Sleep-Disordered Breathing in Patients With Idiopathic Cardiomyopathy.

Banno, Katsuhisa; Shiomi, Toshiaki; Sasanabe, Ryujiro; Otake, Kazuo; Hasegawa, Rumiko; Maekawa, Masato; Itō, Takayuki

doi:10.1253/circj.68.338

Cited by 43 publications

(40 citation statements)

References 25 publications

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“…In addition, it was recently reported that sleep apnea is common in patients with idiopathic cardiomyopathy. 36 Hypertension is a frequent complication of OSAS. It has been reported that the mean blood pressure increases with the severity of the sleep apnea.…”

Section: Discussionmentioning

confidence: 99%

Amelioration of Vascular Endothelial Dysfunction in Obstructive Sleep Apnea Syndrome by Nasal Continuous Positive Airway Pressure-Possible Involvement of Nitric Oxide and Asymmetric NG, NG-Dimethylarginine-

Ohike

Kozaki

Iijima

et al. 2005

Circ J

145

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ndothelial dysfunction is recognized as an early phase of arteriosclerosis 1 and an important cause of that dysfunction is impaired nitric oxide (NO) release from the endothelium. Endothelial NO is a key regulator of vascular homeostasis; it induces vasorelaxation by generating cyclic GMP in the underlying smooth muscle cells, and prevents monocyte adhesion to the endothelium, platelet activation, and smooth muscle cell proliferation. Hence, impaired NO release from injured endothelial cells is regarded as an initiator and promoter of arteriosclerosis.Endothelial NO is produced when L-arginine is con- February 2005 verted to L-citrulline by the enzyme endothelial nitric oxide synthase (eNOS). Endothelial NOS is inhibited by endogenous inhibitors, NG-monomethyl-L-arginine (L-NMMA) and asymmetric dimethylarginine (ADMA), which are structural analogues of L-arginine. 2,3 Plasma ADMA is eliminated by renal excretion and by degradation to citrulline and dimethylamine by the enzyme dimethylarginine dimethylaminohydrolase (DDAH). 4 Increased plasma concentration of ADMA is associated with hypertension, 5 pulmonary hypertension, 6 hypercholesterolemia, 7,8 carotid intima -media thickening, 9 severe peripheral artery occlusive disease, 10 and the clustering of coronary risk factors. 9 These findings suggest that ADMA is responsible for endothelial dysfunction. Obstructive sleep apnea syndrome (OSAS) has been recently attracting attention as a significant disorder. Frequent apnea/hypopnea attacks followed by arousal results in insufficient sleep at night, causing daytime sleepiness, leading to work inefficiency, and even traffic accidents. In addition, OSAS often accompanies hypertension, obesity, glucose intolerance, and dyslipidemia, all of which are factors in metabolic syndrome. Hence, OSAS is recognized as a risk factor for cardiovascular disease. 11-14 It has been Background Asymmetric NG,NG-dimethylarginine (ADMA) is an endogenous inhibitor of endothelial nitric oxide (NO) synthase and its plasma concentration is elevated in patients with cardiovascular risk factors, including hyperlipidemia, hypertension, diabetes, and hyperhomocysteinemia. Obstructive sleep apnea syndrome (OSAS) has been attracting attention as a risk factor for cardiovascular disorders because it often accompanies hypertension, obesity, glucose impairment, and dyslipidemia, all of which are factors in metabolic syndrome and risk factors for cardiovascular disease. Methods and ResultsIn the present study, flow-mediated vasodilatation (FMD) of the brachial artery and plasma concentrations of ADMA were measured before and after nasal continuous positive airway pressure (nCPAP) therapy, which abrogates apnea, in 10 male patients aged 36-69 years old, who were given a diagnosis of OSAS by polysomnography. The percent FMD (%FMD) improved significantly from 3.3±0.3% to 5.8±0.4% (p<0.01) and 6.6±0.3% (p<0.01), before, 1 week, and 4 weeks after nCPAP, respectively. At the same time, the plasma NOx concentrations, metabolites of NO, tended to increase, bu...

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Section: Discussionmentioning

confidence: 99%

Amelioration of Vascular Endothelial Dysfunction in Obstructive Sleep Apnea Syndrome by Nasal Continuous Positive Airway Pressure-Possible Involvement of Nitric Oxide and Asymmetric NG, NG-Dimethylarginine-

Ohike

Kozaki

Iijima

et al. 2005

Circ J

145

View full text Add to dashboard Cite

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“…Obstructive sleep apnea-hypopnea syndrome (OSAHS) is the most common type of sleep-related breathing disorders, which was caused by throat obstruction (1,2). The syndrome associates somnolence and one or two of the following symptoms: severe snoring, nocturnal respiratory arrest, repeated nocturnal awakening, non-recuperative sleep, diurnal fatigue, and altered concentration (3 4).…”

