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Query: UMLS:C0037315 (sleep apnea)
 8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The precise mechanisms that cause atrial fibrillation (AF) are not completely understood. Clinicians should ask themselves whether AF is truly 'lone' or is the effect of an underlying, 'masked' disorder. Atrial fibrillation shares strong epidemiological associations with other cardiovascular diseases such as heart failure, coronary artery disease, valvular heart disease, diabetes mellitus and hypertension. In this review, we discuss the 'new risk factors' and the mechanisms by which they lead to AF. Based on the most recent studies, we present the current knowledge about the relationship between AF occurrence and the following disorders: metabolic syndrome and its components, sleep apnea and inflammation. Moreover, some aspects of the influence of lifestyle (alcohol consumption and physical activity) on AF events are described.
Cardiol J 2010
PMID:Risk factors for atrial fibrillation: Not always severe heart disease, not always so 'lonely'. 2086 72

The difference between maximal and minimal QT interval and corrected QT interval defined as QT dispersion and corrected QT dispersion may represent arrhythmogenic risks. This study sought to evaluate QT dispersion and corrected QT dispersion in childhood obstructive sleep apnoea syndrome. Forty-four children (34 male) with obstructive sleep apnoea syndrome, aged 6.2 plus or minus 3.5 years along with 38 healthy children (25 male), 6.6 plus or minus 2.1 years underwent electrocardiography to measure QT and RR intervals. Means QT dispersion and corrected QT dispersion were significantly higher in obstructive sleep apnoea syndrome than controls, 52 plus or minus 27 compared to 40 plus or minus 14 milliseconds (p equal to 0.014), and 71 plus or minus 29 compared to 57 plus or minus 19 milliseconds (p equal to 0.010), respectively. Interestingly, QT dispersion and corrected QT dispersion in obstructive sleep apnoea syndrome with obesity, 57 plus or minus 30 and 73 plus or minus 31 milliseconds, were significantly higher than in control, 40 plus or minus 14 and 57 plus or minus 19 milliseconds (p equal to 0.009 and 0.043, respectively). However, QT dispersion and corrected QT dispersion in obstructive sleep apnoea syndrome without obesity, 43 plus or minus 20 and 68 plus or minus 26 milliseconds, were not significantly different. In conclusion, QT dispersion and corrected QT dispersion were significantly increased only in childhood obstructive sleep apnoea syndrome with obesity. Obesity may be the factor affecting the increased QT dispersion and corrected QT dispersion.
Cardiol Young 2011 Apr
PMID:QT dispersion in childhood obstructive sleep apnoea syndrome. 2107 Jun 92

Sleep apnea, defined as a pathologic pause in breathing during sleep >10 s, promotes the progression of chronic heart failure and may be a predictor of poor prognosis. It causes, in fact, several mechanical, hemodynamic, chemical and inflammatory changes that negatively compromise cardiovascular homeostasis of heart failure patients. Sleep apnea is recognized as sleep apnea syndrome when specific symptoms, such as sleepiness and headache during the daytime and snoring, are present and is diagnosed with an overnight test called polysomnography. There are two different forms of sleep apnea, central and obstructive. Breathing is interrupted by the loss of respiratory drive and the lack of respiratory effort in the central form, which affects about 40-60% of heart failure patients. In obstructive sleep apnea, breathing stops when throat muscles relax, despite respiratory effort. This form affects about 3% of the general population, while it is present in at least 30% of heart failure patients. The diagnosis of sleep disorders in heart failure becomes very important to help patients adopting lifestyle changes and starting specific therapies to improve quality of life and retard the progression of chronic heart failure.
G Ital Cardiol (Rome) 2010 Nov
PMID:[Sleep apnea and heart failure: pathophysiology, diagnosis and therapy]. 2134 18

