J.F., Leggett J., Mills J., Phillips J., Revenaugh J., Mann J.T., Wilson J., Pattanayak J., Aji J., Strain J., Patel J., Carr J., Moses J., Chen J.-C., Williams J., Greenberg J., Cohn J., Douglas J., Gordon J., Griffin J., Hawkins J., Katopodis J., Lopez J., Marshall J., Wang J., Waltman J., Saucedo J., Galichia J., McClure M., Kozina J., Stella J., Tuma J., Kieval J., Giri K., Ramanathan K., Allen K., Atassi K., Baran K., Khaw K., Clayton K., Croce K., Skelding K., Patel K., Garratt K., Harjai K., Chandrasekhar K., Kalapatapu K., Lin L., Dean L., Barr L., MacDonald L., Cannon L., Satler L., Gruberg L., Tami L., Bikkina M., Shah M., Atieh M., Chauhan M., Litt M., Unterman M., Lechin M., Zughaib M., Fisch M., Grabarczyk M., Greenberg M., Lurie M., Rothenberg M., Stewart M., Purvis M., Hook M., Leesar M., Buchbinder M., Weiss M., Guerrero M., Abu-Fadel M., Ball M., Chang M., Cunningham M., Del Core M., Jones M., Kelberman M., Lim M., Ragosta M., Rinaldi M., Rosenberg M., Savage M., Tamberella M., Kellett M., Vidovich M., Effat M., Mirza M.A., Khan M., Dib N., Laufer N., Kleiman N., Farhat N., Amjadi N., Schechtmann N., Bladuell N., Quintana O., Gigliotti O., Best P., Flaherty P., Hall P., Gordon P., Gurbel P., Ho P., Luetmer P., Mahoney P., Mullen P., Teirstein P., Tolerico P., Ramanathan P., Kerwin P., Lee P.V., Kraft P., Wyman R.M., Gonzalez R., Kamineni R., Dave R., Sharma R., Prashad R., Aycock R., Quesada R., Goodroe R., Magorien R., Randolph R., Bach R., Kettelkamp R., Paulus R., Waters R., Zelman R., Ganim R., Bashir R., Applegate R., Feldman R., Frankel R., Hibbard R., Jobe R., Jumper R., Maholic R., Siegel R., Smith R., Stoler R., Watson R., Wheatley R., Gammon R., Hill R., Sundrani R., Caputo R., Jenkins R., Stella R., Germanwala S., Hadeed S., Ledford S., Dube S., Gupta S., Davis S., Martin S., Waxman S., Dixon S., Naidu S., Potluri S., Cook S., Crowley S., Kirkland S., McIntyre S., Thew S., Lin S., Marshalko S., Guidera S., Hearne S., Karas S., Manoukian S., Rowe S., Yakubov S., Pollock S., Banerjee S., Allaqaband S., Choi S., Mulukutla S., Papadakos S., Bajwa T., Addo T., Schreiber T., Haldis T., and Mathew T.
- Abstract
Importance: Early cardiovascular and bleeding events after coronary stenting are associated with high risk of morbidity and mortality. Objective(s): To assess the prognosis of cardiovascular and bleeding events occurring beyond 1 year after coronary stenting. Design, Setting, and Participant(s): This secondary analysis is derived from data from the Dual Antiplatelet Therapy (DAPT) Study, a multi center trial involving 220 US and in ternational clinical sites from 11 countries. The study dateswere August 2009 to May 2014. Individuals who underwent coronary stenting and completed 12 months of thienopyridine plus aspirin therapy without ischemic or bleeding events remained on an aspirin regimen and were randomized to continued thienopyridine therapy vs placebo for 18 additional months. Individuals were then followed up for 3 additional months while receiving aspirin therapy alone. The analysis began in August 2015. Exposures: Ischemic events (myocardial infarction not related to stent thrombosis, stent thrombosis, and ischemic stroke) and bleeding events (Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Arteries [GUSTO] classification moderate or severe bleeding). Main Outcomes and Measures: Ischemic events (myocardial infarction not related to stent thrombosis, stent thrombosis, and ischemic stroke) and bleeding events (GUSTO classification moderate or severe bleeding). Death at 21 months after randomization (33 months after coronary stenting). Result(s): Intotal, 25 682 individuals older than 18 years with an indication for coronarystentingwere enrolled, and 11 648(meanage,61.3 years; 25.1%female)were randomized. After randomization, 478 individuals (4.1%) had 502 ischemic events (306 with myocardial infarction, 113 with stent thrombosis, and 83 with ischemic stroke), and 232 individuals (2.0%) had 235 bleeding events (155 with moderate and 80 with severe bleeding). Among individuals with ischemic events, 52(10.9%) died. The annualize
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- 2017
15. Pharmacodynamic relationship between PCSK9, alirocumab, and LDL-C lowering in four phase 3 odyssey trials with/without statin background
- Author
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Robinson, J.G., primary, Farnier, M., additional, Kastelein, J.J., additional, Roth, E.M., additional, Taskinen, M.R., additional, Colhoun, H.M., additional, Brunet, A., additional, DiCioccio, A.T., additional, Lecorps, G., additional, Pordy, R., additional, Baccara-Dinet, M.T., additional, and Cannon, C.P., additional
- Published
- 2016
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16. Ezetimibe Added to Statin Therapy after Acute Coronary Syndromes.
- Author
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IMPROVE-IT Investigators, Musliner, T., Tershakovec, A., Gurfinkel, E., Aylward, P., Tonkin, A., Maurer, G., Van de Werf, F., Nicolau, J.C., Theroux, P., Genest, J., Armstrong, P., Corbalan, R., Isaza, D., Spinar, J., Grande, P., Voitk, J., Kesaniemi, A., Bassand, J.P., Farnier, M., Darius, H., Keltai, M., Mathur, A., Mittal, S., Reddy, K., Lewis, B., De Ferrari, G.M., Ophuis, T.O., Jukema, J., White, H., Pedersen, T., Britto, F., Ruzyllo, W., Carrageta, M., Duris, T., Dalby, A., Seung, K.B., Lopez-Sendon, J., Dellborg, M., Mach, F., Guneri, S., Parkhomenko, A., Brady, A., Cannon, C., Blazing, M., Ballantyne, C., de