The effect of the bedtime-dosing doxazosin on nocturnal hypoxia-triggered blood pressure surge in a young adult man with severe obstructive sleep apnea syndrome and a history of three recurrent sleep-onset strokes

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Obstructive sleep apnea syndrome (OSAS) is the most frequent cause of resistant hypertension and nocturnal hypertension, and OSAS increases an individual’s risk of experiencing cardiovascular events 1. OSAS has also been implicated in increased risks of new and recurrent strokes 1. The exaggerated nocturnal blood pressure (BP) surge could subsequently be induced by apneic episodes in patients with OSAS 2 and may contribute toward this association with the occurrence of sleep-onset stroke. However, the existing strategies to assess BP variability including the BP surge associated with sleep apnea episodes in OSAS patients have been difficult to use clinically because neither previous home BP monitoring nor ambulatory BP monitoring measured at fixed intervals could detect the peak sleep BP or the nocturnal BP surge 3.
To resolve this clinical question, we developed a trigger sleep BP (TSP) monitoring method based on an automated fixed-interval measurement function with an additional oxygen-triggered function that takes a BP measurement when the patient’s oxygen desaturation falls below a set variable threshold that is monitored continuously by pulse oximetry 4.
We previously described the case of a young adult man with severe OSAS who showed a prominent BP surge during sleep as measured by this TSP system and then had a recurrence of sleep-onset stroke three times 5. After conservative treatment and discharge, he made an effort to lose weight and accordingly lost 20 kg of body weight (BMI 29.3 kg/m2). His early-morning BP remained high, in contrast to his clinic BP (<130/80 mmHg). Although we proposed the use of continuous positive airway pressure (CPAP) under our supervision, he could not continue because of lack of tolerance. Moreover, we attempted the ambulatory BP monitoring to evaluate his 24-h BP, nocturnal BP, and circadian rhythm toward the goal of preventing further sleep-onset strokes; the patient did not consent to the ambulatory monitoring. We then evaluated his nocturnal BP and hypoxia-related nocturnal systolic blood pressure (SBP) surge again by overnight TSP monitoring for a comparison with his baseline values as he agreed to only nocturnal monitoring.
The results showed a reduced nocturnal SBP surge (peaked to 155 mmHg), whereas the early-morning BP value remained high (139/95 mmHg). We attempted to improve the patient’s hypoxia-triggered nocturnal SBP surge and the level of early-morning BP by chronotherapy. The bedtime dosing of doxazosin (4 mg/day) was initiated, and then we performed overnight TSP to evaluate the effect of this administration. The hypoxia-triggered nocturnal SBP surge was significantly reduced (peaked to 133 mmHg, Fig. 1) and the early-morning BP value was also improved to 119/76 mmHg. Since the time of that evaluation, the patient’s clinic and early-morning BP values have remained in the normal ranges without the recurrence of stroke for over 2 years.
In light of this patient’s case, we suspect that the exaggerated hypoxia-triggered nocturnal BP surge may contribute toward sleep-onset cardiovascular events in OSAS patients, as reported 2. In addition, it is likely that antihypertensive drugs will have different effects in patients with OSAS, but there are few systematic data. We thus need to establish the most effective administration of antihypertensive agents to fully suppress the hypoxia-related nocturnal SBP for preventing sleep-onset cardiovascular events.
To explore this strategy, we previously carried out a clinical study to determine whether the night-time administration of either a vasodilating or a sympatholytic antihypertensive drug might be recommended for the management of hypertensive OSAS patients 6. Compared with nifedipine, carvedilol reduced the peak nocturnal BP, whereas it significantly but less extensively reduced basal BP, resulting in a significant suppression of hypoxia-related nocturnal BP surges 6.

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