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confidence: 99%

The effect of obstructive sleep apnea-hypopnea syndrome on acute myocardial infarction

Zhang¹,

Sun²,

Li³

et al. 2012

BLL

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Background and objectives: Obstructive sleep apnea-hypopnea syndrome (OSAHS) is the most clinically common type of sleep-related breathing disorders. In this study, the effect of OSAHS on ST segment elevation myocardial infarction (STEMI) was investigated. Methods: Seventy-fi ve patients with STEMI were included in this study. The patients were divided into two groups: STEMI accompanied by OSAHS (O + ) group (33 patients) and STEMI without OSAHS (O -) group (42 patients). The differences of the clinical characteristics between the two groups were compared. The relationship between oxyhemoglobin desaturation index (ODI) and Gensini Score, and the relationships between OSAHS and clinical parameters were analyzed by a regression analysis. Results: AMI mainly occurred from 10 pm to 6 am in the O + group (45.5 %) and from 6 am to 2 pm in the O -group (52.3 %). The peak of serous creatine kinase (CK), high-sensitivity C-reactive protein (hs-CRP), N-terminal Pro-brain natriuretic peptide (NT-proBNP), and left ventricle end-diastolic volume index (LVEDVI) were significantly increased in the O + group compared to the O -group, while the left ventricular ejection fraction (LVEF) were signifi cantly decreased. The regression analysis showed that ODI was positively correlated with Gensini Score, while serous CK, hs-CRP, NT-proBNP, and OSAHS were independently associated with left ventricular insuffi ciency (LVI), and the incidence of LVI in O + group was 5.8 times as O -group. Conclusions: In STEMI patients with OSAHS, myocardial infarction mainly occurred from 10 pm to 6 am, and the incidence of LVI was signifi cantly higher than STEMI patients without OSAHS (Tab. 5, Fig. 2 Obstructive sleep apnea-hypopnea syndrome (OSAHS) is the most common type of sleep-related breathing disorders, which was caused by throat obstruction (1, 2). The syndrome associates somnolence and one or two of the following symptoms: severe snoring, nocturnal respiratory arrest, repeated nocturnal awakening, non-recuperative sleep, diurnal fatigue, and altered concentration (3 4). OSAHS may act to cause and promote the progression of hypertension, coronary artery disease (CAD), acute myocardial infarction (AMI) and cerebral vascular disease (1, 5). It is reported that its incidences in adult women is 2 %, and in adult men is 4 % (6). While in China, its incidence is about 3.62 % in people beyond 30 years, which means that there are more than 47 million of patients in China by now (7).Numerous studies showed that OSAHS is closely associated with the development and progression of CAD. The changes of hemodynamics, enhancement of the sympathetic activity, and oxidative stress that are caused by OSAHS can accelerate the process of artherosclerosis (8, 9). Peker et al (10) reported that the incidence of OSAHS is higher in the patients with CAD than in normal people, and OSAHS can raise the mortality of angiocardiopathy, while patients treated by continuous positive airway pressure (CPAP) can reverse this state. The results of Peker et al (10) al...

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“…[2][3][4][5] This breathing disorder may be associated with arterial oxyhemoglobin desaturation and excessive arousals, resulting in sympathetic activation and arrhythmias. 6,7 Because sleep-disordered breathing is also observed in patients with idiopathic cardiomyopathy, 8 the pathophysiological consequences of sleep apnea may further contribute to the mortality of CHF patients with ventricular arrhythmias. Although home oxygen therapy 9 and bi-level positive airway pressure treatment 10,11 improve the clinical condition of sleep apnea syndrome (SAS) in CHF patients, few studies of SAS in CHF with ventricular arrhythmias have been reported and detailed findings and laboratory examinations for arrhythmia in SAS and CHF are needed.…”

mentioning

confidence: 99%

Oxygen Therapy Prevents Ventricular Arrhythmias in Patients With Congestive Heart Failure and Sleep Apnea

Suzuki

Ishihara

Sakurai

et al. 2006

Circ J

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Sleep-Disordered Breathing in Patients With Idiopathic Cardiomyopathy.

Cited by 43 publications

References 25 publications

Amelioration of Vascular Endothelial Dysfunction in Obstructive Sleep Apnea Syndrome by Nasal Continuous Positive Airway Pressure-Possible Involvement of Nitric Oxide and Asymmetric NG, NG-Dimethylarginine-

Amelioration of Vascular Endothelial Dysfunction in Obstructive Sleep Apnea Syndrome by Nasal Continuous Positive Airway Pressure-Possible Involvement of Nitric Oxide and Asymmetric NG, NG-Dimethylarginine-

The effect of obstructive sleep apnea-hypopnea syndrome on acute myocardial infarction

Oxygen Therapy Prevents Ventricular Arrhythmias in Patients With Congestive Heart Failure and Sleep Apnea

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