Lemos, J., Kleiman, N., McGuire, D.K., Centeno, E., Casalins, M., Cartasegna, L., Beltrano, M.C., Guerrero, R., Fanuele, M., Berra, F., Egido, J., Colombo, H., Dellatorre, M., Terns, P., Blumberg, E., Reges, P., Azize, G., Ramos, H., Fernandez, R., Carlessi, C., Milesi, R., Schmuck, R., Duronto, E., Procopio, G., Carlevaro, O., Maffeo, H., Beloscar, J., Viso, M., Hominal, M., Castoldi, M., Bluguermann, J., Mauro, D., Macin, S., Cocco, N., Ruiz, N., Ricart, J., Lozada, A., Nani, S., Turri, D., Fernandez, H., Caruso, O., Zarandon, R., Bono, J., Arias, V., Allall, O., Marino, J., Cusimano, S., Schygiel, P., Buzetti, C., Penaloza, N., Berli, M., Worthley, S., Roach, A., Chew, D., Wright, T., Leitch, J., Hicks, E., Rankin, J., Venn-Edmonds, C., Lehman, R., Morrison, H., Shaw, J., Mak, V., Hii, C., Smith, K., Cross, D., Lilwall, L., Nelson, G., Loxton, A., Horowitz, J., Rose, J., Steinwender, C., Leisch, F., Kammler, J., Brussee, H., Zweiker, R., Niederl, E., Weihs, W., Giorgio, G., Lang, I., Drexel, H., Zanolin, D., Hoppe, U., Atzenhofer-Baumgartner, K., Pichler, M., Hainzer, D., Eber, B., Pichler, F., Foeger, B., Wechselberger, T., Mayr, H., Hofer, J., Stockenhuber, F., Warlits, B., Huber, K., Egger, F., Weidinger, F., Ziegler, B., Jirak, P., Metzler, B., Pachinger, O., Wanitschek, M., Auer, J., Grabscheit, G., Podczeck-Schweighofer, A., Priesnitz, T., Frank, H., El Allaf, D., Marechal, P., Roosen, J., Joly, E., Lefebvre, P., Arend, C., Sinnaeve, P., De Velder, L., Hellemans, S., Vanhauwaert, B., Van Dorpe, A., Heyse, A., Vantomme, C., Striekwold, H., Van Den Broeck, D., Lancellotti, P., Schoors, D., Lemoine, I., Taeymans, Y., De Wolf, L., Brike, C., Vercauteren, S., Tahon, S., Vervoort, G., Mestdagh, I., Pirenne, B., Cardinal, F., Lips, S., Dujardin, K., Debrouwer, K., Dhooghe, G., Holvoet, G., van de Borne, P., Renard, M., De Clippel, M., Lesseliers, H., Van Miert, N., Saraiva, J., Vicente, C., Rossi, P., Dos Santos, L.B., Duda, N., Tognon, A.P., Serrano, C., Gomes, F.L., Manenti, E.R., Silveira, D.S., Maia, L., Mouco, O.M., Paiva, M., Antonangelo, A., de Souza, J., Lino, E.A., Leães, P., Blacher, M.G., Kormann, A., Ultramari, F.T., Dutra, O., Mendelski, A.M., Morgado, S., Ardito, W., Greque, G., Ardito, R.V., Pimentel Filho, P., Zucchetti, C., Alves, A., Seabra, A.M., Mattos, M., Miranda, L.F., Silva, D., Uehara, R.M., Marin Neto, J., Schmidt, A., Braga, J., Rodrigues, A., Abrantes, J., Pinheiro, L., Bodanese, L., Magedanz, É.H., Piegas, L., Dos Santos, E.S., Wainstein, M., Ribeiro, J., Stein, R., Marino, R., Machado, V.M., Moraes Junior, J., Guimarães, S., da Costa, F.A., Ferraz, R.F., Albuquerque, D., Rocha, R.M., de Carvalho Moreira, R., Dohmann, H., Costantini, C., Tarastchuk, J.C., Coelho, O., Cirillo, W., Sousa, A., Almeira, A.S., Stefanini, E., Silva, F., Teixeira, M., da Cunha, C., Précoma, D., Facchi, T.L., Rupka, D., Thiessen, S., Warnica, J., Smith, B., Della Siega, A., Klinke, P., Nelson, S., Dion, D., Gilbert, N., Hui, W., Kvill, L., Sussex, B., Luther, A., Dupuis, R., Ouimet, F., Pandey, A., Clarus, S., Senaratne, M., Ferdinandis, H., Mukherjee, A., Bozek, B., Vizel, S., Markov, G., Zimmermann, R., Stephens, W., Tremblay, B., Wong, G., Uchida, N., Brossoit, R., Peck, C., Van Kieu, C., Forgione, M., Bata, I., Cossett, J., Kostuk, W., Arnold, M., Bone, C., Grondin, F., Bilodeau, N., Gosselin, G., David, M., Giannoccaro, J., Beresford, P., Polasek, P., Roberts, P., Doucet, M., Beaudry, M., Cheung, S., Cleveland, T., Bhargava, R., McCallum, A., Ma, P., Morrissette, J., Cleveland, D., Chadwyn, D., Nigro, F., Weeks, A., Cryderman, C., Leader, R., Houde, G., Rousseau, S., Pearce, M., Radyk, M., Lonn, E., Magi, A., Lefkowitz, C., Sandrin, F., Coffin, N., Lubelsky, B., Coldwell, J., Habot, J., McPherson, C., De Larochelliere, R., Roy, M., Haichin, R., Barber, C., Bhesania, T., Kitagawa, H., To, T., Donnelly, B., Tymchak, W., Harris, L., Kouz, S., Huynh, T., St Jacques, B., Lamy, A., Rizzo, A., Stein, J., Childs, C., Wong, B., Poirier, R., Gupta, M., Dela Cruz, C., Constance, C., Gauthier, M., Ervin, F., Ouellette, M., Kokis, A., Lemay, C., Kwok, K., Leung, C., Lee, D., Nesmith, J., Renton, J., Syan, G., Turek, M., Hogan, D., Griffin, P., Lipson, A., Winestock, J., Abramson, B., Fogel, A., Gagne, C., Bergeron, J., Clarke, A., Slipp, S., Darcel, I., Carling-Chambers, L., Kannampuzha, P., Pallie, S., Krekorian, S., Vertes, G., Roth, S., Lai, K., Heath, J., Perez, L., Arriagada, G., Castro, P., Villa, F., Rodríguez, M., Ramos, G., Baraona, F., Núñez, A., García, M., Jofre, C., Silva, P., Lamich, R., Yovaniniz, P., Escobar, E., Dussaubat, A., Segura, E., Ramirez, M., Lapostol, C., Palma, A., Encina, L., Zapata, M., Baeza, N., Varela, P., Pérez, L., Jaramillo, C., Ruiz, S., Sanchez, G., Perdomo, I., Manzur, F., Cohen, L.E., Velasquez, J., Arana, C., Alvarez, Y., Triana, M., Balaguera, J., de Salazar, D., Rendon, N., Botero, R., Ruiz, A., Saaibi, J., Medina, J., Jaramillo, M., Calderón, M.J., Delgado, J., Bohorquez, R., Medina, M.F., Herrera, M., Rosales, D., Mendoza, F., Martinez, S., Ternera, A., Castro, R., Baiz, A., Martinez, M., Orozco, A., Suarez, M., Fonseca, Y., Beltran, R., Cepeda, M., Jaramillo, N., Valenzuela, C., Gutierrez, M., Sanchez, A., Vitovec, J., Hlinomaz, O., Poloczek, M., Mayer, O., Veselka, J., Vejvoda, J., Soucek, M., Spac, J., Novobilsky, K., Srp, V., Francek, L., Branny, M., Sknouril, L., Motovska, Z., Rohac, F., Stankova, A., Fiala, T., Holub, M., Zeman, K., Pohludkova, L., Pospisilova, E., Tuma, P., Cihalik, C., Oral, I., Podpera, I., Stepanovova, R., Uricar, M., Solar, M., Pelouch, R., Porzer, M., Grussmannova, K., Stipal, R., Reichert, P., Hradec, J., Kral, J., Sejkova, B., Janek, B., Pitha, J., Linhart, A., Polacek, P., Koeber, L., Clemmensen, P., Hebin, C.H., Schmidt, E., Pedersen, M.S., Roseva-Nielsen, N., Kristensen, K., Bang-Hansen, T., Jensen, J., Laage-Petersen, J., Nielsen, H., Stokholm, E., Thayssen, P., Cappelen, H., Jensen, T., Winther-Friis, B., Klausen, I., Hedegaard, B., May, O., Andersen, M., Bottzauw, J., Lush, A., Markenvard, J., Vestager, K.M., Bronnum-Schou, J., Hempel, H., Petersen, J., Nielsen, A.J., Thomsen, K., Nielsen, T., Nygaard, A., Sykulski, R., Jensen, B.S., Ralfkiaer, N., Gottschalck, H., Rasmussen, S., Pedersen, L.R., Dodt, K., Skovsbøl, M., Andersen, O., Tuxen, C., Meier, A.W., Kristensen, T., Rasmussen, O., Lopez, J., Salazar, D., Sanchez, L., Rosero, F., Penaherrera, E., Duarte, Y.C., Marmol, R., Andrade, G., Guzman, E., Morillo, A., Aug, L., Loogna, I., Laanmets, P., Mustonen, J., Mäntylä, P., Kesäniemi, A., Ukkola, O., Kervinen, H., Juhela, S., Juvonen, J., Toppinen, A., Jarvenpaa, J., Syvanne, M., Svahn, T., Voutilainen, S., Huotari, A., Nikkila, M., Raiskinmäki, S., Kotila, M., Rajala, A., Laukkanen, J., Hiltunen, P., Melin, J., Nyman, K., Luukkonen, J., Kosonen, P., Huttunen, M., Seppänen, V., Airaksinen, J., Juonala, M., Lehto, S., Savolainen, K., Halkosaari, M., Sia, J., Palomaki, A., Luoma, J., Utriainen, S., Valpas, S., Tiensuu, T., Lilleberg, J., Kainulainen, R., Schiele, F., Bassand, J., Meneveau, N., Galinier, M., Jean, M., Martelet, M., Mouallem, J., Elbaz, M., Puel, J., Carrié, D., Coisne, D., Varroud-Vial, N., Jaboureck, O., Dujardin, J., Leroy, F., Mansourati, J., Funck, F., Jourdain, P., Guillard, N., Coviaux, F., Gay, A., Dourmap-Collas, C., Froger-Bompas, C., Paillard, F., Tricot, O., Maquin-Mavier, I., Dubois-Rande, J.L., Pongas, D., Paris, A.P., Delahaye, F., Ovize, M., Benyahya, L., Bonnet, J., Belle, L., Mangin, L., Lafitte, B., Zemour, G., Doux, N., Agraou, B., El