Enhanced Ventilatory Response to Exercise in Patients With Chronic Heart Failure and Central Sleep Apnea

Arzt, Michael; Harth, Marion; Luchner, Andreas; Muders, Frank; Holmer, Stephan; Blumberg, Friedrich C.; Riegger, Günter A.J.; Pfeifer, Michael

doi:10.1161/01.cir.0000065227.04025.c2

Cited by 90 publications

(66 citation statements)

References 40 publications

(48 reference statements)

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“…One reason for this could be that, after AMI, patients did not report daytime hypersomnolence. This finding is in accordance with previous reports demonstrating a dissociation of sleep apnoea from hypersomnolence in patients with cardiovascular disease such as HF and stroke [29][30][31]. Furthermore, in the present study, both groups have poor sleep efficiency, similar to previous studies of patients with chronic HF [30].…”

Section: Sleep-related Disorders S Buchner Et Alsupporting

confidence: 94%

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: 94%

Natural course of sleep-disordered breathing after acute myocardial infarction

et al. 2012

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“…CSA events may also originate from unstable breathing control arising from the sleep-awake transition, as well as from cardiac or neurogenic causes (Naughton et al 1993). Periodic breathing patterns in patients with heart failure have been considered to be induced by instability of chemical control during sleep (Arzt et al 2003, Dempsey et al 2004. Unstable plant gain and controller gain cause a reduction in arterial CO 2 (PaCO 2 ) to a level below the apneic threshold, thereby resulting in central apnea.…”

Section: Discussionmentioning

confidence: 99%

Prevalence of Complex Sleep Apnea Among Japanese Patients with Sleep Apnea Syndrome

Endo

Suzuki

Inoue

et al. 2008

Tohoku J. Exp. Med.

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Sleep apnea syndrome (SAS) is basically divided into two types: obstructive and central SAS. Recently, the concept of complex SAS has been advocated. Complex SAS is defined as SAS that initially manifests as primarily obstructive SAS, but is characterized by the frequent central apneas after the removal of upper airway obstruction. To determine the prevalence and clinical significance of complex SAS among Japanese patients with SAS, 1,312 patients with SAS were enrolled in this study. Diagnosis of central SAS was made based on diagnostic polysomnography, and differentiation of obstructive SAS from complex SAS was made from polysomnographic findings for treatment with continuous positive airway pressure, which resolved upper airway obstruction. As a result, obstructive SAS was found in 1,232 of 1,312 patients with SAS (93.9%) and central SAS was found in 14 patients (1.1%). The overall prevalence of complex SAS was 5.0% (n = 66). The prevalence of complex SAS among 1,218 male and 94 female patients with SAS were 5.3% and 1.1%, respectively. Patients with complex SAS had significantly higher apnea/ hypopnea indices than patients with either obstructive or central SAS, but were similar in both mean age and average body mass index to obstructive SAS patients. There were no significant between-group differences in numbers of patients with clinical complications including hypertension, cardiac diseases, or cerebrovascular diseases. In conclusion, the prevalence of complex SAS in Japanese SAS patients is 5.0%, which is lower than previously reported prevalence of complex SAS in the USA and Australia. obstructive sleep apnea syndrome; central sleep apnea syndrome; hypertension; cardiac disease; cerebrovascular disease.

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“…However, in the present study, we found that severity of sleep apnea does not correlate with the novel indexes of CPX in cardiac patients with CSA. Although a ventilatory hypersensitivity to PaCO 2 is considered to be one of the key mechanisms for CSA, 24) the severity of sleep apnea did not correlate with the VE/VCO 2 slope obtained from CPX, which is considered to reflect central chemosensitivity to CO 2 . 25) Although PETCO 2 both at rest and at peak exercise, a parameter reflecting PaCO 2 , significantly correlated with the indexes of cardiopulmonary exercise testing, it did not correlate with the severity of sleep apnea.…”

Section: Discussionmentioning

confidence: 88%

“…Hypopnea was defined as a > 50% reduction of airflow or thoracoabdominal excursions lasting ≥ 10 seconds along with a ≥ 3% drop in pulse oximetric saturation. [22][23][24] CSA was defined as a cessation of thoracoabdominal excursions. OSA was defined when nasal airflow was absent despite the presence of thoracoabdominal excursions.…”

Section: )mentioning

confidence: 99%

Does the Severity of Central Sleep Apnea Correlate With Respiratory Gas Indexes During Cardiopulmonary Exercise Testing?

et al. 2006

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SUMMARYCentral sleep apnea (CSA) is thought to arise as a consequence of chronic heart failure. We have attempted to determine the relationship between the severity of CSA and the respiratory gas indexes during cardiopulmonary exercise testing (CPX), indexes wellknown to reflect the severity of heart failure. Twenty consecutive cardiac patients (59.0 ± 15.3 years) with CSA underwent CPX. End-tidal PCO 2 (PETCO 2 ) was measured at rest and at peak exercise as a substitute for PaCO 2 , along with the peak oxygen uptake (VO 2 ) and the ratio of the increase in ventilation to the increase in CO 2 output (VE/VCO 2 slope). Peak VO 2 , % peak VO 2 , and the VE/VCO 2 slope of the subjects were 15.5 ± 5.8 mL/min/ kg, 52.8 ± 16.7%, and 37.9 ± 12.5, respectively, showing moderate to severely decreased exercise capacity. While PETCO 2 at both rest and peak exercise significantly correlated with peak VO 2 (r = 0.63 and r = 0.51, respectively) and the VE/VCO 2 slope (r = -0.77 and r = -0.91, respectively), none of these 3 parameters correlated with the apnea-hypopnea index. The apnea-hypopnea index in the subjects with lower resting PETCO 2 was not notably different from that in the subjects with relatively high PETCO 2 .Although the severity of CSA is assumed to correlate with the severity of heart failure, and a lowering of PaCO 2 during wakefulness is considered to be one of the mechanisms behind CSA, the severity of CSA does not correlate with the respiratory gas indexes of CPX or the level of PETCO 2 in cardiac patients with moderate to severely decreased exercise capacity. (Int Heart J 2006; 47: 889-900)

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Enhanced Ventilatory Response to Exercise in Patients With Chronic Heart Failure and Central Sleep Apnea

Cited by 90 publications

References 40 publications

Natural course of sleep-disordered breathing after acute myocardial infarction

Natural course of sleep-disordered breathing after acute myocardial infarction

Prevalence of Complex Sleep Apnea Among Japanese Patients with Sleep Apnea Syndrome

Does the Severity of Central Sleep Apnea Correlate With Respiratory Gas Indexes During Cardiopulmonary Exercise Testing?

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