Severity Of Cardiac Dysfunction Research Articles

The influence of sex on heart failure mortality.

Little research has investigated how sex may affect the prognosis of patients with chronic heart failure (HF). The present study was aimed at exploring sex-specific differences in prognosis in a cohort of patients with chronic HF, categorized according to severity of left ventricular dysfunction (HFrEF, HFmrEF and HFpEF), right ventricular (RV) dysfunction and ischemic (IHD) or nonischemic (no-IHD) etiology. This retrospective analysis included 1640 HF patients of whom 24% were females, 759 patients had IHD, 1110 patients had HFrEF, 147 patients had HFmrEF and 383 patients had HFpEF. The median follow-up period was 63 months (25th-75th 27-93). In the no-IHD group, no statistically significant sex differences emerged regarding survival, regardless of age and severity of cardiac dysfunction. In contrast, in the IHD group, females had a significantly lower event rate than males in the age group between 65 and 79 years [hazard ratio (HR) 0.39; 95% confidence interval (CI): 0.86-0.18; P < 0.01]; in addition, a lower event rate was observed in females compared with males among patients with HFrEF (HR 0.47; 95% CI: 0.88-0.25; P < 0.01), among patients without RV dysfunction (HR 0.58; 95% CI: 1.02-0.33; P = 0.048) and among patients without diabetes (HR 0.44; 95% CI: 0.84-0.23; P < 0.01). In nonischemic patients there was no difference between males and females in terms of survival whereas in patients with ischemic etiology survival was better in females among elderly patients, in HFrEF patients, in the absence of RV dysfunction and in the absence of diabetes.

Correlation Between Cystatin C and the Severity of Cardiac Dysfunction in Patients with Systolic Heart Failure.

To investigate the relationship between cystatin C and cardiac dysfunction severity in patients with systolic heart failure. We recruited 100 hospitalized patients with systolic heart failure and 100 age-gender-matched controls. The clinical information of each patient was collected. Blood pressure, heart rate, height, and weight were measured, as were serum concentrations of cholesterol, renal function indices, cystatin C, and B-type natriuretic peptide (BNP). Transthoracic echocardiography was performed on each patient. Cystatin C and other indices of renal function, such as urea nitrogen, creatinine, and uric acid, were significantly elevated in the serum of patients with heart failure and those with more severe cardiac dysfunction. The stepwise regression analyses showed that cystatin C was positively associated with BNP (β = 0.18, P = 0.04, 95% CI: 21.1 ~ 1420.4) and left atrial diameter (LAD) (β = 0.19, P = 0.04, 95% CI: 0.03 ~ 9.21) and was negatively associated with ejection fraction (β = -0.22, P = 0.023, 95% CI: -12.4 ~ -0.93), while creatinine was only positively correlated with BNP (β = 0.23, P = 0.03, 95% CI: 1.11 ~ 20.7). The Receiver Operating Characteristic (ROC) curves demonstrated significantly more severe cardiac dysfunction (NYHA III/IV) in patients with cystatin C ≥ 0.895mg/L (sensitivity was 83.0%, specificity was 80.9%, AUC = 0.893) and creatinine ≥ 91.5μmol/L (sensitivity was 71.7%, specificity was 70.2%, AUC = 0.764). Cystatin C was significantly correlated with cardiac structure and function in patients with systolic heart failure, and it was more valuable than creatinine to evaluate the severity of heart failure.

Changes in the gut microbiota structure and function in rats with doxorubicin-induced heart failure.

