Refractory hypertension and sleep apnoea: effect of CPAP on blood pressure and baroreflex.

This study was undertaken to determine whether abolition of obstructive sleep apnoea (OSA) by continuous positive airway pressure (CPAP) could reduce blood pressure (BP) in patients with refractory hypertension. In 11 refractory hypertensive patients with OSA, the acute effects of CPAP on nocturnal BP were studied during sleep and its longer term effects on 24-h ambulatory BP after 2 months. During a single night's application, CPAP abolished OSA and reduced systolic BP in stage 2 sleep from 138.3 +/- 6.8 to 126.0 +/- 6.3 mmHg. There was also a trend towards a reduction in average diastolic BP (from 77.7 +/- 4.5 to 72.9 +/- 4.5). CPAP usage for 2 months was accompanied by an 11.0 +/- 4.4 mmHg reduction in 24-h systolic BP. In addition, both the nocturnal and daytime components of systolic BP fell significantly by 14.4 +/- 4.4 and 9.3 +/- 3.9 mmHg, respectively. Diastolic BP was reduced significantly at night by 7.8 +/- 3.0 mmHg. In patients with refractory hypertension, acute abolition of obstructive sleep apnoea by continuous positive airway pressure reduces nocturnal blood pressure. These data also suggest that continuous positive airway pressure may reduce nocturnal and daytime systolic blood pressure chronically. Randomised trials are needed to confirm the latter results.     

Effects of continuous positive airway pressure versus supplemental oxygen on 24-hour ambulatory blood pressure

Obstructive sleep apnea (OSA) is associated with recurrent episodes of nocturnal hypoxia and increased risk for development of systemic hypertension. Prior studies have been limited, however, in their ability to show reduction in blood pressure after continuous positive airway pressure (CPAP) therapy, and the effect of supplemental oxygen alone on blood pressure in OSA has not been evaluated. We performed a randomized, double-blind, placebo-controlled study comparing the effects of 2 weeks of CPAP versus sham-CPAP versus supplemental nocturnal oxygen on 24-hour ambulatory blood pressure in 46 patients with moderate-severe OSA. We found that 2 weeks of CPAP therapy resulted in a significant reduction in daytime mean arterial and diastolic blood pressure and nighttime systolic, mean, and diastolic blood pressure (all Ps <0.05). Although nocturnal supplemental oxygen therapy improved oxyhemoglobin saturation, it did not affect blood pressure. We conclude that CPAP therapy reduces both daytime and nighttime blood pressure in patients with OSA, perhaps through mechanisms other than improvement of nocturnal oxyhemoglobin saturation.     

Pulmonary hypertension in obstructive sleep apnoea: effects of continuous positive airway pressure: a randomized, controlled cross-over study.

AIMS: We tested the hypothesis that: (i) obstructive sleep apnoea (OSA) by itself originates pulmonary hypertension (PH); and (ii) the application of continuous positive airway pressure (CPAP) can reduce pulmonary pressure. METHODS AND RESULTS: In this randomized and cross-over trial, 23 middle-aged OSA (apnoea-hypopnoea index, 44.1 +/- 29.3 h(-1)) and otherwise healthy patients and 10 control subjects were included. OSA patients randomly received either sham or effective CPAP for 12 weeks. Echocardiographic parameters, blood pressure recordings, and urinary catecholamine levels were obtained at baseline and after both treatment modalities. At baseline, OSA patients had higher pulmonary artery systolic pressure than control subjects (29.8 +/- 8.8 vs. 23.4 +/- 4.1 mmHg, respectively, P = 0.036). Ten out of 23 patients [43%, (95% CI: 23-64%)] and none of the control subjects had PH at baseline (P = 0.012). Two patients were removed from the study because of inadequate CPAP compliance. Effective CPAP induced a significant reduction in the values for pulmonary systolic pressure (from 28.9 +/- 8.6 to 24.0 +/- 5.8 mmHg, P < 0.0001). The reduction was greatest in patients with either PH or left ventricular diastolic dysfunction at baseline. CONCLUSION: Severe OSA is independently associated with PH in direct relationship with disease severity and presence of diastolic dysfunction. Application of CPAP reduces pulmonary systolic pressure levels.     

