Impact of Renal Denervation on Patients With Obstructive Sleep Apnea and Resistant Hypertension　– Insights From the SYMPLICITY HTN-3 Trial –

Kario, Kazuomi; Bhatt, Deepak L.; Kandzari, David E.; Brar, Sandeep; Flack, John M.; Gilbert, Colleen; Oparil, Suzanne; Robbins, Mark; Townsend, Raymond R.; Bakris, George L.

doi:10.1253/circj.cj-16-0035

Cited by 69 publications

(49 citation statements)

References 39 publications

(19 reference statements)

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“…Some studies have demonstrated that hypoxia‐peak SBP could be reduced by suppressing sympathetic nerve activity. Catheter‐based renal denervation, which ablates the afferent and efferent sympathetic nerves around the renal artery, significantly reduced peak nocturnal SBP values measured by ABPM and hypoxia‐peak SBP detected by TNP by 10 mm Hg in patients with drug‐resistant hypertension who had OSA. Another study showed that bedtime dosing of 20 mg of carvedilol significantly reduced hypoxia‐peak SBP by 23 mm Hg in patients with hypertension who had OSA .…”

Section: Discussionmentioning

confidence: 99%

Polysomnography‐derived sleep parameters as a determinant of nocturnal blood pressure profile in patients with obstructive sleep apnea

Kuwabara

Tomitani

Shiga

et al. 2018

J of Clinical Hypertension

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Obstructive sleep apnea causes blood pressure (BP) surges during sleep, which may lead to increased sleep-onset cardiovascular events. The authors recently developed an oxygen-triggered nocturnal BP monitoring system that initiates BP measurements when oxygen desaturation (SpO ) falls below a variable threshold. The association between nocturnal BP parameters obtained by nocturnal BP monitoring and simultaneously examined polysomnography-derived sleep parameters in 116 patients with obstructive sleep apnea (mean age 57.9 years, 85.3% men) was studied. In multivariable analysis with independent factors of age, body mass index, sex, and polysomnography-derived measures (apnea-hypopnea index, apnea index, arousal index, lowest SpO , and SpO < 90%), apnea-hypopnea index (β = .26, P = .02) and lowest SpO (β = -.34, P < .001) were independent determinants of hypoxia-peak systolic BP (SBP), defined as the maximum SBP value measured by nocturnal BP monitoring. Similarly, apnea-hypopnea index (β = .21, P = .04) and lowest SpO (β = -.49, P < .001) were independent determinants of nocturnal SBP surge, defined as the difference between the hypoxia-peak SBP and the average of the SBP values within 30 minutes before and after the hypoxia-peak SBP, measured by the fixed-interval function in the manner of conventional ambulatory BP monitoring. In conclusion, in polysomnography-derived parameters, lowest SpO , defined as the minimum SpO value during sleep, is the strongest independent determinant of hypoxia-peak SBP and nocturnal SBP surge measured by nocturnal BP monitoring. Our findings suggest that the severity of the decrease in SpO and the frequency of such decreases would be important indicators to identify high-risk patients who are likely to develop cardiovascular events specifically during sleep.

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Section: Discussionmentioning

confidence: 99%

Polysomnography‐derived sleep parameters as a determinant of nocturnal blood pressure profile in patients with obstructive sleep apnea

Kuwabara

Tomitani

Shiga

et al. 2018

J of Clinical Hypertension

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“…This difference might be partially explained by different degrees of baroreceptor reflex dysfunction and of sympathetic nervous activation . In fact, catheter‐based renal denervation (which ablates the afferent and efferent sympathetic nerves around the renal artery) significantly reduced peak nocturnal BP values in drug‐resistant hypertensive patients, especially those with OSA . More directly, the hypoxia‐peak SBP detected by TNP was significantly reduced by 10 mm Hg after renal denervation .…”

Section: Discussionmentioning

confidence: 99%

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

Kuwabara

Hamasaki

Tomitani

et al. 2016

J of Clinical Hypertension

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Obstructive sleep apnea (OSA) causes blood pressure (BP) surges during sleep, which may lead to increased sleeponset 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 (meanAESD: 148.8AE20.5 vs 123.4AE14.2 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.