Mansour, N., Traisnel, G., El Jarroudi, M., Ohlmann, P., Diadema, B., Escande, M., Legros, G., Demarcq, J.M., Haftel, Y., Alsagheer, S., Dambrine, P., Cottin, Y., Ghostine, S., Caussin, C., Gacem, A., Bouvier, J.M., Poulard, J., Davy, J., Furber, A., Prunier, F., Muenzel, T., Genth-Zotz, S., Appel, K., Kretzschmar, D., Ferrari, M., Terres, W., Uher, T., Schulze, H., Ochs, H., Morbach, S., Duengen, H., Gross, M., Oezcelik, C., Tahirovic, E., Heuer, H., Laschewski, B., Kadel, C., Rahn, G., Steiner, S., Kreuzer, J., Tsoy, I., Zeiher, A., Muegge, A., Hanefeld, C., Boehm, S., Boudriot, E., Hodenberg, E., Lippe, B., Hausdorf, C., Sydow, K., Baldus, S., Schlesner, C., Tiroch, K., Haltern, G., Guelker, H., Wilhelm, J., Dietz, S., Ebelt, H., Buerke, M., Rupprecht, H., Rittgen, J., Schaeufele, T., Meinhardt, G., Schieber, M., Honold, M., Sieprath, S., Nienaber, C., Hacker, J., Butter, C., Lapp, H., Hirn, S., Pauschinger, M., Zahn, R., Scheffler, U., Schaefer, A., Schieffer, B., Tebbe, U., Kriete, M., Mudra, H., Raeder, T., Braun, P., Zeymer, U., Kouraki, K., Reppel, M., Schunkert, H., Weil, J., Olbrich, H., Schwaiger, P., Mueller, O., Blessing, E., Buss, I., Bohlscheid, V., Kaddatz, J., Skowasch, D., Nickenig, G., Twelker, K., Osterhues, H., Varghese, T., Burghard, S., Kaeaeb, S., Klauss, V., Sohn, H.Y., Hauptmann, K., Schulze, M., Gall, K., Felix, S., Doerr, M., Mante, J., Gulba, D., Freick, M., Werner, G., Kleinertz, K., Hobbach, H.P., Halbach, M., Mueller-Ehmsen, J., Mueller, M.E., Mitrovic, V., Peil, A., Laufs, U., vom Dahl, J., Baumanns, S., Scholtz, W., Wiemer, M., Haude, M., Van de Loo, A., Pistorius, K., Schaefer, J., Schwinger, R., Goeing, O., Jung, W., Birkemeyer, R., Lee, W., Kong, S., Yu, C., Chui, K., Merkely, B., Szelényi, Z., Polgár, P., Svab, S., Herczeg, B., Bajcsi, É., Vértes, A., Davidovits, S., Nagy, A., Király, C., Lupkovics, G., Kenéz, A., Poór, F., Takács, J., Kirschner, R., Simonyi, G., Koncz, J., Édes, I., Gergely, S., Katona, A., Nagy, E., Kovács, Z., Gyetvai, I., Salamon, C., Kolman, É., Sitkei, É., Csapó, K., Molnar, K., Mező, I., Sereg, M., Reddy, P., Manjunath, C., Narayanappa, S., Kumar, S., Sinha, N., Kapoor, A., Christopher, J., Reddy, G., Rani, M., Oomman, A., Ramamurthee, K., Kumar, N., Pasha, S.S., Rao, C., Murty, G.S., Chopra, A., Kapila, D., Bali, H., Chattree, K., Hasan, O., Suryaprakash, G., Rao, D., Babu, R., Bhargavi, M., Naik, S., Khan, S., Chopra, V., Sapra, R., Kaul, U., Ghose, T., Menon, R., Battikadi, S., Mullasari, A., Subban, V.K., Dani, S., Iby, M., Chandra, P., Sethi, S., Bhargava, M., Arora, P., Tyagi, G., Padmanabhan, T., Malhotra, S., Talwar, K., Shafiq, N., Kasliwal, R., Bansal, M., Eldar, M., Berger, M., Shechter, M., Atar, S., Roguin, N., Kilimnik, M., Hayek, T., Hamoud, S., Katz, A., Plaev, T., Shotan, A., Vazan, A., Weiss, A., Leibowitz, D., Zimlichman, R., Ben-Aharon, J., Hammerman, H., Dragu, R., Rozenman, Y., Witzling, V., Tzivoni, D., Moriel, M., Halkin, A., Sheps, D., Bogomolny, N., Mosseri, M., Khudyak, Y., Halabi, S., Uziel-Iunger, K., Yuval, R., Shimoni, S., Caspi, A., Botwin, S., Gavish, D., Sandler, A., Pollak, A., Kreisberg, B., Hussein, O., Jabal, K., Henkin, Y., Grosbard, A., Rosenschein, U., Rivlin, E., Zeltser, D., Platner, N., Porter, A., Harel, N., Lishner, M., Elis, A., Karny, M., Fuchs, S., Stein, G., Grossman, E., Gealel, Z., Schlaeffer, F., Liberty, I., Golik, A., Tzuman, O., De Ferrari, G., Pavesi, C., Poggio, L., Damiano, S., Pazzano, A.S., Mennuni, M., Paloscia, L., Mascellanti, M., Piovaccari, G., Grosseto, D., Mascia, F., Vetrano, A., Zingarelli, A., Mazzantini, S., Visconti, L., Terzi, G., Senni, M., Gavazzi, A., Scuri, P., Carmelo, M., De Caterina, R., Conti, M., Novo, S., Graceffa, A., Arvigo, L., Lunetta, M., Filardi, P., Chiariello, M., Scala, O., Pirozzi, E., Musella, F., Moretti, L., Testa, M., Vicentini, A., De Feo, S., Biasucci, L., Cardillo, M.T., Puccioni, E., Galli, M., Menegato, A., Margheri, M., Maresta, A., Gatti, C., Guarini, P., Damiano, M., Golino, P., Porcu, M., Fele, N., Gensini, G., Lombardi, A., Ciuti, G., Bernardi, D., Mariani, P., Paolini, E., Marenzi, G., Moltrasio, M., Terrosu, P., Chessa, P., Guglielmino, G., Miccoli, F., Oldoino, E., Ragni, M., Poli, M., Basso, V., Rapezzi, C., Branzi, A., Gallelli, I., Perna, G., Guazzarotti, F., Marra, S., Usmiani, T., Olivari, Z., Calzolari, D., Santoro, G., Minneci, C., Achilli, A., Nassiacos, D., Sommariva, L., Romeo, F., Fedele, F., Foschi, M.L., Bruno, N., Centurion, C., Patrizi, G., De Maria, E., Gonnelli, S., Vichi, V., Cassadonte, F., Rotella, G., Capucci, A., Villani, G., Gaspardone, A., Ferrante, R., Scollo, V., Pancaldi, L., Saccà, S., Gabrielli, D., Ciliberti, D., Savini, E., Binaghi, G., Di Biase, M., Ieva, R., Fattore, L., Cicia, G., Cavallini, C., Tamburino, C., Sacco, A., Mafrici, A., Di Pasquale, G., Pavesi, P.C., Scioli, R., Lioy, E., Occhiuzzi, E., Matino, M.G., Russo, V., Moscogiuri, M.G., Cuccia, C., Forgione, C., Volpe, M., Palano, F., Branca, G., Rossi, R., Modena, M., Olaru, I.A., Zanini, R., Cianflone, D., Cristell, N., Pantaleoni, M., Guiducci, U., Menozzi, C., Gaddi, O., Fasulo, A., Indolfi, C., Emanuele, V., Guerra, F., Iliceto, S., Marotta, C., Morocutti, G., Presbitero, P., Rossi, M., Bonatti, S., Grieco, A., Chiodi, L., Betti, I., Zuppiroli, A., Fanelli, R., Stanco, G., Azzolini, P., Ruggieri, C., Bocconcelli, P., Airoldi, F., Tavano, D., Brunelli, C., Caso, P., Scalzone, A., Ghigliotti, G., Facciorusso, A., Sim, K., Kiam, O., Chee, K., Bin