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In patients with congestive heart failure (CHF), a high prevalence of sleep-disordered breathing has been described. Cheyne-Stokes respiration (CSR) is present in up to 40% of patients with CHF. During the last decade, the medical treatment has been substantially improved. This study was designed to analyze the prognosis of CSR in modern-treated patients with CHF. For this purposes, in 57 patients with CHF who received modern treatment, a 5-year follow-up after initial full night polysomnography was performed. The mean follow-up period was 38 ± 18 months. Mean age was 62 ± 13 years and the mean ejection fraction was 25 ± 7 percent. Respiratory polygraphy revealed CSR with a respiratory disturbance index >5 per hour of sleep in 39 of 57 patients. Twelve patients died. CSR was only characterized by a tendency of worsening (log-rank test, p = 0.25). However, there was a significant difference toward positive outcome for patients who received cardiac resynchronization therapy (log-rank test, p = 0.036). Using Multivariate Cox’s proportional hazard regression with the factors resynchronization and CSR, the effect of resynchronization was almost significant (p = 0.08). In conclusion, no significant change of Cheyne-Stokes prevalence can be found in our small group of modern-treated patients with CHF. Cardiac resynchronization therapy was associated with improved patient outcome.  相似文献   

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BackgroundCheyne-Stokes respiration (CSR) is believed to only occur in supine and sleeping conditions, and thus, CSR treatment is applied to those specific states. Although CSR has also been described in patients with heart failure (HF) during wakefulness, its persistence in an upright position is still unknown.ObjectivesThe purpose of this study was to assess the predictors, clinical correlates, and prognostic value of diurnal CSR in upright position.MethodsOutpatients with systolic HF underwent a comprehensive evaluation, including short-term respiratory monitoring with a head-up tilt test to investigate the presence of upright CSR, assessment of chemoreflex response to hypoxia and hypercapnia, and 24-h cardiorespiratory recording. At follow-up, cardiac death was considered as the endpoint.ResultsOf 574 consecutive patients (left ventricular ejection fraction 32 ± 9%; age 65 ± 13 years; 80% men), 195 (34%) presented supine CSR only, 82 (14%) presented supine and upright CSR, and 297 patients (52%) had normal breathing. Patients with upright CSR had the greatest apnea-hypopnea and central apnea index (at daytime and nighttime), the worst hemodynamic profile and exercise performance, increased plasma norepinephrine and N-terminal pro–B-type natriuretic peptide, and chemosensitivity to hypercapnia, which was the only independent predictor of upright CSR (odds ratio: 3.96; 95% confidence interval [CI]: 1.45 to 10.76; p = 0.007 vs. normal breathing; odds ratio: 4.01; 95% CI: 1.54 to 10.46; p = 0.004 vs. supine CSR). At 8-year follow-up, patients with upright CSR had the worst outcome (log-rank = 14.05; p = 0.001) and the presence of upright CSR independently predicted 8-year cardiac death (hazard ratio: 2.39; 95% CI: 1.08 to 5.29; p = 0.032).ConclusionsUpright CSR in HF patients is predicted by increased chemosensitivity to hypercapnia and is associated with worse clinical conditions and with a greater risk of cardiac death.  相似文献   

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Patients suffering from severe heart failure may develop breathing pattern disorders during sleep, especially in the form of Cheyne-Stokes respiration. Results may be severe disturbances in sleep architecture and worsening of hemodynamics and of prognosis of these patients. Causes of the periodic breathing disorders are probably hypocapnia, hypersensitivity of respiratory control centers, hypoxemia, and prolonged blood circulation time. This study examined the influence of different concentrations of continously administered oxygen during the nighttime on breathing pattern disorders, oxygen saturation, and sleep architecture in 65 patients with severe heart failure (NYHA III–IV). Fifty-two of 65 patients showed an improvement of sleep architecture. Total sleeping time increased significantly (p < 0.01). Fragmentations of sleep by arousals decreased (p < 0.01); time of random eye movement (REM) sleep and non–REM sleep III and IV increased significantly.  相似文献   

