Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Central sleep apnoea (CSA) is highly prevalent in the evolutionary course of chronic heart failure. Such a ventilatory pattern during sleep is independently associated with poor prognosis in people with congestive heart failure. Chronic hyperventilation and daytime hypocapnia are the main mechanisms underlying the frequent association between CSA and cardiac failure. Simplified diagnostic strategies allowing easier recognition of CSA among people with severe heart failure are obviously needed but remain to be validated. Treatment of CSA is essentially aimed at improving cardiac function. When CSA persists, after appropriate adjustment of medication and resynchronisation therapy when indicated, specific ventilatory support during sleep should be considered. Continuous positive airway pressure (CPAP), oxygen, adaptive Servo-ventilation (ASV) and non-invasive ventilation have been proposed. Large randomised trials demonstrating survival and time free from heart transplantation are lacking.
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PMID:Cheyne-Stokes respiration with central sleep apnoea in chronic heart failure: proposals for a diagnostic and therapeutic strategy. 1637 89

Central 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 well-known 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 (V(.)O(2)) and the ratio of the increase in ventilation to the increase in CO(2)output (V(.)E/V(.)CO(2) slope). Peak VO(2), % peak VO(2), and the VE/V(.)CO(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/V(.)CO(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.
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PMID:Does the severity of central sleep apnea correlate with respiratory gas indexes during cardiopulmonary exercise testing? 1726 23

Cheyne-Stokes respiration with central sleep apnea (CSR-CSA) is a form of periodic breathing, commonly observed in patients with heart failure (HF), in which central apneas alternate with hyperpneas that have a waxing-waning pattern of tidal volume. Uniform criteria by which to diagnose a clinically significant degree of CSR-CSA have yet to be established. CSR-CSA is caused by respiratory control system instability characterized by a tendency to hyperventilate. Central apnea occurs when Pa(CO(2)) falls below the threshold for apnea during sleep due to ventilatory overshoot. Patients with CSR-CSA are generally hypocapnic, with a Pa(CO(2)) closer than normal to the apneic threshold such that even slight augmentation in ventilation drives Pa(CO(2)) below threshold and triggers apnea. Factors contributing to hyperventilation in HF include stimulation of pulmonary irritant receptors by pulmonary congestion, increased chemoreceptor sensitivity, reduced cerebrovascular blood flow, and recurrent arousals from sleep. Controversy remains as to whether CSR-CSA is simply a reflection of HF severity, or whether it exerts unique adverse effects on prognosis. The main adverse influence of CSR-CSA on cardiovascular function appears to be excessive sympathetic nervous system activity due to apnea-related hypoxia and arousals from sleep. A number of studies have examined the potential relationship between CSR-CSA and mortality in HF. Most reported that CSR-CSA was associated with an increased risk for mortality, but these studies were small. Further research is therefore needed to elucidate mechanisms which contribute to the pathogenesis of CSR-CSA, and to determine whether its treatment can reduce morbidity and mortality in patients with HF.
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PMID:Central sleep apnea and Cheyne-Stokes respiration. 1825 Feb 16

Central sleep apnoea (CSA) occurs in up to 40% of patients with chronic heart failure (CHF). It is thought to be a consequence of CHF and is associated with an accelerated decline in cardiac function, and increased morbidity and mortality. The optimal treatment of CSA remains unclear. Resolution of CSA has been reported after cardiac transplantation. We report the first case of resolution of CSA 10 months following implantation of a permanent Jarvik 2000 left ventricular assist device (LVAD). The correction of CSA after implantation of the LVAD was associated with improvements in symptoms, exercise capacity, renal function, and increased arterial carbon dioxide levels at rest during wakefulness and also reduction in brain natriuretic peptide.
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PMID:Resolution of central sleep apnoea following implantation of a left ventricular assist device. 1875 59