Ismail, O., Zambahari, R., Ophuis, T., van Nes, E., Werter, C.J., Ophuis, A.J., Troquay, R.P., Hamer, B.J., Lenderink, T., Feld, R.J., van Hessen, M.W., Viergever, E.P., van der Sluis, A., Lok, D.J., Badings, E.A., Nierop, P.R., Danse, I.Y., Hermans, W.R., Holwerda, N.J., Thijssen, H.J., Theunissen, L.J., van der Zwaan, C., Van Den Berg, B.J., Hendriks, I.H., Ronner, E., Withagen, A.J., Dijkshoorn-Giesen, A.H., Ezechiels, J.P., Kuijper, A.F., Den Hartog, F.R., Van Kalmthout, P.M., Buijs, E.M., van der Zeijst, M., Zwart, P.A., Zuidgeest, J.A., van Eck, M., Daniels, M.C., van der Ven-Elzebroek, N., Van 't Hof, A., van Boven, A.J., van der Weerdt, A., Dunselman, P.H., Alings, M.A., van Es, R.F., The, S.H., Gurlek, C., Liem, A.H., van Lennep, H.W., Van Vlies, B., Kalkman, C., Swart, H.P., van der Bij, P., Taverne, R., Ciampricotti, R., van Dam, C., Spierenburg, H., van Ruijven, I., van Kempen, L.H., Willems, F.F., Dirkali, A., Stoel, I., Plomp, J., Veldmeijer, S., Tjeerdsma, G., Nijmeijer, R., Van Hal, J.M., Bartels, G.L., Posma, J.L., Linssen, G.C., Fauser, C.G., Waalewijn, R.A., Groenemeijer, B.E., Pos, L., Fast, J.H., Droste, H.T., Westenburg, J., Veenstra, W., Koolen, J., van Loo, L.W., Smits, W., Milhous, J.G., van Rossum, P., Stuij, S., Scott, R., Richards, A.M., Morrison, Z., Devlin, G., Fisher, R., Stewart, R., Benetar, J., Voss, J., Wong, S., Scott, D., Luke, R., Tang, E., Davidson, L., Hamer, A., Wilson, S., Price, R., Hart, H., Turner, A., Jortveit, J., Calic, S., Gundersen, T., Brunvand, H., Fosse, L., Nygaard, O., Gjellefall, B., Gravdal, S.A., Ringstad, R., Atar, D., Clausen, H., Hysing, J., Arvesen, K., Topper, M., Flagstad, E., Graven, T., Haug, H.H., Dalin, L., Al-Ani, R., Otterstad, J., Ausen, K., Aaser, E., Olufsen, M., Halvorsen, S., Gullestad, L., Stueflotten, W., Waage, K., Stødle, R.M., Hall, C., Aase, O., Nordeng, J., Soyland, E., Fageraas, E.R., Lied, A., Aske, R., Raouf, N., Johansson, J., Herrscher, T., Skogrand, E., Bjornstad, H., Aagnes, I., Arntsen, B.I., Vegsundvaag, J., Skjold, M.E., Velle, H., Aambakk, M.B., Skjetne, O., Byfuglien, A., Rodriguez, J., Galvez, D., Medina, F., Hernandez, H.A., Chavez, V., Morales, R., Huapalla, E., Velasquez, D., Torres, F., Aguirre, O., Yanez, L., Andrade, M., Campos, C., Arce, R., Mogrovejo, W., Osores, F., Bustamante, G., Rodriguez, M., Berrospi, P., Garcia, C., Talledo, M., Navarro, P., Horna, M., Herrera, V., Kadziela, J., Rybicka-Musialik, A., Trusz-Gluza, M., Berger-Kucza, A., Musial, W., Tycinska, A., Gil, R., Gziut, A., Gorny, J., Tyllo, M., Reszka, Z., Mickiewicz-Pawlowska, M., Wrzosek, B., Kosior, J., Staneta, P., Korzeniak, R., Kalarus, Z., Markowicz, E., Miekus, P., Konarzewski, M., Kleinrok, A., Puzniak, M., Grajek, S., Janus, M., Krzyzanowski, M., Hoffmann, A., Muzalewski, P., Polonski, L., Kazik, A., Nowalany-Kozielska, E., Wojciechowska, C., Ponikowski, P., Nawrocka, S., Filipiak, K., Serafin, A., Dubiel, J., Mielecki, W., Ogorek, M., Kopcik, D., Jaworska, K., Skonieczny, G., Kawecka-Jaszcz, K., Bryniarski, L., Tracz, W., Lesniak-Sobelga, A., Jankielewicz, J., Zaluska, R., Trojnar, R., Kawalek, P., Gaciong, Z., Pulkowski, G., Anaszewicz, M., Samul, W., Adamus, J., Cholewa, M., Kubik, L., Szczechowicz, R., Rekosz, J., Kwiatkowska, D., Gajek, J., Mazurek, W., Kominek, M., Siminiak, T., Guzniczak, E., Monteiro, P., Providencia, L., Monteiro, S., Pinho, T., Gavina, C., Sousa, C., Loureiro, J., Ferreira, A.R., Cardoso, A., Araujo, J., Rebolo, I., Catarino, C., Santos, J., Nunes, L.P., Mimoso, J., Marques, N., Leitao, M., Pais, J., Fernandes, A., Diogo, A., Nóbrega, J., Moreira, J.I., Mateus, P., Oliveira, J., Selas, M., Ribeiro, V., Albuquerque, A., Reis, R., Ramos, A., Salazar, F., Nair, D., Ng, C.K., Yeo, D., Wong, A., Funiak, S., Belicova, M., Striezova, I., Krajci, P., Sojka, G., Herman, O., Zemberova, A., Pella, D., Fedacko, J., Banikova, A., Micko, K., Macek, V., Moscovic, M., Vahala, P., Vykoukalova, T., Dzupina, A., Marusakova, M., Stevlik, J., Akubzanova, E., Hatalova, K., Burgess, L., Coetzee, C., Mabin, T., Roos, J., Mohamed, Z., Pillay, T., Corbett, C., Bodenstein, W., Tayob, F., Ebrahim, I., Bolsman, C., Horak, A., Lloyd, E., Pretorius, M., Commerford, P., De 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H., Kelley, M., Diffenback, M., Friedman, B., Zirkle, J., Severa, L., Sample, S., Dignen, K., Raisinghani, A., Ben-Yehuda, O., Ghannadian, B., Moscoso, R., Mankowski, J., Boliek, W., Rukavina, M., Davis, W., Ledbetter, S., Handel, F., Mastouri, R., Mahenthiran, J., Foltz, J., Malhotra, V., Jonas, J., Berk, M., Singh, V., Nelson, M., Elsner, G., Gall, J., Kondo, N., Frank, S., Chandraratna, P., Ranasinghe, S., Ebrahimi, R., Treadwell, M., Walters, B., Hughes, L., Kramer, J., Kumar, K., Mente, T., Lachterman, B., Schifferdecker, B., Munshi, K., Sease, D., Waldo, D., Chandler, G., Manns, D., Nahhas, A., Kamalesh, M., Williams, V., Reich, D., Desalca, M., Sharma, S., Liston, M., Gupta, K., Costa, M., Altschuller, A., Lemmertz, K., Shanes, J., Hansen, C., Therrien, M., Mendelson, R., Ramnarine, R., Myers, G., Donovan, C., Klein, M., Fine, D., Owens, S., Murray, C., Ketroser, R., Heifetz, S., Darnell, Z., Touchon, R., Taghizadeh, B., Bohle, D., Norwood, D., Forrest, T., Jackson, S., Shumate, 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IMPROVE-IT Investigators, Musliner, T., Tershakovec, A., Gurfinkel, E., Aylward, P., Tonkin, A., Maurer, G., Van de Werf, F., Nicolau, J.C., Theroux, P., Genest, J., Armstrong, P., Corbalan, R., Isaza, D., Spinar, J., Grande, P., Voitk, J., Kesaniemi, A., Bassand, J.P., Farnier, M., Darius, H., Keltai, M., Mathur, A., Mittal, S., Reddy, K., Lewis, B., De Ferrari, G.M., Ophuis, T.O., Jukema, J., White, H., Pedersen, T., Britto, F., Ruzyllo, W., Carrageta, M., Duris, T., Dalby, A., Seung, K.B., Lopez-Sendon, J., Dellborg, M., Mach, F., Guneri, S., Parkhomenko, A., Brady, A., Cannon, C., Blazing, M., Ballantyne, C., de