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Sleep Apnea Syndromes: HELP
Articles by Mathias Hohl
Based on 9 articles published since 2008
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Between 2008 and 2019, Mathias Hohl wrote the following 9 articles about Sleep Apnea Syndromes.
 
+ Citations + Abstracts
1 Editorial Too Fatty, Too Salty, Too Western. 2018

Mishima, Ricardo Sadashi / Hohl, Mathias / Linz, Benedikt / Sanders, Prashanthan / Linz, Dominik. ·From the Centre for Heart Rhythm Disorders, South Australian Health and Medical Research Institute (SAHMRI), University of Adelaide and Royal Adelaide Hospital, Australia (R.S.M., P.S., D.L.). · Klinik für Innere Medizin III, Universität des Saarlandes, Homburg/Saar, Germany (M.H., B.L.). ·Hypertension · Pubmed #30354835.

ABSTRACT: -- No abstract --

2 Review Atrial arrhythmogenesis in obstructive sleep apnea: Therapeutic implications. 2016

Linz, Dominik / Linz, Benedikt / Hohl, Mathias / Böhm, Michael. ·Kardiologie, Angiologie und Internistische Intensivmedizin, Universitätsklinikum des Saarlandes, Germany. Electronic address: Dominik.linz@uks.eu. · Kardiologie, Angiologie und Internistische Intensivmedizin, Universitätsklinikum des Saarlandes, Germany. ·Sleep Med Rev · Pubmed #26186892.

ABSTRACT: The prevalence of sleep disordered breathing like obstructive sleep apnea (OSA) among patients with atrial fibrillation (AF) is 40-50%. OSA reduces success rate of catheter based and pharmacological antiarrhythmic treatment. Additionally, efficient treatment of OSA by continuous positive airway pressure ventilation (CPAP), the first line therapy of OSA, has been shown to improve catheter ablation success rates in AF-patients. A systematic literature search using several databases was performed to review the pathophysiology of obstructive apneas in OSA potentially leading to the development of a substrate for AF and to explain potential mechanisms involved in the clinically observed atrial antiarrhythmic effect of effective CPAP therapy.

3 Review Obstructive sleep apnea and atrial arrhythmogenesis. 2014

Hohl, Mathias / Linz, Benedikt / Böhm, Michael / Linz, Dominik. ·Klinik fur Innere Medizin III, Kardiologie, Angiologie und Internistische Intensivmedizin, Universitatsklinikum des Saarlandes, Kirrberger Str. 1, Geb. 40, D-66421 Homburg/ Saar, Germany. Dominik.linz@uks.eu. ·Curr Cardiol Rev · Pubmed #25004989.

ABSTRACT: Atrial fibrillation (AF) is the most common sustained arrhythmia and is associated with relevant morbidity and mortality. Besides hypertension, valvular disease and cardiomyopathy, mainly ischemic and dilated, also other conditions like obesity, alcohol abusus, genetic factors and obstructive sleep apnea (OSA) are discussed to contribute to the progression from paroxysmal to persistent AF. The prevalence of OSA among patients with AF is 40-50%. OSA is characterized by periodic or complete cessation of effective breathing during sleep due to obstruction of the upper airways. Obstructive respiratory events result in acute intrathoracic pressure swings and profound changes in blood gases together leading to atrial stretch and acute sympatho-vagal dysbalance resulting in acute apnea related to electrophysiological and hemodynamic alterations. Additionally, repetitive obstructive events in patients with OSA may lead to sympathetic and neurohumoral activation and subsequent structural and functional changes in the atrium creating an arrhythmogenic substrate for AF in the long run. This review focuses on the acute and chronic effects of negative thoracic pressure swings, changes in blood pressure and sympatho-vagal dysbalance induced by obstructive respiratory events on atrial electrophysiology and atrial structure in patients with obstructive sleep apnea.

4 Article Diagnostic accuracy of overnight oximetry for the diagnosis of sleep-disordered breathing in atrial fibrillation patients. 2018

