The Prognostic Role of Polysomnography Parameters in Heart Failure Patients with Previous Decompensation.

Background: Sleep-disordered breathing (SDB) is a widespread comorbidity in patients with chronic heart failure (HF) and may have a deleterious effect on the pathogenesis of HF. We aimed to evaluate the prognostic role of polysomnography parameters in HF patients with previous decompensation. Methods: 123 patients were included in the prospective cohort study. In addition to the standard examination, all patients underwent polysomnography (PSG). Results: The Kaplan−Meier analysis showed the incidence of the combined endpoint differs between LVEF categories ≤25.5% vs. >25.5% (χ2 = 9.6, log rank p = 0.002), NTpro-BNP > 680 vs. ≤680 pg/mL (χ2 = 12.7, log rank p = 0.001), VO2peak categories <16 vs. ≥16 mL/min/kg (χ2 = 14.2, log rank p = 0.001), VE/VCO2 slope ≥38.5 vs. <38.5 (χ2 = 14.5, log rank p = 0.001), wake after sleep onset >40 min vs. ≤40 min (χ2 = 9.7, log rank p = 0.03), and sleep stage 2 (S2) <44% vs. ≥44% (χ2 = 12.4, log rank p = 0.001). Conclusion: Among the PSG parameters, WASO > 40 min and S2 < 44% were associated with a combined endpoint in patients with previous decompensation of HF. Moreover, higher NT-proBNP and VE/VCO2 slope, lower LVEF, and VO2peak were also independent factors of a poor prognosis.

A new algorithm for optimization of rate-adaptive pacing improves exercise tolerance in patients with HFpEF.

AIM: To develop an algorithm for optimization of rate-adaptive pacing settings in heart failure patients with preserved ejection fraction (HFpEF) and permanent cardiac pacing. METHODS: This is a prospective randomized controlled study. A total of 54 patients with HFpEF, permanent atrial fibrillation (AF), and VVIR pacing were randomized to an intervention group with optimization of rate-adaptation parameters by using cardiopulmonary exercise testing (CPET) and pacemaker stress echocardiography (PASE), and to a control group with conventional programming. CPET, 6-min walk test (6-mwt), echocardiography (echo), Duke Activity Status Index (DASI), and Minnesota questionnaire (MLHFQ) were performed at baseline and after 3 months. PASE was used to exclude exercise-induced ischemia and to determine safe upper sensor rate. Pacing parameters were corrected to achieve optimal heart rate increments of 3-6 bpm for 1 mL/min/kg of VO2 (oxygen uptake). RESULTS: After 3 months, the intervention group demonstrated significant improvement of VO2 peak by 1.64 ± 1.6 mL/min/kg, anaerobic threshold by 1.33 ± 1.3 mL/min/kg, exercise time by 170 ± 98 s, 6-mwt distance by 75 ± 63 m (P < .0001 for all), DASI by 5.23 points (P = .009), MLHFQ-score (reduction by 9 points, P < .0001), and echo parameters (decrease in LA volume from 108 (84; 132) to 95 (85; 130) mL, P = .026; E/e' from 11.7 ± 3.2 to 10.4 ± 2.9, P = .025; systolic pulmonary artery pressure (SPAP) from 44 ± 14 to 39 ± 12 mm Hg, P = .001) compared to the control group. CONCLUSION: An algorithm incorporating CPET and PASE for optimal programming of rate-adaptation parameters is a valuable tool to improve exercise capacity in HFpEF patients with permanent AF and VVIR pacing who remain exercise intolerant after conventional programming.

Is Mixed Apnea Associated with Non-Rapid Eye Movement Sleep a Reversible Compensatory Sign of Heart Failure?

BACKGROUND: Sleep-disordered breathing is common in heart failure (HF), and prolonged circulation time and diminished pulmonary volume are considered the main possible causes of sleep apnea in these patients. However, the impact and interrelation between sleep apnea and HF development are unclear. We report the case of a patient with complete elimination of non-rapid-eye-movement (NREM) sleep-associated mixed apnea in HF after heart transplantation. CASE REPORT: After unsuccessful 12-month conventional treatment with abrupt exacerbation of biventricular HF IV class (according to New York Heart Association Functional Classification), a 26-year-old man was admitted to the hospital. Based on a comprehensive examination including endomyocardial biopsy, dilated cardiomyopathy was diagnosed. Heart transplantation was considered the only possible treatment strategy. Polysomnography showed severe NREM sleep-associated mixed sleep apnea [apnea-hypopnea index 43/h, in rapid eye movement (REM) sleep 3.7/h, in NREM sleep 56.4/h, mean SatO2 93.9%], and periodic breathing. One-month post-transplantation polysomnography did not show sleep-disordered breathing (apnea-hypopnea index 1.0/h; in REM sleep - 2.8/h, in NREM sleep 0.5/h, mean SatO2 97.5%). The patient was discharged from the hospital in improved condition. CONCLUSIONS: NREM sleep-associated mixed apnea occurring in severe systolic HF due to dilated cardiomyopathy might be reversible in case of successful HF treatment. We suggest that mixed sleep apnea strongly associated with NREM sleep occurs in HF, when the brain centers regulating ventilation are intact, and successful HF compensation might be highly effective regarding sleep-breathing disorders without non-invasive ventilation. This is important to know, especially with regard to the recently published data of potentially unfavorable effects of adaptive servoventilation in systolic HF, and the lack of other treatment options.