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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nasal continuous positive airway pressure therapy has recently been studied as a nonpharmacologic adjunct to congestive heart failure therapy. In patients with congestive heart failure, it was reported that continuous positive airway pressure therapy for the condition Cheyne-Stokes respiration with central sleep apnea led to long-term improvements in cardiac function and alleviation of heart failure symptoms. Cheyne-Stokes respiration with central sleep apnea is a frequent breathing disorder well described in patients with congestive heart failure, and is an associated risk factor for increased cardiovascular morbidity and mortality. These apneas cause an increase in sympathetic nervous system activity, which would maintain afterload at a high level or tend to increase it with time, leading to further compromise of ejection fraction. Continuous positive airway pressure appears to benefit the failing heart by increasing intrathoracic pressure, which is believed to cause an increase in cardiac output by decreasing the pressure gradient across the heart wall and allowing the left-ventricular end diastolic volume to decrease, thereby reducing the afterload. This beneficial "resting" of the heart has been documented to increase left-ventricular ejection fraction, increase cardiac index, improve inspiratory muscle strength, lower blood pressure and heart rate, decrease plasma and overnight urinary levels of norepinephrine, lower levels of atrial natriuretic peptide and endothelin-1, and increase heart rate variability. Other benefits include improvement in New York Heart Association functional class status and improvement in dyspnea.
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PMID:Congestive heart failure and continuous positive airway pressure therapy: support of a new modality for improving the prognosis and survival of patients with advanced congestive heart failure. 1197 41

Electrocardiographic ambulatory "Holter" monitoring (AECG) is an essential tool in the diagnostic evaluation of patients with cardiac arrhythmias. Recent advances in digital Holter technology have improved the quality of the ECG signals and new dedicated algorithms have expanded the clinical application of software-based AECG analysis systems. Due to the availability of inexpensive large storage capacities, very long-term (weeks to months) continuous high-quality AECG monitoring will soon be available, together with devices for long-term long-distance telemetric surveillance for high-risk cardiac patients, utilizing trans-telephonic transmission of ECG data. New digital recorders will also have the capability for multichannel simultaneous recordings (currently from 3 to 8 simultaneous leads). Multichannel digital recordings will allow the recording of different biological signals by appropriate sensors, such as respiratory frequency, peripheral oxygen tension, arterial pulse pressure, EEG, and others. This will transform conventional AECG in ambulatory policardiography, allowing the comprehensive evaluation of patients with complex disorders, such as heart failure or sleep apnea syndromes. By this global approach, Holter analysis becomes a real "noninvasive electrophysiological test," to identify potential risk factors for life-threatening cardiac arrhythmias.
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PMID:Advances in modern electrocardiographic equipment for long-term ambulatory monitoring. 1211 36

Often ignored, neurocognitive dysfunction in chronic heart failure represents a daunting morbidity progressing to loss of self-reliance. Although the precise mechanisms arbitrating the development of this disorder remain elusive, microembolization and cerebral hypoperfusion are implicated. Other causes of cognitive decline may include prior cardiac surgery, chronic hypertension, sleep disordered breathing, hyperhomocysteinemia, dementia of aging, and more traditional causes such as Alzheimer's disease. The discovery of neurocognitive defects in heart failure must prompt a well-constructed diagnostic evaluation to search for the underlying causes since this process may be at least partially reversible in many cases.
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PMID:Difficult cases in heart failure: the challenge of neurocognitive dysfunction in severe heart failure. 1214 48

Inadequate splanchnic perfusion is associated with increased morbidity and mortality, particularly if liver dysfunction coexists. Heart failure, increased intra-abdominal pressure, haemodialysis and the presence of obstructive sleep apnoea are among the multiple clinical conditions that are associated with impaired splanchnic perfusion in critically ill patients. Total liver blood flow is believed to be relatively protected when gut blood flow decreases, because hepatic arterial flow increases when portal venous flow decreases (the hepatic arterial buffer response [HABR]). However, there is evidence that the HABR is diminished or even abolished during endotoxaemia and when gut blood flow becomes very low. Unfortunately, no drugs are yet available that increase total hepato-splanchnic blood flow selectively and to a clinically relevant extent. The present review discusses old and new concepts of splanchnic vasoregulation from both experimental and clinical viewpoints. Recently published trials in this field are discussed.
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PMID:Clinical review: splanchnic ischaemia. 1222 96