The rat model of heart failure (HF) induced by doxorubicin (DOX), a broad spectrum and highly effective chemotherapeutic anthracycline with high-affinity to myocardial tissue that causes severe dose-dependent irreversible cardiotoxicity has been widely recognized and applied in HF pathogenesis and drug therapy studies. The gut microbiota (GM) has attracted significant attention due to its potential role in HF, and research in this area may provide beneficial therapeutic strategies for HF. Considering the differences in the route, mode, and total cumulative dose of DOX administration used to establish HF models, the optimal scheme for studying the correlation between GM and HF pathogenesis remains to be determined. Therefore, focusing on establishing the optimal scheme, we evaluated the correlation between GM composition/function and DOX-induced cardiotoxicity (DIC). Three schemes were investigated: DOX (at total cumulative doses of 12, 15 or 18 mg/kg using a fixed or alternating dose via a tail vein or intraperitoneal injection) was administered to Sprague Dawley (SD) for six consecutive weeks. The M-mode echocardiograms performed cardiac function evaluation. Pathological changes in the intestine were observed by H&E staining and in the heart by Masson staining. The serum levels of N-terminal pre-B-type natriuretic peptide (NT-proBNP) and cardiac troponin I (cTnI) were measured by ELISA. The GM was analysed by 16S rRNA gene sequencing. Strikingly, based on the severity of cardiac dysfunction, there were marked differences in the abundance and grouping of GM under different schemes. The HF model established by tail vein injection of DOX (18 mg/kg, alternating doses) was more stable; moreover, the degree of myocardial injury and microbial composition were more consistent with the clinical manifestations of HF. The model of HF established by tail vein injection of doxorubicin, administered at 4mg/kg body weight (2mL/kg) at weeks 1, 3 and 5, and at 2mg/kg body weight (1mL/kg) at weeks 2, 4 and 6, with a cumulative total dose of 18mg/kg, is a better protocol to study the correlation between HF and GM.

Effect of Patisiran on Polyneuropathy and Cardiomyopathy in Patients with hATTR Amyloidosis with V122I/T60A Variants: A Phase 4 Observational Study (S14.005)

Effect of Patisiran on Polyneuropathy and Cardiomyopathy in Patients with hATTR Amyloidosis with V122I/T60A Variants: A Phase 4 Observational Study (S14.005)

Стресс-эхокардиография в диагностике кардиальной дисфункции в раннем постинфарктном периоде

The purpose — to assess the importance of stress echocardiography in identifying the nature and severity of cardiac dysfunction in patients with myocardial infarction. Material and methods.86 patients were examined at the outpatient stage of rehabilitation 6 weeks after myocardial infarction with primary coronary angioplasty with stenting. Results.Echocardiography revealed left ventricular hypertrophy (LVH) in 34 patients with myocardial infarction with concomitant arterial hypertension. Patients with LVH are characterized by more pronounced structural and functional LV remodeling, which is expressed in a lower LVEF and increased LVEDD, LVESVand LVEDV(p&lt;0.05). There were no differences in stroke volume between patients with and without LVH. The performed diastolic stress test in patients with LVH is characterized by significantly lower average early diastolic mitral annular velocity e` (7.6 vs. 9.3 cm/s, p&lt;0.01) without differences in the peak early transmitral Doppler flow velocity E (69.8 vs 78.0, p&gt;0.05) compared with patients without LVH. The revealed differences between patients with and without LVH are due to a higher post-exercise velocity e` in patients with normal LV geometry and a decrease in eccentric LVH subgroup. Conclusions.1) Patients with LVH in the early postinfarction period (6 weeks) have more pronounced LV systolic dysfunction, expressed in a decrease in LVEF and an increase in LVEDD, LVESV, LVEDV compared to patients without LVH.2) Left ventricular hypertrophy, in conditions of myocardial infarction, is associated with latent diastolic dysfunction, which is manifested by a lower average early diastolic mitral annular velocity e` after the stress-test.

Molecular imaging of the brain–heart axis provides insights into cardiac dysfunction after cerebral ischemia

