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An in situ observation of the formation of a laser-irradiation-induced nanodot array on a Si surface was performed using a pulsed-laser-equipped high-voltage electron microscope (laser-HVEM). Under multiple nanosecond (ns) pulsed laser irradiation shots, atomic clusters were first formed and distributed on the surface in order to grow them epitaxially into protruded dots with diameters of ten nanometers or less. This is followed by their diffusion induced by successive laser shots to cannibalize and merge them into a ripple line with aligned, larger dots. We conclude that the present subwavelength two-dimensionally-ordered nanodot array is formed by self-organization under pulsed laser irradiation. [ABSTRACT FROM AUTHOR]

Background and Aims: In patients with heart failure (HF), differences in the association between estimated protein intake (PI) and prognosis in those with and without chronic kidney disease (CKD) remain to be clarified. This study aimed to investigate whether the prognostic effects of the estimated PI differ between patients with HF with and without CKD., Methods: We included patients who required hospitalisation owing to worsening HF between 2015 and 2019 and assessed the estimated PI based on the adjusted Maroni formula using the body mass index and urinary urea nitrogen level. Patients were stratified into the higher and lower estimated PI groups according to the median value of the estimated PI at the time of admission. The primary outcome was all-cause mortality., Results: Among the 694 enrolled patients, 286 had CKD. A lower estimated PI was independently associated with a worse nutritional status. During a median follow-up period of 17.2 months, 175 all-cause deaths occurred, including 99 and 76 in the lower and higher estimated PI groups, respectively. In the Kaplan-Meier curves, the lower estimated PI group was associated with higher overall mortality. However, lower estimated PI was significantly associated with all-cause mortality in patients without CKD, but not in those with CKD, after adjustment for covariates. A significant interaction in terms of prognostic effect was observed between the presence or absence of CKD and estimated PI., Conclusions: Among patients with HF, prognostic effect of the estimated PI may differ between patients with and without CKD., Competing Interests: Declaration of competing interest Yuya Matsue received an honorarium from Otsuka Pharmaceutical Co., Novartis Pharma K.K., Bayer Inc., and AstraZeneca and research grants from Pfizer Japan Inc., Otsuka Pharmaceutical Co., EN Otsuka Pharmaceutical Co., Ltd., and Nippon Boehringer Ingelheim Co., Ltd. Nobuyuki Kagiyama received grants from Philips, Asahi KASEI Corporation, Toho Holdings Co., Ltd., Inter Reha Co., Ltd., EchoNous. Inc., and AMI Inc. outside of the submitted work. Takatoshi Kasai is affiliated with a department-sponsored by Philips Respironics, ResMed, Teijin Home Healthcare, and Fukuda Denshi. The other authors declare no conflicts of interest., (Copyright © 2024 European Society for Clinical Nutrition and Metabolism. Published by Elsevier Ltd. All rights reserved.)

Sleep apnea (SA) is prevalent among patients with heart failure (HF) and contributes to a poor prognosis. Sodium-glucose cotransporter 2 (SGLT2) inhibitors have demonstrated efficacy in reducing the risk of serious clinical events in patients with HF. Additionally, SGLT2 inhibitors may reduce the risk of incident SA and mitigate its severity in patients with cardiovascular disease and T2DM. We aimed to investigate whether the SGLT2 inhibitor tofogliflozin reduced the severity of SA, as assessed using the apnea-hypopnea index (AHI), in patients with HF and T2DM and whether a decrease in AHI correlates with changes in body composition and cardiorenal function parameters. This is a single-arm, prospective pathophysiologic study involving patients with HF, T2DM, and SA, defined as having an AHI of 15 events/h and more. SA was assessed using polysomnography. Changes in AHI before and 6 months after starting oral administration of tofogliflozin (20 mg) were assessed. Additionally, body composition and cardiorenal functions were assessed before and 6 months after tofogliflozin administration. Ten patients with HF, T2DM, and SA were finally enrolled (60% men, 66.9 ± 13.4 years). Tofogliflozin reduced AHI from 43.2 [30.2] to 35.3 [13.1] events/h (p = 0.024) at 6 months. Hemoglobin A1c, body weight, and body water content decreased significantly. However, no significant changes were observed in the cardiorenal function parameters. A linear relationship was observed between the changes in body water content and AHI (r = 0.642, p = 0.045). Tofogliflozin reduced AHI, possibly associated with a reduction in body water content., Competing Interests: Compliance with ethical standards Conflict of interest SI and T Kasai contributed to the study design. AS, SS, HM, JS, SY, AM, MS, T Kato, MH, SN, MK, and FK collected data. SI, RN, KM, and T Kasai performed data and statistical analyses. SI and T Kasai drafted the manuscript. SI, T Kasai, AS, SS, HM, JS, SY, AM, MS, T Kato, MH, SN, MK, and FK performed critical revision, editing, and approval of the final manuscript. SI, T Kasai, HD, and TM are responsible for the overall content of guarantors, (© 2024. The Author(s), under exclusive licence to The Japanese Society of Hypertension.)

