Coronary Artery Disease: Campo G

Daemen J, Simoons ML, Wijns W, Bagust A, Bos G, Bowen JM, Braunwald E, Camenzind E, Chevaliers B, DiMario C, Fajadeto J, Gitt A, Guagliumi G, Hillege HL, James S, Jüni P, Kastrati A, Kloth S, Kristensen SD, Krucoff M, Legrand V, Pfisterer M, Rothman M, Serruys PW, Silber S, Steg PG, Tariah I, Wallentin L, Windecker SW, Aimonetti A, Allocco D, Berenger M, Boam A, Calle JP, Campo G, Carlier S, de Schepper J, Di Bisceglie G, Dobbels H, Farb A, Ghislain JC, Hellbardt S, ten Hoedt R, Isaia C, de Jong P, Lekehal M, LeNarz L, Mhullain FN, Nagai H, Patteet A, Paunovic D, Potgieter A, Purdy I, Raveau-Landon C, Ternstrom S, Van Wuytswinkel J, Waliszewski M, Anonymous00071. · Thoraxcenter, Erasmus MC, Rotterdam, The Netherlands. · EuroIntervention. · Pubmed #19284063 No free full text.

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Ferrari R, Pasanisi G, Notarstefano P, Campo G, Gardini E, Ceconi C. · Division of Cardiology, University Hospital of Ferrara, Corso Giovecca 203, 44100 Ferrara, Italy. · Am J Hypertens. · Pubmed #16125051 No free full text.

Abstract: Perindopril is a long-acting, once-daily lipophilic angiotensin-converting enzyme inhibitor with high tissue angiotensin-converting enzyme affinity, lowering angiotensin II and potentiating bradykinin. Its efficacy, safety, and tolerability are well established in the treatment of hypertension and heart failure. Moreover, large morbidity-mortality trials, such as the EUropean trial on Reduction Of cardiac events with Perindopril in stable coronary Artery disease (EUROPA) and Perindopril pROtection aGainst REcurrent Stroke Study (PROGRESS), have shown that antihypertensive treatment with perindopril reduces and prevents cardiovascular disease in a large range of patients with vascular diseases, whether or not they are hypertensive. Thus, the outcomes of these and other trials support the concept of cardiovascular protective properties of angiotensin-converting enzyme inhibition with perindopril in addition to the obvious blood-pressure-lowering effect. Considering its properties and the clinical evidence on efficacy and tolerability that has been gathered, perindopril fulfils the criteria of the latest guidelines for hypertension and cardiovascular disease management and should therefore be considered as a first-line antihypertensive agent, forming a consistent part of the comprehensive strategy against hypertension and related cardiovascular complications.

Saia F, Piovaccari G, Manari A, Guastaroba P, Vignali L, Varani E, Santarelli A, Benassi A, Liso A, Campo G, Tondi S, Tarantino F, De Palma R, Marzocchi A. · Istituto di Cardiologia, Università di Bologna, Policlinico S. Orsola-Malpighi, Italy. · EuroIntervention. · Pubmed #19577984 No free full text.

Abstract: AIMS: To evaluate the long-term clinical outcome after drug-eluting stents (DES) implantation, and to test if patient selection could enhance their net clinical benefit. METHODS AND RESULTS: We assessed the incidence of major adverse cardiac events (MACE=death, acute myocardial infarction, and target vessel revascularisation, TVR) and angiographic stent thrombosis (ST) during 3-year follow-up in a prospective multicentre registry. Propensity-score analysis to adjust for different clinical, angiographic and procedural characteristics was performed. Overall, 14,115 patients enrolled in the registry received solely BMS (n=9,565) or DES (n=4,550). The incidence of definite ST was 0.6% for BMS and 1.3% for DES (p=0.003). The propensity-score adjusted incidence of cardiac death and myocardial infarction was similar between the two groups (DES 11.9% vs. BMS 12.1%, HR 0.90, 95% CI 0.77-1.04), whereas DES were associated with lower rates of TVR (DES 11.6% vs. BMS 15.2%, HR 0.67, 95% CI 0.59-0.76). The efficacy of DES in reducing TVR increased with increasing likelihood of TVR at baseline. CONCLUSIONS: The beneficial effect of DES in reducing new revascularisations compared to BMS extends out to three years without a significantly worse overall safety profile. The benefit seems more evident in patients with the highest baseline risk of clinical restenosis.

Valgimigli M, Campo G, de Cesare N, Meliga E, Vranckx P, Furgieri A, Angiolillo DJ, Sabatè M, Hamon M, Repetto A, Colangelo S, Brugaletta S, Parrinello G, Percoco G, Ferrari R, Anonymous00068. · Cardiovascular Institute, University of Ferrara, S. Anna Hospital, Corso Giovecca 203, Ferrara, Italy. · Circulation. · Pubmed #19528337 No free full text.

Abstract: BACKGROUND: Inhibition of platelet aggregation after aspirin or clopidogrel intake varies greatly among patients, and previous studies have suggested that poor response to oral antiplatelet agents may increase the risk of thrombotic events, especially after coronary angioplasty. Whether this reflects suboptimal platelet inhibition per se, which might benefit from more potent antiplatelet agents such as tirofiban, is unknown. METHODS AND RESULTS: We screened 1277 patients to enroll 93 aspirin, 147 clopidogrel, and 23 dual poor responders, based on a point-of-care assay, who underwent elective coronary angioplasty at 10 European sites for stable or low-risk unstable coronary artery disease. Patients were randomly assigned in a double-blind manner to receive either tirofiban (n=132) or placebo (n=131) on top of standard aspirin and clopidogrel therapy. The primary end point, consisting of troponin I/T elevation at least 3 times the upper limit of normal, was attained in 20.4% (n=27) in the tirofiban group compared with 35.1% (n=46) in the placebo group (relative risk, 0.58; 95% confidence interval, 0.39 to 0.88; P=0.009). The rate of major adverse cardiovascular events within 30 days in the tirofiban group also was reduced (3.8% versus 10.7%; P=0.031). The overall incidence of bleeding was low, likely explained by a substantial use of the transradial approach, and did not differ between the 2 groups. CONCLUSIONS: In low-risk patients according to clinical presentation who had poor responsiveness to standard oral platelet inhibitors via a point-of-care assay, intensified platelet inhibition with tirofiban lowers the incidence of myocardial infarction after elective coronary intervention.