Portable recording for detecting sleep disorder breathing in patients under the care of a heart failure clinic.

BACKGROUND: Sleep disordered breathing (SDB) has important clinical implications in patients with congestive heart failure (CHF). We performed portable recording in unselected CHF patients on contemporary therapy. Data on the interactions of SDB in patients supervised at heart failure clinics are rare and we illustrate diversities of obstructive sleep apnoea (OSA) and central sleep apnoea (CSA). METHODS: We studied 176 consecutive subjects on contemporary medical therapy with a median left ventricular ejection fraction of 25.0 % (range 7-35%) and median NT-pro BNP levels of 3,413.0 pg/ml (range 305.1-35,000.0 pg/ml). Participants underwent prospective overnight portable recording. RESULTS: 50% presented with an at least moderate form of nocturnal breathing disorder [apnoea-hypopnoea index (AHI) ≥15/h]. Only 15 patients (17.1%) with AHI ≥15/h reported excessive daytime sleepiness. Irrespective of left ventricular ejection fraction, patients with CSA had higher levels of NT-pro BNP compared to patients with OSA (differences in medians = 2,639.0 pg/ml, p = 0.016), and compared to patients with an AHI <15/h (differences in medians = 2,710.0 pg/ml, p < 0.001). OSA affected 26 patients (14.8%). CONCLUSIONS: Patients with severe stable CHF on contemporary therapy have a prevalence of 50.0% of moderate to severe SDB. The natural cascade of the failing heart is initially characterised by absent SDB or OSA, whereas end-stage CHF is associated with CSA.

Pinacidil-primed ATP-sensitive potassium channels mediate feedback control of mechanical power output in isolated myocardium of rats and guinea pigs.

We tested the hypothesis, that ATP-sensitive potassium (K(ATP)) channels limit cardiac energy demand by a feedback control of mean power output at increased cardiac rates. We analysed the interrelationships between rising energy demand of adult rat and guinea pig left ventricular papillary muscle and down-regulatory electromechanical effects mediated by K(ATP) channels. Using the K(ATP)-opener pinacidil the stimulation frequency was increased stepwise and the mechanical parameters and action potentials were recorded. Power output was derived from force-length area or force-time integral calculations, respectively. Simultaneously oxygen availability in the preparations was estimated by flavoprotein fluorescence measurements. ADP/ATP ratios were determined by HPLC. We found highly linear relationships between isotonic power output and the effects of pinacidil on isotonic shortening in both rat (r(2)=0.993) and guinea pig muscles (r(2)=0.997). These effects were solely observed for the descending limb of shortening-frequency relationships. In addition, a highly linear correlation between total force-time integral-derived power and pinacidil effects on action potential duration (APD(50), r(2)=0.92) was revealed. Power output became constant and frequency-independent in the presence of pinacidil at higher frequencies. In contrast, the K(ATP)-blocker glibenclamide produced a lengthening of APD(50) and increased force transiently at higher power levels. Pinacidil prevented core hypoxia and a change in ADP/ATP ratio during high frequency stimulation. We conclude, that pinacidil-primed cardiac K(ATP) channels homeostatically control power output during periods of high energy demand. This effect is associated with a reduced development of hypoxic areas inside the heart muscle by adapting cardiac function to a limited energy supply.