Relationship Between Sleep-Disordered Breathing Level and Acute Onset Time of Congestive Heart Failure

Yoneyama, Kihei; Osada, Naohiko; Sugiyama, Takashi; Ishibashi, Yutaka; Hayashi, Akio; Takahashi, Eiji; Kida, Kenji; Suzuki, Kazuhiro; Tamura, Masachika; Inoue, Kentaro; Akashi, Yoshihiro; Omiya, Kazuto; Miyake, Fumihiko; Izawa, Kazuhiro P.; Watanabe, Satoshi

doi:10.1536/ihj.49.471

Cited by 5 publications

(4 citation statements)

References 23 publications

(21 reference statements)

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“…Hypoxemia plays a crucial role in sympathetic nerve system activation in SAS patients, which is related to nocturnal HTN including secondary HTN and non-dipper blood pressure (BP) pattern, and triggers cardiovascular events [4]. Our previous studies reported the influence of sleep disordered breathing (SDB) on the acute onset time of dyspnea and chest pain in patients with congestive heart failure [5] and acute coronary syndrome [6]. Currently, 24h ambulatory blood pressure monitoring (ABPM) provides accurate BP assessment during sleep.…”

Section: Introductionmentioning

confidence: 99%

Relationship between sleep apnea syndrome and sleep blood pressure in patients without hypertension

Sekizuka

Kida

Akashi

et al. 2010

Journal of Cardiology

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Section: Introductionmentioning

confidence: 99%

Relationship between sleep apnea syndrome and sleep blood pressure in patients without hypertension

Sekizuka

Kida

Akashi

et al. 2010

Journal of Cardiology

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“…1,2 Many investigators have reported that the risk of sudden death, heart failure or acute myocardial infarction increases during sleep in obstructive SAS patients. 5,6,19 These findings suggest that sleep BP control in these patients be desirable.…”

Section: Influential Factors In Circadian Bp Changesmentioning

confidence: 82%

“…Moreover, the incidence of nocturnal cardiovascular events while sleeping increases in these patients. [4][5][6] Chronic kidney disease (CKD) seems to be tightly linked with nocturnal hypertension and morning BP surge. 7 CKD poses a high risk for the onset of cardiovascular disease.…”

Section: Introductionmentioning

confidence: 99%

Relationship between chronic kidney disease and sleep blood pressure in patients with sleep apnea syndrome

et al. 2010

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Chronic kidney disease (CKD) is common disease in patients with sleep apnea syndrome (SAS), which is considered to be responsible for secondary and nocturnal hypertension. In this study, we assessed blood pressure (BP) changes in SAS patients with CKD. Of 460 Japanese outpatients with suspected SAS who underwent ambulatory BP monitoring within 3 months of overnight polysomnography, 198 patients (172 males and 26 females) who were not receiving treatment with antihypertensives or nitroglycerin were enrolled. The estimated glomerular filtration rate (eGFR) was calculated, and the patients were stratified into the high (H; eGFRX60 ml min À1 per 1.73 m 2 ) or the low (L; eGFRo60 ml min À1 per 1.73 m 2 ) group. The patients in the L group were significantly older than those in the H group (Po0.001), and body mass index was significantly smaller in the L group than in the H group (P¼0.025). The rate of patients treated with statin (P¼0.030) and the levels of both triglyceride (P¼0.006) and creatinine (Po0.001) differed significantly between the two groups. The sleep data, 24-h BP, awake BP and morning BP showed no significant differences between the two groups. However, sleep systolic and diastolic BPs were significantly higher in the L group (122.5±16.7 mm Hg and 81.1±12.2 mm Hg, respectively) than in the H group (117.1±11.8 mm Hg, P¼0.033; and 76.1±9.5 mm Hg, P¼0.012, respectively). SAS patients with CKD had elevated sleep BP. This result suggests that appropriate treatments for both SAS and CKD prevent sleep BP elevation, which is considered a risk factor for the onset risk of a cardiovascular event. Keywords: ambulatory blood pressure monitoring; circadian blood pressure; estimated glomerular filtration rate; nocturnal hypertension; polysomnography INTRODUCTIONIt is important to consider blood pressure (BP) outside of a clinic setting when treating patients with hypertension, because BP measurements obtained in a clinic setting are not representative of BP outside of the clinic setting. Abnormal changes in circadian BP are considered to increase the risk of cardiovascular event. Patients with nocturnal hypertension or a morning BP surge tend to have a higher incidence of silent cerebrovascular disease 1 and greater intima-media and relative wall thickness compared with normotensive patients. 2 Nocturnal hypertension and morning BP surge are induced by sleep disordered breathing, which can be observed in 22% of Japanese adult males. 3 Typical clinical features of BP changes in patients with sleep disordered breathing and those with sleep apnea syndrome (SAS) are nocturnal hypertension and non-dipper patterns of circadian BP. As the severity of SAS increases, sleep BP is elevated even in a patient whose BP is within the normal range in the clinic. Moreover, the incidence of nocturnal cardiovascular events while sleeping increases in these patients. [4][5][6] Chronic kidney disease (CKD) seems to be tightly linked with nocturnal hypertension and morning BP surge. 7 CKD poses a high risk for the onset of cardiovascu...