Blood pressure changes after automatic and fixed CPAP in obstructive sleep apnea: relationship with nocturnal sympathetic activity

Treatment of obstructive sleep apnea (OSA) by continuous positive airway pressure (CPAP) usually causes a reduction in blood pressure (BP), but several factors may interfere with its effects. In addition, although a high sympathetic activity is considered a major contributor to increased BP in OSA, a relationship between changes in BP and in sympathetic nervous system activity after OSA treatment is uncertain. This study was undertaken to assess if, in OSA subjects under no pharmacologic treatment, treatment by CPAP applied at variable levels by an automatic device (APAP) may be followed by a BP reduction, and if that treatment is associated with parallel changes in BP and catecholamine excretion during the sleep hours. Nine subjects underwent 24-h ambulatory BP monitoring and nocturnal urinary catecholamine determinations before OSA treatment and 2 months following OSA treatment by APAP (Somnosmart2, Weinmann, Hamburg, Germany). Eight control subjects were treated by CPAP at a fixed level. After APAP treatment, systolic blood pressure (SBP) decreased during sleep (p < 0.05), while diastolic blood pressure (DBP) decreased both during wakefulness (p < 0.05) and sleep (p < 0.02). Similar changes were observed in subjects receiving fixed CPAP. Nocturnal DBP changes were correlated with norepinephrine (in the whole sample: r = .61, p < 0.02) and normetanephrine (r = .71, p < 0.01) changes. In OSA subjects under no pharmacologic treatment, APAP reduces BP during wakefulness and sleep, similarly to CPAP. A reduction in nocturnal sympathetic activity could contribute to the reduction in DBP during sleep following OSA treatment.     

Obstructive Sleep Apnea and Hypertension

Obstructive sleep apnea (OSA) and hypertension commonly coexist. Observational studies indicate that untreated OSA is associated with an increased risk of prevalent hypertension, whereas prospective studies of normotensive cohorts suggest that OSA may increase the risk of incident hypertension. Randomized evaluations of continuous positive airway pressure (CPAP) indicate an overall modest effect on blood pressure. However, these studies do indicate a wide variation in the blood pressure effects of CPAP, with some patients, on an individual basis, manifesting a large antihypertensive benefit. OSA is particularly common in patients with resistant hypertension. The reason for this high prevalence of OSA is not fully explained, but data from our laboratory suggest that it may be related to the high occurrence of hyperaldosteronism in patients with resistant hypertension. We hypothesize that aldosterone excess worsens OSA by promoting accumulation of fluid in the neck, which then contributes to increased upper airway resistance.     

Blood pressure response to antihypertensive therapy: ambulatory versus office blood pressure readings

Blood pressure readings obtained by the physician in his office and ambulatory blood pressures recorded with the semi-automatic Remler device, were compared during a controlled antihypertensive drug trial. Either timolol or methyldopa was administered in in double-blind fashion to 30 patients with uncomplicated essential hypertension. All exhibited a diastolic office blood pressure greater than 95 mmHg at the end of a four-week placebo period. All patients then received a combination of hydrochlorothiazide (25 mg/day) and amiloride (2.5 mg/day). After four weeks of diuretic therapy, timolol (10 mg/day, n = 14) or methyldopa (250 mg/day, n = 16) were added randomly for six weeks. The dose of all antihypertensive agents was doubled after two weeks of therapy with diuretics combined with timolol (n = 7) or methyldopa (n = 16) because of the persistence of diastolic blood pressure levels greater than 90 mmHg at the office. When assessed in the office, the antihypertensive effect of timolol and methyldopa was similar. During ambulatory blood pressure monitoring, however, pressure levels were lower in the patients given timolol (P less than 0.05 for the diastolic). With both regimens, the blood pressure response measured outside the clinic during usual daily activities could not be predicted from that observed with office blood pressure readings. Furthermore the magnitude of the drug induced blood pressure decrease was more reproducible in time when determined outside the clinic. These data suggest that ambulatory blood pressure monitoring is more precise in evaluating the efficacy of antihypertensive therapy than office blood pressure measurement.     

