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Extravascular lung water (EVLW) could increase by permeability pulmonary oedema, cardiogenic oedema, or both. Transthoracic echocardiography examination of a patient allows quantifying B-lines, originating from water-thickened interlobular septa, and the E/Ea ratio, related to pulmonary capillary wedge pressure. The aim of our study was to assess the correlation and the trending ability between EVLW measured by transpulmonary thermodilution and the B-lines score or the E/Ea ratio in patients with ARDS. Twenty-six intensive care unit patients were prospectively included. B-lines score was obtained from four ultrasound zones (anterior and lateral chest on left and right hemithorax). E/Ea was measured from the apical four-chamber view. EVLW was compared with the B-lines score and the E/Ea ratio. A linear mixed effect model was used to take account the repeated measurements. A p value <0.05 was considered significant. A total of 73 measurements were collected. The correlation coefficient between EVLW and B-lines score was 0.66 (EVLW = 0.71 B-lines + 7.64, R 2  = 0.44, p  = 0.001), versus 0.31 for E/Ea ( p  = 0.06). The correlation between EVLW changes and B-lines variations was significant (R 2  = 0.26, p  < 0.01), with a concordance rate of 74 %. A B-lines score ≥6 had a sensitivity of 82 % and a specificity of 77 % to predict EVLW >10 ml/kg, with an AUC equal to 0.86 (0.76–0.93). The gray zone approach identified a range of B-lines between four and seven for which EVLW >10 ml/kg could not be predicted reliably. The correlation between ultrasound B-lines and EVLW was significant, but the B-lines score was not able to track EVLW changes reliably.

Compared to men, women have been reported to have increased morbidity and mortality after ST-elevation myocardial infarction (STEMI); but sex differences in cardiac function in the acute and subacute phases of STEMI are incompletely understood. The objective of this study was to prospectively compare changes in cardiac function over the acute and subacute phases after anterior STEMI with timely reperfusion in women versus men. The Stunning in Takotsubo versus Acute Myocardial Infarction (STAMI) study (NCT04448639) prospectively enrolled 105 men and 41 women with anterior STEMI. Echocardiography and blood sampling were performed within 4 hours of admission and at 1, 2, 3, 7, 14, and 30 days after admission. The primary outcome was akinesia recovery, defined as the difference in the percentage of akinesia observed at baseline versus follow-up. Secondary outcomes included wall motion score index (WMSI), left ventricular ejection fraction (LVEF) and global longitudinal strain (GLS). Mixed effects linear regression or zero-inflated tobit models with random intercepts were used to model echocardiographic parameters over time. Baseline patient characteristics were similar in both groups. The difference between women and men in akinesia recovery at 30 days was 8.3% (95% credible interval 0.8%, 15.5%). The covariate-adjusted posterior probability that akinesia recovery and WMSI improvement at 30 days are greater in women than men were 96.0% and 99.0% respectively. Similar but less pronounced trends towards greater improvement in women than men were observed for LVEF and GLS. In conclusion, cardiac dysfunction recovered to a greater extent in women than in men after anterior STEMI with timely reperfusion.

Cardiovascular disease is the leading cause of death worldwide. Reperfusion therapy is vital to patient survival after a heart attack but can cause myocardial ischemia/reperfusion injury (MI/RI). Nitric oxide (NO) can ameliorate MI/RI and is a key molecule for drug development. However, reactive oxygen species (ROS) can easily oxidize NO to peroxynitrite, which causes secondary cardiomyocyte damage. Herein, L‐arginine‐loaded selenium‐coated gold nanocages (AAS) are designed, synthesized, and modified with PCM (WLSEAGPVVTVRALRGTGSW) to obtain AASP, which targets cardiomyocytes, exhibits increased cellular uptake, and improves photoacoustic imaging in vitro and in vivo. AASP significantly inhibits oxygen glucose deprivation/reoxygenation (OGD/R)‐induced H9C2 cell cytotoxicity and apoptosis. Mechanistic investigation revealed that AASP improves mitochondrial membrane potential (MMP), restores ATP synthase activity, blocks ROS generation, and prevents NO oxidation, and NO blocks ROS release by regulating the closing of the mitochondrial permeability transition pore (mPTP). AASP administration in vivo improves myocardial function, inhibits myocardial apoptosis and fibrosis, and ultimately attenuates MI/RI in rats by maintaining mitochondrial function and regulating NO signaling. AASP shows good safety and biocompatibility in vivo. This findings confirm the rational design of AASP, which can provide effective treatment for MI/RI.