Linz, Dominik / Kadhim, Kadhim / Brooks, Anthony G / Elliott, Adrian D / Hendriks, Jeroen M L / Lau, Dennis H / Mahajan, Rajiv / Gupta, Aashray K / Middeldorp, Melissa E / Hohl, Mathias / Nalliah, Chrishan J / Kalman, Jonathan M / McEvoy, R Doug / Baumert, Mathias / Sanders, Prashanthan. ·Centre for Heart Rhythm Disorders (CHRD), South Australian Health and Medical Research Institute (SAHMRI), University of Adelaide and Royal Adelaide Hospital, Adelaide, Australia. Electronic address: Dominik.Linz@adelaide.edu.au. · Centre for Heart Rhythm Disorders (CHRD), South Australian Health and Medical Research Institute (SAHMRI), University of Adelaide and Royal Adelaide Hospital, Adelaide, Australia. · CRM MicroPort, Australia. · Universitätsklinikum des Saarlandes, Klinik für Innere Medizin III, Homburg, Saar, Germany. · Department of Cardiology, Royal Melbourne Hospital and Department of Medicine, University of Melbourne, Melbourne, Australia. · Adelaide Institute for Sleep Health (AISH) and the School of Medicine, College of Medicine & Public Health, Flinders University, Adelaide, Australia; Sleep Health Service, Respiratory and Sleep Services, Southern Adelaide Local Health Network, Adelaide, Australia. · University of Adelaide, School of Electrical and Electronic Engineering, Adelaide, Australia. ·Int J Cardiol · Pubmed #30057161.

ABSTRACT: BACKGROUND: Sleep-disordered breathing (SDB) is highly prevalent in patients with atrial fibrillation (AF) and its treatment can improve rhythm control. Polysomnography (PSG) is the gold standard for the diagnosis of SDB but its high cost and limited availability constrain its role as a standard SDB screening tool. We sought to assess the diagnostic utility of overnight oximetry in predicting SDB in AF patients. METHODS: We analyzed prospectively collected data on 439 patients with documented AF (62% paroxysmal AF) who underwent PSG. Overnight oximetry was used to determine the oxygen desaturation index (ODI, number of desaturation/h) by a novel automated computer algorithm. ODI was validated against PSG derived apnea-hypopnea index (AHI). RESULTS: The sample consisted of 69% men with a mean age of 59.9 ± 11.3 years and body mass index of 30 ± 5 kg/m CONCLUSIONS: ODI derived from a simple and low-cost overnight oximetry can be used as an accessible and reliable screening tool, particularly to rule out SDB.

5 Article Low-Level But Not High-Level Baroreceptor Stimulation Inhibits Atrial Fibrillation in a Pig Model of Sleep Apnea. 2016

Linz, Dominik / Hohl, Mathias / Khoshkish, Shayan / Mahfoud, Felix / Ukena, Christian / Neuberger, Hans-Ruprecht / Wirth, Klaus / Böhm, Michael. ·Universitätsklinikum des Saarlandes, Klinik für Innere Medizin III, Homburg, Saar, Germany. Dominik.Linz@gmx.de. · Universitätsklinikum des Saarlandes, Klinik für Innere Medizin III, Homburg, Saar, Germany. · Sanofi-Aventis Deutschland GmbH, R&D, Frankfurt, Germany. ·J Cardiovasc Electrophysiol · Pubmed #27235276.

ABSTRACT: BACKGROUND: Obstructive sleep apnea (OSA) increases susceptibility to atrial fibrillation (AF) by a combined sympatho-vagal hyperactivation. The purpose of this study was to investigate the effect of autonomic nervous system modulation by low-level baroreceptor stimulation (LL-BRS) compared to high-level BRS (HL-BRS) on atrial arrhythmogenic changes in a pig model of OSA. METHODS AND RESULTS: Sixteen pigs received tracheotomy under general urethane/chloralose anesthesia. Group 1 pigs (n = 8) received LL-BRS (at 80% of that slowing sinus rate) for 3 hours and group 2 pigs (n = 8) received HL-BRS (slowing sinus rate). Changes in atrial effective refractory period (AERP) and AF-inducibility were determined during applied negative thoracic pressure (NTP) for 2 minutes before and at the end of the 3-hour stimulation protocol. Group 1: LL-BRS prolonged AERP from 150 ± 5 to 172 ± 19 milliseconds (P < 0.001). After 3 hours of LL-BRS, NTP-induced AERP-shortening was diminished from -51 ± 10 milliseconds (-34%) to -22 ± 4 milliseconds (-13%) (P < 0.01). AF-inducibility during NTP maneuvers decreased from 90% at baseline to 15% (P < 0.01). Group 2: HL-BRS shortened AERP from 150 ± 17 to 132 ± 8 milliseconds (P = 0.024). After 3 hours of HL-BRS, NTP-induced AERP-shortening was increased from -55 ± 7 milliseconds (-36%) to -72 ± 11 milliseconds (-54%) (P < 0.05) and AF-inducibility was not affected. NTP-induced changes in blood gases and blood pressure were not different between the groups. CONCLUSION: LL-BRS suppressed NTP-induced AERP-shortening and AF-inducibility. By contrast HL-BRS further perpetuated NTP-induced AERP-shortening and increased AF-inducibility. These findings support only the use of LL-BRS as a novel therapeutic modality to treat AF in OSA.