Sleep disordered breathing (SDB) is a common comorbidity in patients with atrial fibrillation (AF). Patients undergoing pulmonary vein isolation (PVI) for AF have a high prevalence of SDB. In previous studies, some patients with AF had Cheyne-Stokes respiration (CSR). The aim of the present study was to assess the prevalence of SDB and the correlates of SDB severity and CSR in AF patients who have undergone PVI. The study was conducted using a single-center observational design. All participants underwent a home sleep apnea test (ApneaLink Air, ResMed, Australia), which could determine the severity of SDB as assessed by the apnea-hypopnea index (AHI) and the percentage of CSR (%CSR) pattern. 139 AF patients who underwent PVI were included in the study. Overall, 38 (27.3%) patients had no SDB (AHI < 5), 53 (38.1%) had mild SDB (5 ≤ AHI < 15), 33 (23.7%) had moderate SDB (15 ≤ AHI < 30), and 15 (10.8%) had severe SDB (AHI ≥ 30). Correlates of the increased AHI included male sex (β = 0.23, p = 0.004), age (β = 0.19, p = 0.020), high body mass index (β = 0.31, p < 0.001), and β blockers usage (β = 0.18, p = 0.024). Conversely, correlates with the %CSR rate included male sex (β = 0.18, p = 0.020), age (β = 0.19, p = 0.015), non-paroxysmal AF (β = 0.22, p = 0.008), and high glycohemoglobin A1c (β = 0.36, p < 0.001) and N-terminal pro-brain natriuretic peptide (β = 0.24, p = 0.005) levels. SDB is prevalent in patients with AF who have undergone PVI; predisposing factors for SDB include male sex, older age, and obesity. CSR occurs in patients with AF who have undergone PVI; predisposing factors for CSR include male sex, older age, high left ventricular filling pressure, and abnormal blood glucose level., (© 2024. Springer Nature Japan KK, part of Springer Nature.)

Background: Primary percutaneous coronary intervention (PCI) for ST-segment-elevation myocardial infarction (STEMI) complicated by cardiogenic shock (CS) may reduce the risk of subsequent cardiovascular events but remains challenging. The study aim was to evaluate the clinical characteristics and long-term outcomes of patients undergoing primary PCI for STEMI with CS., Methods: We conducted an observational cohort study of patients with STEMI who underwent primary PCI between April 2004 and December 2017 at Juntendo University Shizuoka Hospital. The primary outcome was cardiovascular death (CVD) during the median 3-year follow-up. We performed a landmark analysis for the incidence of CVD from 0 day to 1 year and from 1 to 10 years., Results: Among the 1758 STEMI patients in the cohort, 212 (12.1 %) patients with CS showed significantly higher 30-day CVD rate on admission than those without (26.4 % vs 2.9 %). Landmark Kaplan-Meier analysis showed that CVD from day 0 to year 1 was significantly higher in the patients with CS (log-rank p < 0.0001). Multivariate Cox regression analysis showed that CS was significantly associated with higher cardiovascular mortality (adjusted hazard ratio, 11.8; 95%confidence intervals, 7.78-18.1; p < 0.0001), but the mortality rates from 1 to 10 years were comparable (log-rank p = 0.68)., Conclusion: The cardiovascular 1-year mortality rate for patients with STEMI was higher for those with CS on admission than without, but the mortality rates of >1 year were comparable. Surviving the early phase is essential for patients with STEMI and CS to improve long-term outcomes., Competing Interests: Disclosures None. Declaration of competing interest The authors declare that there is no conflict of interest., (Copyright © 2024 Elsevier Ltd. All rights reserved.)

Background: Both obstructive and central sleep apnea (OSA and CSA) may contribute to nocturnal cardiac arrhythmias (NCA). Data on the prevalence of clinically important nocturnal atrial and ventricular arrythmias in patients with heart failure with reduced ejection fraction (HFrEF) and obstructive (OSA) or central sleep apnea (CSA) are scarce., Research Questions: In a cohort of patients with HFrEF, how does the prevalence of NCA compare among those with OSA, CSA and those with no to mild sleep apnea? Is the severity of OSA or CSA associated with atrial and ventricular NCA?, Methods: This cross-sectional analysis is an ancillary study of the ADVENT-HF trial. We compared the prevalence of NCA (excessive supraventricular ectopic activity [ESVEA], defined as premature atrial complexes [PAC] ≥30/h or supraventricular tachycardia ≥20 beats); atrial fibrillation/flutter [AF]; and >10 premature ventricular complexes [PVC/h]) on ECGs from polysomnograms of HFrEF patients between those with OSA (apnea-hypopnea index [AHI≥15]), those with CSA (AHI≥15/h) and those with no to mild sleep apnea (AHI<15, control)., Results: Compared to controls (n=76), the prevalence of ESVEA was higher in patients with OSA (n=430) and CSA (n=150), 0%, 9% and 12%, respectively. The prevalences of AF in the control, OSA and CSA groups were 9%, 17% and 27%, and of >10 PVC/h 45%, 59% and 63%, respectively. In multivariable regression analyses PAC/h was associated with OSA severity (obstructive AHI) [22.4% increase per 10 events/h (95% confidence interval: 5.2; 42.3); p=0.009], but neither obstructive nor central AHI were associated with AF or >10 PVC/h., Interpretation: In patients with HFrEF, the prevalences of nocturnal ESVEA, AF and PVC >10/h were higher in those with, than in those without OSA or CSA, and OSA severity was related to the burden of nocturnal atrial ectopy. Severity of OSA or CSA were not significantly related to AF or >10 PVC/h., (Copyright © 2024. Published by Elsevier Inc.)