Lemos, J., Kleiman, N., McGuire, D.K., Centeno, E., Casalins, M., Cartasegna, L., Beltrano, M.C., Guerrero, R., Fanuele, M., Berra, F., Egido, J., Colombo, H., Dellatorre, M., Terns, P., Blumberg, E., Reges, P., Azize, G., Ramos, H., Fernandez, R., Carlessi, C., Milesi, R., Schmuck, R., Duronto, E., Procopio, G., Carlevaro, O., Maffeo, H., Beloscar, J., Viso, M., Hominal, M., Castoldi, M., Bluguermann, J., Mauro, D., Macin, S., Cocco, N., Ruiz, N., Ricart, J., Lozada, A., Nani, S., Turri, D., Fernandez, H., Caruso, O., Zarandon, R., Bono, J., Arias, V., Allall, O., Marino, J., Cusimano, S., Schygiel, P., Buzetti, C., Penaloza, N., Berli, M., Worthley, S., Roach, A., Chew, D., Wright, T., Leitch, J., Hicks, E., Rankin, J., Venn-Edmonds, C., Lehman, R., Morrison, H., Shaw, J., Mak, V., Hii, C., Smith, K., Cross, D., Lilwall, L., Nelson, G., Loxton, A., Horowitz, J., Rose, J., Steinwender, C., Leisch, F., Kammler, J., Brussee, H., Zweiker, R., Niederl, E., Weihs, W., Giorgio, G., Lang, I., Drexel, H., Zanolin, D., Hoppe, U., Atzenhofer-Baumgartner, K., Pichler, M., Hainzer, D., Eber, B., Pichler, F., Foeger, B., Wechselberger, T., Mayr, H., Hofer, J., Stockenhuber, F., Warlits, B., Huber, K., Egger, F., Weidinger, F., Ziegler, B., Jirak, P., Metzler, B., Pachinger, O., Wanitschek, M., Auer, J., Grabscheit, G., Podczeck-Schweighofer, A., Priesnitz, T., Frank, H., El Allaf, D., Marechal, P., Roosen, J., Joly, E., Lefebvre, P., Arend, C., Sinnaeve, P., De Velder, L., Hellemans, S., Vanhauwaert, B., Van Dorpe, A., Heyse, A., Vantomme, C., Striekwold, H., Van Den Broeck, D., Lancellotti, P., Schoors, D., Lemoine, I., Taeymans, Y., De Wolf, L., Brike, C., Vercauteren, S., Tahon, S., Vervoort, G., Mestdagh, I., Pirenne, B., Cardinal, F., Lips, S., Dujardin, K., Debrouwer, K., Dhooghe, G., Holvoet, G., van de Borne, P., Renard, M., De Clippel, M., Lesseliers, H., Van Miert, N., Saraiva, J., Vicente, C., Rossi, P., Dos Santos, L.B., Duda, N., Tognon, A.P., Serrano, C., Gomes, F.L., Manenti, E.R., Silveira, D.S., Maia, L., Mouco, O.M., Paiva, M., Antonangelo, A., de Souza, J., Lino, E.A., Leães, P., Blacher, M.G., Kormann, A., Ultramari, F.T., Dutra, O., Mendelski, A.M., Morgado, S., Ardito, W., Greque, G., Ardito, R.V., Pimentel Filho, P., Zucchetti, C., Alves, A., Seabra, A.M., Mattos, M., Miranda, L.F., Silva, D., Uehara, R.M., Marin Neto, 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Ieva, R., Fattore, L., Cicia, G., Cavallini, C., Tamburino, C., Sacco, A., Mafrici, A., Di Pasquale, G., Pavesi, P.C., Scioli, R., Lioy, E., Occhiuzzi, E., Matino, M.G., Russo, V., Moscogiuri, M.G., Cuccia, C., Forgione, C., Volpe, M., Palano, F., Branca, G., Rossi, R., Modena, M., Olaru, I.A., Zanini, R., Cianflone, D., Cristell, N., Pantaleoni, M., Guiducci, U., Menozzi, C., Gaddi, O., Fasulo, A., Indolfi, C., Emanuele, V., Guerra, F., Iliceto, S., Marotta, C., Morocutti, G., Presbitero, P., Rossi, M., Bonatti, S., Grieco, A., Chiodi, L., Betti, I., Zuppiroli, A., Fanelli, R., Stanco, G., Azzolini, P., Ruggieri, C., Bocconcelli, P., Airoldi, F., Tavano, D., Brunelli, C., Caso, P., Scalzone, A., Ghigliotti, G., Facciorusso, A., Sim, K., Kiam, O., Chee, K., Bin Ismail, O., Zambahari, R., Ophuis, T., van Nes, E., Werter, C.J., Ophuis, A.J., Troquay, R.P., Hamer, B.J., Lenderink, T., Feld, R.J., van Hessen, M.W., Viergever, E.P., van der Sluis, A., Lok, D.J., Badings, E.A., Nierop, P.R., 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- Abstract
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. 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 (≥30 days after randomization), or nonfatal stroke. The median follow-up was 6 years. 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 prespecified muscle, gallbladder, and hepatic adverse effects and cancer were similar in the two groups. 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 benef
- Published
- 2015
17. The Controversies of Statin Therapy Weighing the Evidence
- Author
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Jukema, J.W., Cannon, C.P., Craen, A.J.M. de, Westendorp, R.G.J., and Trompet, S.
- Subjects
diabetes mellitus ,adverse effects ,nutritional and metabolic diseases ,cancer ,lipids (amino acids, peptides, and proteins) ,cardiovascular diseases ,cognitive decline ,statins - Abstract
The debate whether statins, 3-hydroxymethyl-3-methylglutaryl coenzyme A reductase inhibitors, are safe to use has been raging since their introduction in 1987. Statins are generally well tolerated and are believed to have minimal adverse effects. However, individual, specific rare adverse events have been reported, such as elevations of liver enzymes, muscle aches, and very rarely, rhabdomyolysis. Discontinuation and/or reduction in the dose of the statin usually leads to resolution of these side effects. Recently, however, debate has focused on the possible negative long-term effects of statin treatment on cognitive decline, the incidence of cancer, and the development of diabetes mellitus. Recently, the U.S. Food and Drug Administration has expanded the warning for statins with a statement that statin use may lead to cognitive impairment. In this review, we discuss all levels of evidence, from case reports to large randomized controlled clinical trials, for the possible adverse effects of statins on cognitive decline, cancer, and diabetes. After careful consideration of all discussed scientific evidence, we conclude that there is no increased risk of cognitive decline or cancer with statin use. However, statin use is related to a small increased risk of type 2 diabetes mellitus. In view of the overwhelming benefit of statins in the reduction of cardiovascular events, we believe the small absolute risk for development of diabetes is outweighed by the cardiovascular benefits in patients for whom statin therapy is recommended. We, therefore, suggest that clinical practice for statin therapy should not be changed on the basis of the most recent Food and Drug Administration informational warnings.
