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Magdalena Januszewicz - One of the best experts on this subject based on the ideXlab platform.
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effects of renal sympathetic denervation on blood pressure Sleep Apnea course and glycemic control in patients with resistant hypertension and Sleep Apnea
Hypertension, 2011Co-Authors: Adam Witkowski, Paweł Śliwiński, Aleksander Prejbisz, Elzbieta Florczak, Jacek Kądziela, Przemyslaw Bielen, Marek Kabat, E Warchol, Ilona Michalowska, Magdalena JanuszewiczAbstract:Percutaneous renal sympathetic denervation by radiofrequency energy has been reported to reduce blood pressure (BP) by the reduction of renal sympathetic efferent and afferent signaling. We evaluated the effects of this procedure on BP and Sleep Apnea severity in patients with resistant hypertension and Sleep Apnea. We studied 10 patients with refractory hypertension and Sleep Apnea (7 men and 3 women; median age: 49.5 years) who underwent renal denervation and completed 3-month and 6-month follow-up evaluations, including polysomnography and selected blood chemistries, and BP measurements. Antihypertensive regimens were not changed during the 6 months of follow-up. Three and 6 months after the denervation, decreases in office systolic and diastolic BPs were observed (median: −34/−13 mm Hg for systolic and diastolic BPs at 6 months; both P P =0.05) and in hemoglobin A1C level (median: 6.1% versus 5.6%; P P =0.059). In conclusion, catheter-based renal sympathetic denervation lowered BP in patients with refractory hypertension and obstructive Sleep Apnea, which was accompanied by improvement of Sleep Apnea severity. Interestingly, there are also accompanying improvements in glucose tolerance. Renal sympathetic denervation may conceivably be a potentially useful option for patients with comorbid refractory hypertension, glucose intolerance, and obstructive Sleep Apnea, although further studies are needed to confirm these proof-of-concept data.
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effects of renal sympathetic denervation on blood pressure Sleep Apnea course and glycemic control in patients with resistant hypertension and Sleep Apnea
Hypertension, 2011Co-Authors: Adam Witkowski, Aleksander Prejbisz, Elzbieta Florczak, Przemyslaw Bielen, Marek Kabat, E Warchol, Ilona Michalowska, Jacek Kądziela, Pawel śliwinski, Magdalena JanuszewiczAbstract:Percutaneous renal sympathetic denervation by radiofrequency energy has been reported to reduce blood pressure (BP) by the reduction of renal sympathetic efferent and afferent signaling. We evaluated the effects of this procedure on BP and Sleep Apnea severity in patients with resistant hypertension and Sleep Apnea. We studied 10 patients with refractory hypertension and Sleep Apnea (7 men and 3 women; median age: 49.5 years) who underwent renal denervation and completed 3-month and 6-month follow-up evaluations, including polysomnography and selected blood chemistries, and BP measurements. Antihypertensive regimens were not changed during the 6 months of follow-up. Three and 6 months after the denervation, decreases in office systolic and diastolic BPs were observed (median: -34/-13 mm Hg for systolic and diastolic BPs at 6 months; both P<0.01). Significant decreases were also observed in plasma glucose concentration 2 hours after glucose administration (median: 7.0 versus 6.4 mmol/L; P=0.05) and in hemoglobin A1C level (median: 6.1% versus 5.6%; P<0.05) at 6 months, as well as a decrease in Apnea-hypopnea index at 6 months after renal denervation (median: 16.3 versus 4.5 events per hour; P=0.059). In conclusion, catheter-based renal sympathetic denervation lowered BP in patients with refractory hypertension and obstructive Sleep Apnea, which was accompanied by improvement of Sleep Apnea severity. Interestingly, there are also accompanying improvements in glucose tolerance. Renal sympathetic denervation may conceivably be a potentially useful option for patients with comorbid refractory hypertension, glucose intolerance, and obstructive Sleep Apnea, although further studies are needed to confirm these proof-of-concept data.
Virend K Somers - One of the best experts on this subject based on the ideXlab platform.