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“…For convenience, subjects with AHI > 20 are designated in the text as having “high levels of OSA activity” and those with AHI < 20 as having “low levels OSA activity.” In a recent study by Gooneratne et al (24), an AHI above 20 was associated with a higher mortality hazard ratio. Further, this cut‐off level has been applied in studies examining how sleep disordered breathing relates to congestive heart failure (25) and outcomes after cardiac resynchronization therapy (25, 26).…”

Section: Methodsmentioning

confidence: 99%

Sleep apnea modifies the long‐term impact of surgically induced weight loss on cardiac function and inflammation

Kardassis

Grote

Sjöström

et al. 2013

Obesity

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Objective: Obesity is frequently associated with obstructive sleep apnea (OSA). Both conditions are proinflammatory and proposed to deteriorate cardiac function. We used a nested cohort study design to evaluate the long-term impact of bariatric surgery on OSA and how weight loss and OSA relate to inflammation and cardiac performance. Design and Methods: At 10-year follow-up in the Swedish Obese Subjects (SOS) study, we identified 19 obese subjects (BMI 31.2 6 5.3 kg m À2 ), who following bariatric surgery at SOS-baseline had displayed sustained weight losses (surgery group), and 20 obese controls (BMI 42.0 6 6.2 kg m À2 ), who during the same time-period had maintained stable weight (control group). All study participants underwent overnight polysomnography examination, echocardiography and analysis of inflammatory markers. Results: The surgery group displayed a lower apnea hypopnea index (AHI) (19.9 6 21.5 vs. 37.8 6 27.7 n/h, P ¼ 0.013), lower inflammatory activity (hsCRP 2.3 6 3.0 vs. 7.2 6 5.0 mg L À1 , P < 0.001), reduced left ventricular mass (165 6 22 vs. 207 6 22 g, P < 0.001) and superior left ventricular diastolic function (E/A ratio 1.24 6 1.10 vs. 1.05 6 0.20, P ¼ 0.006) as compared with weight stable obese controls. In multiple regression analyses including all subjects (n ¼ 39) and controlling for BMI, the AHI remained independently associated with hsCRP (b ¼ 0.09,Conclusions: Patients with sustained weight loss after bariatric surgery display less severe sleep apnea, reduced inflammatory activity, and enhanced cardiac function. Persisting sleep apnea appears to limit the beneficial effect of weight loss on inflammation and cardiac performance.

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Relationship Between Sleep-Disordered Breathing Level and Acute Onset Time of Congestive Heart Failure

Cited by 5 publications

References 23 publications

Relationship between sleep apnea syndrome and sleep blood pressure in patients without hypertension

Relationship between sleep apnea syndrome and sleep blood pressure in patients without hypertension

Relationship between chronic kidney disease and sleep blood pressure in patients with sleep apnea syndrome

Sleep apnea modifies the long‐term impact of surgically induced weight loss on cardiac function and inflammation

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