- Published
- 2012
18. 4B.02
- Author
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Chilton, R., primary, Tikkanen, I., additional, Cannon, C.P., additional, Crowe, S., additional, Hach, T., additional, Woerle, H.J., additional, Broedl, U.C., additional, and Johansen, O.E., additional
- Published
- 2015
- Full Text
- View/download PDF
19. Increased incidence of dyspnoea associated with ticagrelor did not appear to adversely affect cardiovascular outcomes in the PLATO study
- Author
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Storey, R.F., Becker, R.C., Harrington, R.A., Cannon, C.P., Husted, Steen, James, S.K., Wallentin, L., Cools, F., Steg, P.G., and Khurmi, N.
- Subjects
Ticagrelor ,Kardiologi ,Dyspnea ,Cardiology ,Dyspnø - Published
- 2010
20. Prognosis and risk stratification of non obstructive CAD in acute coronary syndrome: observations in TIMI 11B, OPUS-TIMI 16, and PROVE-IT TIMI 22
- Author
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BUGIARDINI, RAFFAELE, MANFRINI, OLIVIA, Murphy SA, De Ferrari GM, Cannon C.P., Bugiardini R, Manfrini O, Murphy SA, De Ferrari GM, and Cannon CP.
- Published
- 2005
21. Long-term prognosis of nonobstructive coronary artery disease in the setting of acute coronary syndrome: A TIMI 22 substudy
- Author
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BUGIARDINI, RAFFAELE, MANFRINI, OLIVIA, Murphy SA, De Ferrari GM, Cannon C.P., Bugiardini R, Manfrini O, Murphy SA, De Ferrari GM, and Cannon CP.
- Published
- 2005
22. Lipoprotein-associated phospholipase A2 and risk of coronary disease, stroke, and mortality: collaborative analysis of 32 prospective studies
- Author
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Thompson, A. (Alexander), Gao, P. (Pei), Orfei, L. (Lia), Watson, S. (Sarah), Angelantonio, E. (Emanuele) di, Kaptoge, S. (Stephen), Ballantyne, C. (Christie), Cannon, C.P., Criqui, M. (Michael), Cushman, M. (Mary Ann), Hofman, A. (Albert), Packard, C. (Chris), Collins, R. (Rory), Danesh, J. (John), Thompson, A. (Alexander), Gao, P. (Pei), Orfei, L. (Lia), Watson, S. (Sarah), Angelantonio, E. (Emanuele) di, Kaptoge, S. (Stephen), Ballantyne, C. (Christie), Cannon, C.P., Criqui, M. (Michael), Cushman, M. (Mary Ann), Hofman, A. (Albert), Packard, C. (Chris), Collins, R. (Rory), and Danesh, J. (John)
- Abstract
Background: Lipoprotein-associated phospholipase A2(Lp-PLA2), an inflammatory enzyme expressed in atherosclerotic plaques, is a therapeutic target being assessed in trials of vascular disease prevention. We investigated associations of circulating Lp-PLA2mass and activity with risk of coronary heart disease, stroke, and mortality under different circumstances. Methods: With use of individual records from 79 036 participants in 32 prospective studies (yielding 17 722 incident fatal or non-fatal outcomes during 474 976 person-years at risk), we did a meta-analysis of within-study regressions to calculate risk ratios (RRs) per 1 SD higher value of Lp-PLA2or other risk factor. The primary outcome was coronary heart disease. Findings: Lp-PLA2activity and mass were associated with each other (r=0·51, 95% CI 0·47-0·56) and proatherogenic lipids. We noted roughly log-linear associations of Lp-PLA2activity and mass with risk of coronary heart disease and vascular death. RRs, adjusted for conventional risk factors, were: 1·10 (95% CI 1·05-1·16) with Lp-PLA2activity and 1·11 (1·07-1·16) with Lp-PLA2mass for coronary heart disease; 1·08 (0·97-1·20) and 1·14 (1·02-1·27) for ischaemic stroke; 1·16 (1·09-1·24) and 1·13 (1·05-1·22) for vascular mortality; and 1·10 (1·04-1·17) and 1·10 (1·03-1·18) for non-vascular mortality, respectively. RRs with Lp-PLA2did not differ significantly in people with and without initial stable vascular disease, apart from for vascular death with Lp-PLA2mass. Adjusted RRs for coronary heart disease were 1·10 (1·02-1·18) with non-HDL cholesterol and 1·10 (1·00-1·21) with systolic blood pressure. Interpretation: Lp-PLA2activity and mass each show continuous associations with risk of coronary heart disease, similar in magnitude to that with non-HDL cholesterol or systolic blood pressure in this population. Associations of Lp-PLA2mass and activity are not exclusive to vascular outcomes, and the vascular associations depend at least partly on lipids. Funding
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- 2010
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23. Prehospital fibrinolysis with dual antiplatelet therapy in ST-elevation acute myocardial infarction: a substudy of the randomized double blind CLARITY-TIMI 28 trial.
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Verheugt, F.W.A., Montalescot, G., Sabatine, M.S., Soulat, L., Lambert, Y., Lapostolle, F., Adgey, J., Cannon, C.P., Verheugt, F.W.A., Montalescot, G., Sabatine, M.S., Soulat, L., Lambert, Y., Lapostolle, F., Adgey, J., and Cannon, C.P.
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Contains fulltext : 52227.pdf (publisher's version ) (Closed access), BACKGROUND: Fibrinolytic therapy for acute ST-elevation myocardial infarction (STEMI) is frequently limited by delays in administration and by incomplete reperfusion or reocclusion of the infarct-related artery. Intensified prehospital management of STEMI may shorten time to treatment and improve outcomes. METHODS: We carried out a prospective substudy in 11 ambulance systems in 216 of the 3,491 patients with STEMI who were enrolled in the CLARITY-TIMI 28 trial. They were randomized in the ambulance to clopidogrel (n = 109) or placebo (n = 107) along with fibrinolysis, aspirin, and heparin. The primary endpoint was the composite of an occluded infarct-related artery (TIMI flow grade 0 or 1), or death or recurrent myocardial infarction before angiography. RESULTS: All patients received a fibrin-specific lytic and the baseline characteristics in both groups were comparable. The incidence of the primary endpoint was 16.5% in the clopidogrel-treated and 27.1% in the placebo patients (adj OR 0.62, 95% CI 0.31-1.21, p = 0.16), an effect that was consistent with the effects seen in the in-hospital patients in the main CLARITY-TIMI 28 trial. Prehospital clopidogrel therapy reduced the incidence of an occluded infarct-related artery on the predischarge angiogram (11.8% vs. 22.3%, adj OR 0.52, 95% CI 0.24-1.13, p = 0.10). The 30-day incidence of cardiovascular death, recurrent MI or recurrent myocardial ischemia requiring urgent revascularization was 12.8% vs. 14.0% (adj OR 1.07, 95% CI 0.48-2.39, p = 0.87). Early TIMI major bleeding occurred in no clopidogrel patients compared with two placebo patients (1.9%). CONCLUSIONS: Addition of clopidogrel to medical reperfusion of STEMI with fibrinolysis, heparin, and aspirin before reaching the hospital is feasible in medically equipped ambulances without an apparent increase in bleeding. Furthermore, prehospital clopidogrel tended to show better early coronary patency compared to placebo, a result consistent with that observed in p
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- 2007
24. 187 Influenza Vaccination and Reduction of Cardiovascular Events-A Systematic Review and Meta-Analysis
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Udell, J.A., primary, Farkouh, M.E., additional, Bhatt, D.L., additional, and Cannon, C.P., additional
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- 2012
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25. American College of Cardiology key data elements and definitions for measuring the clinical management and outcomes of patients with acute coronary syndromes.
