Waist‐to‐hip ratio and mortality in heart failure Streng, Koen W.; Voors, Adriaan A.; Hillege, Hans L. ...
European journal of heart failure,
September 2018, Letnik:
20, Številka:
9
Journal Article
Recenzirano
Odprti dostop
Aims
A higher body mass index (BMI) is associated with better survival in heart failure (HF) patients, also known as the obesity paradox. However, BMI does not account for body composition. We ...therefore analysed the association between abdominal fat, measured via waist‐to‐hip ratio (WHR), BMI and all‐cause mortality in patients with HF.
Methods and results
For this analysis, 1738 patients from the Scottish BIOlogy Study to TAilored Treatment in Chronic Heart Failure (BIOSTAT‐CHF) validation study were included. Patients without waist and hip measurements were excluded. WHR was defined as waist circumference/hip circumference, divided into tertiles and split for sex. A linear regression of principal components from an extensive panel of biomarkers was performed to provide insight in the pathophysiology behind a higher WHR. In total, 1479 patients were included, of which 33% were female and mean age was 75 ±11 years. A higher WHR was independently associated with a higher BMI, a higher prevalence of diabetes and higher New York Heart Association functional class. There was a significant interaction between sex and WHR on its association with mortality (P <0.001). In women, a higher WHR was associated with a higher mortality risk hazard ratio (HR) 2.23, 95% confidence interval (CI) 1.37–3.63; P =0.001, whereas no significant association was found in men (HR 0.87, 95% CI 0.63–1.20; P = 0.409). We found a strong association between a higher WHR and elevated markers of inflammation and MAPK cascade in women, while these associations were less profound in men.
Conclusions
A higher WHR was associated with a higher risk of death in female but not in male HF patients. These findings challenge the obesity paradox, and suggest that fat deposition is pathophysiologically harmful and may be a target for therapy in female patients with HF.
Objective
Despite growing evidence about myocardial injury in hospitalized COronaVIrus Disease 2019 (COVID-19) patients, the mechanism behind this injury is only poorly understood and little is known ...about its association with SARS-CoV-2-mediated myocarditis. Furthermore, definite evidence of the presence and role of SARS-CoV-2 in cardiomyocytes in the clinical scenario is still lacking.
Methods
We histologically characterized myocardial tissue of 40 patients deceased with severe SARS-CoV-2 infection during the first wave of the pandemic. Clinical data were also recorded and analyzed. In case of findings supportive of myocardial inflammation, histological analysis was complemented by RT-PCR and immunohistochemistry for SARS-CoV-2 viral antigens and in situ RNA hybridization for the detection of viral genomes.
Results
Both chronic and acute myocardial damage was invariably present, correlating with the age and comorbidities of our population. Myocarditis of overt entity was found in one case (2.5%). SARS-CoV-2 genome was not found in the cardiomyocytes of the patient with myocarditis, while it was focally and negligibly present in cardiomyocytes of patients with known viral persistence in the lungs and no signs of myocardial inflammation. The presence of myocardial injury was not associated with myocardial inflammatory infiltrates.
Conclusions
In this autopsy cohort of COVID-19 patients, myocarditis is rarely found and not associated with SARS-CoV-2 presence in cardiomyocytes. Chronic and acute forms of myocardial damage are constantly found and correlate with the severity of COVID-19 disease and pre-existing comorbidities.
