[PP.15.13] DIPPING STATUS IS CHARACTERIZED BY AUGMENTED ADMINISTRATION OF BENZODIAZEPINES AND ELEVATED ARTERIAL STIFFNESS

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Abstract

Objective:

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. We hypothesised that dipping status might be correlated with benzodiazepine's administration (sympatholytic action) in the setting of essential hypertension (EH).

Design and method:

Our population consisted of 134 consecutive subjects with stage I-II untreated EH (aged 52 ± 9 years, 72 male, office BP = 151/97 mmHg). 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:

In conclusion, non-dippers compared to dippers hypertensives are characterized by increased benzodiazepine's administration, impaired arterial elasticity and more pronounced activation of proatherogenic mechanisms.

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