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Cannon, C.P., Battler, A. (Alexander), Brindis, R.G. (Ralph), Cox, J.L. (Jafna), Ellis, S.G. (Stephen), Every, N.R. (Nathan), Flaherty, J.T. (Joh), Harrington, R.A. (Robert Alex), Krimholz, H.M., Simoons, M.L. (Maarten), Werf, F.J.J. (Frans) van de, Weintraub, W.S. (William), Cannon, C.P., Battler, A. (Alexander), Brindis, R.G. (Ralph), Cox, J.L. (Jafna), Ellis, S.G. (Stephen), Every, N.R. (Nathan), Flaherty, J.T. (Joh), Harrington, R.A. (Robert Alex), Krimholz, H.M., Simoons, M.L. (Maarten), Werf, F.J.J. (Frans) van de, and Weintraub, W.S. (William)
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- 2001
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26. Practical Implementation of the Guidelines for Unstable Angina/Non-ST-Segment Elevation Myocardial Infarction in the Emergency Department: A Scientific Statement From the American Heart Association Council on Clinical Cardiology (Subcommittee on Acute Cardiac Care), Council on Cardiovascular Nursing, and Quality of Care and Outcomes Research Interdisciplinary Working Group, in Collaboration With the Society of Chest Pain Centers
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Gibler, W.B., primary, Cannon, C.P., additional, and Blomkalns, A.L., additional
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- 2005
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27. Routine vs. Selective Invasive Strategies in Patients With Acute Coronary Syndromes: A Collaborative Meta-analysis of Randomized Trials
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Mehta, S.R., primary, Cannon, C.P., additional, and Fox, K.A.A., additional
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- 2005
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28. Early Initiation of Lipid-lowering Therapy for Acute Coronary Syndromes Improves Compliance With Guideline Recommendations: Observations From the Orbofiban in Patients With Unstable Coronary Syndromes (OPUS–TIMI-16) Trial
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Smith, C.S., primary, Cannon, C.P., additional, McCabe, C.H., additional, Murphy, S.A., additional, Bentley, J., additional, and Braunwald, E., additional
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- 2005
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29. Addition of Clopidogrel to Aspirin and Fibrinolytic Therapy for Myocardial Infarction With ST-Segment Elevation
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Sabatine, M.S., primary, Cannon, C.P., additional, and Gibson, C.M., additional
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- 2005
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30. C-reactive protein levels and outcomes after statin therapy
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Ridker, P.M., primary, Cannon, C.P., additional, and Morrow, D., additional
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- 2005
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31. The effect of routine, early invasive management on outcome for elderly patients with non-ST-segment elevation acute coronary syndromes
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Bach, R.G., primary, Cannon, C.P., additional, and Weintraub, W.S., additional
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- 2004
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32. Comparison of intensive and moderate lipid lowering with statins after acute coronary syndromes
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Cannon, C.P, primary, Braunwald, E, additional, and McCabeet al, C.H, additional
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- 2004
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33. Predictors of major bleeding in acute coronary syndromes: the global registry of acute coronary events (GRACE)
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Moscucci, M., primary, Fox, K.A.A., additional, and Cannon, C.P., additional
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- 2004
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34. Relationship between baseline white blood cell count and degree of coronary artery disease and mortality in patients with acute coronary syndromes. A TACTICS-TIMI 18 substudy
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Sabatine, M.S., primary, Morrow, D.A., additional, and Cannon, C.P., additional
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- 2003
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35. Early coronary intervention following pharmacologic therapy for acute myocardial infarction (the combined TIMI 10B-TIMI 14 experience)
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Schweiger, M.J, primary, Cannon, C.P, additional, and Murphy, S.A, additional
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- 2002
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36. MgO insulated coaxial instrument cable development for FFTF in-vessel temperature and voltage conditions
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Chan, A.I.Y., primary and Cannon, C.P., additional
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- 1978
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37. Recent developments in LOFT advanced fuel rod instrumentation
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Sheen, E.M., primary, Billeter, T.R., additional, Cannon, C.P., additional, Chan, A.I.Y., additional, and Stringer, J.L., additional
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- 1979
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38. Flow distal and not proximal to the lesion is a correlate of clinical outcomes after thrombolysis
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Gibson, M., primary, Sparano, A., additional, Ryan, K., additional, Moynihan, J., additional, Kelley, M., additional, Rizzo, M., additional, Marble, S., additional, McCabe, C., additional, Dodge, T., additional, and Cannon, C.P., additional
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- 1998
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39. Critical pathway for acute ST segment elevation myocardial infarction: evaluation of the potential impact in the TIMI 9 registry
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Cannon, C.P., primary, Antman, E.M., additional, Gibson, C.M., additional, Paul, S.D., additional, and Braunwald, E., additional
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- 1998
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40. A new angiographic method to calculate coronary velocity & its relationship to clinical outcomes after thrombolysis
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Gibson, M., primary, Sparano, A., additional, Ryan, K., additional, Rizzo, M., additional, Moynihan, J., additional, Kelley, M., additional, Marble, S., additional, Dodge, T., additional, Cannon, C.P., additional, and Braunwald, E., additional
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- 1998
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41. Improvements in the treatmant of elderly patients with unstable angina results from the GUARANTEE registry
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Roe, M.T., primary, Moliterno, D.J., additional, Cannon, C.P., additional, Every, N.R., additional, Aquino, F.V., additional, Granger, C.B., additional, Sapp, S., additional, Booth, J., additional, and Ferguson, J.J., additional
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- 1998
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42. The range of QCA velocities for TIMI grades 2 & 3 flow
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Moynihan, J., primary, Ryan, K., additional, Sparano, A., additional, Kelley, M., additional, Rizzo, M., additional, Marble, S., additional, Cannon, C.P., additional, McCabe, C., additional, and Gibson, M., additional
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- 1998
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43. Outcomes of adjunctive PTCA/stenting for TIMI grade 2 flow following thrombolysis
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Gibson, M., primary, Schweiger, M., additional, Sequeira, R.F., additional, Frey, M., additional, Cannon, C.P., additional, Williams, D.O., additional, Van de Wert, F., additional, and Braunwald, E., additional
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- 1998
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44. Oral glycoprotein IIb/IIIa receptor inhibitors in patients with cardiovascular disease: why were the results so unfavourable.
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Leebeek, F.W.G., Boersma, E., Cannon, C.P., van de Werf, F.J.J., and Simoons, M.L.
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- 2002
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45. Cardiovascular outcomes with etoricoxib and diclofenac in patients with osteoarthritis and rheumatoid arthritis in the Multinational Etoricoxib and Diclofenac Arthritis Long-term (MEDAL) programme: a randomised comparison
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Cannon, C.P., Curtis, S.P., FitzGerald, G.A., Krum, H., Kaur, A., Bolognese, J.A., Reicin, A.S., Bombardier, C., Weinblatt, M.E., van der Heijde, D., Erdmann, E., and Laine, L.
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Background: Cyclo-oxygenase-2 (COX-2) selective inhibitors have been associated with an increased risk of thrombotic cardiovascular events in placebo-controlled trials, but no clinical trial has been reported with the primary aim of assessing relative cardiovascular risk of these drugs compared with traditional non-steroidal anti-inflammatory drugs (NSAIDs). The MEDAL programme was designed to provide a precise estimate of thrombotic cardiovascular events with the COX-2 selective inhibitor etoricoxib versus the traditional NSAID diclofenac. Methods: We designed a prespecified pooled analysis of data from three trials in which patients with osteoarthritis or rheumatoid arthritis were randomly assigned to etoricoxib (60 mg or 90 mg daily) or diclofenac (150 mg daily). The primary hypothesis stated that etoricoxib is not inferior to diclofenac, defined as an upper boundary of less than 1.30 for the 95% CI of the hazard ratio for thrombotic cardiovascular events in the per-protocol analysis. Intention-to-treat analyses were also done to assess consistency of results. These trials are registered at http://www.clinicaltrials.gov with the numbers NCT00092703, NCT00092742, and NCT00250445. Findings: 34@?701 patients (24@?913 with osteoarthritis and 9@?787 with rheumatoid arthritis) were enrolled. Average treatment duration was 18 months (SD 11.8). 320 patients in the etoricoxib group and 323 in the diclofenac group had thrombotic cardiovascular events, yielding event rates of 1.24 and 1.30 per 100 patient-years and a hazard ratio of 0.95 (95% CI 0.81-1.11) for etoricoxib compared with diclofenac. Rates of upper gastrointestinal clinical events (perforation, bleeding, obstruction, ulcer) were lower with etoricoxib than with diclofenac (0.67 vs 0.97 per 100 patient-years; hazard ratio 0.69 [0.57-0.83]), but the rates of complicated upper gastrointestinal events were similar for etoricoxib (0.30) and diclofenac (0.32). Interpretation: Rates of thrombotic cardiovascular events in patients with arthritis on etoricoxib are similar to those in patients on diclofenac with long-term use of these drugs.
