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Background: Obesity is a prevalent health issue associated with an increased risk of cardiovascular diseases. While obesity's link to various cardiovascular conditions is well-documented, its specific impact on global longitudinal strain (GLS) requires further investigation. This study aims to explore the relationship between obesity and GLS in an adult population. Materials and Methods: This cross-sectional study included 91 adult participants, categorized into obese (n=59) and non-obese (n=32) groups based on body mass index (BMI). GLS was measured using speckle-tracking echocardiography. Chi-square tests and odds ratios (OR) were used to assess the association between obesity and abnormal GLS. Results: Among the non-obese group, 25.0% had abnormal GLS compared to 20.3% in the obese group. The chi-square test indicated no significant difference in the prevalence of abnormal GLS between the groups (p = 0.60). The odds ratio for abnormal GLS in obese versus non-obese participants was 1.3 (95% CI: 0.4-3.6), indicating no significant association. Conclusion: The study found no significant association between obesity and abnormal GLS, suggesting that BMI alone may not be a reliable predictor of subclinical myocardial dysfunction. These findings highlight the need for a comprehensive approach to cardiovascular risk assessment that includes multiple factors beyond BMI. [ABSTRACT FROM AUTHOR]

Stroke–heart syndrome (SHS), a critical yet underrecognized condition, encompasses a range of cardiac complications that arise following an ischemic stroke. This narrative review explores the pathophysiology, clinical manifestations, and implications of SHS, focusing on the complex interplay between the brain and the heart. Acute ischemic stroke (AIS) triggers autonomic dysfunction, leading to a surge in catecholamines and subsequent myocardial injury. Our review highlights the five cardinal manifestations of SHS: elevated cardiac troponin (cTn) levels, acute myocardial infarction, left ventricular dysfunction, arrhythmias, and sudden cardiac death. Despite the significant impact of these complications on patient outcomes, there is a notable absence of specific guidelines for their management. Through a comprehensive literature search, we synthesized findings from recent studies to elucidate the mechanisms underlying SHS and identified gaps in the current understanding. Our findings underscore the importance of early detection and multidisciplinary management of cardiac complications post-stroke. Future research should focus on establishing evidence-based protocols to improve clinical outcomes for stroke patients with SHS. Addressing this unmet need will enhance the care of stroke survivors and reduce mortality rates associated with cardiac complications. [ABSTRACT FROM AUTHOR]

Pimobendan is not currently approved for use in cats, although its usefulness in feline hypertrophic cardiomyopathy has been suggested. Reports indicate an increase in arrhythmic events following oral administration to healthy cats. Given the greater potency of intravenous administration compared to oral intake, it is conceivable that the incidence of arrhythmias may be increased following pimobendan injection. Therefore, this study aimed to investigate the proarrhythmic effects of pimobendan injection in cats. Five clinically healthy cats underwent physical examination, echocardiography, blood pressure measurements, and 24-hour Holter electrocardiography immediately before and after receiving pimobendan as an intravenous bolus dose of 0.15 mg/kg twice daily for 3 days. Additionally, a 24-hour Holter electrocardiography recording was conducted on the third day of pimobendan or placebo IV administration to assess heart rate, arrhythmias, and heart rate variability. Following pimobendan administration, there was a significant increase in total 24-hour heart rate. Echocardiography revealed a significant increase in mitral valve annulus systolic velocity (S') on the ventricular septal wall side, indicative of enhanced contractility. Only one cat exhibited paroxysmal ventricular tachycardia and an increase in the frequency of arrhythmic events. Conversely, in the remaining cats, a decreasing trend in the number of arrhythmias was observed. These findings indicate that intravenous administration of pimobendan may not be implicated in the onset of arrhythmias. Nevertheless, further research is warranted to explore the effects of intravenous pimobendan administration in cats with myocardial disease. [ABSTRACT FROM AUTHOR]

The objective was to study the dynamics of B-type natriuretic peptide (BNP) and its relationship with hemodynamic parameters during on-pump coronary artery bypass grafting (CABG), and to evaluate the informativeness of the biomarker as a predictor of myocardial dysfunction.Materials and methods. The study involved 127 patients aged 59 [54–66.75] years with ischemic heart disease who underwent CABG. The BNP blood level was determined in the operating room at stages: I – before surgery (BNP1 ), II – at the end of surgery (BNP2 ). Hemodynamic parameters were analyzed at the same stages. Correlation analysis, logistic regression with the calculation of the odds ratio (OR) and 95% confidence interval (95% CI) and ROC analysis with the calculation of the area under the ROC curve (AUC) were used.Results. BNP1 blood level was 49 [25.6–91.6], BNP2 – 90 [47.8–140.2] pg/ml (p < 0.0001). BNP1 correlated with central venous pressure (CVP) at stage I (rho = 0.212; p = 0.017) and with pulmonary artery wedge pressure (PAWP) at stage II (rho = 0.204; p = 0.045). BNP2 correlated with PAWP at stage II (rho = 0.204; p = 0.045). BNP1 > 52.1 pg/ml was the predictor of ICU length of stay > 24 hours (OR 1.0290, 95% CI 1.0154– 1.0427, p < 0.0001, AUC 0.775), BNP1 > 71 pg/ml was the predictor of inotropic index > 5 c. u. (OR 1.0076, 95% CI 1.0015–1.0138, p = 0.014, AUC 0.705) and BNP1 > 90.8 pg/ml was the predictor of vasoactive inotropic index > 10 c. u. (OR 1.0070, 95% CI 1.0014–1.0126, p = 0.013, AUC 0.727). BNP2 > 67.5 pg/ml was the predictor of ICU length of stay > 24 hours (OR 1.0179, 95% CI 1.0073–1.0287, p < 0.0009, AUC 0.763), BNP2 > 94.3 pg/ml was the predictor of inotropic index > 5 c. u. (OR 1.0063, 95% CI 1.0010–1.0117, p = 0.020, AUC 0.713), BNP2 > 144 pg/ml was the predictor of intra-aortic balloon pumping (OR 1.0037, 95% CI 1 .0000–1.0074, p = 0.048, AUC 0.854), BNP2 > 159 pg/ml was the predictor of vasoactive inotropic index > 10 c. u. (OR 1.0072, 95% CI 1.0006–1.0139, p = 0.033, AUC 0.729) and BNP2 > 161 pg/ml was the predictor of early mortality in the ICU (OR 1.0040, 95% CI 1, 0000-1.0080, p = 0.049, AUC 0.845). Conclusion. In 78.7% of patients undergoing on-pump CABG, BNP blood level does not exceed the upper limit of normal; by the end of surgery, the biomarker level increases by 32.9 [17.7–62.0] pg/ml. Before and at the end of surgery, BNP values are weakly correlated with CVP and PAWP and do not correlate with other hemodynamic parameters. Before surgery, BNP blood level in the range of 52.1–90.8 pg/ml are predictors of ICU stay > 24 hours (AUC 0.775), inotropic scale > 5 (AUC 0.705) and vasoactive-inotropic scale > 10 c. u. (AUC 0.727). At the end of surgery, BNP > 67.5 pg/ml is associated with an ICU stay > 24 hours (AUC 0.763), and BNP > 90.4 pg/ml is associated with inotropic scale > 5 c. u. (AUC 0.713). The BNP, increased to 144.0–161.0 pg/ml, indicates severe myocardial dysfunction, including hemodynamic support with intra-aortic balloon pumping (AUC 0.854), vasoactive-inotropic scale > 10 c. u. (AUC 0.729) and the risk of early mortality in the ICU (AUC 0.845).