Ambulatory blood pressure monitoring during antihypertensive treatment: the case of non-responder patients

OBJECTIVE: To analyse the discrepancies between casual and ambulatory blood pressure in hypertensive patients during treatment. PATIENTS AND METHODS: Patients were gathered intio two groups according to casual diastolic blood pressure (DBP) and antihypertensive treatment: group A (responders) with casual DBP < 90 mmHg administered one or more antihypertensive drugs and group B (non-responders) with DBP >/= 95 mmHg taking two or more antihypertensive drugs, maintained during three consecutive visits at 2-week intervals. For all of them casual blood pressure measurements, 24 h ambulatory blood pressure monitoring and assessment of end-organ damage were performed. RESULTS: The difference between casual blood pressure and average 24 h ambulatory blood pressure were significantly higher for group B than those observed for group A (26 versus 7 mmHg systolic, 16 versus 5 mmHg diastolic). Thirty per cent of the patients in group B and 16% in group A had casual blood pressure more than 20 mmHg higher than awake ambulatory blood pressure, whereas 8% in group B and 20% in group A had higher values for ambulatory than for casual blood pressure. In group A 8% of patients had awake DBP higher than 95 mmHg and 8% had awake DBP 85-95 mmHg. Patients of group A with awake DBP >/= 85 mmHg were younger than those with awake DBP < 85 mmHg (41.4+/-8.8 and 52.1+/-13.4 years, respectively). In patients of group B, there was less end-organ damage in the patients with awake DBP < 85 mmHg than there was in patients with awake DBP >/= 95 mmHg (World Health Organization grade I/II-III, 6/10 and 3/20, respectively). CONCLUSION: The differences between casual and ambulatory blood pressures were higher in the 'non-responder' patients. In group A the small percentage of patients who had persistently higher ambulatory blood pressure were younger. In group B one-quarter of the patients had 'normal' ambulatory blood pressure and less end-organ damage. Ambulatory blood pressure monitoring will be useful for better assessment of hypertension control in a subset of hypertensive patients.     

Long-term effect of continuous positive airway pressure on BP in patients with hypertension and sleep apnea

OBJECTIVE: To analyze the long-term effect of continuous positive airway pressure (CPAP) on ambulatory BP in patients with obstructive sleep apnea (OSA) and hypertension, and to identify subgroups of patients for whom CPAP could be more effective. METHODS: We conducted a prospective, long-term follow-up trial (24 months) in 55 patients with OSA and hypertension (mean CPAP use, 5.3 +/- 1.9 h/d [+/- SD]). Twenty-four-hour ambulatory BP monitoring (ABPM) was measured at baseline and after intervention with CPAP on an intention-to-treat basis. In addition, the correlation between the changes in 24-h mean arterial pressure (24hMAP) and CPAP compliance, OSA severity, and baseline ABPM was assessed. RESULTS: At the end of follow-up, a significant decrease was shown only in diastolic BP (- 2.2 mm Hg; 95% confidence interval [CI], - 4.2 to - 0.1; p = 0.03) but not in 24hMAP or other ABPM parameters. However, a correlation between changes in 24hMAP and baseline systolic BP (r = - 0.43, p = 0.001), diastolic BP (r = - 0.38, p = 0.004), and hours of use of CPAP (r = - 0.30, p = 0.02) was observed. A significant decrease in the 24hMAP was achieved in a subgroup of patients with incompletely controlled hypertension at entry (- 4.4 mm Hg; 95% CI, - 7.9 to - 0.9 mm Hg; p = 0.01), as well as in those with CPAP compliance > 5.3 h/d (- 5.3 mm Hg; 95% CI, - 9.5 to - 1.2 mm Hg; p = 0.01). Linear regression analysis showed that baseline systolic BP and hours of CPAP were independent predictors of reductions in BP with CPAP. CONCLUSION: Long-term CPAP reduced BP modestly in the whole sample. However, patients with higher BP at entry and good CPAP compliance achieved significant reductions in BP.     

