Management of Sleep Disordered Breathing in Patients with Heart Failure

Purpose of Review

This paper reviews treatment options for sleep disordered breathing (SDB) in patients with heart failure. We sought to identify therapies for SDB with the best evidence for long-term use in patients with heart failure and to minimize uncertainties in clinical practice by examining frequently discussed questions: what is the role of continuous positive airway pressure (CPAP) in patients with heart failure? Is adaptive servo-ventilation (ASV) safe in patients with heart failure? To what extent is SDB a modifiable risk factor?

Recent Findings

Consistent evidence has demonstrated that the development of SDB in patients with heart failure is a poor prognostic indicator and a risk factor for cardiovascular mortality. However, despite numerous available interventions for obstructive sleep apnea and central sleep apnea, it remains unclear what effect these therapies have on patients with heart failure. To date, all major randomized clinical trials have failed to demonstrate a survival benefit with SDB therapy and one major study investigating the use of adaptive servo-ventilation demonstrated harm.

Summary

Significant questions persist regarding the management of SDB in patients with heart failure. Until appropriately powered trials identify a treatment modality that increases cardiovascular survival in patients with SDB and heart failure, a patient’s heart failure management should remain the priority of medical care.

     

Sleep Disordered Breathing in Patients with Chronic Obstructive Pulmonary Disease

Sleep-related disordered breathing (SDB) and its influence on desaturation were examined in stable COPD patients with waking SpO₂ > 90%. With respiratory inductance plethysmography, thoracic-abdominal respiratory movements for all events with more than 4% desaturation were analyzed in 26 patients. Types of SDB were confirmed by full polysomnography. Irregular breathing induced desaturation, while stable respiration continued during some desaturation events. Three types of altered ventilation were observed: hypoventilation, paradoxical movement and periodic breathing. An unusual type of paradoxical movement, with normal airflow despite progressive desaturation, was observed in REM sleep. Patients were divided into desaturation (15 patients) and non-desaturation (11 patients) groups. Daytime arterial blood gas, lung function values, and 6-min walking distance did not differ. Awake, mode, maximum and minimum nocturnal SpO₂ were lower in the desaturation group. SDB-induced desaturation events in the desaturation group were more frequent (9.2 ± 3.5 vs. 1.8 ± 2.2 times), a greater SpO₂ decrease (11.4 ± 7.1% vs. 5.2 ± 2.1%) and longer duration (73.2 ± 34.8 vs. 18.8 ± 39.0 min). Patterns of SDB in the desaturation group were hypoventilation (74.4 ± 23.4%), paradoxical movement (10.2 ± 14.5%), periodic breathing (12.1 ± 18.3%) and unclassified (5.8 ± 11.2%). These results reveal that lower SpO₂ and SDB influence nocturnal desaturation in stable COPD patients.     

Recent Developments in Oral Appliance Therapy of Sleep Disordered Breathing

Oral appliances are increasingly gaining a place in the treatment of sleep disordered breathing caused by upper airway obstruction. This review of publications since 1995 documents substantial progress in the scientific basis for this therapy. Imaging by several techniques has shown that mandibular advancing oral appliances open the airway in awake and anaesthetized subjects, creating the presumption that this effect is maintained in sleep. Three controlled cross-over treatment trials have shown that patients consistently prefer oral appliance over continuous positive airway pressure therapy, especially when the treatment effect is strong. Appliance design and use indicates a preference for adjustable mandibular advancing appliances. Complications of therapy appear to be infrequent, but evidence for safety of long-term use is still limited. Oral appliance therapy can be an effective therapy for sleep disorders caused by upper airway obstruction. Considering the accumulated evidence, it is no longer tenable to label oral appliance therapy an experimentalÕ procedure.     

Sleep Disordered Breathing in Patients with Heart Failure: Pathophysiology and Management

Sleep disordered breathing (SDB) is common in heart failure patients across the range of ejection fractions and is associated with adverse prognosis. Although effective pharmacologic and device-based treatment of heart failure may reduce the frequency or severity of SDB, heart failure treatment alone may not be adequate to restore normal breathing during sleep. Continuous positive airway pressure (CPAP) is the major treatment for SDB in heart failure, especially if obstructive rather than central sleep apnea (CSA) predominates. Adequate suppression of CSA by PAP is associated with a heart transplant-free survival benefit, although randomized trials are ongoing. Bilevel PAP (BPAP) may be as effective as CPAP in treating SDB and may be preferable over CPAP in patients who experience expiratory pressure discomfort. Adaptive (or auto) servo-ventilation (ASV), which adjusts the PAP depending on the patient’s airflow or tidal volume, may be useful in congestive heart failure patients if CPAP is ineffective. Other therapies that have been proposed for SDB in congestive heart failure include nocturnal oxygen, CO₂ administration (by adding dead space), theophylline, and acetazolamide; most of which have not been systematically studied in outcome-based prospective randomized trials.     