Graphic abstract
Heart failure continues to be a leading cause of hospitalization worldwide, and acute heart failure (AHF) carries significant risk for short-term morbidity and mortality. Despite many trials of ...potential new therapies for AHF, there have been very few advances over the recent decades. In this review, we will examine mortality during and after AHF hospitalization, with an emphasis on available data on mode of death (MOD). We will also review data on the timing of different MOD after AHF and the effect of specific therapies, as well as what is known about the contribution of specific pathophysiological mechanisms. Finally, we discuss the potential utility of further study of MOD data for AHF and its application to drug development, risk stratification, and therapeutic tailoring to improve short- and long-term outcomes in AHF. (Circ J 2016; 80: 17–23)
Summary Background Most patients admitted for acute heart failure have normal or increase blood pressure. Relaxin is a natural human peptide that affects multiple vascular control pathways, ...suggesting potential mechanisms of benefit for such patients. We assessed the dose response of relaxin's effect on symptom relief, other clinical outcomes, and safety. Methods In a placebo-controlled, parallel-group, dose-ranging study, 234 patients with acute heart failure, dyspnoea, congestion on chest radiograph, and increased brain natriuretic peptide (BNP) or N-terminal prohormone of BNP, mild-to-moderate renal insufficiency, and systolic blood pressure greater than 125 mm Hg were recruited from 54 sites in eight countries and enrolled within 16 h of presentation. Patients were randomly assigned, in a double-blind manner via a telephone-based interactive voice response system, to standard care plus 48-h intravenous infusion of placebo (n=62) or relaxin 10 μg/kg (n=40), 30 μg/kg (n=43), 100 μg/kg (n=39), or 250 μg/kg (n=50) per day. Several clinical endpoints were explored to assess whether intravenous relaxin should be pursued in larger studies of acute heart failure, to identify an optimum dose, and to help to assess endpoint selection and power calculations. Analysis was by modified intention to treat. This study is registered with ClinicalTrials.gov , number NCT00520806. Findings In the modified intention-to-treat population, 61 patients were assessed in the placebo group, 40 in the relaxin 10 μg/kg per day group, 42 in the relaxin 30 μg/kg per day group, 37 in the relaxin 100 μg/kg per day group, and 49 in the relaxin 250 μg/kg per day group. Dyspnoea improved with relaxin 30 μg/kg compared with placebo, as assessed by Likert scale (17 of 42 patients 40% moderately or markedly improved at 6 h, 12 h, and 24 h vs 14 of 61 23%; p=0·044) and visual analogue scale through day 14 (8214 mm×h SD 8712 vs 4622 mm×h 9003; p=0·053). Length of stay was 10·2 days (SD 6·1) for relaxin-treated patients versus 12·0 days (7·3) for those given placebo, and days alive out of hospital were 47·9 (10·1) versus 44·2 (14·2). Cardiovascular death or readmission due to heart or renal failure at day 60 was reduced with relaxin (2·6% 95% CI 0·4–16·8 vs 17·2% 9·6–29·6; p=0·053). The number of serious adverse events was similar between groups. Interpretation When given to patients with acute heart failure and normal-to-increased blood pressure, relaxin was associated with favourable relief of dyspnoea and other clinical outcomes, with acceptable safety. Funding Corthera (USA).
BACKGROUNDAtrioventricular node ablation (AVNA) and pacemaker (PM) is performed in symptomatic atrial fibrillation (AF) unresponsive to medical treatment and percutaneous ablation. This meta-analysis ...evaluated results after AVNA and PM. METHODSPrimary and secondary endpoints were early/late overall/cardiac-related mortality and early/late postoperative complications. Meta-regression explored mortality and preoperative characteristics relation. RESULTSWe selected 93 studies with 11,340 patients: 9105 right ventricular (RV)-PM, and 2235 biventricular PM (cardiac resynchronization therapy, CRT). Malignant arrhythmia (2.5%), heart failure (2.4%), and lead dislodgement (2.0%) were most common periprocedural complications. Pooled estimated 30-day mortality was 1.08% (95%CI:0.65-1.77). At 19.9 months median follow-up (IQR: 10.3-34 months), rehospitalization (0.79%/month) and heart failure (0.48%/month) were the most frequent complications. Overall mortality incidence rate (IR) was 0.43%/month (95%CI:0.36-0.51), and cardiac death IR 0.27%/month (95%CI:0.22-0.32). No mortality determinants emerged in the AVNA CRT subgroup. AVNA RV-PM subgroup univariable meta-regression showed inverse relationship between age, ejection fraction (EF), and late cardiac death (Beta = -0.0709 ± 0.0272; p = 0.0092 and Beta = -0.0833 ± 0.0249; p = 0.0008). Coronary artery disease (CAD) was directly associated to follow-up overall/cardiac mortality at univariable (Beta = 0.0550 ± 0.0136, p < 0.0001; Beta = 0.0540 ± 0.0130, p < 0.0001) and multivariable (Beta = 0.0460 ± 0.0189, p = 0.152; Beta = 0.0378 ± 0.0192, p = 0.0491) meta-regression. CONCLUSIONSSolid long-term evidence supporting AVNA and pace is lacking. Younger patients with reduced LVEF% have increased follow-up cardiac mortality after AVNA RV and may require CRT. Alternative strategies to maintain sinus rhythm and ventricular synchronism should be compared to AVNA to support future treatment strategies.
