scholarly journals Obstructive sleep apnea and cardiovascular comorbidity: common pathophysiological mechanisms to cardiovascular disease

2021 ◽  
Vol 17 (4) ◽  
pp. 594-605
Author(s):  
M. V. Agaltsov ◽  
O. M. Drapkina
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Cardiovascular System ◽  
Blood Vessels ◽  
Pressure Fluctuations ◽  
Vascular Wall ◽  
Pathophysiological Mechanisms ◽  
Obstructive Sleep ◽  
Intermittent Hypoxemia ◽  
Eeg Activation

Obstructive sleep apnea (OSA) is associated with many cardiovascular and metabolic diseases. Sleep apnea causes intermittent hypoxemia, chest pressure fluctuations and a reaction from the cerebral cortex in the form of a short awakening during sleep (EEG-activation). The consequences of pathological pathways are studied in experimental models involving cell cultures, animals, and healthy volunteers. At present, the negative impact of intermittent hypoxemia on a variety of pathophysiological disorders of the heart and blood vessels (vascular tone fluctuations, thickening of the intimamedia complex in the vascular wall, direct damaging effect on the myocardium) has a great evidence base. Two other pathological components of OSA (pressure fluctuations and EEG-activation) can also affect cardiovascular system, mainly affecting the increase in blood pressure and changing cardiac hemodynamics. Although these reactions are considered separately in the review, with the development of sleep apnea they occur sequentially and are closely interrelated. As a result, these pathological pathways trigger further pathophysiological mechanisms acting on the heart and blood vessels. It is known that these include excessive sympathetic activation, inflammation, oxidative stress and metabolic dysregulation. In many respects being links of one process, these mechanisms can trigger damage to the vascular wall, contributing to the formation of atherosclerotic lesions. The accumulated data with varying degrees of reliability confirm the participation of OSA through these processes in the formation of cardiovascular disorders. There are factors limiting direct evidence of this interaction (sleep deprivation, causing similar changes, as well as the inability to share the contribution of other risk factors for cardiovascular diseases, in particular arterial hypertension, obesity, which are often associated with OSA). It is necessary to continue the study of processes that implement the pathological effect of OSA on the cardiovascular system.

scholarly journals Pathophysiological Mechanisms Obstructive Sleep Apnea

SLEEP ◽  
1980 ◽  
Vol 3 (3-4) ◽  
pp. 235-246 ◽  
Author(s):  
Colin E. Sullivan ◽  
Faiq O. Issa
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Pathophysiological Mechanisms ◽  
Obstructive Sleep

scholarly journals Obstructive Sleep Apnea in Neurodegenerative Disorders: Current Evidence in Support of Benefit from Sleep Apnea Treatment

2020 ◽  
Vol 9 (2) ◽  
pp. 297 ◽  
Author(s):  
Annie C. Lajoie ◽  
Anne-Louise Lafontaine ◽  
R. John Kimoff ◽  
Marta Kaminska
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Current Knowledge ◽  
Upper Airway ◽  
Current Evidence ◽  
Obstructive Sleep ◽  
Intermittent Hypoxemia ◽  
And Function ◽  
The Impact ◽  
Sleep Apnea Treatment

Obstructive sleep apnea (OSA) is a prevalent disorder characterized by recurrent upper airway obstruction during sleep resulting in intermittent hypoxemia and sleep fragmentation. Research has recently increasingly focused on the impact of OSA on the brain’s structure and function, in particular as this relates to neurodegenerative diseases. This article reviews the links between OSA and neurodegenerative disease, focusing on Parkinson’s disease, including proposed pathogenic mechanisms and current knowledge on the effects of treatment.

scholarly journals Different Associations between Tonsil Microbiome, Chronic Tonsillitis, and Intermittent Hypoxemia among Obstructive Sleep Apnea Children of Different Weight Status: A Pilot Case-Control Study

2021 ◽  
Vol 11 (6) ◽  
pp. 486
Author(s):  
Hai-Hua Chuang ◽  
Jen-Fu Hsu ◽  
Li-Pang Chuang ◽  
Cheng-Hsun Chiu ◽  
Yen-Lin Huang ◽  
...  
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Weight Status ◽  
Oxygen Desaturation ◽  
Chronic Tonsillitis ◽  
Healthy Weight ◽  
Desaturation Index ◽  
Oxygen Desaturation Index ◽  
Obstructive Sleep ◽  
Intermittent Hypoxemia