Overnight increases in arterial stiffness associated with sleep-disordered breathing may adversely affect patients with acute heart failure. Thus, we investigated overnight changes in arterial stiffness and their association with sleep-disordered breathing in patients hospitalized for acute heart failure. Consecutive patients with acute heart failure were enrolled. All participants underwent overnight full polysomnography following the initial improvement of acute signs and symptoms of acute heart failure. The arterial stiffness parameter, cardio-ankle vascular index (CAVI), was assessed before and after polysomnography. Overall, 60 patients (86.7% men) were analyzed. CAVI significantly increased overnight (from 8.4 ± 1.6 at night to 9.1 ± 1.7 in the morning, P < 0.001) in addition to systolic and diastolic blood pressure (from 114.1 mmHg to 121.6 mmHg, P < 0.001; and from 70.1 mmHg to 78.2 mmHg, P < 0.001, respectively). Overnight increase in CAVI (ΔCAVI ≥ 0) was observed in 42 patients (70%). The ΔCAVI ≥ 0 group was likely to have moderate-to-severe sleep-disordered breathing (i.e., apnea-hypopnea index ≥15, 55.6% vs 80.9%, P = 0.047) and greater obstructive respiratory events (29.4% vs 58.5%, P = 0.041). In multivariable analysis, moderate-to-severe sleep-disordered breathing and greater obstructive respiratory events were independently correlated with an overnight increase in CAVI (P = 0.033 and P = 0.042, respectively). In patients hospitalized for acute heart failure, arterial stiffness, as assessed by CAVI, significantly increased overnight. Moderate-to-severe sleep-disordered breathing and obstructive respiratory events may play an important role in the overnight increase in cardio-ankle vascular index., (© 2023. The Author(s), under exclusive licence to The Japanese Society of Hypertension.)

Background: In patients with heart failure and reduced ejection fraction, sleep-disordered breathing, comprising obstructive sleep apnoea (OSA) and central sleep apnoea (CSA), is associated with increased morbidity, mortality, and sleep disruption. We hypothesised that treating sleep-disordered breathing with a peak-flow triggered adaptive servo-ventilation (ASV) device would improve cardiovascular outcomes in patients with heart failure and reduced ejection fraction., Methods: We conducted a multicentre, multinational, parallel-group, open-label, phase 3 randomised controlled trial of peak-flow triggered ASV in patients aged 18 years or older with heart failure and reduced ejection fraction (left ventricular ejection fraction ≤45%) who were stabilised on optimal medical therapy with co-existing sleep-disordered breathing (apnoea-hypopnoea index [AHI] ≥15 events/h of sleep), with concealed allocation and blinded outcome assessments. The trial was carried out at 49 hospitals in nine countries. Sleep-disordered breathing was stratified into predominantly OSA with an Epworth Sleepiness Scale score of 10 or lower or predominantly CSA. Participants were randomly assigned to standard optimal treatment alone or standard optimal treatment with the addition of ASV (1:1), stratified by study site and sleep apnoea type (ie, CSA or OSA), with permuted blocks of sizes 4 and 6 in random order. Clinical evaluations were performed and Minnesota Living with Heart Failure Questionnaire, Epworth Sleepiness Scale, and New York Heart Association class were assessed at months 1, 3, and 6 following randomisation and every 6 months thereafter to a maximum of 5 years. The primary endpoint was the cumulative incidence of the composite of all-cause mortality, first admission to hospital for a cardiovascular reason, new onset atrial fibrillation or flutter, and delivery of an appropriate cardioverter-defibrillator shock. All-cause mortality was a secondary endpoint. Analysis for the primary outcome was done in the intention-to-treat population. This trial is registered with ClinicalTrials.gov (NCT01128816) and the International Standard Randomised Controlled Trial Number Register (ISRCTN67500535), and the trial is complete., Findings: The first and last enrolments were Sept 22, 2010, and March 20, 2021. Enrolments terminated prematurely due to COVID-19-related restrictions. 1127 patients were screened, of whom 731 (65%) patients were randomly assigned to receive standard care (n=375; mean AHI 42·8 events per h of sleep [SD 20·9]) or standard care plus ASV (n=356; 43·3 events per h of sleep [20·5]). Follow-up of all patients ended at the latest on June 15, 2021, when the trial was terminated prematurely due to a recall of the ASV device due to potential disintegration of the motor sound-abatement material. Over the course of the trial, 41 (6%) of participants withdrew consent and 34 (5%) were lost to follow-up. In the ASV group, the mean AHI decreased to 2·8-3·7 events per h over the course of the trial, with associated improvements in sleep quality assessed 1 month following randomisation. Over a mean follow-up period of 3·6 years (SD 1·6), ASV had no effect on the primary composite outcome (180 events in the control group vs 166 in the ASV group; hazard ratio [HR] 0·95, 95% CI 0·77-1·18; p=0·67) or the secondary endpoint of all-cause mortality (88 deaths in the control group vs. 76 in the ASV group; 0·89, 0·66-1·21; p=0·47). For patients with OSA, the HR for all-cause mortality was 1·00 (0·68-1·46; p=0·98) and for CSA was 0·74 (0·44-1·23; p=0·25). No safety issue related to ASV use was identified., Interpretation: In patients with heart failure and reduced ejection fraction and sleep-disordered breathing, ASV had no effect on the primary composite outcome or mortality but eliminated sleep-disordered breathing safely., Funding: Canadian Institutes of Health Research and Philips RS North America., Competing Interests: Declaration of interests Partial funding for this trial, as well as ASV devices, were provided by Philips RS North America. These resources supported the work of all co-authors and trial sites. TDB reports receiving a speaking honorarium from Philips. JSF reports receiving a speaking honorarium and travel expenses from Philips. MA reports receiving speaking honoraria and research grant support from Philips and ResMed. RJK reports receiving speaking honoraria from Eisa and Powell-Mansfield. JMMT reports receiving speaking honoraria from Gebro, Menarini, and Chiesa and research grant support from GSK and AstraZeneca. All other authors declare no competing interests aside from grant support from Philips RS North America to conduct the clinical trial described herein., (Copyright © 2024 Elsevier Ltd. All rights reserved.)