Study of the placebo effect in using the non-invasive ambulatory measurement of blood pressure

The aim of this study is to evaluate the antihypertensive effect of placebo assessed by 24 hr non invasive blood pressure monitoring. 20 patients (16 males, 4 females, 55 +/- 10 years old) with primary hypertension (WHO stage I or II) were included with a diastolic blood pressure greater than or equal to 100 mmHg (mean blood pressure from three clinical readings). Casual blood pressure and blood pressure monitoring (Spacelabs - 4 measurements per hour during a 24 hr period) were established before and at the end of the placebo run in period (one placebo tablet given once daily at 8 h-8 h 30 a.m. for 15 days). Overall sample data: There was no antihypertensive effect of the placebo with casual BP (167 +/- 16-109 +/- 6 mmHg before and 167 +/- 16-109 +/- 7 mmHg after placebo) and with 24 hr B.P. monitoring (142 +/- 14-96 +/- 8 mmHg before and 141 +/- 14-96 +/- 8 mmHg after placebo). The circadian curves were similar. Individual patient data: A clinical placebo effect (B.P. decrease of at least 10 mmHg) was found in 5 patients for the systolic B.P. and in 2 for diastolic B.P. A significant ambulatory placebo effect (p less than 0.05) was found in 5 patients for the 24 hr systolic B.P. and in 4 patients for the 24 hr diastolic B.P. However, patients with clinical placebo effect were not the same as those with ambulatory placebo effect. There was no correlation between the clinical and the ambulatory response to placebo treatment.(ABSTRACT TRUNCATED AT 250 WORDS)     

The effect of continuous positive airway pressure therapy on blood pressure and arterial stiffness in hypertensive patients with obstructive sleep apnea

Aim

We aimed to evaluate the effect of continuous positive airway pressure (CPAP) therapy on blood pressure (BP) and arterial stiffness in hypertensive patients with obstructive sleep apnea (OSA).

Patients and methods

We studied 38 hypertensive patients who suffered from severe OSA. Ambulatory BP measurement was performed at baseline and after at least 3 months of uninterrupted CPAP therapy. In 19 of these patients, we also measured pulse wave velocity (PWV) at baseline, after the first night of CPAP therapy and at 3 months. Fifteen normotensive subjects without OSA comprised the control group.

Results

CPAP therapy reduced systolic BP from 141.5?±?12.1 to 133.5?±?9.7 mmHg (p?=?0.007) and diastolic BP from 87.8?±?6.8 to 83?±?5.4 mmHg (p?=?0.004). CPAP also reduced the PWV from 8.81?±?1.4 to 8.18?±?1 m/s after the first night of CPAP therapy (p?=?0.003) and to 7.37?±?1 m/s at 3 months (p?=?0.007).

Conclusions

To the best of our knowledge, this is the first study demonstrating that CPAP therapy in hypertensive patients with OSA improves arterial stiffness from the first night and that this favorable effect is maintained for at least 3 months of CPAP use. A reduction in BP was also observed, even though BP control was not always achieved.     

Effect of continuous positive airway pressure treatment on pulmonary artery pressure in patients with isolated obstructive sleep apnea: a meta-analysis

Pulmonary hypertension (PH) can occur in patients with obstructive sleep apnea (OSA) in the absence of cardiac or lung disease. Data on the development and severity of PH, and the effect of continuous positive airway pressure (CPAP) therapy on pulmonary artery (PA) pressures in these patients have been inconsistent in the literature. We sought to determine whether CPAP therapy affects PA pressures in patients with isolated OSA in this meta-analysis. We searched PubMed, Medline, EMBASE and other databases from January 1980 to August 2015. Studies of patients with OSA, defined as an apnea–hypopnea index >10 events/h, and PH, defined as PA pressure >25 mmHg were included. Two reviewers independently extracted data and assessed risk of bias. A total of 222 patients from seven studies (341.53 person-years) had reported PA pressures before and after treatment with CPAP therapy. 77 % of participants were men, with a mean age of 52.5 years, a mean apnea–hypopnea index of 58 events/h, and mean PA pressure of 39.3 ± 6.3 mmHg. CPAP treatment duration ranged from 3 to 70 months. Using fixed effects meta-analysis, CPAP therapy was associated with a decrease in PA pressure of 13.3 mmHg (95 % CI 12.7–14.0) in our study population. This meta-analysis found that CPAP therapy is associated with a significantly lower PA pressure in patients with isolated OSA and PH.     