Global left ventricular (LV) myocardial work (MW) indexes can be recognized at ultrasound imaging from the LV pressure/global longitudinal strain (GLS) loop analysis. A total of 4 indexes, global work index (GWI), global constructive work (GCW), global wasted work (GWW), and global work efficiency (GWE), have been demonstrated to overcome the methodological limitations of GLS and provide useful information on myocardial dysfunction in some clinical settings. Although impaired MW indexes have been demonstrated in patients with transthyretin cardiac amyloidosis (ATTR) or with nonobstructive hypertrophic cardiomyopathy (HCM), there are no comparative studies at present. This study aimed to describe the characteristics of MW in both these clinical settings compared with patients with well-controlled hypertension (HTN). A total of 83 patients, 32 with ATTR (aged 70 ± 11 years, 32% mutated, 68% wild-type, 72% men), 29 with HCM (aged 57 ± 17 years), and 22 HTN controls (aged 56 ± 5.6 years, 59% men) were prospectively enrolled at 2 clinical centers. All participants had New York Heart Association class I or II. Overall, the LV mass index was greater in both study groups than in HTN, whereas the LV ejection fraction (EF) was significantly lower in ATTR compared with other groups. Based on this finding, patients with ATTR were further divided into 2 subgroups: ATTR1 (LVEF ≤0.50), n = 14 (44%) and ATTR2 (LVEF >0.50), n = 18 (56%). Overall, the GWI and GCW were lower in all ATTR patients (mostly in ATTR1) than in the other groups (p <0.001), whereas only small differences in GWE and none in GWW were found among the groups. Of interest, the pairwise comparison and receiver operating characteristic analysis in preserved LVEF patients showed that GWI was a better discriminator of ATTR2 from HCM patients than GLS, with the cut-off value ≤1,419 mm Hg% (89% sensitivity; 55% specificity; p = 0.013). In conclusion, MW analysis was confirmed to be a modern way to investigate myocardial function in patients with hypertrophic phenocopies. GWI and GCW were more impaired in patients with ATTR compared with HCM and HTN controls. Furthermore, this study likely revealed an additional discriminative value of GWI over GLS alone in preserved LVEF settings.

BackgroundThe diagnosis of cardiac amyloidosis (CA) is challenging owing to vague symptomatology and non-specific echocardiographic findings.ObjectiveTo describe regional patterns in longitudinal strain (LS) using two-dimensional speckle-tracking echocardiography in CA and to test the hypothesis that regional differences would help differentiate CA from other causes of increased left ventricular (LV) wall thickness.Methods and results55 consecutive patients with CA were compared with 30 control patients with LV hypertrophy (n=15 with hypertrophic cardiomyopathy, n=15 with aortic stenosis). A relative apical LS of 1.0, defined using the equation (average apical LS/(average basal LS + mid-LS)), was sensitive (93%) and specific (82%) in differentiating CA from controls (area under the curve 0.94). In a logistic regression multivariate analysis, relative apical LS was the only parameter predictive of CA (p=0.004).ConclusionsCA is characterised by regional variations in LS from base to apex. A relative ‘apical sparing’ pattern of LS is an easily recognisable, accurate and reproducible method of differentiating CA from other causes of LV hypertrophy.

Background Histone deacetylases (HDACs) play a critical role in modulating myocardial protection and cardiomyocyte survivals. However, Specific HDAC isoforms in mediating myocardial ischemia/reperfusion injury remain currently unknown. We used cardiomyocyte-specific overexpression of active HDAC4 to determine the functional role of activated HDAC4 in regulating myocardial ischemia and reperfusion in isovolumetric perfused hearts. Methods In this study, we created myocyte-specific active HDAC4 transgenic mice to examine the functional role of active HDAC4 in mediating myocardial I/R injury. Ventricular function was determined in the isovolumetric heart, and infarct size was determined using tetrazolium chloride staining. Results Myocyte-specific overexpressing activated HDAC4 in mice promoted myocardial I/R injury, as indicated by the increases in infarct size and reduction of ventricular functional recovery following I/R injury. Notably, active HDAC4 overexpression led to an increase in LC-3 and active caspase 3 and decrease in SOD-1 in myocardium. Delivery of chemical HDAC inhibitor attenuated the detrimental effects of active HDAC4 on I/R injury, revealing the pivotal role of active HDAC4 in response to myocardial I/R injury. Conclusions Taken together, these findings are the first to define that activated HDAC4 as a crucial regulator for myocardial ischemia and reperfusion injury.