Effects of Antihypertensive Therapy on Blood Pressure Variability

Purpose of Review

The study aims to summarize the effect of antihypertensive therapy on various types of BP variability in hypertensives.

Recent Findings

Visit-to-visit, day-by-day, and ambulatory BPV are markers of target organ damage and cardiovascular prognosis, as was shown in the LIFE study, which showed that visit-to-visit variability in BP predicted cardiovascular events in treated hypertensive patients with left ventricular hypertrophy. Long-acting calcium channel blockers (CCBs) may be a preferable treatment in reducing BPV measures. Non-adherence to antihypertensive medication is also a very important component of increased BPV, and improving the adherence is also a key for the favorable prognosis.

Summary

BPV cannot be a target of antihypertensive treatments because of the lack of definitive evidence. However, in high-risk patients, those with cardiovascular or cerebrovascular diseases, the clinical significance should be considered in individual basis. Especially, reduction of BPV would be an important strategy for these patients.

     

Arrhythmia Risk Associated with Sleep Disordered Breathing in Chronic Heart Failure

The intersecting relationships of sleep disordered breathing (SDB), arrhythmogenic risk and chronic heart failure (HF) are complex and most likely multi-directional and synergistic. Autonomic dysfunction is a common pathophysiological feature of each of these entities. Intermittent hypoxia, hypercapnia, mechanical cardiac influences due to upper airway obstruction and rostral fluid shifts are SDB-specific mechanisms which may trigger, perpetuate and exacerbate HF and arrhythmogenesis. Specific pathophysiological mechanisms will vary according to the predominance of central as compared to obstructive sleep apnea. The risk of cardiac arrhythmias and HF attributable to SDB may be considerable given the high prevalence of SDB and its likely physiologic burden. The current review focuses on the data, which have accrued elucidating the specific contributory mechanisms of SDB in cardiac arrhythmias and HF, highlighting the clinical relevance and effects of standard SDB treatment on these outcomes, and describing the role of novel therapeutics.     

阿罗洛尔降压疗效和对睡眠呼吸障碍的影响

目的：阿罗洛尔的抗高血压疗效和对睡眠呼吸状况的影响。方法：随机、单盲、自身对照法。２０例原发性高血压患者在治疗前后分别接受多导睡眠仪和动态血压等监测。结果：患者服药４周，收缩压从２１．７±２．０ｋＰａ（１６３±１５ｍｍＨｇ）降至１８．９±２．５ｋＰａ（１４２±１９ｍｍＨｇ）（Ｐ＝０．０００，ｎ＝２０），舒张压从１３．５±０．９ｋＰａ（１０１±７ｍｍＨｇ）降至１１．７±０．９ｋＰａ（８８±７ｍｍＨｇ）（Ｐ＝０．０００，ｎ＝２０）。合并睡眠呼吸暂停者治疗后呼吸紊乱指数从２４．６０降至１３．１６（Ｐ＜０．０５，ｎ＝５）。超声心动图结果提示患者心功能状态有显著改善。心率无明显下降，治疗后血浆高密度脂蛋白胆固醇增加，血浆肾素浓度降低。结论：阿罗洛尔有较好的降压疗效，可以减轻睡眠呼吸暂停患者的睡眠呼吸障碍，改善心功能，对代谢无不良影响     

Effect of a Novel Calcium Channel Blocker on Abnormal Nocturnal Blood Pressure in Hypertensive Patients