The effect of acebutolol and metoprolol on noninvasive ambulatory blood pressure monitoring system in essential hypertension]

We compared the antihypertensive effects of acebutolol and metoprolol during 2-4 weeks of treatment in patients with mild to moderate essential hypertension. Acebutolol (n = 12) significantly decreased conventionally measured blood pressure from 173/100 mmHg to 148/86 mmHg (p less than 0.005), and metoprolol (n = 11) decreased it from 164/106 mmHg to 138/87 mmHg (p less than 0.01). Based on data derived from automated 24-hour ambulatory blood pressure monitoring, both drugs significantly decreased the blood pressure in the early morning (5:00-10:00). Moreover, in the metoprolol group, there were significant falls in day-time blood pressure (7:30-19:30) and night-time blood pressure (23:00-7:00). In contrast, acebutolol showed significant antihypertensive effect on day-time blood pressure, but not effect on night-time blood pressure. The study confirmed the efficacy and character of metoprolol and acebutolol. We must choose an effective beta-blocker when using an automated 24-hour ambulatory blood pressure monitoring system to get adequate blood pressure reduction for the whole 24 hours.     

The effects of continuous positive airway pressure on prehypertension and masked hypertension in men with severe obstructive sleep apnea

Obstructive sleep apnea and hypertension are common conditions that frequently coexist. Continuous positive airway pressure (CPAP) reduces blood pressure in patients with obstructive sleep apnea and sustained hypertension. However, the impact of CPAP on patients with obstructive sleep apnea and prehypertension and masked hypertension, conditions associated with increased cardiovascular risk, is unknown. Thirty-six male patients (age, 43 ± 7 years; body mass index, 28.8 ± 3.0 kg/m(2)) with untreated severe obstructive sleep apnea (apnea-hypopnea index, 56 ± 22 events/hr on polysomnography) with diagnostic criteria for prehypertension and/or masked hypertension, based on office and 24-hour ambulatory blood pressure monitoring, respectively, were studied. The patients randomized to no treatment (control; n=18) or CPAP (n=18) for 3 months had similar frequency of prehypertension and masked hypertension at study entry. There were no significant changes in blood pressure in patients randomized to the control group. In contrast, patients randomized to CPAP presented significant reduction in office systolic (from 126 ± 5 to 121 ± 7 mm Hg; P=0.001) and a trend for diastolic blood pressure (from 75 ±7 to 73 ± 8 mm Hg; P=0.08) as well as a significant decrease in daytime and nighttime systolic and diastolic blood pressure (P<0.05 for each comparison). There was a significant reduction in the frequency of prehypertension (from 94% to 55%; P=0.02) and masked hypertension (from 39% to 5%; P=0.04) only in the CPAP group. In conclusion, effective CPAP therapy promotes significant reduction in the frequency of prehypertension and masked hypertension by promoting significant blood pressure reductions in patients with severe obstructive sleep apnea.     

Blood pressure effects of CPAP in nonresistant and resistant hypertension associated with OSA: A systematic review of randomized clinical trials

Obstructive sleep apnea (OSA) is a rather common chronic disorder, associated with increased prevalence of hypertension. The pathophysiological mechanisms for hypertension in OSA are at least in part linked to intermittent hypoxia developed during nightly hypopneas and apneas. Hypoxemia stimulates sympathetic overactivity, systemic inflammation, oxidative stress, and endothelial dysfunction. However, it appears that intermittent hypoxemia is not the only factor in the development of hypertension in OSA. Supplemental oxygen therapy that improved oxyhemoglobin saturation to similar levels to those achieved with CPAP treatment did not reduce BP. In this scenario, it could be proposed that hypoxemia acts as a trigger of sympathetic overdrive, which when set is the main factor in the development of hypertension in OSA. This review appraises evidence provided by randomized controlled trials on the BP-lowering effectiveness of continuous positive airway pressure (CPAP) treatment of OSA patients with nonresistant and resistant hypertension. It suggests that CPAP treatment is more effective in treating resistant hypertension than nonresistant hypertension. A possible explanation is that sympathetic overactivity and altered vascular reactivity in OSA could be more severe in resistant hypertension than in nonresistant hypertension. An intricate interaction among compliance, adherence, and their interaction with demographic characteristics, genetic factors, and comorbidities of the population included might explain the differences found between trials on their influence over the antihypertensive effectiveness of CPAP. Further long-term trials are needed in hypertensive OSA patients to assess whether CPAP treatment in OSA patients consistently restores physiological nocturnal BP fall and adjusts resting and circadian heart rate.     

