The Relationship Between Obstructive Sleep Apnea Hypopnea Syndrome and Inflammatory Markers and Quality of Life in Subjects With Acute Coronary Syndrome

Abstract

BACKGROUND: The objective of this work was to examine the relationship between obstructive sleep apnea (OSA) and inflammatory markers and quality of life in patients with acute coronary syndrome, especially undergoing percutaneous coronary intervention. METHODS: One hundred eighteen subjects were admitted with acute coronary syndrome over 1 y who had symptoms of OSA and positive polysomnography on admission. Of these subjects, 53 underwent primary percutaneous coronary intervention during their admission, and 65 had medical management. We then compared inflammatory markers by OSA status. We also assessed cardiac symptoms using the Seattle Angina Questionnaire and sleep symptoms using the Epworth Sleepiness Scale. RESULTS: Subjects in the percutaneous coronary intervention group had a higher oxygen desaturation index (ODI) (P ‫؍‬ .02) and apnea-hypopnea index (AHI) (P ‫؍‬ .048) compared with those in the medical management group. In percutaneous coronary intervention subjects, the moderate-severe OSA group (AHI > 15/h) had a higher hematocrit (P ‫؍‬ .047), homocysteine (P ‫؍‬ .01), and highsensitivity C-reactive protein (P ‫؍‬ .045) compared with those with no or mild OSA (AHI < 15/h). There was a significant correlation between high-sensitivity C-reactive protein and both AHI (r ‫؍‬ 0.46, P ‫؍‬ .001) and ODI (r ‫؍‬ 0.47, P < .001). Those with moderate-severe OSA had higher Epworth Sleepiness Scale (P ‫؍‬ .002), greater physical limitation (P ‫؍‬ .01), and lower treatment satisfaction and disease perception (P ‫؍‬ .007), as judged by subscales of the Seattle Angina Questionnaire, compared with those with no or mild OSA. Finally, subjects undergoing percutaneous coronary intervention with lower AHI (r ‫؍‬ 0.48, P < .001) and ODI (r ‫؍‬ 0.49, P < .001) reported higher treatment satisfaction. CONCLUSIONS: Subjects with acute coronary syndrome undergoing percutaneous coronary intervention who had moderate-severe OSA showed higher levels of inflammatory mediators and lower treatment satisfaction and disease perception. These factors may increase the risk of adverse sequelae by increasing the systemic inflammatory response.

Plasma Homocysteine and Autonomic Nervous Dysfunction: Association and Clinical Relevance in OSAS

“…Similarly, a previous study demonstrated an association between homocysteine and OSAS severity in males [18]. Consistently, subjects with acute coronary syndrome in the moderate-severe OSAS group had a higher homocysteine compared with those with no or mild OSAS [19]. Although the exact mechanism remains…”

“…Similarly, a previous study demonstrated an association between homocysteine and OSAS severity in males [ 18 ]. Consistently, subjects with acute coronary syndrome in the moderate-severe OSAS group had a higher homocysteine compared with those with no or mild OSAS [ 19 ]. Although the exact mechanism remains incompletely clarified, another study has also demonstrated that the severity of OSAS is significantly associated with an elevated level of homocysteine in ischemic stroke patients [ 20 ].…”

Resistance Training Improves Sleep and Anti-Inflammatory Parameters in Sarcopenic Older Adults: A Randomized Controlled Trial

“…Furthermore, this immune cascade also activates phagocytic cells, such as neutrophils, monocytes, and macrophages, which can also increase the production of these inflammatory cytokines [ 61 , 62 ]. IL-1, in particular, has been postulated as an important somnogenic factor [ 63 ] associated with poor sleep, increased sleep latency, daytime sleepiness, fatigue [ 64 , 65 , 66 ], and obstructive sleep apnea syndrome [ 67 ]. In addition, IL-1 is associated with circadian disruption [ 63 ] and skeletal muscle reduction [ 68 ].…”

Mean apnea–hypopnea duration (but not apnea–hypopnea index) is associated with worse hypertension in patients with obstructive sleep apnea

“…In the long-term, the sleep fragmentation in OSA elicits events such as constriction of blood vessels due to increased sympathetic activity and the severer nocturnal hypoxaemia of OSA. Longer MAD also triggers systemic inflammation [17,27] and metabolic dysregulation, [28] which can lead to short-term and long-term rises in arterial blood pressure eventually leading to chronic hypertension. [29] …”