The authors examined the effect of cilnidipine, a unique L/N‐type calcium channel blocker, on abnormal nocturnal blood pressure (BP) dipping in Japanese hypertensive patients in the real world. The Ambulatory Blood Pressure Control and Home Blood Pressure (Morning and Evening) Lowering by N‐Channel Blocker Cilnidipine (ACHIEVE‐ONE), a large‐scale clinical study, was designed to evaluate the effects of cilnidipine in daily medical practice. Among the study, 24‐hour ambulatory BP data were obtained from 615 patients and classified according to their nocturnal dipping status as extreme dippers, dippers, nondippers, or risers. A 12‐week treatment with cilnidipine significantly reduced 24‐hour BP in all groups (P<.001). Changes in nocturnal systolic BP (SBP) from baseline were −17.9 mm Hg from 154.6 mm Hg in risers and −11.9 mm Hg from 142.1 mm Hg, −6.6 mm Hg from 128.5 mm Hg, and 0.1 mm Hg from 115.8 mm Hg in nondippers, dippers, and extreme dippers, respectively. Changes from baseline in nocturnal SBP reduction rate were 8.2% in risers (P<.001) but −7.0% in extreme dippers (P<.001), while no change was observed in the nighttime SBP reduction rate for the total patients (−0.2%±9.6%, P=.617). Cilnidipine partially, but significantly, restored abnormal nocturnal dipping status toward a normal dipping pattern in hypertensive patients.

A number of studies have demonstrated that nocturnal nondipping¹, ², ³ and extreme dipping of blood pressure (BP)⁴, ⁵, ⁶ are associated with organ damage. A lack of nocturnal dipping has also been related to risk of cardiovascular events,⁷, ⁸, ⁹, ¹⁰, ¹¹ even if BP measured at the clinic or at home is normal. Diuretics, angiotensin‐converting enzyme inhibitors, angiotensin II receptor blockers, and aldosterone antagonists are partially effective in restoring normal BP dipping.¹², ¹³, ¹⁴ However, evidence‐based studies of antihypertensive medication for the treatment of abnormal nocturnal dipping are lacking. In current daily medical practice, antihypertensive medication for reducing 24‐hour BP as well as normalizing dipping status need to be individualized and optimized in each hypertensive patient with different backgrounds such as age and comorbidities.Cilnidipine is a unique L/N‐type calcium channel blocker (CCB) that inhibits norepinephrine release at sympathetic nerve endings by blocking N‐type calcium channels and directly dilates vascular vessels by blocking L‐type calcium channels.¹⁵, ¹⁶, ¹⁷, ¹⁸ Recently, we demonstrated that cilnidipine reduced BP and pulse rate (PR) in patients with morning hypertension suggested to be characterized by increased sympathetic activity using data measured at home obtained from the Ambulatory Blood Pressure Control and Home Blood Pressure (Morning and Evening) Lowering by the N‐Channel Blocker Cilnidipine (ACHIEVE‐ONE) trial.¹⁹ The investigation is a large‐scale clinical study designed to evaluate the effects of cilnidipine in daily medical practice on BP and PR in patients with essential hypertension measured at the clinic and at home. In a portion of these patients, measurement was performed by 24‐hour ambulatory BP (ABP) monitoring (ABPM).In the present study, we examined the effects of cilnidipine on abnormal nocturnal dipping in hypertensive patients.     

Poor Blood Pressure and Urinary Albumin Excretion Responses to Home Blood Pressure-Based Antihypertensive Therapy in Depressive Hypertensive Patients

J Clin Hypertens (Greenwich). There has been no report comparing the changes in home blood pressure (HBP) and target organ damage between depressive and nondepressive hypertensives receiving antihypertensive therapy based on HBP monitoring. This study was a multicenter prospective study conducted by 7 doctors at 2 institutions. The authors prospectively studied 42 hypertensive patients with home systolic blood pressure >135 mm Hg. Participants were divided into a depression group (Beck Depression Inventory score >10; n=21) and a nondepression group (Beck Depression Inventory score <9, matched for HBP level; n=21). The authors performed antihypertensive therapy to reduce home systolic blood pressure to below 135 mm Hg and, 6 months later, evaluated the urinary albumin/creatinine ratio (UACR). Although patients in the depression group tended to require the addition of a greater number of medications than those in the nondepression group (2.3±1.0 vs 1.7±1.0 drugs, P<.05), HBP was reduced similarly in both groups at 6 months (depression group: 150±17/78±11 mm Hg to 139±11/73±8 mm Hg, P<.001; nondepression group: 150±11/76±9 mm Hg to 135±9/70±8 mm Hg, P<.01). The reduction of UACR was smaller in the depression group than in the nondepression group (2.4 vs 10.1 mg/gCr, P<.05). Depressive hypertensive patients required a larger number of antihypertensive drugs to control HBP, and showed a smaller reduction in UACR than nondepressive hypertensives.     