A 60-year-old man with hypertension and dyslipidemia complained of chest pain upon ascending from a maximum depth of 27 meters while diving. After reaching the shore, his chest pain persisted, and he called an ambulance. When a physician checked him on the doctor's helicopter, his electrocardiogram (ECG) was normal, and there were no bubbles in his inferior vena cava or heart on a portable ultrasound examination. The physician still suspected that he had acute coronary syndrome instead of decompression illness; therefore, he was transported to our hospital. After arrival at the hospital, standard cardiac echography showed a flap in the ascending aorta. Immediate enhanced computed tomography revealed Stanford type A aortic dissection. The patient obtained a survival outcome after emergency surgery. To our knowledge, this is the first reported case of aortic dissection potentially associated with scuba diving. It highlights the importance of considering aortic dissection in patients with sudden-onset chest pain during physical activity. In addition, this serves as a reminder that symptoms during scuba diving are not always related to decompression. This report also suggests the usefulness of on-site ultrasound for the differential diagnosis of decompression sickness from endogenous diseases that induce chest pain. Further clinical studies of this management approach are warranted., Competing Interests: The authors of this paper declare no conflicts of interest exist with this submission., (Copyright© Undersea and Hyperbaric Medical Society.)

Hyperuricemia is influenced by diet and can cause gout. Whether it is a potential risk factor for cardiovascular disease (CVD) remains controversial, and the mechanism is unclear. Similar to CVDs, gout attacks occur more frequently in the morning and at night. A possible reason for this is the diurnal variation in uric acid (UA), However, scientific data regarding this variation in patients with CVD are not available. Thus, we aimed to investigate diurnal variations in serum levels of UA and plasma levels of xanthine, hypoxanthine, and xanthine oxidoreductase (XOR) activity, which were measured at 18:00, 6:00, and 12:00 in male patients with coronary artery disease. Thirty eligible patients participated in the study. UA and xanthine levels significantly increased from 18:00 to 6:00 but significantly decreased from 6:00 to 12:00. By contrast, XOR activity significantly increased both from 18:00 to 6:00 and 6:00 to 12:00. Furthermore, the rates of increase in UA and xanthine levels from night to morning were significantly and positively correlated. In conclusion, UA and xanthine showed similar diurnal variations, whereas XOR activity showed different diurnal variations. The morning UA surge could be due to UA production. The mechanism involved XOR activity, but other factors were also considered.