Ischemic stroke imparts elevated risk of heart failure though the underlying mechanisms remain poorly described. We aimed to characterize the influence of cerebral ischemic injury on cardiac function using multimodality molecular imaging to investigate brain and cardiac morphology and tissue inflammation in two mouse models of variable stroke severity. Transient middle cerebral artery occlusion (MCAo) generated extensive stroke damage (56.31 ± 40.39 mm3). Positron emission tomography imaging of inflammation targeting the mitochondrial translocator protein (TSPO) revealed localized neuroinflammation at 7 days after stroke compared to sham (3.8 ± 0.8 vs 2.6 ± 0.7 %ID/g max, p < 0.001). By contrast, parenchyma topical application of vasoconstrictor endothelin-1 did not generate significant stroke damage or neuroinflammatory cell activity. MCAo evoked a modest reduction in left ventricle ejection fraction at both 1 weeks and 3 weeks after stroke (LVEF at 3 weeks: 54.3 ± 5.7 vs 66.1 ± 3.5%, p < 0.001). This contractile impairment was paralleled by elevated cardiac TSPO PET signal compared to sham (8.6 ± 2.4 vs 5.8 ± 0.7%ID/g, p = 0.022), but was independent of leukocyte infiltration defined by flow cytometry. Stroke size correlated with severity of cardiac dysfunction (r = 0.590, p = 0.008). Statistical parametric mapping identified a direct association between neuroinflammation at 7 days in a cluster of voxels including the insular cortex and reduced ejection fraction (ρ = − 0.396, p = 0.027). Suppression of microglia led to lower TSPO signal at 7 days which correlated with spared late cardiac function after MCAo (r = − 0.759, p = 0.029). Regional neuroinflammation early after cerebral ischemia influences subsequent cardiac dysfunction. Total body TSPO PET enables monitoring of neuroinflammation, providing insights into brain–heart inter-organ communication and may guide therapeutic intervention to spare cardiac function post-stroke.

Cardiac dysfunction in relation to vascular brain injury, cognitive impairment and depressive symptoms; The Heart-Brain Connection Study

Abstract Introduction Cardiovascular disease is an independent contributor to cognitive impairment. With an imminent rise in chronic cardiovascular disease, a better understanding of its effects on brain health is warranted. Impaired blood flow to the brain is one of the main hypothesized mechanisms linking cardiovascular disease with abnormal brain aging. Purpose To investigate relations between (subclinical) cardiac dysfunction and vascular brain injury, cognitive impairment and depressive symptoms, with a side-by-side comparison of cardiac biomarkers and imaging parameters. Methods Multicenter, cross-sectional, observational cohort study among 559 participants: 431 with manifest cardiovascular disease (heart failure [HF], carotid occlusive disease or vascular cognitive impairment) and 128 control participants, all without dementia. Participants underwent 3T heart-brain MRI and cognitive testing. Determinants were cardiac biomarkers (NT-proBNP and high-sensitive Troponin-I) and left ventricular (LV) functional parameters by MRI (LV ejection fraction, cardiac output, LV global function index). Outcome measures were cerebral small vessel disease (CSVD) by MRI (presence of white matter hyperintensities, microbleeds, lacunar infarcts or perivascular spaces), CSVD score (0–4), cognitive impairment in ≥1 domain (memory, language, attention-psychomotor speed and executive functioning) and depressive symptoms (Geriatric Depression Scale-15 score &amp;gt;5). Interaction analyses were used to investigate effect modification by patient group; results are reported pooled or stratified accordingly. Results In patients with cardiovascular disease and controls, but not in those with manifest HF, LV functional parameters were associated with CSVD and cognitive impairment, with the following associations: LVEF &amp;lt;50% with CSVD (OR 4.67 [1.37–15.95]) and CSVD score (RR 1.38 [1.06–1.81]); LV global function index with CSVD (OR 0.71 [0.58–0.86]), CSVD score (RR 0.90 [0.84–0.96]) and cognitive impairment (OR 0.84 [0.72–0.97]). LV global function index (OR 0.82 [0.71–0.95]) and cardiac output (OR 0.81 [0.71–0.93]) were also associated with depressive symptoms in all. These relations were independent from age, sex, hypertension, diabetes, waist-hipratio, history of ischemic heart disease, transient ischemic attack or stroke. Cardiac biomarkers were univariably associated with brain outcome measures, but not in multivariable analysis. Conclusion This study indicates that subclinical cardiac dysfunction, as assessed by cardiovascular MRI, is independently associated with vascular brain injury, cognitive impairment and depressive symptoms. Of all parameters, LV global function index showed the most robust relations, indicating that global cardiac performance is more closely related to poorer brain outcome than merely LV systolic function. In those with clinically manifest HF, the severity of cardiac dysfunction was related to depressive symptoms but not to other brain outcome measures. Funding Acknowledgement Type of funding sources: Public grant(s) – National budget only. Main funding source(s): The Netherlands CardioVascular Research Initiative; The Dutch Heart Foundation

