Literature DB >> 23355129

Smoking selectively accelerates carotid atherosclerosis in hypertensive patients.

Raffaele Izzo1, Gianfranco Di Renzo, Nicola De Luca, Valentina Trimarco, Francesco Buono, Salvatore Crispo, Renata Giudice, Frazer Lowe, Mike McEwan, Francesco Rozza, Antonella Bassi, Alfredo Nunziata, Lucio Annunziato, Bruno Trimarco.   

Abstract

BACKGROUND AND OBJECTIVES: Left ventricular hypertrophy, carotid atherosclerosis and renal dysfunction are indicators of target organ damage in hypertension, and independent risk factors for both fatal and non-fatal cardio- and cerebrovascular events. In the general population, smoking is associated with increases in left ventricular mass and carotid intima-media thickness (IMT), and impaired renal function. The aim of the present study was to evaluate whether smoking affects the development of target organ damage in patients with arterial hypertension.
METHODS: 3192 hypertensive patients referred to the Hypertension Clinic of the "Federico II" University of Naples from January 2000 to July 2006 were retrospectively analysed. Subjects were aged from 18 to 75 years. Among these patients, 1391 were smokers and 1801 non-smokers.
RESULTS: The duration and severity of hypertension was significantly shorter in smokers when compared with non-smokers. The maximum arterial IMT was significantly higher in smokers compared with non-smokers (1.7 ± 0.1 mm vs 1.5 ± 0.1, p < 0.0001), while left ventricular mass index was comparable between the two groups. In contrast, glomerular filtration rate was observed to be higher in smokers compared with non-smokers. Logistic regression analysis showed that smoking, age, sex, duration of hypertension, systolic blood pressure and diastolic blood pressure were significantly correlated with IMT. Furthermore, a strong correlation was found between the number of cigarettes smoked per day and IMT.
CONCLUSIONS: Together, these data indicate that in hypertensive patients who have a high risk of developing atherosclerosis, smoking could potentiate the development of atherosclerotic plaques.

Entities:  

Year:  2013        PMID: 23355129     DOI: 10.2165/0151642-200815040-00006

Source DB:  PubMed          Journal:  High Blood Press Cardiovasc Prev        ISSN: 1120-9879


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