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Sleep Apnea and cardiovascular disease
Circulation, 2008Co-Authors: Virend K Somers, Raouf S. Amin, David P White, William T Abraham, Fernando Ferreira Costa, Antonio Culebras, Stephen R Daniels, John S Floras, Carl E Hunt, Lyle J OlsonAbstract:Sleep-related breathing disorders are highly prevalent in patients with established cardiovascular disease. Obstructive Sleep Apnea (OSA) affects an estimated 15 million adult Americans and is present in a large proportion of patients with hypertension and in those with other cardiovascular disorders, including coronary artery disease, stroke, and atrial fibrillation.1–14 In contrast, central Sleep Apnea (CSA) occurs mainly in patients with heart failure.15–19 The purpose of this Scientific Statement is to describe the types and prevalence of Sleep Apnea and its relevance to individuals who either are at risk for or already have established cardiovascular disease. Special emphasis is given to recognizing the patient with cardiovascular disease who has coexisting Sleep Apnea, to understanding the mechanisms by which Sleep Apnea may contribute to the progression of the cardiovascular condition, and to identifying strategies for treatment. This document is not intended as a systematic review but rather seeks to highlight concepts and evidence important to understanding the interactions between Sleep Apnea and cardiovascular disease, with particular attention to more recent advances in patient-oriented research. Implicit in this first American Heart Association/American College of Cardiology Scientific Statement on Sleep Apnea and Cardiovascular Disease is the recognition that, although holding great promise, this general area is in need of a substantially expanded knowledge base. Specific questions include whether Sleep Apnea is important in initiating the development of cardiac and vascular disease, whether Sleep Apnea in patients with established cardiovascular disease accelerates disease progression, and whether treatment of Sleep Apnea results in clinical improvement, fewer cardiovascular events, and reduced mortality. Experimental approaches directed at addressing these issues are limited by several considerations. First, the close association between obesity and OSA often obscures differentiation between the effects of obesity, the effects of OSA, and the effects of synergies between these conditions. Second, multiple comorbidities, …
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obstructive Sleep Apnea
Annals of Internal Medicine, 2005Co-Authors: Sean M Caples, Apoor S Gami, Virend K SomersAbstract:Obstructive Sleep Apnea remains an important public health problem because of its neurocognitive sequelae. This review covers the epidemiology, clinical presentation, and diagnosis of obstructive s...
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sympathetic neural mechanisms in obstructive Sleep Apnea
Journal of Clinical Investigation, 1995Co-Authors: Virend K Somers, Mark Eric Dyken, Mary P Clary, Francois M AbboudAbstract:Blood pressure, heart rate, sympathetic nerve activity, and polysomnography were recorded during wakefulness and Sleep in 10 patients with obstructive Sleep Apnea. Measurements were also obtained after treatment with continuous positive airway pressure (CPAP) in four patients. Awake sympathetic activity was also measured in 10 age- and sex-matched control subjects and in 5 obese subjects without a history of Sleep Apnea. Patients with Sleep Apnea had high levels of nerve activity even when awake (P < 0.001). Blood pressure and sympathetic nerve activity did not fall during any stage of Sleep. Mean blood pressure was 92 +/- 4.5 mmHg when awake and reached peak levels of 116 +/- 5 and 127 +/- 7 mmHg during stage II Sleep (n = 10) and rapid eye movement (REM) Sleep (n = 5), respectively (P < 0.001). Sympathetic activity increased during Sleep (P = 0.01) especially during stage II (133 +/- 9% above wakefulness; P = 0.006) and REM (141 +/- 13%; P = 0.007). Peak sympathetic activity (measured over the last 10 s of each apneic event) increased to 299 +/- 96% during stage II Sleep and to 246 +/- 36% during REM Sleep (both P < 0.001). CPAP decreased sympathetic activity and blood pressure during Sleep (P < 0.03). We conclude that patients with obstructive Sleep Apnea have high sympathetic activity when awake, with further increases in blood pressure and sympathetic activity during Sleep. These increases are attenuated by treatment with CPAP.
Adam Witkowski - One of the best experts on this subject based on the ideXlab platform.
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effects of renal sympathetic denervation on blood pressure Sleep Apnea course and glycemic control in patients with resistant hypertension and Sleep Apnea
Hypertension, 2011Co-Authors: Adam Witkowski, Paweł Śliwiński, Aleksander Prejbisz, Elzbieta Florczak, Jacek Kądziela, Przemyslaw Bielen, Marek Kabat, E Warchol, Ilona Michalowska, Magdalena JanuszewiczAbstract:Percutaneous renal sympathetic denervation by radiofrequency energy has been reported to reduce blood pressure (BP) by the reduction of renal sympathetic efferent and afferent signaling. We evaluated the effects of this procedure on BP and Sleep Apnea severity in patients with resistant hypertension and Sleep Apnea. We studied 10 patients with refractory hypertension and Sleep Apnea (7 men and 3 women; median age: 49.5 years) who underwent renal denervation and completed 3-month and 6-month follow-up evaluations, including polysomnography and selected blood chemistries, and BP measurements. Antihypertensive regimens were not changed during the 6 months of follow-up. Three and 6 months after the denervation, decreases in office systolic and diastolic BPs were observed (median: −34/−13 mm Hg for systolic and diastolic BPs at 6 months; both P P =0.05) and in hemoglobin A1C level (median: 6.1% versus 5.6%; P P =0.059). In conclusion, catheter-based renal sympathetic denervation lowered BP in patients with refractory hypertension and obstructive Sleep Apnea, which was accompanied by improvement of Sleep Apnea severity. Interestingly, there are also accompanying improvements in glucose tolerance. Renal sympathetic denervation may conceivably be a potentially useful option for patients with comorbid refractory hypertension, glucose intolerance, and obstructive Sleep Apnea, although further studies are needed to confirm these proof-of-concept data.