Iron deficiency is an independent risk factor of increased myocardial energy expenditure in chronic heart failure patients

Chronic heart failure (CHF) is a major public health burden and is associated with high morbidity, mortality, and cost. Recent studies demonstrated iron metabolism and myocardial energy metabolism were altered in CHF patients. In this study, we aimed to analyze the effects and correlations of iron metabolism on myocardial energy metabolism in CHF. One hundred and thirty patients with CHF [age: 66.2±11.5 years, males: 58.5% and New York Heart Association (NYHA) class (II/III/IV): 67/43/20] were included. Serum concentrations of ferritin, transferrin saturation (Tsat), and soluble transferrin receptor (sTfR) were quantified as the indexes of iron metabolism, and echocardiography was used to assess myocardial energy expenditure (MEE) levels. Iron deficiency (ID) was defined as ferritin <100 or 100-300 µg/L with Tsat <20%. Patients with CHF were divided into two groups based on iron status. The prevalence of ID in CHF was 36.9%, and increased with the severity of CHF, reaching 80.0% in those with NYHA class IV (NYHA class II/III/IV: 17.9% vs. 46.5% vs. 80.0%, P=0.000). The demographic characteristics [age, sex, body mass index (BMI), blood pressure, and heart rate] and hemoglobin (HGB) concentrations in two groups were similar (all P>0.05). MEE was significantly higher in the ID group (92.7±23.0 vs. 65.6±20.8 cal/min, P=0.000), while NYHA classes II and III was significantly higher in the ID group (71.6±16.4 vs. 60.3±14.8 cal/min, P=0.022; 88.9±10.4 vs. 69.1±20.1 cal/min, P=0.000). In univariable linear regression models, the presence of ID, higher NYHA class, increased N-terminal pro-B-type natriuretic peptide (NT-proBNP), sTfR, left ventricular internal diastolic diameter (LVIDd), as well as reduced ferritin, Tsat levels, and lower left ventricular ejection fraction (LVEF) were associated with elevated MEE levels (all P<0.05). In multivariable regression models, the presence of ID, reduced Tsat. and increased sTfR remained independent predictors of elevated MEE levels after adjustment for all variables that showed a significant association with MEE (all P<0.05). The prevalence of ID is high in CHF and is associated with the severity of cardiac dysfunction. The presence of ID as well as reduced Tsat and increased sTfR concentrations are associated with elevated MEE levels in CHF.

Serum Meteorin-like is associated with weight loss in the elderly patients with chronic heart failure.

BackgroundUnintentional weight loss (cachexia) has been associated with poor outcomes in chronic heart failure (CHF). Meteorin‐like (Metrnl) is a novel myokine with protective effects on cardiovascular diseases. However, the change of Metrnl concentrations and its role in elderly patients with CHF remains unclear. The aim of this study was to evaluate the association of serum Metrnl with weight loss and outcomes in elderly patients with CHF.MethodsA total of 931 consecutive elderly patients (aged 60 years and older) with CHF and 135 age‐matched and sex‐matched control subjects were enrolled. Serum Metrnl concentration was measured by enzyme‐linked immunosorbent assay. Body weight was measured at baseline and 12 months.ResultsMedian of serum Metrnl levels was lower in CHF patients when compared with controls [201.31 (184.95–261.16) pg/mL vs. 168.68 (103.15–197.54) pg/mL, P < 0.001]. Patients with the lowest levels of Metrnl had higher N‐terminal pro brain natriuretic peptide (NT‐proBNP) levels but lower left ventricular eject fraction (LVEF) and estimated glomerular filtration rate (P < 0.001). Lower serum Metrnl was associated with a higher risk of >5% weight loss from baseline to 12 months [odds ratio = 6.13, 95% confidence interval (CI) = 2.57–14.62 per log decrease; P < 0.001]. Serum Metrnl levels were decreased as LVEF decreased (P < 0.001) and were positively correlated with LVEF (r = 0.267, P < 0.001) but negatively correlated with NT‐proBNP levels (r = −0.257, P < 0.001). Cox regression analysis suggested that lower serum Metrnl was associated with higher cardiovascular mortality [hazard ratio (HR) = 6.71, 95% CI = 3.41–13.18 per log decrease; P < 0.001], CHF rehospitalization (HR = 3.07, 95% CI = 1.82–5.17 per log decrease; P < 0.001), and the combined major adverse cardiac event(s) (MACEs) (HR = 5.38, 95% CI = 3.51–8.25 per log decrease; P < 0.001). The Kaplan–Meier survival curves showed that low concentration of Metrnl was a prognostic indicator of MACEs in patients with CHF.ConclusionsOur study suggests that lower serum Metrnl level is correlated with weight loss and the severity of cardiac dysfunction in elderly patients with CHF.