Abstract Background Patients with diabetes have an increased risk of developing heart failure with preserved ejection fraction (HFpEF). This study aimed to compare indices of myocardial deformation and perfusion between patients with type 2 diabetes mellitus (T2DM) with and without HFpEF and to investigate the relationship between myocardial strain and perfusion reserve. Methods This study included 156 patients with T2DM without obstructive coronary artery disease (CAD) and 50 healthy volunteers who underwent cardiac magnetic resonance (CMR) examination at our center. Patients with T2DM were subdivided into the T2DM–HFpEF (n = 74) and the T2DM–non-HFpEF (n = 82) groups. The parameters of left ventricular (LV) and left atrial (LA) strain as well as stress myocardial perfusion were compared. The correlation between myocardial deformation and perfusion parameters was also assessed. Mediation analyses were used to evaluate the direct and indirect effects of T2DM on LA strain. Results Patients with T2DM and HFpEF had reduced LV radial peak systolic strain rate (PSSR), LV circumferential peak diastolic strain rate (PDSR), LA reservoir strain, global myocardial perfusion reserve index (MPRI), and increased LA booster strain compared to patients with T2DM without HFpEF (all P

Background: Patients with diabetes have an increased risk of developing heart failure with preserved ejection fraction (HFpEF). This study aimed to compare indices of myocardial deformation and perfusion between patients with type 2 diabetes mellitus (T2DM) with and without HFpEF and to investigate the relationship between myocardial strain and perfusion reserve. Methods: This study included 156 patients with T2DM without obstructive coronary artery disease (CAD) and 50 healthy volunteers who underwent cardiac magnetic resonance (CMR) examination at our center. Patients with T2DM were subdivided into the T2DM–HFpEF (n = 74) and the T2DM–non-HFpEF (n = 82) groups. The parameters of left ventricular (LV) and left atrial (LA) strain as well as stress myocardial perfusion were compared. The correlation between myocardial deformation and perfusion parameters was also assessed. Mediation analyses were used to evaluate the direct and indirect effects of T2DM on LA strain. Results: Patients with T2DM and HFpEF had reduced LV radial peak systolic strain rate (PSSR), LV circumferential peak diastolic strain rate (PDSR), LA reservoir strain, global myocardial perfusion reserve index (MPRI), and increased LA booster strain compared to patients with T2DM without HFpEF (all P < 0.05). Furthermore, LV longitudinal PSSR, LA reservoir, and LA conduit strain were notably impaired in patients with T2DM without HFpEF compared to controls (all P < 0.05), but LV torsion, LV radial PSSR, and LA booster strain compensated for these alterations (all P < 0.05). Multivariate linear regression analysis demonstrated that LA reservoir and LA booster strain were independently associated with global MPRI (β = 0.259, P < 0.001; β = − 0.326, P < 0.001, respectively). Further, the difference in LA reservoir and LA booster strain between patients with T2DM with and without HFpEF was totally mediated by global MPRI. Global stress PI, LA booster, global rest PI, and global MPRI showed high accuracy in diagnosing HFpEF among patients with T2DM (areas under the curve [AUC]: 0.803, 0.790, 0.740, 0.740, respectively). Conclusions: Patients with T2DM and HFpEF exhibited significant LV systolic and diastolic deformation, decreased LA reservoir strain, severe impairment of myocardial perfusion, and elevated LA booster strain that is a compensatory response in HFpEF. Global MPRI was identified as an independent influencing factor on LA reservoir and LA booster strain. The difference in LA reservoir and LA booster strain between patients with T2DM with and without HFpEF was totally mediated by global MPRI, suggesting a possible mechanistic link between microcirculation impairment and cardiac dysfunction in diabetes. Myocardial perfusion and LA strain may prove valuable for diagnosing and managing HFpEF in the future. [ABSTRACT FROM AUTHOR]

Objective: To study the prevalence of macrophage activation syndrome (MAS) in children with Kawasaki disease (KD) and to devise a classification tree for predicting MAS in early KD based on easily available clinical and laboratory information using artificial intelligence (AI) technology. Methods: A cross-sectional observational study was conducted (March 2020–October2021) during which hospitalized children aged 1–18 years with KD were consecutively enrolled. Those with a positive RTPCR test or IgM/IgG serology for COVID-19 were excluded. The clinical and laboratory profiles of children with and without MAS were studied. A multivariable logistic regression (LR) model was developed utilizing backward elimination method to determine the relationship between select candidate predictor variables and MAS in patients with KD. A classification tree was created based on these using artificial intelligence algorithms. Results: Sixty-two children were diagnosed with KD during the study period, of these, 42 children with KD were included; 14 (33.3 %) were diagnosed with MAS. The median (IQR) duration of fever (days) was significantly more in MAS than those without MAS [7 (5, 15) vs 5 (5, 9), P < 0.05]. Serum albumin (g/dL) was significantly lower in those with MAS [2.3 (2.2, 2.7) vs 2.8 (2.3, 3.1), P = 0.03]. The classification tree constructed using the AI-based algorithm predicted that in children with KD who had myocardial dysfunction, serum albumin < 2.8 g/dL and fever > 6 days duration at admission had an increased likelihood of developing MAS. In children without myocardial dysfunction, alanine transaminase (ALT) levels > 70 U/L and fever > 5 days were equally predictive of MAS. Conclusion: Nearly one-third of the children with KD had MAS. Clinicians should consider screening all children with KD for MAS at admission. A classification tree based on the presence of myocardial dysfunction, duration of fever > 6 days, ALT levels and hypoalbuminemia can identify MAS in the course of KD. [ABSTRACT FROM AUTHOR]

Purpose: The assessment of cardiac performance in septic new-borns is crucial for detecting hemodynamic instability and predicting outcome. The aim of the study is to assess myocardial performance in neonates with sepsis for the early identification of cardiac dysfunction. Patients and methods: A case control study was carried out from September 2022 to May 2023 at the Neonatal Intensive care unit, Kasturba Medical College, Manipal. A total of 68 neonates were included in the study, with 33 females and 35 males. The study population was further subdivided into 3 groups namely preterm septic neonates (n = 21), term septic neonates (n = 10) and non-septic healthy controls (n = 37). The cardiac structure and function were assessed using conventional method, Tissue Doppler imaging (Sm) and speckle tracking echocardiography (GLS). The study was approved by the Institutional Ethics Committee at Kasturba Medical College, Manipal (approval number IEC: 90/2022). The CTRI registration number for the study is CTRI/2022/09/045437 and was approved on September 12, 2022. Prior to the neonate's enrolment, informed consent was obtained from their mothers or legal guardians. Results: Out of the total 68 neonates, 31 were cases and 37 were controls which included 33 females and 35 males. LV systolic function was not statistically significant between cases and controls. E/A ratio of the mitral valve was significantly lower in septic newborns than in healthy neonates. (1.01 ± 0.35 vs 1.18 ± 0.31, p < 0.05) preterm neonates showed significantly lower Lateral E' and RV E' velocities than term neonates. TAPSE was significantly lower in septic preterm neonates. (8.61 ± 1.28 vs. 10.7 ± 2.11, p < 0.05) No significant difference was noted in the Myocardial Performance Index between septic neonates and healthy neonates. LV Global Longitudinal Strain was slightly lower in preterm septic neonates than in term neonates with sepsis. Conclusion: Septic newborns are associated with LV diastolic dysfunction, RV systolic dysfunction and substantially higher pulmonary systolic pressures. [ABSTRACT FROM AUTHOR]