The 2011 Canadian Cardiovascular Society Heart Failure (HF) Guidelines Focused Update reviews the recently published clinical trials that will potentially impact on management. Also reviewed is the less studied but clinically important area of sleep apnea. Finally, patients with advanced HF represent a group of patients who pose major difficulties to clinicians. Advanced HF therefore is examined from the perspectives of HF complicated by renal failure, the role of palliative care, and the role of mechanical circulatory support (MCS). All of these topics are reviewed from a perspective of practical applications. Important new studies have demonstrated in less symptomatic HF patients that cardiac resynchronization therapy will be of benefit. As well, aldosterone receptor antagonists can be used with benefit in less symptomatic HF patients. The important role of palliative care and the need to address end-of-life issues in advanced HF are emphasized. Physicians need to be aware of the possibility of sleep apnea complicating the course of HF and the role of a sleep study for the proper assessment and management of the conditon. Patients with either acute severe or chronic advanced HF with otherwise good life expectancy should be referred to a cardiac centre capable of providing MCS. Furthermore, patients awaiting heart transplantation who deteriorate or are otherwise not likely to survive until a donor organ is found should be referred for MCS.
Can J Cardiol
PMID:The 2011 Canadian Cardiovascular Society heart failure management guidelines update: focus on sleep apnea, renal dysfunction, mechanical circulatory support, and palliative care. 2188 42

Cerebral ischemia and ischemic heart diseases, common entities nowadays, are the main manifestation of circulatory diseases. Cardiovascular diseases, followed by stroke, represent the leading cause of mortality worldwide. Both entities share risk factors, pathophisiology and etiologic aspects by means of a main common mechanism, atherosclerosis. However, each entity has its own particularities. Ischemic stroke shows a variety of pathogenic mechanisms not present in ischemic heart disease. An ischemic stroke increases the risk of suffering a coronary heart disease, and viceversa. The aim of this chapter is to review data on epidemiology, pathophisiology and risk factors for both entities, considering the differences and similarities that could be found in between them. We discuss traditional risk factors, obtained from epidemiological data, and also some novel ones, such as hyperhomocisteinemia or sleep apnea. We separate risk factors, as clasically, in two groups: nonmodifiables, which includes age, sex, or ethnicity, and modifiables, including hypertension, dyslipidemia or diabetis, in order to discuss the role of each factor in both ischemic events, ischemic stroke and coronary heart disease.
Curr Cardiol Rev 2010 Aug
PMID:Epidemiology and risk factors of cerebral ischemia and ischemic heart diseases: similarities and differences. 2180 73

A 78-year-old man presented with dyspnea and mild heart failure with Cheyne-Stokes respiration (CSR). Workup revealed inferolateral ischemia in the setting of significant triple vessel coronary disease, and nil else to adequately explain his dyspnea and eventual respiratory failure. After he underwent surgical revascularization, his ventricular function improved, leading to resolution of his respiratory failure and, of interest, his CSR. CSR is a central sleep apnea common in heart failure patients and has been associated with increased mortality. Here, we present the first English-literature report of CSR abating with surgical coronary revascularization, and briefly review the literature.
Can J Cardiol
PMID:Cheyne-Stokes respiration due to chronic heart failure abates with coronary artery revascularization. 2226 Nov 83

Post-traumatic stress disorder (PTSD) is gaining increasing recognition as a risk factor for morbidity and mortality. The aim of this study was to examine the impact of PTSD and abnormal cardiovascular biomarkers on mortality in military veterans. Eight hundred ninety-one patients presenting for routine echocardiography were enrolled. Baseline clinical data and serum samples for biomarker measurement were obtained and echocardiography was performed at the time of enrollment. Patients were followed for up to 7.5 years for the end point of all-cause mortality. Ninety-one patients had PTSD at the time of enrollment. There were 33 deaths in patients with PTSD and 221 deaths in those without PTSD. Patients with PTSD had a trend toward worse survival on Kaplan-Meier analysis (p = 0.057). Among patients with elevated B-type natriuretic peptide (>60 pg/ml), those with PTSD had significantly increased mortality (p = 0.024). Among patients with PTSD, midregional proadrenomedullin (MR-proADM), creatinine, and C-terminal proendothelin-1 were significant univariate predictors of mortality (p = 0.006, p = 0.024, and p = 0.003, respectively). In a multivariate model, PTSD, B-type natriuretic peptide, and MR-proADM were independent predictors of mortality. In patients with PTSD, MR-proADM was a significant independent predictor of mortality after adjusting for B-type natriuretic peptide, cardiovascular risk factors, cancer, and sleep apnea. Adding MR-proADM to clinical predictors of mortality increased the C-statistic from 0.572 to 0.697 (p = 0.007). In conclusion, this study demonstrates an association among PTSD, abnormal cardiac biomarker levels, and increased mortality.
Am J Cardiol 2012 Apr 15
PMID:Cardiac biomarkers, mortality, and post-traumatic stress disorder in military veterans. 2230 6