Patients with chronic congestive cardiac failure (CCF) frequently suffer from central sleep apnoea syndrome (CSAS). Continuous positive airway pressure (CPAP) has been suggested as a treatment. The authors hypothesised that bilevel ventilation might be easier to initiate and superior to CPAP at correcting the sleep-related abnormality of breathing in patients with CCF. After excluding those with a history suggestive of obstructive sleep apnoea, 35 patients with CCF (left ventricular ejection fraction <35%) were screened with overnight oximetry and the diagnosis of CSAS was established with polysomnography in 18. Two 14-day cycles of CPAP (0.85 kPa (8.5 mbar)) or bilevel ventilation (0.85/0.3 kPa (8.5/3 mbar)) in random order, were compared in a crossover study. Sixteen patients (13 males), mean age 62.0+/-7.4 yrs completed the study. The pretreatment apnoea/hypopnoea index of 26.7+/-10.7 was significantly reduced by CPAP and bilevel ventilation to 7.7+/-5.6 and 6.5+/-6.6, respectively. The arousal index fell from 31.1+/-10.0 per hour of sleep to 15.7+/-5.4 and 16.4+/-6.9, respectively. Significant and equal improvements with CPAP and bilevel ventilation were found for sleep quality, daytime fatigue, circulation time and New York Heart Association class. The authors conclude that continuous positive airway pressure and bilevel ventilation equally and effectively improve Cheyne-Stokes respiration in patients with congestive cardiac failure.
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PMID:Assisted ventilation for heart failure patients with Cheyne-Stokes respiration. 1241 86

Recent epidemiologic studies indicate that approximately 40 to 50% of stable patients with congestive heart failure (CHF) suffer from either obstructive sleep apnea (SA) or Cheyne-Stokes respiration with central SA. In either type of sleep apnea, several mechanisms contribute to significant mechanical and adrenergic stresses upon the failing myocardium. These include hypoxemia, reductions in intrathoracic pressure, rises in systemic arterial pressure, increases in left ventricular afterload, and arousals from sleep worsening the sleep architecture. Consequently, sympathetic activation and parasympathetic withdrawal are the hallmark of sleep-related sleeping disorders that contribute to the progression of heart failure and may adversely affect its prognosis. On the other hand, recent studies indicate that successful treatment of either type of SA with continuous positive airway pressure in patients with CHF results in objective and subjective improvement in the severity of heart failure increases in left ventricular ejection fraction, and reductions in sympathetic nervous system activity. Therefore, the early diagnosis and specific treatment of either obstructive or central SA in patients with CHF is highly warranted.
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PMID:Cardiovascular implications of sleep apnea in patients with congestive heart failure. 1244 40

Obstructive sleep apnoeas are common among stroke patients and, as different from central apnoeas, they do not decline during stroke rehabilitation. Cerebral and cardiovascular changes display a different pattern during central and obstructive sleep apnoeas. The cerebral blood flow velocity according to transcranial Doppler increases during an obstructive apnoea and decreases after apnoea termination concomitant with changes in arterial pressure. The changes in cerebral circulation during obstructive apnoeas could be an immediate effect of rapid changes in blood pressure because cerebral autoregulation is overridden. Low cerebral blood flow, low arterial pressure and hypoxemia after apnoea termination may predispose to nocturnal cerebral ischaemia. The opposite pattern is seen during a central apnoea, with a decrease in cerebral blood flow velocity during apnoea and an increase after apnoea termination. Changes during obstructive apnoeas are probably hazardous, with adverse cardiovascular effects including stroke. This may not be the case during central apnoeas, as Cheyne-Stokes respiration with central apnoeas is a result of an underlying disorder such as heart failure and stroke and is not a disease entity in itself. It is suggested that obstructive sleep apnoea is a risk factor for stroke as it is common among stroke victims and cerebral hypoperfusion occurs after an obstructive apnoea. The treatment of sleep apnoea should also be taken into account among stroke patients. Large cohort studies, treatment studies and further studies of possible mechanisms for apnoea-induced stroke are, however, essential in order to evaluate whether obstructive sleep apnoea is an independent risk factor for stroke.
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PMID:Cerebral haemodynamics in obstructive sleep apnoea and Cheyne-Stokes respiration. 1250 76

Sleep apnoea in heart failure increases mortality risk, possibly as a result of greater activation of the sympathetic nervous system. In healthy subjects, simulated central apnoeas (holding breath) and obstructive apnoeas (Mueller manoeuvres) increase muscle sympathetic activity equally, primarily through chemoreceptor stimulation. In heart failure, however, Mueller manoeuvres cause greater reductions in blood pressure than breath holds. We hypothesized that in heart failure, the summation of arterial baroreceptor unloading and chemoreceptor stimulation would increase sympathetic activity more during obstructive than central apnoeas. Healthy human subjects and heart failure patients (seven of each) performed 15-s breath holds and 15-s Mueller manoeuvres. Breath holds evoked a progressive increase in muscle sympathetic nerve activity in both groups, but had no effect on blood pressure. In healthy subjects, breath holds and Mueller manoeuvres caused equal peaks in sympathetic activity. In contrast, in heart failure patients, Mueller manoeuvres caused a progressive decrease in blood pressure (P < 0.05) and greater increases in sympathetic activity than breath holds (P < 0.01). In heart failure, simulated obstructive apnoea elicits greater increases in sympathetic activity than simulated central apnoea, due to its additional hypotensive effect. These present findings offer novel insight into the potential role of sleep apnoea in augmenting sympathetic activity and accelerating disease progression in heart failure.
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PMID:Augmented sympathetic neural response to simulated obstructive apnoea in human heart failure. 1260 77