Background: Isoproterenol is a drug used for the treatment of bradycardia that has many side effects due to its non-selective β-adrenoceptor agonist properties. Aim: In this study, we evaluated an in vivo experimental model for isoproterenol (ISO) cardiac injury using BALB/c mice and protective treatment with a combined optimized dose of Arctiin (AR) and Lactobacillus plantarum (LP) (ARLP; 30 mg/kg b.w. AR and viable 106 CFU/mL LP p.o.) together. Introduction: Isoproterenol causes cardiac injury in many instances. Arctiin is a naturally occurring lignin glycoside present in many herbal medicinal plants that has many beneficial effects for humans. Lactobacillus plantarum is yet another beneficial probiotic that benefits largely to humans. Materials and Methods: Male BALB/c mice in appropriate groups (6 animals each) were treated with ARLP for 7 days with ISO administration (100 mg/kg i.p.) on days 5 and 6. On the 8th day, animals were sacrificed. Serum and heart samples were collected for further processing. CK-MB, cardiac troponin, AST, ALT, LDH, GST, GPx, CAT, SOD, GSH, GSSG, MDA, nuclear factor kappa B (NFκB), TNF-α, and IL-6 by ELISA and gene expressions of nuclear factor erythroid 2-related factor 2 (Nrf2) were estimated in samples. Results: Mice administered with ISO showed a prominent rise in the serum marker enzyme activities and tissue oxidative stress markers (MDA and GSSG). Furthermore, marked reductions in body weight and enzymatic and non-enzymatic antioxidant levels were noticed in ISO toxicity. Alterations in proinflammatory cytokines (TNF-α and IL-6) and Nrf2 levels by RT-PCR were analyzed. Histopathology of the heart also indicated cardiac injury in ISO-intoxicated mice. ARLP pretreatment prevented all these cardiac injuries and exerted significant (p ≤ 0.05) prophylactic protection toward cardiac tissue. Further, we analyzed the possible interactions between AR and LP in vitro, to understand the influence of ARonLP, which showed no significant suppressive/antibacterial activity on LP. Conclusion: In conclusion, ARLP exerts a strong cardioprotective and anti-inflammatory activity in cardiovascular injury. [ABSTRACT FROM AUTHOR]

Background: Ferroptosis is an important type of cell death contributing to myocardial dysfunction induced by whole body ischemia reperfusion following cardiac arrest (CA) and resuscitation. Sulforaphane (SFN), known as the activator of the nuclear factor E2-related factor 2 (Nrf2), has been proven to effectively alleviate regional myocardial ischemia reperfusion injury. The present study was designed to investigate whether SFN could improve post-resuscitation myocardial dysfunction by inhibiting cardiomyocytes ferroptosis and its potential regulatory mechanism. Methods and results: An in vivo pig model of CA and resuscitation was established. Hypoxia/reoxygenation (H/R)-stimulated AC16 cardiomyocytes was constructed as an in vitro model to simulate the process of CA and resuscitation. In vitro experiment, SFN reduced ferroptosis-related ferrous iron, lipid reactive oxygen species, and malondialdehyde, increased glutathione, and further promoted cell survival after H/R stimulation in AC16 cardiomyocytes. Mechanistically, the activation of Nrf2 with the SFN decreased interferon regulatory factor 1 (IRF1) expression, then reduced its binding to the promoter of glutathione peroxidase 4 (GPX4), and finally recovered the latter’s transcription after H/R stimulation in AC16 cardiomyocytes. In vivo experiment, SFN reversed abnormal expression of IRF1 and GPX4, inhibited cardiac ferroptosis, and improved myocardial dysfunction after CA and resuscitation in pigs. Conclusions: SFN could effectively improve myocardial dysfunction after CA and resuscitation, in which the mechanism was potentially related to the inhibition of cardiomyocytes ferroptosis through the regulation of Nrf2/IRF1/GPX4 pathway.

Background Coronary microvascular dysfunction (CMD) could be a potential underlying mechanism for myocardial disease in HIV. Methods Comparisons of coronary flow reserve corrected for heart rate-blood pressure product (CFRCOR) were made among people with HIV (PWH) with no known history of cardiovascular disease (CVD) or diabetes mellitus, persons without HIV (PWOH), and persons with diabetes (PWDM) and no known history of CVD or HIV. Results PWH (n = 39, 74% male, age 55 [7] years, body mass index [BMI] 32.3 (26.8-34.9) kg/m2, duration of antiretroviral therapy 13 [5] years, CD4+ count 754 [598-961] cells/μL) were similar to PWOH (n = 69, 74% male, age 55 [8] years, BMI 32.2[25.6-36.5] kg/m2) and PWDM (n = 63, 63% male, age 55 [8] years, BMI 31.5 [28.6-35.6] kg/m2). CFRCOR was different among groups: PWOH 2.76 (2.37-3.36), PWH 2.47 (1.92-2.93), and PWDM 2.31 (1.98-2.84); overall P =.003. CFRCOR was reduced comparing PWH to PWOH (P =.04) and PWDM to PWOH (P =.007) but did not differ when comparing PWH to PWDM (P =.98). A total 31% of PWH had CFRCOR < 2.0, a critical cutoff for CMD, compared to 14% of PWOH and 27% with PWDM. A total 40% of women with HIV had a CFRCOR < 2.0 compared to 6% of women without HIV (P =.02). Conclusions Subclinical CMD is present among chronically infected and well-treated, asymptomatic PWH who are immunologically controlled. This study demonstrates CFR is reduced in PWH compared to PWOH and comparable to PWDM, further highlighting that well-treated HIV infection is a CVD-risk enhancing factor for CMD similar to diabetes. Clinical Trials Registration: NCT02740179 [ABSTRACT FROM AUTHOR]

Sepsis-induced cardiomyopathy is a clinical entity rarely reported in the literature. It lacked an objective and agreedupon definition, and although there are clinical criteria, there are no diagnostic guidelines or specific treatment; its identification, approach, and management imply a challenge for the clinician. Its presence increases mortality by up to 70%. It is considered an acute onset complication that manifests with alterations in systolic and diastolic function, finally showing reversibility in a period of seven to ten days. When this entity is suspected, the gold standard for diagnosis is the echocardiogram. Infection control, life support, and hemodynamic measures associated with the use of vasopressors and inotropes are the main therapeutic tools that have shown a decrease in mortality. However, this entity usually requires advanced organic support, even requiring ventricular assistance devices such as an intraaortic balloon pump (IABP) or extra corporeal membrane oxygenation (ECMO), which have shown promising results in the treatment of this pathology. Despite this, mortality is high, and the prognosis continues to be unfavorable without early identification, hence the importance of unifying criteria, establishing risk factors, validated diagnostic tools as well as differentiating it from other clinical entities, thereby improving its outcome and prognosis. [ABSTRACT FROM AUTHOR]