Effect of Continuous Positive Airway Pressure on Blood Pressure Variability in Patients With Obstructive Sleep Apnea

Obstructive sleep apnea (OSA) is a common risk factor for cardiovascular disease. Continuous positive airway pressure (CPAP) improves OSA symptoms and blood pressure (BP) control. The effect of CPAP on BP variability (BPV) in patients with and without hypertension treated with autotitrating CPAP (APAP) for 2 weeks was studied. A total of 78 participants (76.9% men, 49% hypertensive, mean body mass index 36.2 [6.9] kg/m², age 49.0 [12.9] years) underwent 2 weeks of APAP therapy. Office BP, BPV (standard deviation of three BP measurements), and pulse rate were measured before and after treatment. Systolic BPV (5.3±4.9 vs 4.2±3.4 mm Hg, P=.047) and pulse rate (78.0±14.5 vs 75.5±15.8 beats per minute, P=.032) decreased after treatment, particularly in hypertensive participants. Mask leak was independently associated with reduced changes in systolic BPV (r=−0.237, P=.048). Short‐term APAP treatment reduced BPV and pulse rate, particularly in hypertensive patients with OSA.

Obstructive sleep apnea (OSA) is a well‐recognized risk factor for cardiovascular (CV) disease.¹ Its prevalence is rising as a result of the current obesity epidemic.² OSA is caused by recurrent obstructions of the upper airway when asleep. These obstructions result in apneas and hypopneas, which lead to repeated oxygen desaturations and arousals from sleep, and hence activation of the sympathetic nervous system.³ Increased sympathetic tone impacts on blood pressure (BP), heart rate,⁴ and importantly on the risk of CV morbidity.Continuous positive airway pressure (CPAP) maintains upper airway patency and abolishes or reduces obstructive events in patients with OSA,⁵ also reducing BP.⁶ Recent studies have revealed that optimal CPAP control reduces BP, with more marked effects in patients with resistant hypertension,⁷ implying a role of the autonom ous nervous system in relation to changes in BP.BP variability (BPV) is a marker of autonomic nervous system output and an independent predictor of CV morbidity and mortality.⁸ It is defined as the fluctuation of BP between different measurements over a defined time interval.⁹ Visit‐to‐visit BPV comparison is related to an increased risk of CV events.¹⁰, ¹¹ Patients with OSA are known to have an increased sympathetic tone, which causes increased BPV¹², ¹³ and leads to raised levels of absolute BP and increased risk of CV morbidity and mortality. Patients with hypertension exhibit higher BPV when compared with normotensives as expression of an enhanced sympathetic tone.⁹ We aimed to investigate how CPAP treatment modifies the risk of increased sympathetic activation, through its impact on BPV, in patients with obstructive sleep apnea.     

Novel Triggered Nocturnal Blood Pressure Monitoring for Sleep Apnea Syndrome: Distribution and Reproducibility of Hypoxia‐Triggered Nocturnal Blood Pressure Measurements

Obstructive sleep apnea (OSA) causes blood pressure (BP) surges during sleep, which may lead to increased sleep‐onset cardiovascular events. The authors recently developed a triggered nocturnal BP monitoring system that initiates BP measurements when oxygen desaturation falls below a variable threshold. The distribution and reproducibility of hypoxia‐triggered nocturnal BP parameters compared with those of fixed‐interval nocturnal BP parameters for two consecutive nights in 147 OSA patients (mean age 59.4 years, 86.4% men) were evaluated. The mean and distribution (standard deviation [SD]) of the hypoxia‐peak systolic BP (SBP) were significantly greater than that of the mean nocturnal SBP (mean±SD: 148.8±20.5 vs 123.4±14.2 mm Hg, P<.001). The repeatability coefficient (expressed as %MV) of hypoxia‐peak SBP between night 1 and night 2 was comparable to that of mean nocturnal SBP (43% vs 32%). In conclusion, hypoxia‐peak nocturnal BP was much higher than mean nocturnal BP, and it was as reproducible as mean nocturnal BP.     

