Obstructive sleep apnoea inhibits the recovery of left ventricular function in patients with acute myocardial infarction

Nakashima, Hiroshi; Katayama, Toshiro; Takagi, Chisa; Amenomori, Kentarou; Ishizaki, Masahiko; Honda, Yukiharu; Suzuki, Shin

doi:10.1093/eurheartj/ehl219

Cited by 106 publications

(78 citation statements)

References 35 publications

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“…The prevalence of sleep apnoea in the acute phase after a first AMI in the current study is confirmed by several previous studies [5,6,[25][26][27]. NAKASHIMA et al [6] and YUMINO et al [25] performed their sleep studies between 14-21 days after primary PCI, whereas other previous studies used a similar time-point to the present study to assess sleep apnoea at baseline (,5 days after AMI) [5,26,28].…”

Section: Sleep-related Disorders S Buchner Et Alsupporting

confidence: 86%

“…1) Sleep apnoea may contribute to the progression of HF by exposing the heart to intermittent hypoxia, increased pre-load and afterload, sympathetic activation and vascular endothelial dysfunction. For example, in a previous observational study the presence of sleep apnoea early after AMI was linked to impaired recovery of cardiac function [6]. Ultimately, both OSA and CSA confer an increased mortality risk in patients with chronic HF [7][8][9].…”

mentioning

confidence: 95%

“…acute myocardial infarction (AMI) [4][5][6]. The interactions between sleep apnoea and heart failure (HF) are bi-directional.…”

mentioning

confidence: 99%

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Natural course of sleep-disordered breathing after acute myocardial infarction

et al. 2012

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The aim of this study was to test whether an improvement of left ventricular ejection fraction (EF) in the early phase after acute myocardial infarction is associated with a reduction of the severity of central and obstructive sleep apnoea.40 consecutive patients with acute myocardial infarction underwent polysomnography and cardiovascular magnetic resonance imaging within 5 days and 12 weeks after the event to assess sleep apnoea and cardiac function. We stratified the sample in patients who improved their left ventricular EF within 12 weeks by o5% (improved EF group, DEF 9¡1%, n516) and in those who did not (unchanged EF group, DEF -1¡1%, n524).Prevalence of sleep apnoea (o15 apnoea and hypopnoea events?h -1 ) within f5 days after myocardial infarction was 55%. Apnoea and hypopnoea events?h -1 were significantly more reduced in the improved EF group compared with the unchanged EF group (-10¡3 versus 1¡3 events?h -1 ; p50.036). This reduction was based on a significant alleviation of obstructive events (-7¡2 versus 4¡3 events?h -1 ; p50.009), while the reduction of central events was similar between groups (p50.906).An improvement of cardiac function early after myocardial infarction is associated with an alleviation of sleep apnoea. This finding suggests that re-evaluation of treatment indication for sleep apnoea is needed when a change in cardiac function occurs.

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Section: Sleep-related Disorders S Buchner Et Alsupporting

confidence: 86%

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confidence: 95%

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Natural course of sleep-disordered breathing after acute myocardial infarction

et al. 2012

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“…After the first acute myocardial infarction, 65.7% of patients had an apnea-hypopnea index ≥ 15/h 35 . In other studies, the prevalence of OSA in patients with artery heart disease ranged from 43 to 66.4% 36,37,38,39 . The prevalence of a high risk of coronary artery disease associated with OSA in our survey was within these estimates.…”

Section: Discussionmentioning

confidence: 75%

Obstructive sleep apnea, detected by the Berlin Questionnaire: an associated risk factor for coronary artery disease

et al. 2012

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Obstructive sleep apnea (OSA), a risk factor for coronary artery disease, remains under diagnosed. We investigated if OSA identified by the Berlin Questionnaire (BQ) is associated with the risk of coronary artery disease. Cases were patients referred for elective coronariography. The cases were classified with significant coronary lesions (stenosis > 50% in an epicardial coronary) or without significant coronary lesions. Controls were selected from a population-based sample. Positive BQ results were identified in 135 (41.2%) of 328 cases, in contrast with 151 (34.4%) of 439 control subjects (p = 0.03). In a multinomial logistic analysis, the risk for OSA identified by the BQ was independently associated with coronary artery disease in cases with lesions of at least 50% (OR = 1.53; 95%CI: 1.02-2.30; p = 0.04). The risk from OSA identified by the BQ was higher in younger subjects (40-59 years) (OR = 1.76; 95%CI: 1.05-2.97; p = 0.03) and in women (OR = 3.56; 95%CI: 1.64-7.72; p = 0.001). In conclusion, OSA identified by the BQ greatly increases the risks of coronary artery disease in patients having significant coronary artery lesions indicated by anangiogram, particularly in younger individuals and in women.

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“…To date diagnosis or treatment of sleep apnoea is not part of the recommended or standard care of patients early after acute myocardial infarction [6]. Since sleep apnoea is associated with increased cardiac workload [7] and myocardial damage [8] in the early phase after myocardial infarction, intervention trials are warranted to assess the safety and efficacy of PAP treatment in this time period. @ERSpublications Recovery of left ventricular function after acute myocardial infarction leads to attenuation of sleep apnoea http://ow.ly/kslug…”

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confidence: 99%

Recovery of left ventricular function and sleep apnoea after acute myocardial infarction

2013

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Obstructive sleep apnoea inhibits the recovery of left ventricular function in patients with acute myocardial infarction

Abstract: The novel finding is that OSA may inhibit the recovery of LV function in patients with AMI.

Cited by 106 publications

References 35 publications

Natural course of sleep-disordered breathing after acute myocardial infarction

Natural course of sleep-disordered breathing after acute myocardial infarction

Obstructive sleep apnea, detected by the Berlin Questionnaire: an associated risk factor for coronary artery disease

Recovery of left ventricular function and sleep apnoea after acute myocardial infarction

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