Applied cardio-oncology in hematological malignancies refers to the integration of cardiovascular care and management for patients with blood cancer, particularly leukemia, lymphoma, and multiple myeloma. Hematological cancer therapy-related cardiotoxicity deals with the most common cardiovascular complications of conventional chemotherapy, targeted therapy, immunotherapy, chimeric antigen receptor T (CAR-T) cell and tumor-infiltrating lymphocyte therapies, bispecific antibodies, and hematopoietic stem cell transplantation. This narrative review focuses on hematological cancer-therapy-related cardiotoxicity's definition, risk stratification, multimodality imaging, and use of cardiac biomarkers to detect clinical and/or subclinical myocardial dysfunction and electrical instability. Moreover, the most common cardiotoxic profiles of the main drugs and/or therapeutic interventions in patients with hematological malignancies are described thoroughly. [ABSTRACT FROM AUTHOR]

Abstract Background Coronary slow flow (CSF) often links to inflammation and endothelial function disturbance. While conventional ejection fraction measurements fall short in identifying myocardial dysfunction, left ventricular global longitudinal strain (LV GLS) has shown superior efficacy in this regard. Our study aimed to explore subclinical left ventricular systolic dysfunction by assessing LV GLS in patients diagnosed with coronary slow flow (CSF). Methods The study included sixty patients with CSF and sixty control individuals without CSF. Coronary angiography employed the Thrombolysis in Myocardial Infarction (TIMI) frame count (TFC) to identify CSF. LV GLS values were evaluated and compared between the two groups. Results Significantly reduced LV GLS was evident in the CSF group compared to the control group (− 16.18 ± 1.25 vs. − 19.34 ± 1.33, p

Stroke–heart syndrome (SHS), a critical yet underrecognized condition, encompasses a range of cardiac complications that arise following an ischemic stroke. This narrative review explores the pathophysiology, clinical manifestations, and implications of SHS, focusing on the complex interplay between the brain and the heart. Acute ischemic stroke (AIS) triggers autonomic dysfunction, leading to a surge in catecholamines and subsequent myocardial injury. Our review highlights the five cardinal manifestations of SHS: elevated cardiac troponin (cTn) levels, acute myocardial infarction, left ventricular dysfunction, arrhythmias, and sudden cardiac death. Despite the significant impact of these complications on patient outcomes, there is a notable absence of specific guidelines for their management. Through a comprehensive literature search, we synthesized findings from recent studies to elucidate the mechanisms underlying SHS and identified gaps in the current understanding. Our findings underscore the importance of early detection and multidisciplinary management of cardiac complications post-stroke. Future research should focus on establishing evidence-based protocols to improve clinical outcomes for stroke patients with SHS. Addressing this unmet need will enhance the care of stroke survivors and reduce mortality rates associated with cardiac complications.

Myocardial dysfunction is common in patients admitted to the intensive care unit (ICU). Septic disease frequently results in cardiac dysfunction, and sepsis represents the most common cause of admission and death in the ICU. The association between left ventricular (LV) systolic dysfunction and mortality is not clear for critically ill patients. Conversely, LV diastolic dysfunction (DD) seems increasingly recognized as a factor associated with poor outcomes, not only in sepsis but also more generally in critically ill patients. Despite recent attempts to simplify the diagnosis and grading of DD, this remains relatively complex, with the need to use several echocardiographic parameters. Furthermore, the current guidelines have several intrinsic limitations when applied to the ICU setting. In this manuscript, we discuss the challenges in DD classification when applied to critically ill patients, the importance of left atrial pressure estimates for the management of patients in ICU, and whether the study of cardiac dysfunction spectrum during critical illness may benefit from the integration of left ventricular and left atrial strain data to improve diagnostic accuracy and implications for the treatment and prognosis. [ABSTRACT FROM AUTHOR]

In this study, we aimed to investigate the effect and underlying mechanism of betulinic acid (BA) on myocardial dysfunction in septic rats. Twenty‐four male Sprague–Dawley rats were randomly allocated into four groups (n = 6 rats/group): the sham operation (Control) group, the cecal ligation and puncture (CLP) group, the BA 10 mg/kg group, and the BA 50 mg/kg group. The septic rat model was induced through cecal ligation and puncture in the CLP and BA groups, except for the Control group. Then, cardiac function parameters were assessed using echocardiography, myocardial injury markers were quantified via biochemical assays, and myocardial histopathological injuries were observed through H&E staining. Inflammatory factors in the serum were measured using ELISA assays, immunohistochemistry and qRT‐PCR were performed to determine macrophage numbers and the expression of iNOS, CD86, Arg‐1, and Mrc1 in myocardial tissue. The protein expression levels of TLR4, Myd88, and NF‐κB in myocardial tissue were assessed through western blot analysis. The results showed that BA significantly improved cardiac function, reduced myocardial injury, and attenuated inflammation in CLP rats. Specifically, BA decreased LVEDD and LVESD while increasing LVEF and LVFS. Furthermore, BA upregulated the levels of BNP, cTnT, CK‐MB, LDH, IL‐6, IL‐1β, and TNF‐α in CLP rat serum. Additionally, BA reduced macrophage infiltration, inhibited M1/M2 gene expression, and downregulated TLR4, Myd88 and NF‐κB protein expression in CLP rats myocardial tissues. In conclusion, BA can inhibit myocardial inflammation and prevent sepsis‐induced myocardial dysfunction by inhibiting TLR4/MyD88/NF‐κB signaling, thereby promoting M2 macrophage polarization in myocardial tissues. [ABSTRACT FROM AUTHOR]

Myocardial ischemia caused by coronary artery disease (CAD) and the presence of metabolic abnormalities and microvascular impairments detected in patients with diabetes mellitus (DM) are a common cause of left ventricular (LV) dysfunction. Transthoracic echocardiography is the most-used, non-invasive imaging method for the assessment of myocardial contractility. The accurate evaluation of LV function is crucial for identifying patients who are at high risk or may have worse outcomes. Myocardial work (MW) is emerging as an alternative tool for the evaluation of LV systolic function, providing additional information on cardiac performance when compared to conventional parameters such as left ventricular ejection fraction (LVEF) and global longitudinal strain (GLS) because it incorporates deformation and load into its analysis. The potential of MW in various conditions is promising and it has gained increased attention. However, larger studies are necessary to further investigate its role and application before giving an answer to the question of whether it can have widespread implementation into clinical practice. The aim of this review is to summarize the actual knowledge of MW for the analysis of LV dysfunction caused by myocardial ischemia and hyperglycemia. [ABSTRACT FROM AUTHOR]