The chemoreflexes are important modulators of sympathetic activation. The peripheral chemoreceptors located in the carotid bodies respond primarily to hypoxaemia. Central chemoreceptors located in the region of the brainstem respond to hypercapnia. Activation of either the hypoxic or hypercapnic chemoreflex elicits both hyperventilation and sympathetic activation. During apnoea, when the inhibitory influence of stretch of the pulmonary afferents is eliminated, there is a potentiation of the sympathetic response to both hypoxia and hypercapnia. This inhibitory influence of the pulmonary afferents is more marked on the sympathetic response to peripheral compared with central chemoreceptor activation. The arterial baroreflexes also have a powerful inhibitory influence on the chemoreflexes. This inhibition is again more marked with respect to the peripheral compared with central chemoreflexes. In patients with hypertension, there is a marked increase in the sympathetic and ventilatory response to hypoxaemia. During apnoea, with elimination of the inhibitory influence of breathing, the sympathetic response in untreated mild hypertensive patients is strikingly greater than that seen in matched normotensive controls. This potentiated peripheral chemoreflex sensitivity in hypertension may be explained in part by impaired baroreflex function in these patients. Enhanced peripheral chemoreflex sensitivity is also evident in patients with obstructive sleep apnoea. This peripheral chemoreflex enhancement is not explained by obesity, as obese individuals have a selective potentiation of the central chemoreceptors with peripheral chemoreflex responses similar to those seen in lean controls. Increased sensitivity to hypoxaemia has important implications in patients with obstructive sleep apnoea who experience repetitive and severe hypoxaemic stress. Tonic activation of the chemoreflex may also contribute to the high levels of sympathetic activity evident even during normoxic daytime wakefulness in sleep apnoea patients. Administration of 100% oxygen in patients with sleep apnoea results in reductions in heart rate, blood pressure and central sympathetic outflow. In patients with heart failure, the central chemoreflex response to hypercapnia is markedly and selectively enhanced. This increased central chemoreflex sensitivity may contribute to the development of central sleep apnoea in heart failure patients. Administration of 100% oxygen does not lower sympathetic activity in patients with heart failure, providing further evidence against any peripheral chemoreflex potentiation. The peripheral and central chemoreflexes have powerful effects on sympathetic activity in both health and disease and may contribute importantly to disease pathophysiology, particularly in conditions such as hypertension, obstructive sleep apnoea and heart failure.
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PMID:Chemoreflexes--physiology and clinical implications. 1260 9

Plasma noradrenaline (NA) concentrations relate both to the severity of heart failure, and to its impact on survival, but have shortcomings that limit their usefulness as measures of sympathetic discharge. Neural recordings and the isotopic dilution method for determining organ-specific rates of NA spillover into plasma have enhanced our understanding of mechanisms responsible for sympathetic activation. Because the arterial baroreceptor reflex control of heart rate is impaired in heart failure, a parallel reduction in the reflex inhibition of sympathetic outflow has been assumed. However, human heart failure is characterized by rapidly responsive arterial baroreflex regulation of muscle sympathetic nerve activity (MSNA), attenuated cardiopulmonary reflex modulation of MSNA, and activation of a cardiac-specific sympatho-excitatory reflex related to increased cardiopulmonary filling pressures. Together, these baroreceptor mediated mechanisms account only, in part, for the time course and magnitude of adrenergic activation in heart failure. Non-baroreflex sympatho-excitatory mechanisms include: a metaboreflex arising from exercising skeletal muscle, mediated, in part, by adenosine, co-existing sleep apnoea, and pre-junctional facilitation of NA release. Thus, sympathetic activation in the setting of impaired systolic function reflects the net balance and interaction between augmented excitatory and diminished inhibitory influences. Variation, between patients, in the dynamics, magnitude and progression of sympathetic activation mandates an individualized approach to investigation and therapy. Excessive sympathetic outflow to the heart and periphery can be addressed by several complimentary strategies: attenuating these sympatho-excitatory stimuli, modulating the neural regulation of NA release, and blocking the actions of catecholamines at post-junctional receptors.
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PMID:Sympathetic activation in human heart failure: diverse mechanisms, therapeutic opportunities. 1260 11


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