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Hypertension. 2007;49:784-791
Published online before print February 19, 2007, doi: 10.1161/01.HYP.0000259739.64834.d4
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(Hypertension. 2007;49:784.)
© 2007 American Heart Association, Inc.

Original Articles

Morning Blood Pressure Surge as a Destabilizing Factor of Atherosclerotic Plaque

Role of Ubiquitin–Proteasome Activity

Raffaele Marfella; Mario Siniscalchi; Michele Portoghese; Clara Di Filippo; Franca Ferraraccio; Concetta Schiattarella; Basilio Crescenzi; Paolo Sangiuolo; Giuseppe Ferraro; Silvio Siciliano; Francesca Cinone; Gennaro Mazzarella; Simone Martis; Mario Verza; Ludovico Coppola; Francesco Rossi; Michele D’Amico; Giuseppe Paolisso

From the Departments of Geriatric and Metabolic Diseases (R.M., M.S., C.S., G.F., F.C., M.V., L.C., G.P.), Experimental Medicine (C.D.F.), and Clinical and Preventive Medicine (F.F., G.M., S.M.) and the Cardiovascular Research Center (R.M., C.D.F., F.R., G.P.), Second University of Naples, Naples, Italy; the Cardiovascular Surgery Unit (M.P., F.R., M.D.), Sassari Hospital, Italy; and the Cardiovascular Surgery Unit (B.C., P.S.) and Cardiology Department (S.S.), Hospital V. Monaldi, Naples, Italy.

Correspondence to Raffaele Marfella, Via Emilio Scaglione 141, 80145 Napoli, Italy. E-mail raffaele.marfella{at}unina2.it

Whether morning blood pressure surge influences the molecular mechanisms of plaque progression toward instability is not known. Recently, we have demonstrated enhanced activity of the ubiquitin–proteasome system in human plaques and evidenced that it is associated with inflammatory-induced plaque rupture. We evaluated the inflammatory infiltration and ubiquitin–proteasome activity in asymptomatic carotid plaques of hypertensive patients with different patterns of morning blood pressure surge. Plaques were obtained from 32 hypertensive patients without morning blood pressure surge and 28 with morning blood pressure surge enlisted to undergo carotid endarterectomy for extracranial high-grade (>70%) internal carotid artery stenosis. Plaques were analyzed for macrophages, T-lymphocytes, human leukocyte antigen–DR+cells, ubiquitin–proteasome activity, nuclear factor-{kappa}B, inhibitor kB-ß, tumor necrosis factor-{alpha}, nitrotyrosine, matrix metalloproteinase-9, and collagen content (immunohistochemistry and ELISA). Compared with plaques obtained from hypertensive patients without morning blood pressure surge, plaques from with morning blood pressure surge had more macrophages, T-lymphocytes, human leukocyte antigen–DR+cells (P<0.001), ubiquitin-proteasome activity, tumor necrosis factor-{alpha}, nuclear factor-kB (P<0.001), nitrotyrosine, and matrix metalloproteinase-9 (P<0.01), along with a lesser collagen content and IkB-ß levels (P<0.001). Enhanced ubiquitin–proteasome activity in atherosclerotic lesions of patients with morning blood pressure surge is associated with inflammatory-dependent unstable plaque phenotype. These data suggest a potential interplay between morning blood pressure surge and ubiquitin–proteasome activity in atherosclerosis pathophysiology.


Key Words: morning blood pressure • atherosclerotic plaque • inflammation • ubiquitin–proteasome activity


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