Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0037315 (sleep apnea)
 8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a case of an adult male in whom, one week after an anterior acute myocardial infarction, we documented nocturnal episodes of type II second degree atrio-ventricular heart block, including advanced heart block episodes (4:1). An electrophysiologic study did not show atrio-ventricular conduction abnormalities, so we suspected a possible sleep apnea syndrome, which was confirmed with a polysomnographic study. It was observed that advanced heart block episodes were preceded by significant decreases in arterial oxygen saturation. These episodes disappeared with continuous positive air pressure ventilation.
Rev Esp Cardiol 1998 Jun
PMID:[Advanced auriculoventricular block of atypical presentation after acute myocardial infarct in sleep apnea syndrome]. 966 4

A 40-year-old man with severe sleep apnoea syndrome presented significant sinus pauses during a 48 h electrocardiogram Holter recording. Holter analysis showed one sinus pause of 6.4 s duration, and many pauses greater than 3 s. The 48 h Holter reevaluation, after a continuous positive air pressure device was applied, showed no pauses. The electrophysiological study was negative for sick sinus syndrome.
Int J Cardiol 1998 Dec 31
PMID:Excessive sinus pauses and their elimination in a patient with sleep apnea syndrome. 989 10

A 26-year-old woman developed congestive heart failure (CHF) secondary to idiopathic dilated cardiomyopathy. Despite aggressive pharmacological therapy, her disease progressed over the next year, causing massive edema and dyspnea at rest. Although a sleep study showed no clinically significant sleep apnea, she was treated with nocturnal continuous positive airway pressure (CPAP). Following application of CPAP, a remarkable improvement in her condition was observed, with resolution of her edema and alleviation of dyspnea. Left ventricular ejection fraction increased from 29% to 43% and left ventricular dimensions decreased. Previous studies have demonstrated that nocturnal CPAP exerts a number of favourable effects on cardiovascular function in patients with CHF who suffer from a coexisting sleep apnea disorder. This report illustrates that CPAP can also have beneficial long term effects on the failing heart even in the absence of clinically significant sleep apnea.
Can J Cardiol 1999 Sep
PMID:Long term treatment of refractory congestive heart failure by continuous positive airway pressure. 1050 75

Obstructive sleep apnea syndrome is characterized by obesity, nocturnal breathing abnormalities, arterial hypertension, and an increased number of cardiovascular events. Sympathetic activity is increased during nocturnal apneic episodes, which may mediate the cardiovascular complications of sleep apnea. We studied 15 male subjects with obstructive sleep apnea syndrome and associated hypertension, 54 subjects with mild to moderate essential hypertension, and 25 healthy normotensive men. Cardiovascular autonomic control was assessed using frequency domain measures of heart rate variability (HRV) during a controlled breathing test and during orthostatic maneuver. Compared with normotensive and hypertensive groups, total power and low- and high-frequency components of HRV during controlled breathing were significantly (analysis of variance, p<0.0001) lower in the obstructive sleep apnea syndrome. During the orthostatic maneuver, the change in total power of HRV was different between the 3 groups (analysis of variance, p = 0.004). The total power of HRV tended to increase in the normotensive (4.11+/-12.29 ms2) and in hypertensive (2.31+/-12.65 ms2) groups, but decreased (1.13+/-1.23 ms2) in the hypertensive group with obstructive sleep apnea syndrome. According to multivariate regression analysis, age and sleep apnea were the major independent determinants of HRV. This study found that an abnormal response to autonomic nervous tests characterizes hypertension in overweight subjects with obstructive sleep apnea syndrome. This could be due to autonomic withdrawal or supersaturation of the end-organ receptors by excessive and prolonged sympathetic stimulation. Our results also show the reduced response of orthostatic maneuver and controlled breathing in the hypertensive group compared with the normotensive group.
Am J Cardiol 2000 Jan 15
PMID:Comparison of autonomic withdrawal in men with obstructive sleep apnea syndrome, systemic hypertension, and neither condition. 1095 83

Twenty-nine patients in whom severe bradyarrhythmias occurred exclusively during obstructive sleep apnea and in whom advanced sinus node disease or atrioventricular conduction system dysfunction had been excluded by invasive electrophysiologic evaluation were prospectively followed on nasal continuous positive airway pressure. During 54 +/- 10 months follow-up, no syncope and no sudden deaths were observed, suggesting that patients with sleep apnea-associated bradyarrhythmias and a normal electrophysiologic study appear to have a favorable prognosis with continuous positive airway pressure.
Am J Cardiol 2000 Sep 15
PMID:Outcome of patients with sleep apnea-associated severe bradyarrhythmias after continuous positive airway pressure therapy. 1098 Feb 27