Tei指数对BiPAP改善冠心病合并睡眠呼吸障碍病人右心功能的疗效评价

目的：探讨右室 Tei指数评价双水平气道正压通气（BiPAP）治疗冠心病合并不同类型睡眠呼吸障碍的疗效。方法对2011年1月—2012年12月南京医科大学附属江宁医院呼吸科睡眠监测室进行多导睡眠监测（PSG）的人群进行筛选,共入选病人60例,根据 PSG检查结果分为中枢性 SDB组、阻塞性 SDB组、混合性 SDB组,每组20例。所有人群均测定 PSG指标[睡眠呼吸暂停低通气指数（AHI）、SaO2〈90%时间]、右心功能指标（Tei指数）和血管内皮功能指标（内皮素1和一氧化氮）;病人经 BiPAP治疗并随访1个月,记录治疗前后的各项指标并比较。结果经 BiPAP治疗后,3组 PSG指标、右心功能及血管内皮功均能得到明显改善（P〈0.05）。结论 BiPAP治疗能明显改善与呼吸暂停有关的低氧状态,从而调节血管内皮的功能,改善右心功能,可能会成为治疗冠心病合并 SDB的重要途径。     

Microalbuminuria in Patients with Non-Insulin-dependent Diabetes Mellitus Relates to Nocturnal Systolic Blood Pressure

PURPOSE: Microalbuminuria predicts early mortality in non-insulin-dependent-diabetes mellitus patients (NIDDM). Our objective in the present study was to compare and assess the relationship between 24-hour, day and nocturnal ambulatory blood pressure (BP) and urinary albumin excretion rate (UAE) in microalbuminuric and normoalbuminuric NIDDM and in normal control subjects.PATIENTS AND METHODS: In the present cross-sectional study, 24 hour ambulatory BP (daytime BP and nocturnal BP) and HbA1c were compared in microalbuminuric (n = 10) and nonmicroalbuminuric NIDDM patients (n = 10) and in nondiabetic controls (n = 9). None of the patients were taking antihypertensive agents.RESULTS: In the microalbuminuric group, whereas 24 hour and daytime systolic BP differed significantly from control values (P <0.025 and P <0.05 respectively), there was no difference between diabetic groups. However, nocturnal systolic BP in the microalbuminuric group was significantly higher than in the normoalbuminuric diabetic patients (139 vs. 125) (P <0.05) and a significant difference was also found between the NIDDM patients and the control group (139, 125 vs. 114) (P <0.025). In multiple regression analysis, only nocturnal systolic BP showed a significant relationship with UAE (P <0.05).CONCLUSIONS: We suggest that the higher nocturnal systolic blood pressure seen in our microalbuminuric NIDDM patients may contribute to the increased morbidity in this group.     

Differential Effects of Amlodipine on Ambulatory Blood Pressure in Elderly Hypertensive Patients With Different Nocturnal Reductions in Blood Pressure

Previous studies have discovered that amlodipine given once daily can reduce blood pressure (BP) throughout the day and night. The effects of amlodipine on day and night BP have not been fully investigated in groups of hypertensives with different diurnal variations. In a prospective study, we performed 24-h ambulatory BP monitoring before and after once-daily use of amlodipine in three groups of asymptomatic elderly hypertensive patients with different nocturnal BP reductions, as follows: 10 extreme dippers with nocturnal reduction of systolic BP ≥ 20% of daytime systolic BP, 17 dippers (reduction by ≥ 10% to < 20%), and 23 nondippers (reduction by < 10%). At baseline, the office and the awake BP were similar in all three groups, whereas the nighttime BP was significantly higher in the nondippers than in the dippers and in the dippers than in the extreme dippers. After treatment, the office and the daytime BP were both equally reduced in all three groups. On the other hand, the nighttime BP was significantly reduced both in the nondippers and, to a lesser extent, in the dippers. In the extreme dippers, however, no further reductions of nocturnal BP were found. Significant positive correlations were found between baseline BP levels and the BP reduction after amlodipine therapy was begun. No BP reduction > 10 mm Hg was observed when the baseline systolic/diastolic BP was < 120/70 mm Hg. Multiple linear regression analysis disclosed that the nighttime BP reduction afforded by amlodipine was dependent on the baseline nighttime BP levels, but not on the baseline nocturnal fall of BP. Once-daily use of amlodipine reduced BP levels throughout the day and night in hypertensive patients who show minimal or mild nocturnal BP fall, but it had no effects on nocturnal BP in those who show a substantial nighttime BP reduction. Thus, when we controlled using daytime office BP, amlodipine might not further reduce nocturnal BP to the extent that it accelerates the brain ischemia in some hypertensive patients with marked nocturnal BP reduction.     