Chronic congestive heart failure is a highly prevalent and progressive disorder associated with excess morbidity and mortality; it has huge economic impact. Left heart failure may be systolic or may occur as isolated diastolic dysfunction. The diastolic form predominates in older people. Sleep disorders are frequent in both types. Most systematic studies have been performed in patients with systolic heart failure. Prospective studies show the presence of obstructive and central sleep apnea, periodic limb movements, and significant alterations in sleep architecture, characterized by poor efficiency, excess stage 1 and arousals, and lack of deep sleep. Both obstructive sleep apnea and central sleep apnea occur in patients with heart failure and have been shown to be associated with excess mortality. Obstructive sleep apnea is best treated with continuous positive airway pressure (CPAP) devices. Central sleep apnea is also best treated with CPAP, but only about 50% of the patients are considered responders. Survival improves when heart failure patients are effectively treated with CPAP for both central and obstructive sleep apnea. A new positive airway pressure device, a pressure support servo-ventilator, is the next best choice for heart failure patients whose central sleep apnea does not respond to CPAP. Nocturnal oxygen should be used for patients whose central sleep apnea does not respond to positive pressure devices. Both periodic limb movements and insomnia could have adverse hemodynamic consequences for the failing heart. There are no guidelines or long-term studies regarding treatment of these conditions in heart failure. For restless legs syndrome with or without periodic limb movements, pramipexole and ropinirole have been approved. Treatment of insomnia comorbid with heart failure depends on the cause. In the absence of any known cause, a trial of ramelteon is the first choice.
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PMID:Sleep dysfunction in heart failure. 1878 5

Obstructive sleep apnea (OSA) is present in at least 2% to 4% of the general population. Central sleep apnea (CSA), though less common, is highly prevalent in patients with heart failure. Both forms of sleep apnea exert strong modulatory effects on the autonomic nervous system at night through a number of mechanisms including central respiratory-cardiac coupling in the brainstem, chemoreflex stimulation, baroreflexes, and reflexes relating to lung inflation. Arousals also contribute to the autonomic disturbance. Although sleep is normally a time when parasympathetic modulation of the heart predominates and myocardial electrical stability is enhanced, OSA and CSA disturb this quiescence, creating an autonomic profile in which both profound vagal activity leading to bradyarrhythmias, and sympatho-excitation favoring ventricular ectopy are observed. The resulting tendency toward cardiac arrhythmia may directly contribute to sudden cardiac death and premature mortality in patients with sleep apnea. Therapy consists largely of treatment with continuous positive airway pressure, which has been shown to improve autonomic profile and reduce nocturnal arrhythmias.
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PMID:Sleep-disordered breathing: autonomic mechanisms and arrhythmias. 1911 Jan 34

Sleep plays a large role in patients with heart failure. In normal subjects, sleep is usually in a supine position with reduced sympathetic drive, elevated vagal tone and as such a relatively lower cardiac output and minute ventilation, allowing for recuperation. Patients with heart failure may not experience the same degree of autonomic activity change and the supine position may place a large strain on the pulmonary system. More than half of all heart failure patients have one of two types of sleep apnea: either obstructive or central sleep apnea. Some patients have both types. Obstructive sleep apnea is likely to be a cause of heart failure due to large negative intrathoracic pressures, apnea related hypoxemia and hypercapnia, terminated by an arousal and surge in systemic blood pressure associated with endothelial damage and resultant premature atherosclerosis. Reversal of obstructive sleep apnea improves blood pressure, systolic contraction and autonomic dysfunction however mortality studies are lacking. Central sleep apnea with Cheyne Stokes pattern of respiration (CSA-CSR) occurs as a result of increased central controller (brainstem driving ventilation) and plant (ventilation driving CO2) gain in the setting of a delayed feed back (i.e., low cardiac output). It is thought this type of apnea is a result of moderately to severely impaired cardiac function and is possibly indicative of high mortality. Treatment of CSA-CSR is best undertaken by treating the underlying cardiac condition which may include with medications, pacemakers, transplantation or continuous positive airway pressure (CPAP). In such patients CPAP exerts unique effects to assist cardiac function and reduce pulmonary edema. Whether CPAP improves survival in this heart failure population remains to be determined.
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PMID:Sleep in heart failure. 1911 Jan 35