6 Article Impact of obstructive and central apneas on ventricular repolarisation: lessons learned from studies in man and pigs. 2016

Linz, Dominik / Denner, Alisa / Illing, Susanne / Hohl, Mathias / Ukena, Christian / Mahfoud, Felix / Ewen, Sebastian / Reil, Jan C / Wirth, Klaus / Böhm, Michael. ·Klinik für Innere Medizin III, Universitätsklinikum des Saarlandes, 66421, Homburg/Saar, Germany. dominik.linz@uks.eu. · Klinik für Innere Medizin III, Universitätsklinikum des Saarlandes, 66421, Homburg/Saar, Germany. ·Clin Res Cardiol · Pubmed #26809960.

ABSTRACT: BACKGROUND: Sleep apnea (SA) is associated with sudden cardiac death. Compared to central apneas, obstructive apneas are associated with negative intrathoracic pressure swings inducing autonomic imbalance, which may disturb ventricular repolarisation resulting in arrhythmias. OBJECTIVES: To identify the influence of obstructive apneas versus central apneas on ventricular repolarisation. METHODS: In 14 patients with SA, duration (RT-intervals) and dispersion of ventricular repolarisation [Tpeak-to-Tend-interval (TpTe)] were determined during central apneas compared to obstructive apneas. To identify mechanisms, hypoxia alone or hypoxia with applied negative thoracic pressure was applied in a pig model for SA before and after atropine (n = 7), atenolol (n = 5) and sympathetic renal denervation (RDN, n = 7). RESULTS: In patients with SA, obstructive apneas during sleep were always associated with a prolongation of RT- as well as TpTe intervals. By contrast central apneas did not affect ventricular repolarisation significantly in the same patients. In the pig model for SA, 2 min of acute tracheal occlusion with applied negative thoracic pressure resulted in a prolongation in RT- and TpTe-interval. These changes in ventricular repolarisation could be inhibited by atenolol as well as by RDN and were not influenced by parasympathetic blockade by atropine. By contrast hypoxia alone did not affect ventricular repolarisation. CONCLUSIONS: Intrathoracic pressure swings during obstructive apneas contribute to changes in ventricular repolarisation, which are not observed with central apneas. These changes are mainly driven by sympathetic activation and may represent mechanisms for increased occurrence of sudden cardiac death in obstructive SA.

7 Article Obstructive respiratory events and premature atrial contractions after cardioversion. 2015

Linz, Dominik / Hohl, Mathias / Ukena, Christian / Mahfoud, Felix / Wirth, Klaus / Neuberger, Hans-Ruprecht / Böhm, Michael. ·Universitätsklinikum des Saarlandes, Klinik für Innere Medizin III, Homburg/Saar, Germany. ·Eur Respir J · Pubmed #25745047.

ABSTRACT: Recurrence of atrial fibrillation (AF) after electrical cardioversion (ECV) is increased in patients with obstructive sleep apnoea (OSA). In patients with persistent AF, with (n=40) and without (n=32) obstructive respiratory events (OREs) during sedation for ECV, we determined the occurrence of premature atrial contractions (PACs) before and after insertion of a nasopharyngeal tube. The influence of acute obstructive respiratory events on atrial electrophysiology after termination of AF was studied in pigs. Incidence of PACs directly after ECV was higher in patients with OREs compared to those without OREs (7±2 versus 1±1 per 10 s, respectively; p<0.01). Occurrence of PACs could be reduced by 79% by insertion of a nasopharyngeal tube. In a subsequent sleeping study, patients with OREs had higher apnoea-hypopnoea indices and more PACs during night. 16 patient with and four patients without OREs had a relapse of AF during 1 week after ECV (p<0.01). In pigs, acute OREs after 30 min of AF increased occurrence of PACs and vulnerability for reinduction of AF, which could be attenuated by atropine, beta-blockers and renal denervation. OREs are associated with increased occurrence of PACs and more early relapse of AF. OREs increase occurrence of PACs and vulnerability for reinduction of AF by sympathovagal imbalance.

8 Article Effect of obstructive respiratory events on blood pressure and renal perfusion in a pig model for sleep apnea. 2014

Linz, Dominik / Mahfoud, Felix / Linz, Benedikt / Hohl, Mathias / Schirmer, Stephan H / Wirth, Klaus J / Böhm, Michael. ·Klinik für Innere Medizin III, Universitätsklinikum des Saarlandes, Homburg/Saar, Germany; dominik.linz@uks.eu. · Klinik für Innere Medizin III, Universitätsklinikum des Saarlandes, Homburg/Saar, Germany; · Sanofi-Aventis Deutschland GmbH, R&D, Frankfurt, Germany. ·Am J Hypertens · Pubmed #24622919.