The tonsil microbiome is associated with chronic tonsillitis and obstructive sleep apnea (OSA) in children, and the gut microbiome is associated with host weight status. In this study, we hypothesized that weight status may be associated with clinical profiles and the tonsil microbiome in children with OSA. We prospectively enrolled 33 non-healthy-weight (cases) and 33 healthy-weight (controls) pediatric OSA patients matched by the proportion of chronic tonsillitis. Differences in the tonsil microbiome between the non-healthy-weight and healthy-weight subgroups and relationships between the tonsil microbiome and clinical variables were investigated. Non-healthy weight was associated with significant intermittent hypoxemia (oxygen desaturation index, mean blood saturation (SpO2), and minimal SpO2) and higher systolic blood pressure percentile, but was not related to the tonsil microbiome. However, chronic tonsillitis was related to Acidobacteria in the non-healthy-weight subgroup, and oxygen desaturation index was associated with Bacteroidetes in the healthy-weight subgroup. In post hoc analysis, the children with mean SpO2 ≤ 97% had reduced α and β diversities and a higher abundance of Bacteroidetes than those with mean SpO2 > 97%. These preliminary findings are novel and provide insights into future research to understand the pathogenesis of the disease and develop personalized treatments for pediatric OSA.

741Pharmacological inhibition of the acetylcholine-regulated potassium channel (IK,ACh) prevents atrial arrhythmogenic changes in a rat model for obstructive sleep apnea

EP Europace ◽  
2020 ◽  
Vol 22 (Supplement_1) ◽  
Author(s):  
B Linz ◽  
K Rombouts ◽  
A H Thostrup ◽  
M Hohl ◽  
K Wirth ◽  
...  
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Airway Pressure ◽  
Pressure Fluctuations ◽  
Upper Airway ◽  
Intrathoracic Pressure ◽  
P Wave ◽  
Atrial Pacing ◽  
Obstructive Sleep ◽  
Atrial Activation

Abstract Background In obstructive sleep apnea (OSA), intermittent hypoxemia and intrathoracic pressure fluctuations may increase vagal tone, resulting in an increased acetylcholine-regulated potassium current (IK,ACh). Here we elucidated acute atrial electrophysiological effects of obstructive respiratory events simulated by intermittent negative upper airway pressure (INAP) and the role of atrial IKACh activation. Methods In sedated spontaneously breathing rats (2% isoflurane), either IK,ACh-inhibitor (XAF-1407: 1mg/kg) or a buffer-based vehicle was perfused (Control). INAP was applied non-invasively by a negative pressure device 14 times throughout 70 minutes. Simulated apneas were maintained for one minute with a four minute resting period. Atrial effective refractory period (AERP), inducible atrial fibrillation (AF)-durations and atrial activation time were acquired by a programmed atrial pacing protocol before, during and after applied INAP throughout the study. Results During single INAP applications atrial activation times prolonged transiently in both groups (Control: INAP vs. pre-INAP p = 0.034; XAF-1407: INAP vs. pre-INAP p = 0.039). In control-rats, seventy minutes of repetitive INAP prolonged P-wave duration (+10.8 ± 2.7% vs. baseline, p = 0.008) and decreased AERP by 14.6 ± 3.1% (vs. baseline p = 0.001). AERP shortening correlated with the cumulative pressure applied per body weight (Pearson r= -0.773; p= 0.025). XAF-1407 could prevent P-wave prolongation and AERP shortening. Inducible AF-durations (CTR 0.94 ± 0.34s vs. XAF-1407 0.1 ± 0.09s p = 0.049) were shorter in XAF-1407 treated rats. Drops in oxygen saturation or applied INAP were comparable in control and XAF-1407 rats. Conclusion Short-term simulated OSA is associated with AF-related arrhythmogenic changes, which could be prevented by pharmacological IK,ACh inhibition. Moreover, the cumulative negative airway pressure applied determined aERP shortening and may represent a target for OSA treatment. These findings have important implications for the antiarrhythmic management of AF patients with OSA.

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