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effects of renal sympathetic denervation on blood pressure Sleep Apnea course and glycemic control in patients with resistant hypertension and Sleep Apnea
Hypertension, 2011Co-Authors: Adam Witkowski, Aleksander Prejbisz, Elzbieta Florczak, Przemyslaw Bielen, Marek Kabat, E Warchol, Ilona Michalowska, Jacek Kądziela, Pawel śliwinski, Magdalena JanuszewiczAbstract:Percutaneous renal sympathetic denervation by radiofrequency energy has been reported to reduce blood pressure (BP) by the reduction of renal sympathetic efferent and afferent signaling. We evaluated the effects of this procedure on BP and Sleep Apnea severity in patients with resistant hypertension and Sleep Apnea. We studied 10 patients with refractory hypertension and Sleep Apnea (7 men and 3 women; median age: 49.5 years) who underwent renal denervation and completed 3-month and 6-month follow-up evaluations, including polysomnography and selected blood chemistries, and BP measurements. Antihypertensive regimens were not changed during the 6 months of follow-up. Three and 6 months after the denervation, decreases in office systolic and diastolic BPs were observed (median: -34/-13 mm Hg for systolic and diastolic BPs at 6 months; both P<0.01). Significant decreases were also observed in plasma glucose concentration 2 hours after glucose administration (median: 7.0 versus 6.4 mmol/L; P=0.05) and in hemoglobin A1C level (median: 6.1% versus 5.6%; P<0.05) at 6 months, as well as a decrease in Apnea-hypopnea index at 6 months after renal denervation (median: 16.3 versus 4.5 events per hour; P=0.059). In conclusion, catheter-based renal sympathetic denervation lowered BP in patients with refractory hypertension and obstructive Sleep Apnea, which was accompanied by improvement of Sleep Apnea severity. Interestingly, there are also accompanying improvements in glucose tolerance. Renal sympathetic denervation may conceivably be a potentially useful option for patients with comorbid refractory hypertension, glucose intolerance, and obstructive Sleep Apnea, although further studies are needed to confirm these proof-of-concept data.
Brent M Egan - One of the best experts on this subject based on the ideXlab platform.
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renal sympathetic denervation a novel intervention for resistant hypertension insulin resistance and Sleep Apnea
Hypertension, 2011Co-Authors: Brent M EganAbstract:See related article, pp 559–565 “Effects of renal sympathetic denervation on blood pressure, Sleep Apnea course and glycemic control in patients with resistant hypertension and Sleep Apnea” by Witkowski et al is an illuminating report.1 The authors confirm that renal denervation lowers blood pressure (BP) in patients with stage 2 (BP ≥160/≥100 mm Hg) treatment-resistant hypertension adherent to optimal doses of ≥3 antihypertensive medications, including a diuretic.2,3 Their report also endorses the work of Mahfoud et al4 documenting that renal denervation in humans improves indices of insulin action and glucose metabolism. It should be noted, however, that glycosylated hemoglobin levels declined significantly among patients in the current but not the previous report.1,4 The current publication extends previous work by documenting that the BP and metabolic benefits of renal denervation include patients with Sleep Apnea. However, this is not surprising, because most hypertensive patients with treatment-resistant hypertension have Sleep Apnea,1 and it is unlikely that renal denervation would have been effective in previous studies if benefits did not extend to patients with Sleep Apnea. The novel aspect of the current work is that renal sympathetic denervation improved Sleep Apnea in 7 of 8 patients with obstructive Sleep Apnea and 1 of 2 patients with both obstructive and central components. Although the mechanism(s) by which renal denervation may improve obstructive Sleep Apnea is unknown, the authors' hypothesis that changes in sodium-volume status are …
Alfredo Halpern - One of the best experts on this subject based on the ideXlab platform.
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obesity and obstructive Sleep Apnea hypopnea syndrome
Obesity Reviews, 2008Co-Authors: A G De Sousa, Cintia Cercato, Marcio C Mancini, Alfredo HalpernAbstract:Summary Obstructive Sleep Apnea-hypopnea syndrome involves recurring episodes of total obstruction (Apnea) or partial obstruction (hypopnea) of airways during Sleep. Obstructive Sleep Apnea-hypopnea syndrome affects mainly obese individuals and it is defined by an Apnea-hypopnea index of five or more episodes per hour associated with daytime somnolence. In addition to anatomical factors and neuromuscular and genetic factors, Sleep disorders are also involved in the pathogenesis of Sleep Apnea. Obesity affects upper airway anatomy because of fat deposition and metabolic activity of adipose tissue. Obstructive Sleep Apnea-hypopnea syndrome and metabolic syndrome have several characteristics such as visceral obesity, hypertension and insulin resistance. Inflammatory cytokines might be related to the pathogenesis of Sleep Apnea and metabolic syndrome. Sleep Apnea treatment includes obesity treatment, use of equipment such as continuous positive airway pressure, drug therapy and surgical procedures in selected patients. Currently, there is no specific drug therapy available with proven efficacy for the treatment of obstructive Sleep Apnea-hypopnea syndrome. Body-weight reduction results in improvement of Sleep Apnea, and obesity treatment must be emphasized, including lifestyle changes, anti-obesity drugs and bariatric surgery.