Central sleep apnea is highly prevalent in association with heart failure, some neurological diseases and chronic opioids use. There are two main categories of central sleep apnea respectively related with different underlying conditions. Some hypocapnic patients exhibit respiratory control system instability and central apnea occurs when PaCO(2) falls below the threshold for apnea during sleep. The other group are patients with chronic hypercapnia mainly in the context of neuromuscular disorders or obesity hypoventilation syndrome. All these patients should be assessed by recording blood gases, polysomnography and ventilatory responses to CO(2). Cardiologic assessment should include pro-brain natriuretic factor (pro-BNP) and cardiac echography whereas neurological examination requires brain imaging and/or electromyography. Ventilatory supports used for treating central sleep apnea are non-invasive ventilation and servo-assisted ventilation in hypercapnic and hypocapnic patients respectively.
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PMID:[Management of central sleep apnea]. 1978 53

In patients with heart failure (HF), the predominant type of sleep apnoea can change over time in association with alterations in circulation time. The aim of this study was to determine whether, in some patients with HF, a spontaneous shift from mainly central (>50% central events) to mainly obstructive (>50% obstructive events) sleep apnoea (CSA and OSA, respectively) over time coincides with improvement in left ventricular ejection fraction (LVEF). Therefore, sleep studies and LVEFs of HF patients with CSA from the control arm of the Canadian Continuous Positive Airway Pressure for Patients with Central Sleep Apnea and Heart Failure (CANPAP) trial were examined to determine whether some converted to mainly OSA and, if so, whether this was associated with an increase in LVEF. Of 98 patients with follow-up sleep studies and LVEFs, 18 converted spontaneously to predominantly OSA. Compared with those in the nonconversion group, those in the conversion group had a significantly greater increase in the LVEF (2.8% versus -0.07%) and a significantly greater fall in the lung-to-ear circulation time (-7.6 s versus 0.6 s). In patients with HF, spontaneous conversion from predominantly CSA to OSA is associated with an improvement in left ventricular systolic function. Future studies will be necessary to further examine this relationship.
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PMID:Shift in sleep apnoea type in heart failure patients in the CANPAP trial. 2019 Mar 31

Chronic heart failure is a clinical syndrome with a high mortality and morbidity. Despite optimal therapy, five-year survival is still only 50%. Central sleep apnoea syndrome is seen in approximately 40% of patients with congestive heart failure. Sleep apnoea syndrome can be divided into two forms in these patients: obstructive sleep apnoea syndrome (OSAS) and central sleep apnoea syndrome (CSAS, Cheyne-Stokes respiration), of which CSAS is the most common. CSAS is a form of sleep apnoea in congestive heart failure which is driven by changes in pCO(2). As a consequence of apnoea-hypopnoea an imbalance in myocardial oxygen delivery/consumption ratio will develop, sympathetic and other neurohormonal systems will be activated and right and left ventricular afterload will be increased. Sleep apnoea is associated with an increased mortality in patients with systolic heart failure. Treatment of sleep apnoea increases left ventricular ejection fraction and transplant-free survival. Because of its high prevalence, poor quality of life, poor outcome, and the beneficial effects of treatment, physicians treating patients with heart failure should be aware of central sleep apnoea. There are different treatment options, but the exact effects and indications of each option have not yet been fully determined. Further studies should be done to further investigate its prevalence, and to establish the most adequate therapy for the individual patient. (Neth Heart J 2010;18:260-3.).
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PMID:Central sleep apnoea syndrome in chronic heart failure: an underestimated and treatable comorbidity. 2050


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