Comparison of empirical continuous positive airway pressure (CPAP) treatment versus initial portable sleep monitoring followed by CPAP treatment for patients with suspected obstructive sleep apnoea

Background: Polysomnography is labour‐intensive for diagnosing obstructive sleep apnoea (OSA). We compared two algorithms for initiating continuous positive airway pressure (CPAP) treatment for patients with suspected OSA. Methods: Symptomatic OSA patients were randomised into either algorithm I or II. Algorithm I consisted of an empirical CPAP trial whereas algorithm II utilised an Apnea Risk Evaluation System, a wireless device applied on the forehead, for establishing a diagnosis before a CPAP trial for 3 weeks. Primary outcome was success of CPAP trial, defined as CPAP usage > 4 h/night and willingness to continue CPAP. Subjective usefulness of CPAP, accuracy of Apnea Risk Evaluation System versus polysomnography and CPAP adherence at 6 months were secondary end‐points. Results: Altogether 138 patients in algorithm I and 110 patients in algorithm II completed the CPAP trial. There were no significant differences between these algorithms with respect to the primary end‐point. The sensitivity and specificity of algorithm I versus II as a diagnostic test for OSA were 0.3, 0.8 versus 0.31, 1.00 respectively. In predicting CPAP adherence at 6 months, the likelihood ratio positive for algorithms I and II was 2.7 and 5.27 respectively. The mean (SE) time taken from the first consultation to the end of CPAP trial in algorithm I and algorithm II was 60 (2) and 98 (5) days, respectively, P < 0.01. Conclusion: An ambulatory approach with portable sleep monitoring for diagnosing OSA before a CPAP trial can identify more patients who would adhere to CPAP at 6 months than empirical CPAP treatment alone.     

Cost-effectiveness of ambulatory blood pressure: a reanalysis

Accurate diagnosis of hypertension and prognosis for future cardiovascular events can be enhanced through the use of 24-hour ambulatory blood pressure monitoring. It has been suggested that the use of ambulatory monitoring as a secondary screening for hypertension might be cost-effective. Many needed studies that are related to the calculation of cost-effectiveness for ambulatory monitoring have become available in recent years. More accurate estimates for cost of care, costs for testing, prevalence of white-coat hypertension, and incidence of the transition from normal pressures to hypertension have been reported. This study presents calculations of the cost savings likely to take place when ambulatory blood pressure monitoring is implemented for newly detected hypertensive subjects. These calculations are based on current estimates for cost of testing, cost of treatment, prevalence of white-coat hypertension at baseline, and varying the incidence of new hypertension after the initial screening. The results indicate a potential savings of 3% to 14% for cost of care for hypertension and 10% to 23% reduction in treatment days when ambulatory blood pressure monitoring is incorporated into the diagnostic process. At current reimbursement rates, the cost of ambulatory blood pressure monitoring for secondary screening on an annual basis would be <10% of treatment costs. Calculated savings for use of ambulatory blood pressure monitoring can take place when annual treatment costs are as little as 300 dollars. These estimates should be considered for the management of recently detected hypertension, especially when the risk of future cardiovascular is disease is low.     

Causes and consequences of blood pressure alterations in obstructive sleep apnea

The obstructive sleep apnea (OSA) syndrome has been considered to be a cause of both transient blood pressure elevations during sleep and sustained hypertension during the awake state. The purpose of this review was to examine critically the existing literature regarding (1) the blood pressure alterations associated with OSA, (2) causal mechanisms relating specific blood pressure alterations to OSA, and (3) potential consequences of the systemic circulatory abnormalities associated with OSA. Particular attention was directed at studies that assessed the prevalence of OSA in patients with hypertension and that examined the effects on blood pressure of treatment of OSA. We conclude that patients with OSA have abnormal sleep blood pressure patterns, manifested most frequently by apnea-associated blood pressure elevations. Confounding factors such as obesity and antihypertensive drug therapy, and conflicting evidence regarding changes in daytime blood pressure after therapy for OSA, make it premature to conclude that OSA and daytime hypertension are directly associated. Circumstantial evidence suggests that the blood pressure alterations that occur during sleep could contribute to the high cardiovascular morbidity in patients with OSA. Further research into the relationship between OSA and hypertension should improve the future care of patients with these conditions and enhance our understanding of cardiopulmonary pathophysiology.     