Serum uric acid (UA) level is associated with the high cumulative incidence or prevalence of coronary artery disease (CAD), and hyperuricemia is considered as an independent risk marker for CAD. Sleep-disordered breathing (SDB) is also associated with an increased risk of CAD. Several studies have shown that SDB is associated with hyperuricemia, but the mechanisms are unclear. We measured serum levels of UA and xanthine oxidoreductase (XOR) activity and urinary levels of 8-hydroxy-2'-deoxyguanosine (8-OHdG), all of which were assessed at 6 p.m. and the following 6 a.m. in males with CAD. In addition, nocturnal pulse oximetry was performed for the night. Overall 32 eligible patients with CAD were enrolled. Serum UA levels significantly increased overnight. (5.32 ± 0.98 mg/dl to 5.46 ± 1.02 mg/dl, p < 0.001) Moreover, XOR activity and urinary 8-OHdG levels significantly increased from 6 p.m. to 6 a.m. Furthermore, 3% Oxygen desaturation index (ODI) was correlated with the overnight changes in XOR activity (r = 0.36, P = 0.047) and urinary 8-OHdG levels (r = 0.41, P = 0.02). In addition, 3%ODI was independently correlated with the changes in XOR activity (correlation coefficient, 0.36; P = 0.047) and 8-OHdG (partial correlation coefficient, 0.63; P = 0.004) in multivariable analyses. SDB severity was associated with the overnight changes in XOR activity and urinary 8-OHdG, suggesting that SDB may be associated with oxidative stress via UA production. This trial is registered at University Hospital Medical Information Network (UMIN), number: UMIN000021624., (© 2023. The Author(s), under exclusive licence to The Japanese Society of Hypertension.)

Background and Aims: Heart failure with concomitant sarcopenia has a poor prognosis; therefore, simple methods for evaluating the appendicular skeletal muscle mass index (ASMI) are required. Recently, a model incorporating anthropometric data and the sarcopenia index (i.e., serum creatinine-to-cystatin C ratio [Cre/CysC]), was developed to estimate the ASMI. We hypothesized that this model was superior to the traditional model, which uses only anthropometric data to predict prognosis. This retrospective cohort study compared the prognostic value of low ASMI as defined by the biomarker and anthropometric models in patients with heart failure., Methods and Results: Among 847 patients, we estimated ASMI using an anthropometric model (incorporating age, body weight, and height) in 791 patients and a biomarker model (incorporating age, body weight, hemoglobin, and Cre/CysC) in 562 patients. The primary outcome was all-cause mortality. Overall, 53.4% and 39.1% of patients were diagnosed with low ASMI (using the Asian Working Group for Sarcopenia cut-off) by the anthropometric and biomarker models, respectively. The two models showed a poor agreement in the diagnosis of low ASMI (kappa: 0.57, 95% confidence interval: 0.50-0.63). Kaplan-Meier curves showed that a low ASMI was significantly associated with all-cause death in both models. However, this association was retained after adjustment for other covariates in the biomarker model (hazard ratio: 2.32, p = 0.001) but not in the anthropometric model (hazard ratio: 0.79, p = 0.360)., Conclusion: Among patients hospitalized with heart failure, a low ASMI estimated using the biomarker model, and not the anthropometric model, was significantly associated with all-cause mortality., Competing Interests: Declaration of competing interest The authors declare no conflicts of interest., (Copyright © 2023 The Italian Diabetes Society, the Italian Society for the Study of Atherosclerosis, the Italian Society of Human Nutrition and the Department of Clinical Medicine and Surgery, Federico II University. Published by Elsevier B.V. All rights reserved.)

We investigated the clinical and prognostic implications of hyaluronic acid, a liver fibrosis marker, in patients with heart failure. We measured hyaluronic acid levels on admission in 655 hospitalized patients with heart failure between January 2015 and December 2019. Patients were stratified into three groups according to hyaluronic acid level: low (< 84.3 ng/mL, n = 219), middle (84.3-188.2 ng/mL, n = 218), and high (≥ 188.2 ng/mL, n = 218). The primary endpoint was all-cause death. The high hyaluronic acid group had higher N-terminal pro-brain-type natriuretic peptide levels, larger inferior vena cava, and shorter tricuspid annular plane systolic excursion than the other two groups. During the follow-up period (median 485 days), 132 all-cause deaths were observed: 27 (12.3%) in the low, 37 (17.0%) in the middle, and 68 (31.2%) in the high hyaluronic acid (P < 0.001) groups. Cox proportional hazards analysis revealed that higher log-transformed hyaluronic acid levels were significantly associated with all-cause death (hazard ratio, 1.38; 95% confidence interval, 1.15-1.66; P < 0.001). No significant interaction was observed between hyaluronic acid level and reduced/preserved left ventricular ejection fraction on all-cause death (P = 0.409). Hyaluronic acid provided additional prognostic predictability to pre-existing prognostic factors, including the fibrosis-4 index (continuous net reclassification improvement, 0.232; 95% confidence interval, 0.022-0.441; P = 0.030). In hospitalized patients with heart failure, hyaluronic acid was associated with right ventricular dysfunction and congestion and was independently associated with prognosis regardless of left ventricular ejection fraction., (© 2023. Springer Nature Japan KK, part of Springer Nature.)

