The impact of sleep disordered breathing on cardiac troponin in acutely decompensated heart failure.

PURPOSE: Sleep disordered breathing in decompensated heart failure has physiological consequences (e.g., intermittent hypoxemia) that may predispose to subclinical myocardial injury, yet a temporal relationship between sleep apnea and troponin elevation has not been established. METHODS: We assessed the feasibility of performing respiratory polygraphy and measuring overnight high-sensitivity cardiac troponin T change in adults admitted to the hospital with acutely decompensated heart failure. Repeat sleep apnea tests (SATs) were performed to determine response to optimal medical heart failure therapy. Multivariable logistic regression was used to identify associations between absolute overnight troponin change and sleep apnea characteristics. RESULTS: Among the 19 subjects with acutely decompensated heart failure, 92% of SATs demonstrated sleep disordered breathing (apnea-hypopnea index [AHI] > 5 events/h). For those with repeat SATs, AHI increased in 67% despite medical management of heart failure. Overnight troponin increase was associated with moderate to severe sleep apnea (vs. no to mild sleep apnea, odds ratio (OR = 18.4 [1.51-224.18]), central apnea index (OR = 1.11 [1.01-1.22]), and predominantly central sleep apnea (vs. obstructive, OR = 22.9 [1.29-406.32]). CONCLUSIONS: Sleep apnea severity and a central apnea pattern may be associated with myocardial injury. Respiratory polygraphy with serial biomarker assessment is feasible in this population, and combining this approach with interventions (e.g., positive airway pressure) may help establish if a link exists between sleep apnea and subclinical myocardial injury.

Addition of frontal EEG to adult home sleep apnea testing: does a more accurate determination of sleep time make a difference?

RATIONALE: Home sleep apnea testing (HSAT) typically does not include electroencephalogram (EEG) monitoring for sleep assessment. In patients with insomnia and low sleep efficiency, overestimation of the sleep period can result from absence of EEG, which will reduce sleep disordered breathing (SDB) indices and may lead to a false-negative result. OBJECTIVE: To validate a single channel frontal EEG for scoring sleep versus wake against full EEG during polysomnography, and then to examine the utility of adding this single channel EEG to standard HSAT to prevent false-negative results. METHODS: Epoch-by-epoch validation for sleep scoring of single channel EEG versus full PSG was first performed in 21 subjects. This was followed by a separate retrospective analysis of 207 consecutive HSATs in adults performed in a university-affiliated sleep center using the Somte (Compumedics) HSAT with one frontal EEG as well as chin EMG, nasal airflow, oxyhemoglobin saturation, respiratory effort, pulse rate, and body position. Each study was scored twice, with (HSATEEG) and without the EEG signal visible (HSATPolygraphy), to calculate AHI4 and RDI and the effect on OSA diagnosis and severity. Analyses were repeated in 69 patients with poor sleep suggesting insomnia plus Epworth Sleepiness Scale < 7 as well as in 38 patients ultimately shown to have sleep efficiency < 70% on HSAT with EEG. MEASUREMENTS AND MAIN RESULTS: Single channel and full EEG during polysomnography agreed on sleep versus wake in 92-95% of all epochs. HSAT without EEG overestimated the sleep period by 20% (VST = 440 ± 76 min vs TST = 356 ± 82 min), had a false-negative rate of 8% by AHI4 criteria, and underestimated disease severity in 11% of all patients. Sub-group analysis of patients with subjective poor sleep suggesting insomnia did not change the results. Patients later shown to have low sleep efficiency had lower SDB indices and a 20.8% false negative rate of sleep apnea diagnosis. CONCLUSIONS: Although overall false negative rates using HSATPolygraphy were moderate, suggesting utility for ruling out OSA, there was a specific subgroup in whom there were significant missed diagnoses. However, we were unable to identify this subgroup a priori.