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“…Suppressing effects of sympathetic activation by RDN may blunt or reverse this response. 5,12,13 In a proof-of-concept observational study, we showed for the first time that catheter-based renal sympathetic denervation lowers BP in resistant hypertensive patients with OSA. This was accompanied by an improvement in severity of OSA.…”

mentioning

confidence: 89%

“…1,2 In most of the trials, including Symplicity HTN-3 and the recent SPYRAL HTN-OFF MED (Global Clinical Study of Renal Denervation With the Symplicity Spyral Multi-Electrode Renal Denervation System in Patients With Uncontrolled Hypertension in the Absence of Antihypertensive Medications), RDN effects on BP showed considerable variability. [3][4][5][6] It was postulated that identification of specific subsets of patients who could potentially benefit from RDN, or clinical features that may help to predict outcomes after the procedure, might be of importance. 2,7,8 Obstructive sleep apnea (OSA) is considered as a contributing factor to the development of hypertension and is especially associated with resistant hypertension.…”

mentioning

confidence: 99%

Renal Denervation in Resistant Hypertension and Obstructive Sleep Apnea

Warchoł-Celińska

Prejbisz

Kądziela³

et al. 2018

Hypertension

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Abstract-It has been postulated that catheter-based renal denervation (RDN) may lower blood pressure (BP) and improve severity of obstructive sleep apnea (OSA) in resistant hypertensive patients. The aim of our study (NCT01366625) was to investigate in a prospective randomized trial the effect of RDN on BP and clinical course of OSA. Sixty patients with true resistant hypertension coexisting with moderate-to-severe OSA (apnea/hypopnea index, ≥15) were randomly allocated to RDN group (30 patients) and to control group (30 patients). The primary end point was reduction in office systolic BP at 3 months. Secondary end points included reduction in diastolic office and ambulatory BP, change in apnea/hypopnea index and biochemical measurements at 3 months, and change in echocardiographic measurements at 6 months. There were no differences in clinical characteristics between the groups. At 3 months in the RDN group, both office and ambulatory BP were significantly reduced, and a significant decrease in OSA severity (apnea/hypopnea index, 39.4 versus 31.2 events per hour; P=0.015) was observed. Between-group difference in apnea/hypopnea index change was significant at 0.05. At 6 months in the RDN group, reductions in office and ambulatory BP were sustained and were accompanied by significant improvement in echocardiographic measures of global longitudinal strain. There were no differences in metabolic variables in follow-up in both groups. In a randomized controlled trial, RDN lowered both office and ambulatory BP in patients with resistant hypertension and OSA. This was accompanied by improvement of the clinical severity of OSA. Clinical Trial Registration-URL: http://www.clinicaltrials.gov. Unique identifier: NCT01366625.

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Impact of Renal Denervation on Patients With Obstructive Sleep Apnea and Resistant Hypertension　– Insights From the SYMPLICITY HTN-3 Trial –

Cited by 69 publications

References 39 publications

Polysomnography‐derived sleep parameters as a determinant of nocturnal blood pressure profile in patients with obstructive sleep apnea

Polysomnography‐derived sleep parameters as a determinant of nocturnal blood pressure profile 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

Renal Denervation in Resistant Hypertension and Obstructive Sleep Apnea

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Impact of Renal Denervation on Patients With Obstructive Sleep Apnea and Resistant Hypertension – Insights From the SYMPLICITY HTN-3 Trial –

Cited by 69 publications

References 39 publications

Polysomnography‐derived sleep parameters as a determinant of nocturnal blood pressure profile in patients with obstructive sleep apnea

Polysomnography‐derived sleep parameters as a determinant of nocturnal blood pressure profile 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

Renal Denervation in Resistant Hypertension and Obstructive Sleep Apnea

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Impact of Renal Denervation on Patients With Obstructive Sleep Apnea and Resistant Hypertension　– Insights From the SYMPLICITY HTN-3 Trial –