Plasma free fatty acid is associated with ischemic cardiomyopathy and cardiac dysfunction severity in systolic heart failure patients with diabetes.

Plasma free fatty acid is associated with ischemic cardiomyopathy and cardiac dysfunction severity in systolic heart failure patients with diabetes.

Association between severity of cardiac dysfunction caused by ventricular pre-excitation-led dyssynchrony and cardiac function recovery after ablation in children.

To investigate the associationbetween the severity of cardiac dysfunction caused by ventricular pre-excitation-led dyssynchrony and cardiac function recovery time after catheter ablation and identify predictors of cardiac function recovery after ablation. A total of 49 children underwent successful ablation (median 2.92 years). This study included 23 patients with mild cardiac dysfunction (left ventricular ejection fraction [LVEF]: 45% ≤ LVEF ≤ 55%), 15 with moderate (30% ≤ LVEF < 45%), and 11 with severe (LVEF <30%). The time for mean LVEF reaching 55% was 0.75, 3, and more than 12 months, respectively. The mean LVEF of children with severe cardiac dysfunction aged ≤6 years normalized within 12 months of follow-up (63.00% ± 1.41%). Mean LVEF of those aged more than 6 years did not normalize at 12 months of follow-up (38.67% ± 10.97%). LVEF recovery time was significantly different between these two age groups (median 11 months vs >12 months, χ2 = 4.55; P = .04). Cox regression analysis showed that preablation smaller left ventricular diastolic diameter (LVDd) Z score and higher LVEF were predictors of cardiac dysfunction recovery time (hazard ratio [HR] = 0.91, 95% confidence interval [CI] = 0.82-0.99, P = .04; HR = 1.09, 95% CI = 1.03-1.15, P = .01). Patients with higher LVDd Z scores and lower LVEF tend to have slower improvement in cardiac function after ablation. Patients with LVEF less than 30% and aged more than 6 years need more than 12 months to fully recover, and some might not even completely recover. Early catheter ablation is suggested once ventricular pre-excitation-led cardiac dysfunction is suspected.

Early postnatal changes of circulating N-terminal-pro-B-type natriuretic peptide in neonates with congenital diaphragmatic hernia

BackgroundSeverity of lung hypoplasia, pulmonary hypertension (PH) and cardiac dysfunction are major contributors to mortality in congenital diaphragmatic hernia (CDH). Therefore, early assessment and management is important to improve outcome. NT-proBNP is an established cardiac biomarker with only limited data for early postnatal risk assessment in CDH newborns. AimsTo investigate the correlation of NT-proBNP at birth, 6 h, 12 h, 24 h, and 48 h with PH and cardiac dysfunction and the prognostic information of NT-proBNP for the use of ECMO support or mortality. Subjects44 CDH newborns treated at our institution (December 2014–October 2017) were prospectively enrolled. Outcome measuresPrimary clinical endpoint was either need for ECMO or death within the first 48 h (group A). Infants not receiving ECMO support were allocated to group B. Mortality was tested as secondary endpoint. ResultsNT-proBNP levels measured at 6 h, 12 h, 24 h and 48 h postpartum correlated significantly with PH severity following NICU admission and at 24 h, and with severity of cardiac dysfunction at birth, 24 h, 48 h and after 7 days of life. There was no difference in NT-proBNP levels between survivors and non-survivors. NT-proBNP levels were significantly higher in group A at 6 h (p = 0.007), 12 h (p = 0.036), and 24 h (p = 0.007), but not at birth (p = 0.785) or 48 h (p = 0.15) compared to group B. ConclusionNT-proBNP analysis in the first 48 h of life may be useful to assess PH and cardiac dysfunction in CDH newborns and to predict the need for ECMO support.