Resistant hypertension, obstructive sleep apnoea and aldosterone

Obstructive sleep apnoea (OSA) and hypertension commonly coexist. Observational studies indicate that untreated OSA is strongly associated with an increased risk of prevalent hypertension, whereas prospective studies of normotensive cohorts suggest that OSA may increase the risk of incident hypertension. Randomized evaluations of continuous positive airway pressure (CPAP) indicate an overall modest effect on blood pressure (BP). Determining why OSA is so strongly linked to having hypertension in cross-sectional studies, but yet CPAP therapy has limited BP benefit needs further exploration. The CPAP studies do, however, indicate a wide variation in the BP effects of CPAP, with some patients manifesting a large antihypertensive benefit such that a meaningful BP effect can be anticipated in some individuals. OSA is particularly common in patients with resistant hypertension (RHTN). The reason for this high prevalence of OSA is not fully explained, but data suggest that it may be related to the high occurrence of hyperaldosteronism in patients with RHTN. In patients with RHTN, it has been shown that aldosterone levels correlate with severity of OSA and that blockade of aldosterone reduces the severity of OSA. Overall, these findings are consistent with aldosterone excess contributing to worsening of underlying OSA. We hypothesize that aldosterone excess worsens OSA by promoting accumulation of fluid within the neck, which then contributes to increased upper airway resistance.     

Continuous Positive Airway Pressure in Patients With Obstructive Sleep Apnea and Resistant Hypertension: A Meta‐Analysis of Randomized Controlled Trials

This study aimed to analyze the effect of continuous positive airway pressure (CPAP) on blood pressure (BP) in patients with obstructive sleep apnea (OSA) and resistant hypertension. Randomized controlled trials (RCTs) that evaluated the effect of CPAP on BP in patients with OSA and resistant hypertension, indexed in MEDLINE, Embase, and the Cochrane Library from inception until March 20, 2015, were included in the meta‐analysis. A total of five RCTs were identified to meet the inclusion criteria. The pooled changes after CPAP treatment for 24‐hour ambulatory systolic BP and diastolic BP (DBP) were −4.78 mm Hg (95% confidence interval [CI], −7.95 to −1.61) and −2.95 mm Hg (95% CI, −5.37 to −0.53) in favor of the CPAP group. CPAP was also associated with reduction in nocturnal DBP (mean difference, −1.53 mm Hg, 95% CI, −3.07 to 0). The results indicated a favorable reduction in BP with CPAP treatment in patients with OSA and resistant hypertension.     

Assessment of the anti-hypertensive effect of diltiazem in delayed-action capsules by ambulatory monitoring of arterial pressure]

The aim of this parallel controlled-placebo study was to assess the antihypertensive effect of diltiazem in a slow release formulation in monotherapy by the ambulatory blood pressure monitoring (ABPM). Twenty patients with moderate essential hypertension entered the trial. Whole day ambulatory blood pressure (BP) monitoring, with a COLIN ABPM 630, was done after a wash-out period, after placebo administration and 60 days of therapy with diltiazem in a 120 or 180 mg once or twice daily administration. We verified by ABPM that placebo administration did not have an antihypertensive effect (146 +/- 10 mmHg/87 +/- 7 mmHg at base line to 145 +/- 8 mmHg/84 +/- 6 mmHg with placebo p = ns). Eithy four percent of the patients showed a significant systolic and diastolic BP decrease after 60 days of therapy (from 146 +/- 10 mmHg/87 +/- 7 mmHg at base line to 132 +/- 7/77 +/- 6 mmHg - p less than 0.025). In 56% of the patients this was achieved with 180 mg/day and this effect was sustained throughout the 24 hours. We did not find a significant decrease on heart rate. The ABPM is a valuable technique to assess the effect of antihypertensive drugs and demonstrated that diltiazem in a slow release formulation was effective in decreasing systolic and diastolic BP, throughout the day even in patients with low doses, once daily.