Background: Coronary slow flow (CSF) often links to inflammation and endothelial function disturbance. While conventional ejection fraction measurements fall short in identifying myocardial dysfunction, left ventricular global longitudinal strain (LV GLS) has shown superior efficacy in this regard. Our study aimed to explore subclinical left ventricular systolic dysfunction by assessing LV GLS in patients diagnosed with coronary slow flow (CSF). Methods: The study included sixty patients with CSF and sixty control individuals without CSF. Coronary angiography employed the Thrombolysis in Myocardial Infarction (TIMI) frame count (TFC) to identify CSF. LV GLS values were evaluated and compared between the two groups. Results: Significantly reduced LV GLS was evident in the CSF group compared to the control group (− 16.18 ± 1.25 vs. − 19.34 ± 1.33, p < 0.001). A notable correlation (r = 0.492, p < 0.001) between LV GLS and TFC was observed in the CSF group. Multivariate logistic regression analysis highlighted reduced LV-GLS (OR 2.2, 95% CI 1.57–3.09, p < 0.001) and smoking (OR 11.55, 95% CI 3.24–41.2, p < 0.001) as significant predictors for CSF presence. The receiver operating characteristic curve established that an LV GLS value of ≥ − 17.8% accurately predicted the presence of CSF (AUC: 0.958, 95% CI: 0.924–0.991, p < 0.001) with 90% specificity and 91.7% sensitivity. Conclusion: Our study indicates that reduced LV GLS is associated with CSF presence, offering a valuable means to early detect subclinical left ventricular systolic dysfunction in high-risk patients susceptible to heart failure. Trial registration: ZU-IRB#7038/12-7-2021 Registered 12 July 2021, email: IRB_123@medicine.zu.edu.eg. [ABSTRACT FROM AUTHOR]

Clinical evidence indicates that COVID‐19 is a multiorgan disease that significantly impacts the cardiovascular system. However, little is known about the predictors of myocardial dysfunction after SARS‐CoV‐2 infection. Therefore, this research aimed to evaluate the clinical and electrocardiographic correlates of myocardial dysfunction after SARS‐CoV‐2 infection in nonhospitalised patients without previously diagnosed cardiovascular disease. This observational study included 448 patients selected from the database of 4142 patients in the Polish Long‐Covid Cardiovascular study. All patients underwent a 12‐lead electrocardiogram (ECG); 24‐h Holter ECG monitoring, 24/7 ambulatory blood pressure monitoring, echocardiography, and cardiac magnetic resonance imaging. According to the results of diagnostic tests, patients were divided into two groups depending on the occurrence of myocardial dysfunction after COVID‐19. Group 1–without myocardial dysfunction after COVID‐19–consisted of 419 patients, with a mean age of 48.82 (SD ± 11.91), and Group 2 (29 patients)–with myocardial dysfunction after COVID‐19, with a mean age of 51.45 (SD ± 12.92). When comparing the analysed groups, there were significantly more men in Group 2 (p = 0.006). QRS (corresponds to the time of ventricular contraction in an electrocardiographic examination) fragmentation (p = 0.031), arrhythmias (atrial fibrillation, supraventricular extrasystole, ventricular extrasystole) (p = 0.008), and male gender (p = 0.007) were independently associated with myocardial dysfunction after COVID‐19. The study showed that myocardial damage after COVID‐19 affects men more often and is independent of typical clinical factors and the severity of the disease course. The QRS fragmentation and arrhythmias observed in the ECG indicate the possibility of myocardial dysfunction in patients after COVID‐19, which may be a valuable marker for physicians. [ABSTRACT FROM AUTHOR]

Sepsis-induced myocardial dysfunction (SIMD) has become one of the most lethal complications of sepsis, while the treatment was limited by a shortage of pertinent drugs. Epigallocatechin-3-gallate (EGCG) is the highest content of active substances in green tea, and its application in cardiovascular diseases has broad prospects. This study was conducted to test the hypothesis that EGCG was able to inhibit lipopolysaccharide (LPS) induced myocardial dysfunction and investigate the underlying molecular mechanisms. The cardiac systolic function was assessed by echocardiography. The cardiomyocyte apoptosis was determined by TUNEL staining. The expression of inflammatory factors and apoptosis-related protein, cardiac markers were examined by Western Blot and qRT-PCR. EGCG effectively improve LPS-induced cardiac function damage, enhance left ventricular systolic function, and restore myocardial cell vitality. It can effectively inhibit the upregulation of TLR4 expression induced by LPS and inhibit IκB α/NF- κB/p65 signaling pathway, thereby inhibiting cardiomyocyte apoptosis and improving myocarditis. In conclusion, EGCG protects against SIMD through anti-inflammatory and anti-apoptosis effects; it was mediated by the inhibition of the TLR4/NF-κB signal pathway. Our results demonstrated that EGCG might be a possible medicine for SIMD prevention and treatment.

Abstract Background Extracellular vesicles (EVs) derived from various cell sources exert cardioprotective effects during cardiac ischemic injury. Our previous study confirmed that EVs derived from ischemic-reperfusion injured heart tissue aggravated cardiac inflammation and dysfunction. However, the role of EVs derived from normal cardiac tissue in myocardial ischemic injury remains elusive. Results In the present study, normal heart-derived EVs (cEVs) and kidney-derived EVs (nEVs) were isolated and intramyocardially injected into mice after myocardial infarction (MI). We demonstrated that administration of both cEVs and nEVs significantly improved cardiac function, reduced the scar size, and alleviated inflammatory infiltration into the heart. In addition, cardiomyocyte apoptosis was inhibited, whereas angiogenesis was enhanced in the hearts receiving cEVs or nEVs treatment. Moreover, intramyocardial injection of cEVs displayed much better cardiac protective efficacy than nEVs in murine MI models. RNA-seq and protein-protein interaction (PPI) network analysis revealed the protective mRNA clusters in both cEVs and nEVs. These mRNAs were involved in multiple signaling pathways, which may synergistically orchestrate to prevent the heart from further damage post MI. Conclusions Collectively, our results indicated that EVs derived from normal heart tissue may represent a promising strategy for cardiac protection in ischemic heart diseases.

Diabetic ketoacidosis in children is associated with a wide gamut of complications, which can be either disease- or therapy-related. Common complications in children with DKA include cerebral edema, acute kidney injury, hypokalemia, hypoglycemia, etc. As opposed to asymptomatic hypophosphatemia, which is common during the management of DKA, severe symptomatic hypophosphatemia leading to life-threatening complications like rhabdomyolysis, hemolysis, respiratory failure secondary to muscle weakness, and cardiac complications are rare. The authors present a case of a newly diagnosed T1DM patient who, during the course of management, developed severe hypophosphatemia leading to arrhythmias and cardiac dysfunction, which improved with prompt recognition and correction. [ABSTRACT FROM AUTHOR]

Sepsis-induced myocardial dysfunction (SMD) is the major cause of death in sepsis. Nucleotide-binding oligomerization domain-like receptor family pyrin domain containing 3 (NLRP3)-mediated pyroptosis contributes to the occurrence and development of SMD. Although Apelin confers direct protection against SMD, the potential mechanisms remain unclear. This study aimed to determine whether Apelin protects against SMD via regulation of NLRP3-mediated pyroptosis of cardiomyocytes. Experimental SMD was induced in wild-type (WT) control mice and Apelin knockout (Apelin−/−) mice by cecal ligation and puncture (CLP). Neonatal mouse cardiomyocytes (NMCs) were treated with lipopolysaccharide (LPS) to simulate the physiological environment of SMD in vitro. The expression of Apelin was greatly decreased in the plasma from septic patients and septic mouse heart. Knockout of Apelin aggravated SMD, evidenced by decreased cardiac function, and increased cardiac fibrosis and NLRP3 inflammasome and pyroptosis levels in CLP-treated Apelin−/− mice compared with WT mice. Overexpression of Apelin activated the AMPK pathway and thereby inhibited NLRP3 inflammasome–mediated pyroptosis of NMCs induced by LPS in vitro These protective effects were partially abrogated by AMPK inhibitor. In conclusion, Apelin attenuated SMD by inhibiting NLRP3-mediated pyroptosis via activation of the AMPK pathway. Apelin may serve as a promising therapeutic target for SMD.