Cerebral cortical microinfarcts: A novel MRI marker of vascular brain injury in patients with heart failure

BackgroundPatients with heart failure (HF) are at risk for vascular brain injury. Cerebral cortical microinfarcts (CMIs) are a novel MRI marker of vascular brain injury. This study aims to determine the occurrence of CMIs in patient with HF and their clinical correlates, including haemodynamic status. MethodsFrom the Heart-Brain Study, a multicenter prospective cohort study, 154 patients with clinically stable HF without concurrent atrial fibrillation (mean age 69.5 ± 10.1, 32% female) and 124 reference participants without HF (mean age 65.6 ± 7.4, 47% females) were evaluated for CMIs on 3 T MRI. CMI presence in HF was tested for associations with vascular risk profile, cardiac function and history, MRI markers of vascular brain injury and cognitive profile. ResultsCMI occurrence was higher in patient with HF (17%) than reference participants (7%); after correction for age and sex OR 2.5 [95% CI 1.1–6.0] p = .032; after additional correction for vascular risk factors OR 2.7 [1.0–7.1] p = .052. In patients with HF, CMI presence was associated with office hypertension (OR 2.7 [1.2–6.5] p = .021) and a lower cardiac index (B = -0.29 [−0.55−−0.04] p = .023 independent of vascular risk factors), but not with cause or duration of HF. Presence of CMIs was not associated with cognitive performance in patients with HF. ConclusionsCMIs are a common occurrence in patients with HF and related to an adverse vascular risk factor profile and severity of cardiac dysfunction. CMIs thus represent a novel marker of vascular brain injury in these patients.

Figures of the Heart Failure Association (HFA): Dr. Rudolf de Boer, HFA Board Member (2014-2020), Chair of the Basic Science Section (2016-2018), coordinator of the Study Group on Heart Failure with Preserved Ejection Fraction, and member of the HFA study groups of Translational Research and Cardio-oncology.

Figures of the Heart Failure Association (HFA): Dr. Rudolf de Boer, HFA Board Member (2014-2020), Chair of the Basic Science Section (2016-2018), coordinator of the Study Group on Heart Failure with Preserved Ejection Fraction, and member of the HFA study groups of Translational Research and Cardio-oncology.

Ultrasonic cardiogram and MiRNA-21 analysis of cardiac dysfunction in patients with cardiac arrest following cardiopulmonary resuscitation

PurposeTo explore correlations between the serum level of miRNA-21 expression and cardiac dysfunction severity after cardiopulmonary resuscitation (CPR) using ultrasonic cardiogram. MethodsThirty-nine patients with cardiopulmonary arrest receiving successful CPR and forty-one healthy participants were recruited in the study. Reverse Transcription-Polymerase Chain Reaction (RT-PCR) and immunochemiluminometric assays was used to examine the serum miRNA-21 level and the concentration of cardiac troponins T and I, respectively. Indices of Electrocardiogram (ECG) and cardiac dysfunction measured by ultrasound of patients in the case group were used to assess cardiac function after CPR. Furthermore, the correlation between the serum level of miRNA-21 expression and severity of cardiac dysfunction was analyzed by Spearman correlation analysis. ResultsAs compared to the control group, the serum level of miRNA-21 expression, as well as cardiac troponin T and I levels in the case group were significantly higher (p = 0.000). The miRNA-21 expression level in the patients at IV grade of cardiac function were substantially higher than patients at III grade (p = 0.015). There was no significant difference in level of cardiac troponins T and I between patients at III grade and patients at IV grade (p > 0.05). Further, Spearman correlation analysis revealed that the level of miRNA-21 expression was negatively correlated with cardiac function index in the ultrasound imaging: E peak, E/A value, LVEF and LVEDD (r = 0.617, 0.535, 0.612, 0.573, P = 0.012, 0.009, 0.008, 0.011), but was positively correlated with the level of cardiac troponins T and I (r = 0.546,0.582, P = 0.006,0.007) and the severity of cardiac dysfunction (r = 0.859, p < 0.05). ConclusionThe level of miRNA-21 is higher after CPR is closely related to the severity of cardiac dysfunction that is measured by ultrasound, suggesting that it may serve as a potential biomarker.