Despite years of investigation our fundamental and clinical knowledge of the major public health problem, obesity-hypertension, is relatively meager and certainly inadequate. We are at a loss to explain why the pathophysiological mechanisms of obesity and hypertension are so inextricably intertwined. Adding to this frustration is the inadequacy of the treatment for obesity. Hemodynamically, we recognize that the expanded plasma volume caused by obesity imparts a significant volume overload on the heart, thereby increasing cardiac output, while the hypertension compounds this ventricular stress by an associated pressure overload. Thus, the ventricle has an eccentric as well as a concentric adaptive hypertrophy. Associated with obesity is an increased burden of pressor (e.g., catecholamine, angiotensin II); peptide (e.g., endothelin, insulin, leptin, natriuretic); hormonal (e.g., growth, steroids, thyroid); and neural mechanisms. Further complicating these alterations are electrolytic, lipid, uric acid, and other metabolic factors. Both diseases (obesity and hypertension) are exacerbated by frequently encountered comorbid pathophysiological disorders including atherosclerosis, ventricular dysfunction, diabetes mellitus, hyperlipidemias, and sleep apnea. To add to these issues, therapy for obesity-hypertension is suboptimal. Behavioral modification (of overweight and obesity) is commonly characterized by recidivism, and pharmacotherapy of obesity is woefully inadequate; the present agents either raise arterial pressure or are fraught with adverse effects. Fortunately, there are no contraindications imparted by obesity that complicate the drug treatment of the associated hypertension. Each of the lifestyle modifications and seven classes of antihypertensive therapy that is discussed herein is done in light of the coexistent hypertension and comorbid diseases.
Cardiol Rev
PMID:Clinical management of the obese hypertensive patient. 1204 91

In an adult population, the prevalence of sleep apnea is 4% for men and 2% for women. Generally, nasal positive pressure ventilation is the best therapeutic option. To date, and in spite of the possible presence of marked brady-arrhythmias during sleep apnea, there is no recognised indication for Pacemaker implantation. However, recent data show the potential benefit of permanent cardiac stimulation in these patients. Increasing heart rate (using atrial pacing) improves cardiac output, and reduces pulmonary congestion and pulmonary vagal afferent nerves are no longer stimulated. The incidence of central sleep apnea is thereby reduced. Excessive nocturnal vagal tone increases snoring and sleep apnea, because of excessive relaxation of the oropharyngeal muscles. In patients with bradycardia, atrial stimulation may oppose increased vagal tone, by stimulating the sympathetic system or maintaining it at a minimal level. It is therefore possible that cardiac stimulation will become part of the treatment of sleep apnea in patients with documented bradycardia and/or heart failure.
Ann Cardiol Angeiol (Paris) 2003 Aug
PMID:[Sleep apnea and cardiac pacing: mechanisms of action and perspectives]. 1460 5

Central sleep apnoea is often recognized in patients with heart failure. Although the medical treatment to improve cardiac function is effective for sleep apnoea, direct evidence that improved cardiac function ameliorates sleep apnoea has not been reported due to the fact that a particular drug may affect a multitude of organs. We present a chronic heart failure patient with central sleep apnoea whose nocturnal desaturation was improved by percutaneous coronary intervention that resulted in improved cardiac function. This is the first case where percutaneous coronary intervention improved sleep apnoea, suggesting that the improved cardiac function led to amelioration of sleep apnoea.
Acta Cardiol 2004 Feb
PMID:Percutaneous coronary intervention for central sleep apnoea with ischaemic cardiomyopathy. 1503 Jan 36

Stroke and sleep-disordered breathing (SDB) are both common and are associated with significant morbidity and mortality. Several recent large epidemiologic studies have shown a strong association between these two disorders independent of known risk factors for stroke. This review will outline the scientific basis for this relationship and suggest SDB as a modifiable risk factor for stroke. Several studies have shown a characteristic circadian rhythmicity in stroke. The authors discussed the influence of normal sleep states as well as the effect of SDB on cerebral hemodynamics. The hemodynamic, metabolic, and hematologic changes during SDB in the form of decreased cerebral perfusion and increased coagulability are the possible pathogenetic mechanisms for stroke. There are accumulating lines of evidence that SDB may indeed cause diurnal hypertension. However, the increased risk of stroke in patients with SDB appears to be independent of coexisting hypertension, but the presence of hypertension would greatly increase the risk even further. Furthermore, several studies have documented high prevalence of sleep apnea in patients with transient ischemic attacks and stroke. SDB appears to contribute as a risk factor for stroke through hemodynamic and hematologic changes. Because of high prevalence of SDB in this population, patients with transient ischemic attacks and stroke should be screened for these disorders.
Prev Cardiol 2003
PMID:Sleep-disordered breathing: implications in cerebrovascular disease. 1531 84

Chronic heart failure (CHF) is a common condition and is associated with excess morbidity and mortality, in spite of the many advances in its treatment. Chronic stable heart failure is also associated with an increased incidence of sleep-related breathing disorders, such as central sleep apnoea (CSA) and Cheyne Stokes respiration (CSR). Continuous positive airways pressure (CPAP) has been shown to alleviate the symptoms of CHF, improve left ventricular function and oxygenation. To a certain extent, CPAP also abolishes sleep-related breathing disorders in patients with chronic heart failure. In patients with acute pulmonary oedema, the use of positive pressure ventilation improves cardiac haemodynamic indices, as well as symptoms and oxygenation, and is associated with a lower need for intubation. However, some studies have cast doubts about its safety and suggest a higher rate of myocardial infarction associated with its use. In our opinion, non-invasive positive pressure ventilation and CPAP offers an adjunctive mode of therapy in patients with acute pulmonary oedema and chronic heart failure, who may not be suitable for intubation and in those not responsive to conventional therapies. Non-invasive ventilation also helps to improve oxygenation in those patients with exhaustion and respiratory acidosis. Many trials are still ongoing and the results of these studies would throw more light on the present role of non-invasive ventilation in the management of CHF.
Int J Cardiol 2005 Mar 18
PMID:Positive pressure ventilation in the management of acute and chronic cardiac failure: a systematic review and meta-analysis. 1638 32


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