Malnutrition frequently coexists with heart failure (HF), leading to series of negative consequences. Cheyne-Stokes respiration (CSR) is predominantly detected in patients with HF. However, the effect of CSR and malnutrition on the long-term prognosis of patients with acute decompensated HF (ADHF) remains unclear. We enrolled 162 patients with ADHF (median age, 62 years; 78.4% men). The presence of CSR was assessed using polysomnography and the controlling nutritional status score was assessed to evaluate the nutritional status. Patients were divided into four groups based on CSR and malnutrition. The primary outcome was all-cause mortality. In total, 44% of patients had CSR and 67% of patients had malnutrition. The all-cause mortality rate was 26 (16%) during the 35.9 months median follow-up period. CSR with malnutrition was associated with lower survival rates (log-rank p < 0.001). Age, hemoglobin, albumin, lymphocyte count, total cholesterol, triglyceride, low-density lipoprotein cholesterol, creatinine, estimated glomerular filtration rate, B-type natriuretic peptide, administration of loop diuretics, apnea-hypopnea index and central apnea-hypopnea index were significantly different among all groups ( p < 0.05). CSR with malnutrition was independently associated with all-cause mortality. In conclusion, CSR with malnutrition is associated with a high risk of all-cause mortality in patients with ADHF.

Background: Identifying patients at risk for poor clinical outcomes following acute heart failure (AHF) is essential. However, data regarding the prognostic effect of sleep-disordered breathing (SDB) and treatment with positive airway pressure (PAP) on clinical outcomes of hospitalized patients following AHF is lacking., Objectives: This study investigated the prognostic effect of SDB, PAP treatment, and compliance with PAP treatment on patient clinical outcomes. Polysomnography was performed in hospitalized patients whose left ventricular ejection fraction was < 50%. Patients were divided into groups based on whether SDB was defined as an apnea-hypopnea index ≥ 15 and if they had received PAP treatment. Furthermore, patients with SDB and PAP were subdivided into more and less compliant groups. We assessed the incidences of deaths and rehospitalizations due to heart failure., Results: Overall, 241 patients were enrolled; 73% had SDB and 29% were initiated on PAP treatment. At a median follow-up of 1.7 years, 74 clinical events (32 deaths, 42 rehospitalizations) occurred. In the multivariable analysis, compared with the non-SDB group, SDB without PAP treatment was associated with an increased risk of clinical outcomes (hazard ratio [HR] 1.79, P = 0.049), whereas SDB with PAP treatment was not (HR 0.78, P = 0.582). Among patients with PAP treatment, a more compliant group was also inversely associated with clinical events (HR 0.11, P = 0.012)., Conclusions: In hospitalized patients with AHF, untreated SDB was associated with worse clinical outcomes that might be reversible by PAP treatment. However, this potential may be suppressed in less compliant patients., (© 2021. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany.)

Mid-aortic syndrome (MAS) is a rare vascular disorder that causes refractory hypertension. A 76-year-old woman was hospitalized for acute heart failure (HF) with drug-resistant hypertension; other comorbidities included epigastric artery rupture, old myocardial infarction, an intraventricular thrombus, and a cerebral artery aneurysm. Angiography revealed severe narrowing of the descending aorta, which led to the diagnosis of MAS. Although intensive medical treatment improved her HF, optimal blood pressure (BP) could not be achieved. Percutaneous coronary intervention and surgical bypass for diseased aorta was then performed in two stages, resulting in the achievement of optimal BP and alleviation of HF.

Background: Although short-term mortality of acute myocardial infarction (AMI) has decreased dramatically in the past few decades, sudden cardiac arrest remains a serious complication. The aim of the study was to assess the clinical characteristics and predictors of prognosis in AMI patients who experienced out-of-hospital cardiac arrest (OHCA)., Methods: We retrospectively registered consecutive AMI patients who were treated with emergency percutaneous coronary intervention (PCI) between 2004 and 2017. Clinical characteristics and outcomes were compared between patients with OHCA and those without OHCA., Results: Among 2101 AMI patients, 95 (4.7%) presented with OHCA. Younger age (odds ratio [OR]: 0.95; 95% confidence interval [CI]: 0.93-0.97; p < 0.0001), absence of diabetes mellitus (OR, 0.51; 95% CI, 0.30-0.85; p = 0.01) or dyslipidemia (OR, 0.56; 95% CI, 0.36-0.88; p = 0.01), left main trunk (LMT) or left anterior descending artery (LAD) as the culprit lesion (OR, 3.26; 95% CI, 1.99-5.33; p < 0.0001), and renal deficiency (OR, 3.64; 95% CI, 2.27-5.84; p < 0.0001) were significantly associated with incidence of OHCA. Thirty-day mortality was 32.6% in patients with OHCA and 4.5% in those without OHCA. Multivariate logistic analysis revealed LMT or LAD as the culprit lesion (OR, 12.18; 95% CI, 2.27-65.41; p = 0.004), glucose level (OR, 1.01; 95% CI, 1.00-1.01; p = 0.01), and renal deficiency (OR, 3.35; 95% CI, 1.07-10.53; p = 0.04) as independent predictors of 30-day mortality among AMI patients with OHCA., Conclusions: In patients with AMI who underwent emergency PCI, 30-day mortality was six times greater in those having presented initially with OHCA compared with those without OHCA. Younger age, absence of diabetes mellitus or dyslipidemia, LMT or LAD as the culprit lesion, and renal deficiency were independent predictors of OHCA. OHCA patient with higher blood glucose level on admission, LMT or LAD as the culprit lesion, or renal deficiency showed worse clinical outcomes., (© 2022. The Author(s).)