Background: Cardiac complications due to non-traumatic subarachnoid hemorrhage (SAH) are usually described using classical echocardiographic evaluation. Strain imaging appears to have better sensitivity than standard echocardiographic markers for the diagnosis of left ventricular dysfunction. The aim of this study was to determine the prevalence of cardiac dysfunction defined as a Global Longitudinal Strain (GLS) ≥ − 20% in patients with good-grade SAH (WFNS 1 or 2). Methods: Seventy-six patients with good-grade SAH were prospectively enrolled and analyzed at admission for neurocritical care. Transthoracic echocardiography was performed on days 1, 3, and 7 after hemorrhage. Routine measurements, including left ventricular ejection fraction (LVEF), were performed, and off-line analysis was performed by a blinded examiner, to determine 2-, 3-, and 4-cavity longitudinal strain and left ventricular GLS. GLS was considered altered if it was ≥ − 20%, we also interested the value of ≥ − 17%. LVEF was considered altered if it was < 50%. Results: On day 1, 60.6% of patients had GLS ≥ − 20% and 21.2% of patient had GLS ≥ − 17%. In comparison, alteration of LVEF was present in only 1.7% of patients. The concordance rate between LVEF < 50% and GLS ≥ − 20% and LVEF ≥ 50% and GLS < − 20% was 46%. Conclusion: Strain imaging showed a higher prevalence (60.6%) of left ventricular dysfunction during the acute phase of good-grade SAH (WFNS 1 or 2) than previously described. [ABSTRACT FROM AUTHOR]

Background: Extracellular vesicles (EVs) derived from various cell sources exert cardioprotective effects during cardiac ischemic injury. Our previous study confirmed that EVs derived from ischemic-reperfusion injured heart tissue aggravated cardiac inflammation and dysfunction. However, the role of EVs derived from normal cardiac tissue in myocardial ischemic injury remains elusive. Results: In the present study, normal heart-derived EVs (cEVs) and kidney-derived EVs (nEVs) were isolated and intramyocardially injected into mice after myocardial infarction (MI). We demonstrated that administration of both cEVs and nEVs significantly improved cardiac function, reduced the scar size, and alleviated inflammatory infiltration into the heart. In addition, cardiomyocyte apoptosis was inhibited, whereas angiogenesis was enhanced in the hearts receiving cEVs or nEVs treatment. Moreover, intramyocardial injection of cEVs displayed much better cardiac protective efficacy than nEVs in murine MI models. RNA-seq and protein-protein interaction (PPI) network analysis revealed the protective mRNA clusters in both cEVs and nEVs. These mRNAs were involved in multiple signaling pathways, which may synergistically orchestrate to prevent the heart from further damage post MI. Conclusions: Collectively, our results indicated that EVs derived from normal heart tissue may represent a promising strategy for cardiac protection in ischemic heart diseases. [ABSTRACT FROM AUTHOR]

Background Increased renin angiotensin aldosterone system (RAAS) activity may contribute to excess cardiovascular disease in people with HIV (PWH). We investigated how RAAS blockade may improve myocardial perfusion, injury, and function among well-treated PWH. Methods Forty PWH, on stable ART, without known heart disease were randomized to eplerenone 50 mg PO BID (n = 20) or identical placebo (n = 20) for 12 months. The primary endpoints were (1) myocardial perfusion assessed by coronary flow reserve (CFR) on cardiac PET or stress myocardial blood flow (sMBF) on cardiac MRI or (2) myocardial inflammation by extracellular mass index (ECM i) on cardiac MRI. Results Beneficial effects on myocardial perfusion were seen for sMBF by cardiac MRI (mean [SD]: 0.09 [0.56] vs −0.53 [0.68] mL/min/g; P =.03) but not CFR by cardiac PET (0.01 [0.64] vs −0.07 [0.48]; P =.72, eplerenone vs placebo). Eplerenone improved parameters of myocardial function on cardiac MRI including left ventricular end diastolic volume (−13 [28] vs 10 [26] mL; P =.03) and global circumferential strain (GCS; median [interquartile range 25th–75th]: −1.3% [−2.9%–1.0%] vs 2.3% [−0.4%–4.1%]; P =.03), eplerenone versus placebo respectively. On cardiac MRI, improvement in sMBF related to improvement in global circumferential strain (ρ = −0.65, P =.057) among those treated with eplerenone. Selecting for those with impaired myocardial perfusion (CFR <2.5 and/or sMBF <1.8), there was a treatment effect of eplerenone versus placebo to improve CFR (0.28 [0.27] vs −0.05 [0.36]; P =.04). Eplerenone prevented a small increase in troponin (0.00 [−0.13–0.00] vs 0.00 [0.00–0.74] ng/L; P =.03) without effects on ECM i (0.9 [−2.3–4.3] vs −0.7 [−2.2–−0.1] g/m2; P =.38). CD4+ T-cell count (127 [−38–286] vs −6 [−168–53] cells/μL; P =.02) increased in the eplerenone- versus placebo-treated groups. Conclusions RAAS blockade with eplerenone benefitted key indices and prevented worsening of myocardial perfusion, injury, and function among PWH with subclinical cardiac disease when compared with placebo. Clinical Trials Registration NCT02740179 (https://clinicaltrials.gov/ct2/show/NCT02740179?term=NCT02740179&draw=2&rank=1). [ABSTRACT FROM AUTHOR]

The aim of the study was to perform a comprehensive fundamental analysis of the factors of inflammation, oxidative stress, fibrosis, myocardial dysfunction, ischemia and omega-3 index associated with postoperative atrial fibrillation (POAF) after coronary artery bypass graft (CABG) surgery in patients with coronary artery disease. The study involved 158 patients who were admitted to the hospital to undergo CABG surgery. Patients were divided into two groups: group 1 comprised 111 patients without POAF (82% males, median age—62.0 (56.0; 66.0) years), and group 2 comprised 47 patients with POAF (84.4% males, median age—65.0 (61.0; 70.0) years). POAF occurred 5.2 (2.0; 7.0) days after CABG. In all the patients, we evaluated laboratory tests before and 3–4 days after CABG. All the patients also underwent echocardiography. According to results of multifactorial regression analysis, the odds ratio of POAF development for left atrial diameter >41 mm was 4.3 (95% confidence interval (CI) 2.0–9.7, p < 0.001), interleukin (IL)-6 postoperative levels >22.07 pg/mL—3.0 (95% CI 1.4–8.2, p = 0.006), IL-8 postoperative levels >9.67 pg/mL—2.3 (95% CI 1.2–7.3, p = 0.006), superoxide dismutase postoperative levels in plasma >1100.5 U/g—3.2 (95% CI 1.4–9.2, p = 0.03), glutathione postoperative levels ≤0.194 micromole/g of hemoglobin—1.9 (95% CI 1.2–6.3, p < 0.001), glutathione peroxidase postoperative levels ≤17.36 millimole/g of hemoglobin—2.2 (95% CI 1.1–8.2, p < 0.001), glutathione reductase postoperative levels ≤2.99 millimole/g of hemoglobin—2.3 (95% CI, 1.1–5.7, p < 0.001), malondialdehyde postoperative levels >1.25 micromole/g of hemoglobin—2.0 (95% CI, 1.2–7.9, p < 0.001), NO postoperative levels in plasma >36.4 micromole/L—1.5 (95% CI, 1.1–5.9, p < 0.001) and omega-3 index ≤1.59%—2.6 (95% CI 1.5–9.1, p < 0.001). Our study showed that increased left atrial diameter, high postoperative levels of inflammatory factors, oxidative stress, fibrosis indicators and omega-3 index were associated with POAF in patients who underwent CABG. [ABSTRACT FROM AUTHOR]