Imaging in patients with suspected acute heart failure: timeline approach position statement on behalf of the Heart Failure Association of the European Society of Cardiology.

Acute heart failure is one of the main diagnostic and therapeutic challenges in clinical practice due to a non-specific clinical manifestation and the urgent need for timely and tailored management at the same time. In this position statement, the Heart Failure Association aims to systematize the use of various imaging methods in accordance with the timeline of acute heart failure care proposed in the recent guidelines of the European Society of Cardiology. During the first hours of admission the point-of-care focused cardiac and lung ultrasound examination is an invaluable tool for rapid differential diagnosis of acute dyspnoea, which is highly feasible and relatively easy to learn. Several portable and stationary imaging modalities are being increasingly used for the evaluation of cardiac structure and function, haemodynamic and volume status, precipitating myocardial ischaemia or valvular abnormalities, and systemic and pulmonary congestion. This paper emphasizes the central role of the full echocardiographic examination in the identification of heart failure aetiology, severity of cardiac dysfunction, indications for specific heart failure therapy, and risk stratification. Correct evaluation of cardiac filling pressures and accurate prognostication may help to prevent unscheduled short-term readmission. Alternative advanced imaging modalities should be considered to assist patient management in the pre- and post-discharge phase, including cardiac magnetic resonance, computed tomography, nuclear studies, and coronary angiography. The Heart Failure Association addresses this paper to the wide spectrum of acute care and heart failure specialists, highlighting the value of all available imaging techniques at specific stages and in common clinical scenarios of acute heart failure.

Dectin-1 Contributes to Myocardial Ischemia/Reperfusion Injury by Regulating Macrophage Polarization and Neutrophil Infiltration.

Macrophage-associated immune response plays an important role in myocardial ischemia/reperfusion (IR) injury. Dectin-1, expressed mainly on activated myeloid cells, is crucial for the regulation of immune homeostasis as a pattern recognition receptor. However, its effects and roles during the myocardial IR injury remain unknown. Genetic ablation, antibody blockade, or Dectin-1 activation, along with the adoptive bone marrow transfer chimeric model, was used to determine the functional significance of Dectin-1 in myocardial IR injury. Immune cell filtration and inflammation were examined by flow cytometry, quantitative real-time polymerase chain reaction, and immunohistochemistry. Moreover, Dectin-1+ cells were analyzed by flow cytometry in the blood of patients with ST-segment-elevation myocardial infarction and stable patients with normal coronary artery (control). We demonstrated that Dectin-1 expression observed on the bone marrow-derived macrophages is increased in the heart during the early phase after IR injury. Dectin-1 deficiency and antibody-mediated Dectin-1 inhibition led to a considerable improvement in cardiac function, accompanied by a reduction in cardiomyocyte apoptosis, which was associated with a decrease in M1 macrophage polarization and Ly-6C+ monocyte and neutrophil infiltration. Activation of Dectin-1 with its agonist had the opposite effects. Furthermore, Dectin-1 contributed to neutrophil recruitment through the regulation of Cxcl1 and granulocyte colony-stimulating factor expression. In addition, Dectin-1-dependent interleukin-23/interleukin-1β production was shown to be essential for interleukin-17A expression by γδT cells, leading to neutrophil recruitment and myocardial IR injury. Furthermore, we demonstrated that circulating Dectin-1+CD14++CD16- and Dectin-1+CD14++CD16+ monocyte levels were significantly higher in patients with ST-segment-elevation myocardial infarction than in controls and positively correlated with the severity of cardiac dysfunction. Our results reveal a crucial role of Dectin-1 in the process of mouse myocardial IR injury and provide a new, clinically significant therapeutic target.

Increased Serum Interleukin-34 Levels Are Related to the Presence and Severity of Cardiac Dysfunction in Patients With Ischemic Cardiomyopathy.