Background: Renal dysfunction includes glomerular dysfunction (GD) and tubular dysfunction (TD); however, there is limited information regarding the prevalence, coexistence, and prognostic relevance of TD and GD among patients with acute heart failure (AHF)., Methods and results: This study reviewed 489 patients with AHF who had undergone testing at the time of their admission to identify GD (estimated glomerular filtration rate <60 mL/min/1.73 m 2 ) and TD (urinary β-2-microglobulin ≥300 µg/gCr). Patients were grouped according to the presence/absence of GD and TD as having neither condition (n=116), isolated TD (n=101), isolated GD (n=83), or coexisting GD plus TD (n=189). During a median follow up of 466 days (interquartile range: 170-871 days), 107 deaths were observed. Kaplan-Meier curve analysis revealed that, relative to the absence of a GD and TD group, higher mortality rates were observed in the groups with isolated TD, isolated GD, and coexisting GD plus TD (log-rank P<0.001). Similarly, the adjusted Cox regression analyses revealed that significantly higher risks of mortality were associated with isolated TD, isolated GD, and coexisting GD plus TD. Moreover, isolated GD and isolated TD were both independently associated with increased risks of all-cause mortality., Conclusions: As a significant proportion of patients with AHF had isolated TD and an increased risk of mortality, patients with AHF should be screened for TD even if they do not have GD.

Pulmonary arteriovenous malformation (PAVM) is a probable cause of thromboembolic diseases such as acute myocardial infarction (MI); however, few cases have been reported. A woman in her early 40s developed acute-onset chest pain; an ECG showed ST-elevated MI. Emergency catheter angiography showed that the culprit lesion was a thrombus that was treated successfully with aspiration. She had a history of deep venous thrombosis and CT revealed PAVM. It was likely that the venous thrombus had moved into the coronary artery through the PAVM. Catheter embolisation of the PAVM was performed and she did not experience any other cardiac event until 6 months after embolisation., Competing Interests: Competing interests: None declared., (© BMJ Publishing Group Limited 2022. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)

Aims: Urinary liver-type fatty acid-binding protein (L-FABP) is expressed in proximal tubular epithelial cells and excreted into the urine during tubular injury. We hypothesized that high urinary L-FABP is associated with poor prognosis in patients with acute heart failure (AHF)., Methods and Results: We analysed 623 patients (74 ± 13 years old; 60.0% male patients) with AHF. Urinary L-FABP levels were measured at the time of admission and adjusted for the urinary creatinine concentration. The primary endpoint was all-cause mortality. The median value and interquartile range of urinary L-FABP levels were 6.66 and 3.37-21.1 μg/gCr, respectively. Urinary L-FABP levels were significantly correlated with both beta-2 microglobulin and cystatin C levels; the correlation with the former was higher than that with the latter. During the follow-up of 631 (interquartile range: 387-875) days, 142 deaths occurred. A high tertile of urinary L-FABP level was associated with high mortality; this association was retained after adjusting for other covariates (second tertile hazard ratio 1.40, P = 0.152 vs. first tertile; third tertile hazard ratio 1.94, P = 0.005 vs. first tertile)., Conclusions: Urinary L-FABP is more closely associated with tubular dysfunction than with glomerular dysfunction. Tubular dysfunction, which was evaluated based on urinary L-FABP levels, in patients with AHF is associated with all-cause mortality and is independent of pre-existing risk factors. L-FABP should be considered for use in the prognosis of AHF., (© 2021 The Authors. ESC Heart Failure published by John Wiley & Sons Ltd on behalf of European Society of Cardiology.)

Study Objectives: Patients with sleep-disordered breathing have cyclic variation of heart rate (CVHR) in response to respiratory events. However, limited data are available regarding the utility of CVHR as a screening tool for sleep-disordered breathing in patients with mixed heart failure (HF) and those without HF., Methods: We enrolled consecutive patients with and without HF who underwent full polysomnographies with simultaneous Holter electrocardiogram monitoring. We determined the temporal position of the individual dips comprising the CVHR score using time-domain methods., Results: The data of 101 patients, including 70 with and 31 without HF, were analyzed. The CVHR score was significantly correlated with the apnea-hypopnea index ( r = .667, P < .001) and limits of agreement between the apnea-hypopnea index and CVHR score were -21.8 to 35.2. The receiver operating characteristic analysis demonstrated that the CVHR score (best cut-off of 23.5 events/h) identified severe sleep-disordered breathing with a sensitivity of 83.3%, specificity of 79.5%, and the area under the curve of 0.856. In addition, there was no interaction between the presence or absence of HF and the apnea-hypopnea index-CVHR score relationship ( P = .323)., Conclusions: The CVHR score, determined by Holter electrocardiogram monitoring, is a useful tool for evaluating sleep-disordered breathing even in patients with mixed HF and patients without HF., Citation: Yatsu S, Kasai T, Naito R, et al. Utility of cyclic variation of heart rate score as a screening tool for sleep-disordered breathing in patients with heart failure. J Clin Sleep Med . 2021;17(11):2187-2196., (© 2021 American Academy of Sleep Medicine.)