Pediatric septic shock is defined as progressive multi-organ dysfunction and cardiovascular dysfunction accompanying sepsis. Studies showing myocardial dysfunction associated with pediatric septic shock are very limited. The aim of this study was to evaluate the relationship between myocardial functions calculated by echocardiography, disease severity, and clinical outcomes in children with septic shock. This observational prospective study was conducted in a pediatric intensive care at a university-affiliated tertiary hospital. The patients diagnosed with septic shock between January 2021 and February 2022 were included in the study. The study was conducted with 56 patients. The rate of myocardial dysfunction (systolic and/or diastolic dysfunction) was 50%. Of these, 39.3% (n = 22) had systolic dysfunction, 17.9% (n = 10) had diastolic dysfunction, and 8.9% (n = 5) had both systolic and diastolic dysfunction. PRISM III score (p = 0.004), VIS (p < 0.001), lactate (p = 0.002), CK-MB (p = 0.023), troponin (p = 0.038), EF (p = 0.004) EF z-score (p = 0.003), MAPSE z-score (p = 0.049), TAPSE (p = 0.010), TAPSE z-score (p = 0.003), and mitral valve E/e ´z-score (p = 0.028) were statistically significant difference with mortality. No significant difference was found for mortality with MAPSE (p = 0.090), mitral valve E/A (p = 0.624), and mitral valve E/A z-score (p = 0.327). EF z-score was found to be associated with 30-day mortality (OR = 0,681, 95% CI 0,480 to 0.991, p = 0,045). We found the TAPSE z-score to be the most significant parameter with 30-day mortality (OR = 0,690, 95% CI 0,489 to 0.998, p = 0,032). Conclusion: We found left ventricular dysfunction associated factor with mortality. TAPSE showing right ventricular dysfunction was found to be the independent risk factor most associated with mortality. What is Known: • Studies showing myocardial dysfunction associated with pediatric septic shock are limited. • Little is known about the use of echocardiography in pediatric septic shock, and there are no specific guidelines for treatment and follow-up in pediatric patients. What is New: • Characteristics, echocardiographic measurements, and outcomes were comprehensively assessed in children with septic shock. • As a result of our analysis, we found that TAPSE, which is easily measured at the bedside, is the most critical parameter in relation to mortality. • We offer recommendations for its use in the follow-up of children with septic shock. [ABSTRACT FROM AUTHOR]

Abstract Background Sepsis is the leading cause of death in intensive care units. Sepsis-induced myocardial dysfunction, one of the most serious complications of sepsis, is associated with higher mortality rates. As the pathogenesis of sepsis-induced cardiomyopathy has not been fully elucidated, there is no specific therapeutic approach. Stress granules (SG) are cytoplasmic membrane-less compartments that form in response to cellular stress and play important roles in various cell signaling pathways. The role of SG in sepsis-induced myocardial dysfunction has not been determined. Therefore, this study aimed to determine the effects of SG activation in septic cardiomyocytes (CMs). Methods Neonatal CMs were treated with lipopolysaccharide (LPS). SG activation was visualized by immunofluorescence staining to detect the co-localization of GTPase-activating protein SH3 domain binding protein 1 (G3BP1) and T cell-restricted intracellular antigen 1 (TIA-1). Eukaryotic translation initiation factor alpha (eIF2α) phosphorylation, an indicator of SG formation, was assessed by western blotting. Tumor necrosis factor alpha (TNF-α) production was assessed by PCR and enzyme-linked immunosorbent assays. CMs function was evaluated by intracellular cyclic adenosine monophosphate (cAMP) levels in response to dobutamine. Pharmacological inhibition (ISRIB), a G3BP1 CRISPR activation plasmid, and a G3BP1 KO plasmid were employed to modulate SG activation. The fluorescence intensity of JC-1 was used to evaluate mitochondrial membrane potential. Results LPS challenge in CMs induced SG activation and resulted in eIF2α phosphorylation, increased TNF-α production, and decreased intracellular cAMP in response to dobutamine. The pharmacological inhibition of SG (ISRIB) increased TNF-α expression and decreased intracellular cAMP levels in CMs treated with LPS. The overexpression of G3BP1 increased SG activation, attenuated the LPS-induced increase in TNF-α expression, and improved CMs contractility (as evidenced by increased intracellular cAMP). Furthermore, SG prevented LPS-induced mitochondrial membrane potential dissipation in CMs. Conclusion SG formation plays a protective role in CMs function in sepsis and is a candidate therapeutic target.

Applied cardio-oncology in hematological malignancies refers to the integration of cardiovascular care and management for patients with blood cancer, particularly leukemia, lymphoma, and multiple myeloma. Hematological cancer therapy-related cardiotoxicity deals with the most common cardiovascular complications of conventional chemotherapy, targeted therapy, immunotherapy, chimeric antigen receptor T (CAR-T) cell and tumor-infiltrating lymphocyte therapies, bispecific antibodies, and hematopoietic stem cell transplantation. This narrative review focuses on hematological cancer-therapy-related cardiotoxicity’s definition, risk stratification, multimodality imaging, and use of cardiac biomarkers to detect clinical and/or subclinical myocardial dysfunction and electrical instability. Moreover, the most common cardiotoxic profiles of the main drugs and/or therapeutic interventions in patients with hematological malignancies are described thoroughly.

The growing global prevalence of heart failure (HF) necessitates innovative methods for early diagnosis and classification of myocardial dysfunction. In recent decades, non-invasive sensor-based technologies have significantly advanced cardiac care. These technologies ease research, aid in early detection, confirm hemodynamic parameters, and support clinical decision-making for assessing myocardial performance. This discussion explores validated enhancements, challenges, and future trends in heart failure and dysfunction modeling, all grounded in the use of non-invasive sensing technologies. This synthesis of methodologies addresses real-world complexities and predicts transformative shifts in cardiac assessment. A comprehensive search was performed across five databases, including PubMed, Web of Science, Scopus, IEEE Xplore, and Google Scholar, to find articles published between 2009 and March 2023. The aim was to identify research projects displaying excellence in quality assessment of their proposed methodologies, achieved through a comparative criteria-based rating approach. The intention was to pinpoint distinctive features that differentiate these projects from others with comparable objectives. The techniques identified for the diagnosis, classification, and characterization of heart failure, systolic and diastolic dysfunction encompass two primary categories. The first involves indirect interaction with the patient, such as ballistocardiogram (BCG), impedance cardiography (ICG), photoplethysmography (PPG), and electrocardiogram (ECG). These methods translate or convey the effects of myocardial activity. The second category comprises non-contact sensing setups like cardiac simulators based on imaging tools, where the manifestations of myocardial performance propagate through a medium. Contemporary non-invasive sensor-based methodologies are primarily tailored for home, remote, and continuous monitoring of myocardial performance. These techniques leverage machine learning approaches, proving encouraging outcomes. Evaluation of algorithms is centered on how clinical endpoints are selected, showing promising progress in assessing these approaches’ efficacy.

