Prognostic Significance of Insomnia in Heart Failure

Kanno, Yuki; Yoshihisa, Akiomi; Watanabe, Susumu; Takiguchi, Masafumi; Yokokawa, Tetsuro; Sato, Akihiko; Miura, Satoshi; Shimizu, Takeshi; Nakamura, Yūichi; Abe, Satoshi; Sato, Toshio; Suzuki, Satoshi; Oikawa, Masayoshi; Saitoh, Shu‐ichi; Takeishi, Yasuchika

doi:10.1253/circj.cj-16-0205

Cited by 56 publications

(63 citation statements)

References 41 publications

(23 reference statements)

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“…It may be associated with increased level of renin . However, renin level in this study was lower than that in previous reports; the effect of freeze/thaw cycles therefore may be limited.…”

Section: Limitationscontrasting

confidence: 85%

Clinical determinants and prognostic implications of renin and aldosterone in patients with symptomatic heart failure

et al. 2020

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Aims Activation of the renin-angiotensin-aldosterone system plays an important role in the pathophysiology of heart failure (HF) and has been associated with poor prognosis. There are limited data on the associations of renin and aldosterone levels with clinical profiles, treatment response, and study outcomes in patients with HF. Methods and results We analysed 2,039 patients with available baseline renin and aldosterone levels in BIOSTAT-CHF (a systems BIOlogy study to Tailored Treatment in Chronic Heart Failure). The primary outcome was the composite of all-cause mortality or HF hospitalization. We also investigated changes in renin and aldosterone levels after administration of mineralocorticoid receptor antagonists (MRAs) in a subset of the EPHESUS trial and in an acute HF cohort (PORTO). In BIOSTAT-CHF study, median renin and aldosterone levels were 85.3 (percentile 25-75 = 28-247) μIU/mL and 9.4 (percentile 25-75 = 4.4-19.8) ng/dL, respectively. Prior HF admission, lower blood pressure, sodium, poorer renal function, and MRA treatment were associated with higher renin and aldosterone. Higher renin was associated with an increased rate of the primary outcome [highest vs. lowest renin tertile: adjusted-HR (95% CI) = 1.47 (1.16-1.86), P = 0.002], whereas higher aldosterone was not [highest vs. lowest aldosterone tertile: adjusted-HR (95% CI) = 1.16 (0.93-1.44), P = 0.19]. Renin and/or aldosterone did not improve the BIOSTAT-CHF prognostic models. The rise in aldosterone with the use of MRAs was observed in EPHESUS and PORTO studies. Conclusions Circulating levels of renin and aldosterone were associated with both the disease severity and use of MRAs. By reflecting both the disease and its treatments, the prognostic discrimination of these biomarkers was poor. Our data suggest that the "point" measurement of renin and aldosterone in HF is of limited clinical utility.Categorical variables are described as frequencies (percentages), and continuous variables are described as means ± 954 M. Kobayashi et al. ESC Heart Failure 2020; 7: 953-963

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“…It may be associated with increased level of renin . However, renin level in this study was lower than that in previous reports; the effect of freeze/thaw cycles therefore may be limited.…”

Section: Limitationscontrasting

confidence: 85%

Clinical determinants and prognostic implications of renin and aldosterone in patients with symptomatic heart failure

et al. 2020

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“…Breath-by-breath oxygen consumption (VO2), carbon dioxide production (VCO2), and minute ventilation (VE) were measured during exercise using an AE-300S respiratory monitor (Minato Medical Science, Osaka, Japan). 12 Peak VO2 was measured as an average of the last 30 seconds of exercise. Ventilatory response to exercise (slope of the relationship between ventilation and carbon dioxide production, VE/VCO2 slope) was calculated as the regression slope relating VE to CO2 from the start of exercise until the respiratory compensation point.…”

mentioning

confidence: 99%

“…Ventilatory response to exercise (slope of the relationship between ventilation and carbon dioxide production, VE/VCO2 slope) was calculated as the regression slope relating VE to CO2 from the start of exercise until the respiratory compensation point. 12 Parametric variables are presented as mean ± SD, nonparametric variables (e.g., ferritin, vitamin B12, erythropoietin, C-reactive protein, BNP, and troponin I) are presented as median and interquartile range, and categorical variables are expressed as numbers and percentages. The chi-square test was used for comparisons of categorical variables.…”

mentioning

confidence: 99%

Relation of Testosterone Levels to Mortality in Men With Heart Failure

Yoshihisa

Suzuki

Sato

et al. 2018

The American Journal of Cardiology

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We aimed to investigate the impact of testosterone on the prognosis of heart failure (HF), as well as the underlying cardiac function, cardiac damage, and exercise capacity. We analyzed consecutive 618 men with HF (age 65.9 years). These patients were divided into quartiles based on their serum levels of total testosterone (TT): first (TT > 631 ng/dl, n = 154), second (462 < TT ≤ 631 ng/dl, n = 155), third (300 < TT ≤ 462 ng/dl, n = 156), and fourth (TT ≤ 300 ng/dl, n = 153) quartiles. In the Kaplan-Meier analysis (mean 1,281 days), all-cause mortality progressively increased throughout from the first to the fourth groups. In the multivariable Cox proportional hazard analysis, TT was found to be an independent predictor of all-cause mortality (hazard ratio 0.929, p = 0.042). In addition, we compared the parameters of echocardiography and cardiopulmonary exercise testing, as well as levels of B-type natriuretic peptide and cardiac troponin I, among the 4 groups. Left ventricular ejection fraction and B-type natriuretic peptide did not differ among the groups. In contrast, the fourth quartile, compared with the first, second, and third groups, had higher levels of troponin I and lower peak VO (p <0.05, respectively). Decreased serum testosterone is associated with myocardial damage, lower exercise capacity, and higher mortality in men with HF.

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“…Hence, we clearly mentioned this point in the limitations of our study. 1 Third, when analyzed separately based on sex in the Cox proportional hazard analysis, insomnia was a predictor of cardiac events in both male and female patients (male, HR 1.961, P<0.001; female, HR 1.754, P=0.003), and there was no interaction between the effect of insomnia and sex difference in our study population (P=0.543). In addition,…”

mentioning

confidence: 61%