Sleep disordered breathing including obstructive sleep apnea (OSA) and central sleep apnea (CSA) with Cheyne-Stokes respiration (CSR) is often accompanied by heart failure. Treatment of OSA centered on continuous positive airway pressure (CPAP) is established. However, treatment of CSR-CSA is still controversial. Since CSR-CSA occurs as a consequence of heart failure, optimization of heart failure is essential to treat CSR-CSA. For treatment directed at CSR-CSA itself, a variety of treatment approaches including night oxygen therapy and noninvasive positive pressure ventilation have been applied. Among them, night oxygen therapy improves patients' symptoms, quality of life (QOL), and left ventricular function, but had yet been shown to improve clinical outcome. For CPAP, there are responders and non-responders and for responders CPAP can also improve survival. Adaptive servo-ventilation (ASV), which most effectively treats CSR-CSA, improves exercise capacity, QOL, and cardiac function. Recent reports suggested ASV may also prevent cardiac events in patients with heart failure. However, further studies are needed to conclude that this treatment improves patient survival.
J Cardiol 2012 Mar
PMID:Treatment of Cheyne-Stokes respiration-central sleep apnea in patients with heart failure. 2237 Jan 66

Sleep apnea is frequently observed in patients with heart failure (HF). In general, sleep apnea consists of two types: obstructive and central sleep apnea (OSA and CSA, respectively). OSA results from upper airway collapse, whereas CSA arises from reductions in central respiratory drive. In patients with OSA, blood pressure is frequently elevated as a result of sympathetic nervous system overactivation. The generation of exaggerated negative intrathoracic pressure during obstructive apneas further increases left ventricular (LV) afterload, reduces cardiac output, and may promote the progression of HF. Intermittent hypoxia and post-apneic reoxygenation cause vascular endothelial damage and possibly atherosclerosis and consequently coronary artery disease and ischemic cardiomyopathy. CSA is also characterized by apnea, hypoxia, and increased sympathetic nervous activity and, when present in HF, is associated with increased risk of death. In patients with HF, abolition of coexisting OSA by continuous positive airway pressure (CPAP) improves LV function and may contribute to the improvement of long-term outcomes. Although treatment options of CSA vary compared with OSA treatment, CPAP and other types of positive airway ventilation improve LV function and may be a promising adjunctive therapy for HF patients with CSA. Since HF remains one of the major causes of mortality in the industrialized countries, the significance of identifying and managing sleep apnea should be more emphasized to prevent the development or progression of HF.
J Cardiol 2012 Aug
PMID:Sleep apnea and heart failure. 2282 95

Cardiac cachexia and alterations in muscle metabolism are a co-morbidity that can develop in advanced stages of chronic heart failure (HF). Up to 15% of ambulatory patients with HF are affected and present with a loss of different tissue types including muscle mass. Whilst cardiac cachexia has long been a neglected clinical entity, current HF guidelines of the European Society of Cardiology (ESC) include a section on weight management in patients with HF at risk of cardiac cachexia. This article highlights some recent studies of metabolic and functional alterations of the muscle in HF that were presented at the annual meeting of the ESC in August 2012 in Munich, Germany. The studies presented were focused on dysfunction of respiratory and limb skeletal musculature as well as metabolic features of myocardium in HF. Strategies improving muscle function and peak oxygen consumption in HF such as (inspiratory) muscle training and treatment of central sleep apnea by adaptive servoventilation are described. The latter shows promising results regarding HF symptoms and exercise capacity but still has to prove survival benefits in larger trials. A rat model highlights the value of microRNAs to regulate exercise-induced skeletal muscle angiogenesis. Another study provides evidence for changes in substrate utilisation depending on the functional status of mitochondria in the failing heart and points to mitochondrial dysfunction as a potential mediator of metabolic remodelling. Though treatments remain to be established, these findings may pave the way for effective therapeutic approaches to altered muscle function and cardiac cachexia.
Int J Cardiol 2012 Nov 29
PMID:Muscle in heart disease: highlights from the European Society of Cardiology's Annual Meeting 2012. 2312 13


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