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Cheyne-Stokes respiration is a pattern of alternating central apnea and hyperpnea. It is well described in adults with congestive heart failure, but not in children.We report the case of a 17-year-old boy whose systolic heart failure was complicated by Cheyne-Stokes respiration. He was given supportive therapy until heart transplant, after which his Cheyne-Stokes respiration clinically resolved. Clinicians should be aware of this uncommon condition in pediatric and adolescent patients who have advanced heart failure and irregular breathing.  相似文献   

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Definition: Cheyne-Stokes respiration is a breathing disorder characterized by recurrent central sleep apneas, mainly during sleep, alternating with a crescendo-decrescendo pattern of tidal volume. Pathophysiology and Prognosis: The pathophysiology of Cheyne-Stokes respiration, involving the cardiovascular, pulmonary and sympathetic nervous system, is still not well understood. Although 50% of moderate to severe congestive heart failure patients suffer from significant Cheyne-Stokes respiration, studies been undertaken to determine the prevalence of this phenomenon and its implications regarding patients' life expectancy and quality of life were conducted only in recent years. Other studies suggest that Cheyne-Stokes respiration has a negative prognostic value upon congestive heart failure patients. Treatment: Novel therapeutic approaches have been attempted in order to treat Cheyne-Stokes respiration; they include oxygen delivery, various pharmaceutical treatments aimed to stabilize the ventilatory system and other pharmaceutical treatments aimed to improve the left ventricular ejection fraction. However, none of them was effective. Objectives: This review summarizes some of the current knowledge regarding Cheyne-Stokes respiration pathophysiology, prevalence, prognostic implication and available treatments. Definition: Das Cheyne-Stokes-Atemmuster wurde erstmalig zu Beginn des 19. Jahrhunderts beschrieben und kennzeichnet eine Atemstörung, bei der vor allem während des Schlafs Atempausen (Apnoephasen) auftreten. Diese Apnoephasen wechseln mit einem Atemmuster mit Kreszendo/Dekreszendo-Charakter ab. Pathophysiologie und Prognose: Die Pathophysiologie der Cheyne-Stokes-Atmung, die kardiovaskuläre, pulmonale und zentralvenöse Aspekte umfasst, ist noch weitgehend unklar. Obwohl nahezu 50% der Patienten mit schwerer Herzinsuffizienz eine Cheyne-Stokes-Atmung aufweisen, wurden erst in den letzten Jahren die Prävalenz dieser Begleiterkrankung und die möglichen Auswirkungen auf die Lebenserwartung und die Lebensqualität charakterisiert. Erste Studien lassen vermuten, dass Patienten mit Cheyne-Stokes-Atmung eine deutlich schlechtere Prognose als Patienten mit Herzinsuffizienz ohne Cheyne-Stokes-Atmung aufweisen. Behandlung: Ziel der bisher eingesetzten Therapie ist es, das Atemsystem zu stabilisieren und die kardiovaskuläre Funktion zu optimieren, um dadurch das Leben der Patienten zu verlängern. Doch weder die Verabreichung von Sauerstoff noch der Einsatz verschiedener pharmakotherapeutischer Konzepte zeigten bisher einen nachhaltigen Erfolg. Gegenstand: In dieser Übersicht werden wichtige Aspekte der Pathophysiologie der Cheyne Stokes Atmung, seine prognostische Bedeutung sowie vorhandene Therapiekonzepte besprochen und kritisch bewertet.  相似文献   

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Opinion statement Both atrial and ventricular arrhythmias are very common in patients with congestive heart failure, and their presence is associated with symptoms, significant morbidity, and mortality. Studies have attempted to determine the prognostic significance of atrial and ventricular arrhythmias in patients with heart failure. Whether atrial fibrillation is an independent risk factor of mortality remains controversial. The presence of ventricular arrhythmias in patients with ischemic cardiomyopathy identifies patients at high risk for sudden death. However, in patients with nonischemic cardiomyopathy there is not a strong correlation between ventricular arrhythmias and increased risk for sudden death. Multiple trials using antiarrhythmic drugs, pharmacologic therapy, and implantable cardioverter defibrillators have been performed in an attempt to improve survival in patients 1) post-myocardial infarction; 2) with congestive heart failure, with and without nonsustained ventricular tachycardia; and 3) with sustained ventricular tachycardia and those who have survived an out-of-hospital cardiac arrest. The purpose of this article is to present an overview of arrhythmias in patients with heart failure and discuss the prevalence, prognostic significance, complications, mechanisms, and trials that have formed the current therapies presently used.  相似文献   