ABSTRACT: BACKGROUND: Obstructive sleep apnea (OSA) is associated with hypertension and the progression of chronic kidney disease (CKD). Renal sympathetic innervation contributes to either condition. METHODS: We investigated the effect of renal sympathetic denervation (RDN) on blood pressure (BP), renal perfusion, and neurohumoral responses during and after repetitive obstructive apneas in a pig model for OSA. BP, femoral artery, and renal artery flow were measured in 29 spontaneously breathing urethane-chloralose-anesthetized pigs. The effect of RDN (n = 14) and irbesartan (n = 3) was investigated. Repetitive tracheal occlusions for 2 minutes with applied negative tracheal pressure at -80 mbar were performed over 4 hours. RESULTS: Spontaneous breathing attempts during tracheal occlusion caused an intra-apneic breathing synchronous oscillating pattern of renal flow. Renal flow oscillations were > 2-fold higher compared with femoral flow that almost showed changes proportional to the BP alterations (2.9%/mm Hg vs. 1.3%/mm Hg; P < 0.0001). A marked postapneic BP rise from 102 ± 3 to 172 ± 8 mm Hg (P < 0.00001) was associated with renal hypoperfusion (from 190 ± 24 to 70 ± 20 ml/min; P < 0.00001) occurring after application of obstructive respiratory events. RDN, but not irbesartan, inhibited postapneic BP rises and renal hypoperfusion and attenuated increased plasma renin activity and aldosterone concentration induced by repetitive tracheal occlusions. Additionally, increased urinary protein/creatinine ratio was significantly reduced by RDN, whereas intra-apneic hemodynamic changes or blood gases were not modified by RDN. CONCLUSIONS: Repetitive obstructive respiratory events result in postapneic BP rises and renal hypoperfusion, as well as neurohumoral responses and increased protein/creatinine ratio. These changes are mainly sympathetically driven because they could be attenuated by RDN.

9 Article Effect of renal denervation on neurohumoral activation triggering atrial fibrillation in obstructive sleep apnea. 2013

Linz, Dominik / Hohl, Mathias / Nickel, Alexander / Mahfoud, Felix / Wagner, Michael / Ewen, Sebastian / Schotten, Ulrich / Maack, Christoph / Wirth, Klaus / Böhm, Michael. ·Klinik für Innere Medizin III, Universitätsklinikum des Saarlandes, 66421 Homburg, Saar, Germany. Dominik.Linz@uks.eu. ·Hypertension · Pubmed #23959548.

ABSTRACT: Obstructive sleep apnea is characterized by repetitive collapses of the upper airway, negative thoracic pressure periods, and intermittent hypoxia, stimulating the autonomic nervous system. The increased sympathetic drive during obstructive sleep apnea results in postapneic blood pressure rises and neurohumoral activation potentially involved in the initiation and progression to permanent atrial fibrillation (AF). In a pig model mimicking obstructive sleep apnea, we studied the effects of repetitive obstructive respiratory events for 4 hours on the occurrence of spontaneous AF episodes, postapneic blood pressure rises, and neurohumoral activation. In addition, renal sympathetic denervation was performed to investigate the impact of the sympathetic nervous system. Repetitive obstructive respiratory events caused pronounced postapneic blood pressure rises, prolonged duration of spontaneous AF episodes triggered by spontaneous atrial beats, and increased plasma renin activity and aldosterone concentrations. This was associated with increased nicotinamide adenine dinucleotide phosphate-oxidase activity, reduced antioxidative capacity, and elevated expression of connective tissue growth factor, a redox-sensitive mediator of fibrosis. Renal sympathetic denervation inhibited postapneic blood pressure rises and decreased plasma renin activity and aldosterone concentrations. The occurrence and duration of spontaneous AF were reduced comparable with a combined pharmacological blockade of angiotensin receptor and β-adrenoceptor. Increased atrial oxidative stress, together with the activation of profibrotic pathways and intermittent hypoxia, was not attenuated after renal sympathetic denervation. Repetitive obstructive respiratory events triggered spontaneous AF, increased atrial oxidative stress, and activated profibrotic pathways in the atrium. Renal sympathetic denervation reduced spontaneous AF and postapneic blood pressure rises by combined reduction of sympathetic drive and components of the circulating renin-angiotensin system. However, the generation of atrial oxidative stress was not modulated.