Aims: Relationships between cardiac acoustic biomarkers (CABs) measured by acoustic cardiography and clinical outcomes have been reported in heart failure (HF) patients. However, no studies have investigated the temporal change of CABs and the corresponding changes in HF status. The purpose of this study was to assess whether the temporal changes of CABs in patients with acute decompensated heart failure (ADHF) reflect changes in cardiac function and status., Methods and Results: Sixty ADHF patients were enrolled prospectively. CABs and echocardiography data were collected at admission, before discharge, and at the first clinic visit. CABs included electromechanical activation time (EMAT); the time interval from Q wave onset on electrocardiography to the first heart sound (S1), QoS2; the time interval from Q wave onset on electrocardiography to the second heart sound (S2); and third heart sound (S3) and fourth heart sound (S4) intensities, defined as the peak-to-peak amplitudes of S3 and S4. EMATc (EMAT/RR) (P = 0.001), S3 intensity (P < 0.001), and S4 intensity (P < 0.001) were significantly decreased, and QoS2 (P = 0.005) was significantly increased from admission to discharge. The change in S3 intensity was significantly correlated with that of E/A (ρ = 0.571, P < 0.001), and the extended QoS2 was also significantly correlated with the increase in the stroke volume index (ρ = 0.383, P = 0.004)., Conclusions: Some CABs in ADHF patients changed significantly in the normal direction throughout the treatment course and could be useful biomarkers in ADHF management., (© 2021 The Authors. ESC Heart Failure published by John Wiley & Sons Ltd on behalf of European Society of Cardiology.)

Background: Although urinary alpha-1-microglobulin has been used as a marker of tubular dysfunction, its clinical and prognostic values in patients with acute heart failure have not been validated., Methods: We analyzed 623 patients (74 ± 13 years old, 60.0% male) with acute heart failure in whom urinary alpha-1-microglobulin (A1MG) levels were measured as tubular markers at the time of admission. The primary endpoint was all-cause mortality., Results: The median levels of urinary alpha-1-microglobulin with and without correction for urinary creatinine concentration were 8.80 (interquartile range: 4.20-17.7) mg/dL and 12.9 (5.92-30.7) mg/gCr, respectively. Urinary A1MG levels were significantly correlated with all of beta-2-microglobulin (r = 0.77), N-acetyl-β-D-glucosaminidase (r = 0.51), and estimated glomerular filtration rate (r = -0.42); however, alpha-1-microglobulin was most often predicted using beta-2-microglobulin or N-acetyl-β-D-glucosaminidase. During the 488-day (interquartile range: 185-938 days) follow-up, 141 deaths occurred. Higher A1MG levels were associated with higher mortality even after adjustment for other covariates. Only A1MG, but not beta-2-microglobulin or N-acetyl-β-D-glucosaminidase, yielded incremental prognostic information in addition to the preexisting prognostic factors (net-reclassification improvement: 0.254, P = 0.023; integrated discrimination improvement: 0.015, P = 0.028)., Conclusions: In patients hospitalized due to acute heart failure, urinary alpha-1-microglobulin was a marker of tubular dysfunction. High alpha-1-microglobulin was associated with all-cause mortality independent of glomerular function and was a better predictor of mortality than urinary beta-2-microglobulin., (Copyright © 2021 Elsevier B.V. All rights reserved.)

Aims: Although both hypercapnia and hypocapnia are common in acute heart failure (AHF) patients, routine assessment of arterial blood gas is not recommended. Additionally, no association between hypercapnia and increased mortality has been found, and the prognostic value of hypocapnia in AHF patients remains to be elucidated. In this observational study, we aimed to investigate the relationship between partial pressure of arterial carbon dioxide (PaCO2), especially low PaCO2, and long-term mortality in AHF patients., Methods and Results: Acute heart failure patients hospitalized in the cardiac intensive care unit of our institution between 2007 and 2011 were screened. All eligible patients were divided into two groups based on the inflection point (i.e. 31.0 mmHg) of the 3-knot cubic spline curve of the hazard ratio (HR), with a PaCO2 of 40 mmHg as a reference. The association between PaCO2 levels and all-cause mortality was assessed using Cox proportional hazards regression models. Among 435 patients with a median follow-up of 1.8 years, 115 (26.4%) died. Adjusted analysis with relevant variables as confounders indicated that PaCO2 <31 mmHg was significantly associated with increased all-cause mortality [HR 1.71, 95% confidence interval (CI) 1.05-2.79; P = 0.032]. When PaCO2 was considered as a continuous variable, the lower was the log-transformed PaCO2, the greater was the increased risk of mortality (HR 0.71, 95% CI 0.52-0.96; P = 0.024)., Conclusions: In AHF patients, lower PaCO2 at admission was associated with increased long-term mortality risk., (Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2021. For permissions, please email: journals.permissions@oup.com.)