Patients with acute heart failure (AHF) require urgent in‐hospital treatment for relief of symptoms. The main reason for hospitalization is congestion, rather than low cardiac output. Although ...congestion is associated with a poor prognosis, many patients are discharged with persistent signs and symptoms of congestion and/or a high left ventricular filling pressure. Available data suggest that a pre‐discharge clinical assessment of congestion is often not performed, and even when it is performed, it is not done systematically because no method to assess congestion prior to discharge has been validated. Grading congestion would be helpful for initiating and following response to therapy. We have reviewed a variety of strategies to assess congestion which should be considered in the care of patients admitted with HF. We propose a combination of available measurements of congestion. Key elements in the measurement of congestion include bedside assessment, laboratory analysis, and dynamic manoeuvres. These strategies expand by suggesting a routine assessment of congestion and a pre‐discharge scoring system. A point system is used to quantify the degree of congestion. This score offers a new instrument to direct both current and investigational therapies designed to optimize volume status during and after hospitalization. In conclusion, this document reviews the available methods of evaluating congestion, provides suggestions on how to properly perform these measurements, and proposes a method to quantify the amount of congestion present.
Aims
We evaluated the added prognostic value of a multi‐time point‐based multimarker panel of biomarkers in patients with acute heart failure (AHF).
Methods and results
Seven circulating biomarkers ...NT‐proBNP, high sensitivity cardiac troponin T (hs‐cTnT), soluble ST2 (sST2), growth differentiation factor 15 (GDF‐15), cystatin‐C, galectin‐3, and high sensitivity C‐reactive protein (hs‐CRP) were measured at baseline and on days 2, 5, 14, and 60 in 1161 patients enrolled in the RELAX‐AHF trial. Patients with BNP ≥350 ng/L or NT‐proBNP ≥1400 ng/L, mild to moderate renal impairment, and systolic blood pressure >125 mmHg were included in the trial. Time‐dependent Cox regression analysis was utilized to evaluate the incremental value of serial measurement of biomarkers. Added value of individual biomarkers and their combination, on top of a pre‐specified baseline model, was quantified with the gain in the C‐index. Serial biomarker evaluation showed incremental predictive value over baseline measurements alone for the prediction of 180‐day cardiovascular mortality except for galectin‐3. While a repeat measurement as early as day 2 was adequate for NT‐proBNP and cystatin‐C in terms of maximizing discriminatory accuracy, further measurements on days 14 and 60 provided added value for hs‐cTnT, GDF‐15, sST2, and hs‐CRP. Individual biomarker additions on top of the baseline model showed additional prognostic value. The greatest prognostic gain was, however, attained with the combination of NT‐proBNP, hs‐cTnT, GDF‐15, and sST2, which yielded 0.08 unit absolute increment in the C‐index to 0.87 (95% confidence interval 0.83–0.91.
Conclusion
In patients with AHF and mild to moderate renal impairment, a multimarker approach based on a panel of serially evaluated biomarkers provides the greatest prognostic improvement unmatched by a single time point‐based single marker strategy.
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