Abstract 12398: Administration of Benzodiazepines Coincides With Non Dipping Status and Elevated Arterial Stiffness
Introduction: Blunted reduction of blood pressure (BP) fall as well as psychological stress have both been related to adverse cardiovascular prognosis and potentially share the altered sympathetic tone as a common pathophysiological substrate. Hypothesis: We hypothesized that benzodiazepine's administration (sympatholytic action) might be correlated with altered dipping status in the setting of essential hypertension (EH).
Methods: We studied134 consecutive subjects with stage I-II untreated EH (aged 52±9 years, 72 male, office BP=151/97 mm Hg). They were classified according to the nocturnal BP fall on 24-hour ambulatory BP monitoring, to non-dippers (those with <10% nocturnal systolic and diastolic BP fall, n=36) and dippers (the remaining subjects, n=98). All participants underwent arterial stiffness evaluation on the basis of carotid to femoral pulse wave velocity (c-f PWV) by means of a computerized method (Complior SP). Anthropometric data were recorded and venous blood samples were drawn for estimation of high sensitivity C-reactive protein ( hs-CRP) and homocysteine levels. Self-reported data about benzodiazepine's administration were obtained via interview.
Results : Non-dippers compared to dippers did not differ regarding age, gender, body mass index, office and 24-hour systolic and diastolic BP (p=NS for all cases). Non-dippers had significantly increased 24-hour pulse pressure (54±8 vs 49±9 mmHg, p<0.05). Additionally, they exhibited higher c-f PWV values (8.5 vs 7.6 m/sec, p<0.05), increased hs-CRP (2.8 ± 0.8 vs 2.1 ± 0.6 mg/L, p<0.05) and homocysteine levels (14.6 ± 6.8 vs 11.9 ± 5.4 mmol/L, p<0.05). Benzodiazepine's administration as anxiolytic therapy, was significantly more prevalent among non-dippers compared to dippers (78% vs 23%, p<0.05).
Conclusions: Benzodiazepine's administration in hypertensives is associated with non - dipping status, impaired arterial elasticity and more pronounced activation of proatherogenic mechanisms.
- © 2012 by American Heart Association, Inc.