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陈-施呼吸(CSR)是中枢性睡眠呼吸紊乱的一种形式,以潮气量周期性渐进性减弱-消失-增强为特征。CSR最多见于心力衰竭患者,但也可见于急性肺水肿恢复期、进展性肾衰、中枢性神经系统损伤患者。重度心力衰竭可能是CSR最重要的危险因素,而CSR反过来也会增加心力衰竭患者的发病率和死亡率。  相似文献   

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Purpose of Review

This review aims to summarize and discuss heart failure outcomes for current glucose-lowering agents in patients with type 2 diabetes mellitus.

Recent Findings

Current regulations require cardiovascular outcomes trials for new glucose-lowering therapies to establish that there is no unacceptable increase in cardiovascular risk prior to approval. These cardiovascular outcomes trials include glucagon-like peptide 1 receptor agonists, dipeptidyl peptidase-4 inhibitors, and sodium-glucose cotransporter-2 inhibitors. Overall, 87,162 patients have been studied in 10 published cardiovascular outcomes trials. There was no significant increase in major adverse cardiovascular events including cardiovascular mortality, myocardial infarction, and stroke in any of these trials. Heart failure was a component of the secondary endpoint of all of these trials, but only two of these studies show a significant improvement in rates of hospitalization for heart failure.

Summary

Expanded regulatory labeling for reduction in cardiovascular mortality (empagliflozin) and reduction in major adverse cardiovascular events (liraglutide) has recently been established. Saxagliptin and to a lesser part alogliptin have been associated with an increased rate of hospitalization for heart failure. Canagliflozin and empagliflozin are the only two medications that have shown a clear benefit in rates of heart failure hospitalization in treatment of patients with type 2 diabetes mellitus.
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Heart failure results from injury to the myocardium from a variety of causes, including ischemic and nonischemic etiologies. Severe heart failure carries a 50% 5-year mortality rate and is responsible for more than one-third of cardiovascular deaths in the United States.1 Heart failure progression is accompanied by activation of neurohormonal and cytokine systems as well as a series of adaptive changes within the myocardium, collectively referred to as left ventricular remodelling. The unfavorable alterations may be categorized broadly into changes that occur in the cardiac myocytes and changes that occur in the volume and composition of the extracellular matrix.2 Since remodelling in heart failure is progressive and eventually becomes detrimental, the majority of treatment strategies are aimed at stopping or reversing this process. Although medical management, cardiac resychronization therapy, and long-term or destination mechanical circulatory support have been successful in this regard, a considerable number of patients still progress to end-stage heart failure with limited therapeutic options. For these patients, stem cell therapies are being investigated as a safe treatment strategy for decreasing cardiac remodelling on top of conventional medical and device treatment.  相似文献   

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Historically, patients with heart failure were advised to avoid exertion due to fear that the added myocardial stress would worsen heart function. However, between 1979 and 1991, five uncontrolled trials demonstrated that moderate exercise training can partially reverse the exercise intolerance common among patients with heart failure. Since 1991, numerous randomized exercise trials demonstrated a 12% to 33% improvement in exercise capacity, as measured by oxygen consumption. The mechanisms by which this improvement occurs are now being studied. Potential mechanisms include improved cardiac output due to increases in both peak stroke volume and reversal of chronotropic incompetence; improved regional blood flow to the metabolically more active skeletal muscle; and partial reversal of skeletal muscle histochemical abnormalities such as increased oxidative enzymes and a re-shift in fiber type toward increased type I fibers. Improved sympathetic function has also been noted with exercise training, evidenced by decreased norepinephrine spillover and increased heart rate variability. Exercise training can be of benefit in selected patients with stable New York Heart Association class II or III heart failure.  相似文献   

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