Effect of Continuous Positive Airway Pressure Therapy on Aortic Stiffness in Patients with Obstructive Sleep Apnea Syndrome

Objective: The most significant complications seen in patients with obstructive sleep apnea syndrome (OSAS) are associated with the cardiovascular system. The present study assessed aortic stiffness in patients with OSAS and evaluated the effect of continuous positive airway pressure (CPAP) therapy on aortic stiffness. Method: Twenty‐four patients with newly diagnosed, previously untreated, moderate or severe OSAS (apnea‐hypopnea index > 15) and a control group of 17 healthy patients were included in the study. M‐mode recordings of the ascending aorta were taken from the parasternal long axis by echocardiograhy, and systolic and diastolic diameters of the aorta were measured. Aortic elastic parameters, aortic strain, and distensibility were calculated. Measurements were repeated after 6 months of CPAP therapy in patients with OSAS and were compared with baseline values. Results: In patients with OSAS, compared with the control group, aortic strain (6.7%± 2.1% vs. 12.4%± 3.1%; P < 0.001) and aortic distensibility (2.8 ± 0.9 × 10^?6 cm² dyn^?1 vs. 5.5 ± 1.7 × 10^?6 cm² dyn^?1; P < 0.001) were evidently lower, and there was a significant correlation between aortic elastic parameters and AHI. After a 6‐month course of CPAP therapy, significant increases were observed in aortic strain (6.1%± 1.5% vs. 7.3%± 1.7%; P < 0.001) and aortic distensibility (2.5 ± 0.7 × 10^?6 cm² dyn^?1 vs. 3.1 ± 0.9 × 10^?6 cm² dyn^?1; P < 0.001) in patients with OSAS. Conclusion: Aortic strain and distensibility were lower in patients with OSAS than in control patients, and CPAP treatment provided improvement in aortic elastic parameters. (ECHOCARDIOGRAPHY, Volume 26, November 2009)     

Effect of Seven Different Modalities of Antihypertensive Therapy on Pulse Pressure in Patients with Newly Diagnosed Stage I Hypertension

In this study, we investigated the effect of different antihypertensive agents on pulse pressure (PP). The study was designed in a prospective manner and patients were sequentially allocated to one of the seven different therapy groups, according to the order of enrollment (every first patient to group I, every second patient to group II, and etc). Patients in group I received 10 mg of lisinopril, in group II 10/6.25 mg of lisinopril/hydrochlorothiazide, in group III 80 mg of valsartan, in group IV 80/6.25 mg of valsartan/hydrochlorothiazide, in group V 5 mg of amlodipine, in group VI 1.25 mg of indapamide, and finally those in group VII received 50 mg of atenolol. The reduction in PP was more significant in patients receiving lisinopril, lisinopril hydrochlorothiazide, valsartan, and valsartan hydrochlorothiazide, when compared with patients receiving indapamide, atenolol, and amlodipine (P < 0.05 for each group). Factors such as age, gender, and body mass index were not found to significantly influence the effectiveness of antihypertensive agents on PP. The reduction in PP was more apparent with lisinopril, lisinopril hydrochlorothiazide, valsartan, and valsartan hydrochlorothiazide in diabetic patients, when compared with those without diabetes (P < 0.001, P < 0.05). And also patients on therapy with 3‐hydroxy‐3‐methyl‐glutaryl‐CoA (HMG‐CoA) reductase inhibitors had a greater reduction in PP with lisinopril, lisinopril hydrochlorothiazide, valsartan, and valsartan hydrochlorothiazide (P < 0.001, P < 0.05).     

Effects of Nighttime Single‐Dose Administration of Vasodilating vs Sympatholytic Antihypertensive Agents on Sleep Blood Pressure in Hypertensive Patients With Sleep Apnea Syndrome

Obstructive sleep apneas syndrome (OSAS) is associated with nocturnal hypertension with higher sleep blood pressure (BP) and its variability, both of which increase cardiovascular risk. In this crossover design study, the effect of nighttime single‐dose administration of vasodilating (nifedipine 40 mg) vs sympatholytic (carvedilol 20 mg) antihypertensive agents on sleep BP in 11 hypertensive OSAS patients was evaluated. The authors recently developed a trigger sleep BP monitor with an oxygen‐triggered function that initiates BP measurement when oxygen desaturation falls. The BP‐lowering effects of nifedipine on the mean (P<.05) and minimum sleep systolic BPs (SBPs) (P<.01) were stronger than those of carvedilol. Sleep SBP surge (difference between the hypoxia‐peak SBP measured by oxygen‐triggered function and SBPs within 30 minutes before and after the peak SBP) was only significantly reduced by carvedilol (P<.05). The nighttime dosing of both vasodilating and sympatholytic antihypertensive drugs is effective to reduce sleep BP but with different BP‐lowering profiles.