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Adaptive servoventilation improves cardiac function and respiratory stability

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      Abstract

      Cheyne–Stokes respiration (CSR) in patients with chronic heart failure (CHF) is of major prognostic impact and expresses respiratory instability. Other parameters are daytime pCO2, VE/VCO2-slope during exercise, exertional oscillatory ventilation (EOV), and increased sensitivity of central CO2 receptors. Adaptive servoventilation (ASV) was introduced to specifically treat CSR in CHF. Aim of this study was to investigate ASV effects on CSR, cardiac function, and respiratory stability. A total of 105 patients with CHF (NYHA ≥ II, left ventricular ejection fraction (EF) ≤ 40%) and CSR (apnoea–hypopnoea index ≥ 15/h) met inclusion criteria. According to adherence to ASV treatment (follow-up of 6.7 ± 3.2 months) this group was divided into controls (rejection of ASV treatment or usage <50% of nights possible and/or <4 h/night; n = 59) and ASV (n = 56) adhered patients. In the ASV group, ventilator therapy was able to effectively treat CSR. In contrast to controls, NYHA class, EF, oxygen uptake, 6-min walking distance, and NT-proBNP improved significantly. Moreover, exclusively in these patients pCO2, VE/VCO2-slope during exercise, EOV, and central CO2 receptor sensitivity improved. In CHF patients with CSR, ASV might be able to improve parameters of SDB, cardiac function, and respiratory stability.

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      Most cited references 36

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      The six-minute walk test.

       P Enright (2003)
      The American Thoracic Society has issued guidelines for the 6-minute walk test (6MWT). The 6MWT is safer, easier to administer, better tolerated, and better reflects activities of daily living than other walk tests (such as the shuttle walk test). The primary measurement is 6-min walk distance (6MWD), but during the 6MWT data can also be collected about the patient's blood oxygen saturation and perception of dyspnea during exertion. When conducting the 6MWT do not walk with the patient and do not assist the patient in carrying or pulling his or her supplemental oxygen. The patient should walk alone, not with other patients. Do not use a treadmill on which the patient adjusts the speed and/or the slope. Do not use an oval or circular track. Use standardized phrases while speaking to the patient, because your encouragement and enthusiasm can make a difference of up to 30% in the 6MWD. Count the laps with a lap counter. If the 6MWD is low, thoroughly search for the cause(s) of the impairment. Better 6MWD reference equations will be published in the future, so be sure you are using the best available reference equations.
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        Sympathetic nervous system activation in human heart failure: clinical implications of an updated model.

        Disturbances in cardiovascular neural regulation, influencing both disease course and survival, progress as heart failure worsens. Heart failure due to left ventricular systolic dysfunction has long been considered a state of generalized sympathetic activation, itself a reflex response to alterations in cardiac and peripheral hemodynamics that is initially appropriate, but ultimately pathological. Because arterial baroreceptor reflex vagal control of heart rate is impaired early in heart failure, a parallel reduction in its reflex buffering of sympathetic outflow has been assumed. However, it is now recognized that: 1) the time course and magnitude of sympathetic activation are target organ-specific, not generalized, and independent of ventricular systolic function; and 2) human heart failure is characterized by rapidly responsive arterial baroreflex regulation of muscle sympathetic nerve activity (MSNA), attenuated cardiopulmonary reflex modulation of MSNA, a cardiac sympathoexcitatory reflex related to increased cardiopulmonary filling pressure, and by individual variation in nonbaroreflex-mediated sympathoexcitatory mechanisms, including coexisting sleep apnea, myocardial ischemia, obesity, and reflexes from exercising muscle. Thus, sympathetic activation in the setting of impaired systolic function reflects the net balance and interaction between appropriate reflex compensatory responses to impaired systolic function and excitatory stimuli that elicit adrenergic responses in excess of homeostatic requirements. Recent observations have been incorporated into an updated model of cardiovascular neural regulation in chronic heart failure due to ventricular systolic dysfunction, with implications for the clinical evaluation of patients, application of current treatment, and development of new therapies.
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          Influence of ejection fraction on cardiovascular outcomes in a broad spectrum of heart failure patients.

          Left ventricular function is a principal determinant of cardiovascular risk in patients with heart failure. The growing number of patients with preserved systolic function heart failure underscores the importance of understanding the relationship between ejection fraction and risk. We studied 7599 patients with a broad spectrum of symptomatic heart failure enrolled in the Candesartan in Heart failure: Assessment of Reduction in Mortality and morbidity (CHARM) Program. All patients were randomized to candesartan at a target dose of 32 mg once daily or matching placebo and followed up for a median of 38 months. We related left ventricular ejection fraction (LVEF), measured before randomization at the sites, to cardiovascular outcomes and causes of death. Mean LVEF in patients enrolled in CHARM was 38.8+/-14.9% (median LVEF 36%). Patients with lower LVEF tended to have higher baseline New York Heart Association class. The hazard ratio for all-cause mortality increased by 39% for every 10% reduction in ejection fraction below 45% (hazard ratio 1.39, 95% CI 1.32 to 1.46), with adjustment for baseline covariates. All-cause mortality, cardiovascular death, and all components of cardiovascular death declined with increasing ejection fraction until an ejection fraction of 45%, after which the risk of these outcomes remained relatively stable with increasing LVEF. The absolute change in rate per 100 patient-years for each 10% reduction in LVEF was greatest for sudden death and heart failure-related death. The effect of candesartan in reducing cardiovascular outcomes was consistent across LVEF categories. LVEF is a powerful predictor of cardiovascular outcome in heart failure patients across a broad spectrum of ventricular function. Nevertheless, once elevated to a range above 45%, ejection fraction does not further contribute to assessment of cardiovascular risk in heart failure patients.
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            Author and article information

            Affiliations
            [1 ]Department of Cardiology, Heart and Diabetes Centre North Rhine Westphalia, University Hospital, Ruhr University Bochum, Georgstrasse 11, 32545 Bad Oeynhausen, Germany
            [2 ]Cardiac Research Unit, Heart and Diabetes Centre North Rhine Westphalia, Ruhr University Bochum, Bad Oeynhausen, Germany
            [3 ]Department of Business Administration and Economics, University of Bielefeld, Bielefeld, Germany
            Contributors
            +49-5731-971258 , +49-5731-972194 , akleemeyer@hdz-nrw.de
            Journal
            Clin Res Cardiol
            Clinical Research in Cardiology
            Springer-Verlag (Berlin/Heidelberg )
            1861-0684
            1861-0692
            12 September 2010
            12 September 2010
            February 2011
            : 100
            : 2
            : 107-115
            3033509
            20835903
            216
            10.1007/s00392-010-0216-9
            © Springer-Verlag 2010
            Categories
            Original Paper
            Custom metadata
            © Springer-Verlag 2011

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