Background: Several inflammatory factors have been demonstrated with diagnostic or prognostic value in patients with ischemic cardiomyopathy (ICM). Interleukin 34 (IL-34), an additional ligand of colony stimulating factor-1 receptor (CSF-1R), has been identified as a biomarker of coronary artery disease (CAD) and chronic kidney disease (CKD). However, the potential effect of IL-34 in ICM remains unknown.Methods: Serum IL-34 levels were detected in 360 subjects with ICM and in 465 subjects without ICM; the latter group included 233 controls without CAD and 232 patients with CAD and normal cardiac function. Uni- and multivariable logistic regression analyses were conducted to analyze the relationship between IL-34 and ICM.Results: IL-34 levels were significantly increased in patients with ICM compared with both groups of subjects without ICM (122.52 ± 115.30 vs. 95.02 ± 101.43 vs. 82.57 ± 84.24 pg/ml, respectively; P < 0.001). Moreover, serum IL-34 level was significantly positively correlated to NT-proBNP level (r = 0.223, P < 0.001), left ventricular end diastolic diameter and New York Heart Association (NYHA) functional class, indicating that a higher IL-34 level reflects more severe heart failure (HF). Multivariable regression analyses revealed that IL-34 was remarkably associated with the presence and severity of ICM after adjusting for age, sex, conventional risk factors as well as medication [odds ratio (OR): 1.501, 95% confidence interval (CI): 1.249–1.803, P < 0.001, per SD increase]. The predictive value of IL-34 value remained significant in patients already diagnosed with CAD.Conclusion: Increased IL-34 levels are relevant to the presence and severity of ischemic HF in all subjects and in patients with CAD. IL-34 may be used as a novel clinical biomarker of ICM with predictive value.

Pathogenesis of sepsis-induced myocardial dysfunction

Sepsis is a common disease in intensive care units (ICU), and the resulted multi-organ dysfunction syndrome (MODS) is the main cause of death in patients with severe sepsis. The cardiovascular system is one of the most important target organ for sepsis. The severity of cardiac dysfunction is closely related to the clinical prognosis of patients with sepsis. Studies have reported that various cytokines are expressed during sepsis. They have influence on myocardial contractile function, mitochondrial function and self-regulation. Where after, it will induce cardiomyocyte apoptosis, which can lead to myocardial dysfunction. In this article, the pathogenesis of sepsis-induced myocardial dysfunction (SIMD) were reviewed to further clarify the pathogenesis of SIMD, and provide theoretical basis for subsequent research.

Restoration of Circulating MFGE8 (Milk Fat Globule-EGF Factor 8) Attenuates Cardiac Hypertrophy Through Inhibition of Akt Pathway.

Cardiac hypertrophy occurs in response to numerous stimuli like neurohumoral stress, pressure overload, infection, and injury, and leads to heart failure. Mfge8 (milk fat globule-EGF factor 8) is a secreted protein involved in various human diseases, but its regulation and function during cardiac hypertrophy remain unexplored. Here, we found that circulating MFGE8 levels declined significantly in failing hearts from patients with dilated cardiomyopathy. Correlation analyses revealed that circulating MFGE8 levels were negatively correlated with the severity of cardiac dysfunction and remodeling in affected patients. Deleting Mfge8 in mice maintained normal heart function at basal level but substantially exacerbated the hypertrophic enlargement of cardiomyocytes, reprogramming of pathological genes, contractile dysfunction, and myocardial fibrosis after aortic banding surgery. In contrast, cardiac-specific Mfge8 overexpression in transgenic mice significantly blunted aortic banding-induced cardiac hypertrophy. Whereas MAPK (mitogen-activated protein kinase) pathways were unaffected in either Mfge8-knockout or Mfge8-overexpressing mice, the activated Akt/PKB (protein kinase B)-Gsk-3β (glycogen synthase kinase-3β)/mTOR (mammalian target of rapamycin) pathway after aortic banding was significantly potentiated by Mfge8 deficiency but suppressed by Mfge8 overexpression. Inhibition of Akt with MK-2206 blocked the prohypertrophic effects of Mfge8 deficiency in angiotensin II-treated neonatal rat cardiomyocytes. Finally, administering a recombinant human MFGE8 in mice in vivo alleviated cardiac hypertrophy induced by aortic banding. Our findings indicate that Mfge8 is an endogenous negative regulator of pathological cardiac hypertrophy and may, thus, have potential both as a novel biomarker and as a therapeutic target for treatment of cardiac hypertrophy.