Left ventricular (LV) global longitudinal strain (GLS) has established itself in the last decade as a reliable, more objective method for the evaluation of LV systolic function, able to detect subtle abnormalities in LV contraction even in the presence of preserved ejection fraction (EF). However, recent studies have demonstrated that GLS, similar to LV EF, has important load dependency. Non-invasive myocardial work (MW) quantification has emerged in the last years as an alternative tool for myocardial function assessment. This new method, incorporating measurement of strain and LV pressure, has shown to overcome GLS and LV EF limitations and provide a loading-independent evaluation of myocardial performance. The presence of a commercially available echocardiographic software for the non-invasive MW calculation has allowed the application of this new method in different settings. This review sought to provide an overview on the current knowledge of non-invasive MW estimation, showing its potential applications and possible added value in clinical practice.

Del Nido cardioplegia (DNC), a blood‐and‐crystalloid solution containing high and low concentrations of potassium and calcium, respectively, is used as a single‐dose antegrade infusion to induce immediate cardiac arrest in the surgery of patients with cardiovascular diseases requiring extracorporeal circulation. Adding cardioprotective molecules may further reduce the damage‐triggered ischemia/reperfusion (I/R) injury. Angiotensin‐(1–9) (Ang‐(1–9)) and angiotensin‐(1–7) (Ang‐(1–7)), members of the counter‐regulatory renin‐angiotensin system, have shown cardioprotective effects in cardiac hypertrophy and I/R models. This study aimed to evaluate the effects of Ang‐(1–9) and Ang‐(1–7), as adjuvants of the DNC, on cardioprotection and ventricular function in isolated rat hearts subjected to I/R and in cultured neonatal rat ventricular myocytes subjected to simulated I/R (sI/R). The addition of DNC and Ang‐(1–9) and Ang‐(1–7) decreased lactic dehydrogenase (LDH) release in cultured cardiomyocytes subjected to sI/R in comparison to those cardiomyocytes subjected to sI/R and incubated with DNC alone. Moreover, hearts treated with Ang‐(1–9) during reperfusion after DNC + I/R exhibited fewer arrhythmias and required less time to reach left ventricular developed pressure stability. Overall, reperfusion with DNC and Ang‐(1–9) improves the recovery of the left ventricular function of the heart.

TNFα is crucially involved in the pathogenesis and progression of myocardial ischemia/reperfusion injury and heart failure. The formation and release of TNFα and its downstream signal transduction cascade following activation of its two receptor subtypes are characterized. Myocardial TNFα and TNF receptor activation have an ambivalent role in myocardial ischemia/reperfusion injury and protection from it. Excessive TNFα expression and subsequent cardiomyocyte TNF receptor type 1 stimulation induce contractile dysfunction, hypertrophy, fibrosis and cell death, while a lower TNFα concentration and subsequent cardiomyocyte TNF receptor type 2 stimulation are protective. Apart from its concentration and receptor subtype, the myocardial action of TNFα depends on the duration of its exposure and its localization. While detrimental during sustained ischemia, TNFα contributes to ischemic preconditioning protection, no matter whether it is the first, second or third window of protection, and both TNF receptors are involved in the protective signal transduction cascade. Finally, the available clinical attempts to antagonize TNFα in cardiovascular disease, notably heart failure, are critically discussed.

Muscarinic acetylcholine (ACh) receptors (also known as M receptors) are widely distributed in all organs and tissues of the body, mainly playing a role in cholinergic nerve conduction. There are five known subtypes of muscarinic ACh receptors, but their pharmacological mechanisms of action on myocardial function have remained to be clearly defined. Functional myocardial diseases and myocardial injuries, such as arrhythmia, myocardial ischemia, myocarditis and myocardial fibrosis, may be affected by muscarinic ACh receptors. This article reviews the research progress of the regulation of myocardial function by muscarinic ACh receptors and related diseases, with the aim of developing better strategies and providing references for further revealing and clarifying the signal transduction and mechanisms of muscarinic ACh receptors in cardiomyocytes, and finding potential myocardial protective drugs that act on muscarinic ACh receptors.