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Time rate of blood pressure variation: a new factor associated with coronary atherosclerosis

Manios, Efstathiosa; Stamatelopoulos, Kimona; Tsivgoulis, Georgiosb; Barlas, Gerasimosa; Koroboki, Elenia; Tsagalis, Georgiosa; Michas, Fotiosa; Vemmos, Konstantinosa; Zakopoulos, Nikolaosa

doi: 10.1097/HJH.0b013e3283454ff4
Original papers: Blood pressure measurement
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Objectives Previous studies have demonstrated that the time rate of blood pressure (BP) variation was associated with early carotid atherosclerosis, independent of peripheral and central BP levels. We evaluated the association between the rate of BP variation, derived from ambulatory BP monitoring (ABPM) data analysis, and the severity and topography of coronary artery lesion in a cohort of normotensive patients with suspected coronary artery disease.

Methods ABPM and coronary angiography were performed in 162 normotensive patients with suspected coronary artery disease. The topography and severity of coronary artery lesions were assessed by Gensini score. The time rate of BP variation was defined as the first derivative of the BP values against time.

Results Patients with coronary artery disease (n = 123) presented significantly (P = 0.005) higher daytime rate of systolic BP variation than control patients (n = 39). Multiple linear regression models revealed independent determinants of Gensini score in the following rank order: diabetes mellitus (β: +0.286, P < 0.001), daytime rate of systolic BP variation (β: +0.277, P < 0.001), daytime systolic BP (β: +0.216, P = 0.002), smoking (β: +0.178, P = 0.008) and hypercholesterolemia (β: +0.158, P = 0.020). A 0.1 mmHg/min increase in the daytime rate of systolic BP variation correlated with an increment of 4.935 in the Gensini score (95% CI 2.432–7.438).

Conclusion Steeper BP variations may produce a greater stress on the arterial wall and may have an additive role to vascular risk factors and BP parameters in the detection of the severity of coronary artery lesions in normotensive individuals with suspected coronary artery disease.

aDepartment of Clinical Therapeutics, University of Athens, Greece

bDepartment of Neurology, Democritus University of Thrace, Greece

Received 31 August, 2010

Revised 26 December, 2010

Accepted 2 February, 2011

Correspondence to Efstathios Manios, MD, Ierolochiton 60, 12244 Athens, Greece Tel: +30 2105696691; fax: +30 210 6742604; e-mail: stathismanios@yahoo.gr

© 2011 Lippincott Williams & Wilkins, Inc.