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- 2006
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46. Techniques in endoprosthetic reconstruction
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Cannon, C.P., Zeegen, E., and Eckardt, J.J.
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Malignant primary bone tumors are frequently treated with limb-salvage surgery. A variety of techniques are available to reconstruct the limb after tumor resection. Current endoprostheses are an attractive option because of their excellent function, cosmesis, emotional acceptance, and relatively low complication rate. Also, unlike allografts, endoprostheses are universally available and carry no risk of disease transmission. This article describes the operative techniques for an endoprosthetic reconstruction in the most common sites-distal femur, proximal tibia, proximal femur, and proximal humerus. Postoperative rehabilitation and management is also discussed.
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- 2004
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47. Racial differences in the management of unstable angina: Results from the multicenter GUARANTEE registry
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Scirica, B.M., Moliterno, D.J., Every, N.R., Anderson, H., Aguirre, F.V., Granger, C.B., Lambrew, C.T., Rabbani, L.E., Sapp, S.K., Booth, J.E., Ferguson, J.J., and Cannon, C.P.
- Abstract
Background Prior studies, usually conducted with the use of insurance databases, have shown differences in the use of cardiac procedures between black patients and white patients hospitalized with various types of coronary artery disease. However, few data are available in prospectively collected cohorts of patients with unstable angina or on the use of appropriate medications or interventions. Methods and Results We evaluated 2948 consecutive patients with unstable angina admitted to 35 hospitals across the United States in 1996, comparing nonwhite and white patients. Seventy-seven percent of patients were white, 14% were black, 4% were Hispanic, 1% were Asian, and 3% were other or unknown race. Differences were seen in coronary risk profile, with a higher incidence of hypertension and diabetes mellitus in nonwhites. Cardiac catheterization was performed less often in nonwhites compared with whites (36% vs 53%, P = .001). Even in patients meeting the criteria for appropriate catheterization in the Agency for Health Care Policy Research unstable angina guidelines, fewer nonwhites underwent catheterization (44% vs 61%, P = .001), but among these, fewer nonwhites had significant coronary stenosis (72% vs 90%, P = .001). However, among patients catheterized who had indications for revascularization, angioplasty and coronary artery bypass grafting were performed equally often in nonwhites and whites. Conclusions Current guidelines would recommend more aggressive use of cardiac catheterization for nonwhite patients. However, our findings suggest that racial differences may need to be included in the diagnostic and interventional algorithms. (Am Heart J 1999;138:1065-72.)
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- 1999
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48. Methodologic drift in the assessment of TIMI grade 3 flow and its implications with respect to the reporting of angiographic trial results
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Gibson, C., Ryan, K.A., Kelley, M., Rizzo, M.J., Mesley, R., Murphy, S., Swanson, J., Marble, S.J., Dodge, J., Giugliano, R.P., Cannon, C.P., and Antman, E.M.
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Background The Thrombolysis In Myocardial Infarction (TIMI) Study Group originally defined TIMI grade 3 flow (complete perfusion) as antegrade flow into the bed distal to the obstruction that occurs as promptly as antegrade flow into the bed proximal to the obstruction. Recently, several groups have defined TIMI grade 3 flow as opacification of the coronary artery within 3 cardiac cycles. Methods and Results On the basis of heart rate data at the time of the cardiac catheterization and the time for dye to go down the artery (TIMI frame count/30 = seconds), we estimated the number of patients who would meet the 3 cardiac cycle criterion and compared this with the number of patients with TIMI grade 3 flow by using the original definition in 1157 patients from 3 recent TIMI trials (10 A, 10B, and 14). In 74 patients without acute myocardial infarction and normal coronary arteries, the fraction of a cardiac cycle required for dye to traverse the artery was a mean of 0.93 +/- 0.34 cardiac cycles (n = 74) (median 0.80, minimum 0.44, maximum 2.1, none >3.0 cycles). The mean heart rate at 90 minutes after thrombolysis in the TIMI 14 trial was 79.6 +/- 16.8 beats/min (n = 194), and the duration of 3 cardiac cycles was a mean of 2.36 seconds, or a TIMI frame count of 70.8 frames. In all trials, the rate of TIMI grade 3 flow was 57.3% (n = 663/1157) with the original definition and 66.8% (n = 743/1113) with the <3 cardiac cycle definition (P < .001). Conclusions A duration of 3 cardiac cycles for dye to traverse the artery lies approximately 6 SD above that observed in normal coronary arteries. A 3 cardiac cycle definition of TIMI grade 3 flow results in rates of normal perfusion that are approximately 10% higher than if the original definition of TIMI grade 3 flow is applied. Application of this simple correction factor may help place data reported with the 3 cardiac cycle definition of TIMI grade 3 flow in context. (Am Heart J 1999;137:1179-5.)
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- 1999
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49. Relation between injections before 90-minute angiography and coronary patency: Results of the Thrombolysis in Myocardial Infarction 4 Trial*
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Gibson, C., Marble, S.J., Rizzo, M.J., Moynihan, J., McLean, C., Ryan, K., Sparano, A., Piana, R.N., McCabe, C., and Cannon, C.P.
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The current goal of thrombolytic therapy is to achieve both full (Thrombolysis in Myocardial Infarction [TIMI] grade 3) and early reperfusion. Newer reperfusion strategies may now achieve a high degree of reperfusion even earlier than the traditional 90-minute end point. To determine whether injections before 90 minutes affect this traditional end point, the relation between the number of injections before 90-minute angiography and patency was examined in the TIMI 4 trial. The number of injections before 90-minute angiography was no different between occluded arteries (TIMI grade 0/1 flow) (2.46 +/- 1.78; n = 94) and patent arteries (TIMI grade 2/3 flow) (2.71 +/- 2.42; n = 295) (p = 0.24). The incidence of any injections before 90 minutes was no different in patent versus closed arteries (80.6% [77/98] vs 72.4% [22/304]; p = 0.10). The number of injections before 90 minutes was insignificantly smaller in patients with TIMI grade 3 flow (2.53 +/- 2.53 [n = 184] vs 2.76 +/- 2.03 [n = 204]; p = 0.31) but the incidence of any injections before 90 minutes was significantly smaller in patients with TIMI grade 3 flow (68.8% [132/192] vs 79.5% [167/210]; p = 0.01). No relation was identified between the number of injections before 90-minute angiography and patency at this traditional time point. This observation justifies the judicious use of a limited number of ''earlier snapshots'' of the infarct-related artery before 90 minutes to ascertain just how rapidly newer thrombolytic regimens achieve patency. Patients with TIMI grade 3 flow had a slightly lower incidence of injections before 90 minutes, perhaps because they did not require as urgent a definition of coronary anatomy. (Am Heart J 1997;134:351-4.)
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- 1997
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50. Relation of coagulation parameters to patency and recurrent ischemia in the Thrombolysis in Myocardial Infarction (TIMI) Phase II Trial
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Tracy, R.P., Kleiman, N.S., Thompson, B., Cannon, C.P., Bovill, E.G., Brown, R., Collen, D., Mahan, E., Mann, K.G., Rogers, W.J., Sopko, G., Stump, D.C., Williams, D.O., and Zaret, B.L.
- Abstract
Current protocols for use of tissue-type plasminogen activator in acute myocardial infarction include heparin estimated by the activated partial thromboplastin time (aPTT). Recent reports indicate a risk of recurrent ischemic events with long aPTT values. Longer aPTT values in the Thrombolysis in Myocardial Infarction-II (TIMI II) Trial, obtained within the first 48 hours, were associated with patency at 18 to 48 hours and better left ventricular function at discharge (average 9.6 days), but also with emergency catheterizations within the first 48 hours and, weakly, with recurrent ischemia during the first 18 hours. A moderate decrease in fibrinogen, compared with a ''small'' decrease, was also associated with patency, but a ''large'' decrease was associated with hemorrhagic events. Patency was associated with higher fibrinogen values and higher plasminogen values at baseline. The aPTT results support frequent monitoring during the first 24 to 48 hours to ensure optimal clinical outcome. The coagulation factor results suggest that there may be an optimum window for fibrinogenolysis in this setting. (Am Heart J 1998;135:29-37.)
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- 1998
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