The exact interaction of factors leading to myocardial dysfunction and fibrosis of the systemic right ventricle (SRV) is not completely understood. Myocardial ischemia and injury associated with a supply-demand mismatch of the pressure overloaded SRV are thought to play an important role, however studies confirming this are lacking. Adult SRV patients were included in this single centre cohort study. All patients underwent a comprehensive diagnostic and imaging workup. A two-day stress-rest SPECT was performed to assess myocardial perfusion. SRV ischemia was defined as decreased segmental tracer uptake during exercise with significant improvement at rest. Contrast enhanced cardiac magnetic resonance imaging (CMR) was also performed in a subgroup of patients without contraindication, to assess focal myocardial fibrosis. Differences between patients with and without SRV ischemia were assessed. Twenty-three SRV patients (15 with transposition of the great arteries after atrial switch procedure and 8 with congenitally corrected transposition of the great arteries; 5 (22%) females; mean age 38 ± 11 years) were included. Seven (30%) patients had SRV ischemia on SPECT. Late gadolinium enhancement on CMR was more common in patients with SRV ischemia (p = 0.002). However, there was no association between SRV ischemia and different echocardiographic or CMR parameters of SRV systolic function, laboratory markers (high-sensitivity troponin I and NT-proBNP) and exercise capacity. Our multimodality study showed that SRV ischemia in adult SRV patients was associated with more focal myocardial fibrosis, but not with functional or imaging markers of SRV function. • The role of myocardial ischemia in dysfunction of the systemic right ventricle is unknown. • Myocardial ischemia of the systemic right ventricle was evident in 30% of adult patients with systemic right ventricle. • Patients with ischemia more commonly had focal myocardial fibrosis. • Myocardial ischemia had no impact on functional or imaging markers of systemic right ventricular function. [ABSTRACT FROM AUTHOR]

Pathomechanisms responsible for recovery from acute myocarditis (MCD) or progression to non-ischemic cardiomyopathy have not been comprehensively investigated. Iron, positioned at the crossroads of inflammation and the energy metabolism of cardiomyocytes, may contribute to the pathophysiology of inflammatory myocardial disease. The aim of this study was to evaluate whether systemic iron parameters are related to myocardial dysfunction in MCD patients. We prospectively enrolled 42 consecutive patients hospitalized for MCD. Their iron status and their clinical, laboratory, and echocardiographic indices were assessed during hospitalization and during ambulatory visits six weeks after discharge. A control group comprising healthy volunteers was recruited. The MCD patients had higher serum ferritin and hepcidin and lower serum iron concentration and transferrin saturation (TSAT) than the healthy controls (all p < 0.01). Six weeks after discharge, the iron status of the MCD patients was already comparable to that of the control group. During hospitalization, lower serum iron and TSAT correlated with higher NT-proBNP (both p < 0.05). In-hospital lower serum iron and TSAT correlated with both a lower left ventricular ejection fraction (LVEF) and worse left ventricular global longitudinal strain at follow-up visits (all p < 0.05). In conclusion, in patients with acute MCD, iron status is altered and normalizes within six weeks. Low serum iron and TSAT are related to greater in-hospital neurohormonal activation and subtle persistent left ventricular dysfunction. [ABSTRACT FROM AUTHOR]

Abstract Background Celiac disease (CD) is a chronic immune-mediated disorder with multiple extraintestinal manifestations. The increased incidence of cardiac morbidities in celiac patients highlights the importance of early detection of subclinical myocardial dysfunctions. In this study, we aimed to assess the cardiac functions and explore early subclinical myocardial dysfunctions in celiac patients by tissue Doppler imaging. Results A cross-sectional analytical study which included 42 celiac patients with CD and 36 age- and sex-matched controls. They were subjected to full medical history and examination and complete transthoracic echocardiography including tissue Doppler imaging to assess cardiac functions. Evidences of early subclinical systolic and diastolic dysfunctions were found in our patients; they had significantly lower tricuspid E/A ratio; lower S, E′, a′ in both ventricles; reduced mitral E′/a′ (2.13 ± 0.87, 2.94 ± 0.061 respectively, p

Introduction: The Global Registry of Acute Coronary Events (GRACE) risk score is widely recommended for risk assessment in patients with acute myocardial infarction (AMI). Variable degrees of impairment in left ventricular (LV) systolic and diastolic function might be found after AMI. Tei index is an echocardiography parameter that represents both systolic and diastolic LV performance. Previous studies demonstrate Tei index as an independent predictor of Major Adverse Cardiovascular Events (MACE) after AMI. This study investigates whether the addition of Tei index could improve the GRACE risk score performance to predict inhospital MACE after AMI.

Abstract Background Subjects with Type 1 diabetes mellitus (T1DM) have an increased incidence of heart failure (HF). Several pathophysiological mechanisms have been involved in its development. The aim of this study was to analyze the potential contribution of the advanced lipoprotein profile and plasma glycosylation (GlycA) to the presence of subclinical myocardial dysfunction in subjects with T1DM. Methods We included subjects from a Danish cohort of T1DM subjects (Thousand & 1 study) with either diastolic and/or systolic subclinical myocardial dysfunction, and a control group without myocardial dysfunction, matched by age, sex and HbA1c. All underwent a transthoracic echocardiogram and an advanced lipoprotein profile obtained by using the NMR-based Liposcale® test. GlycA NMR signal was also analyzed. Systolic dysfunction was defined as left ventricular ejection fraction ≤ 45% and diastolic dysfunction was considered as E/e′≥12 or E/e′ 8–12 + volume of the left atrium > 34 ml/m2. To identify a metabolic profile associated with the presence of subclinical myocardial dysfunction, a multivariate supervised model of classification based on least squares regression (PLS-DA regression) was performed. Results One-hundred forty-six subjects had diastolic dysfunction and 18 systolic dysfunction. Compared to the control group, patients with myocardial dysfunction had longer duration of diabetes (p = 0.005), and higher BMI (p = 0.013), serum NTproBNP concentration (p = 0.001), systolic blood pressure (p

Background: Sepsis is the leading cause of death in intensive care units. Sepsis-induced myocardial dysfunction, one of the most serious complications of sepsis, is associated with higher mortality rates. As the pathogenesis of sepsis-induced cardiomyopathy has not been fully elucidated, there is no specific therapeutic approach. Stress granules (SG) are cytoplasmic membrane-less compartments that form in response to cellular stress and play important roles in various cell signaling pathways. The role of SG in sepsis-induced myocardial dysfunction has not been determined. Therefore, this study aimed to determine the effects of SG activation in septic cardiomyocytes (CMs). Methods: Neonatal CMs were treated with lipopolysaccharide (LPS). SG activation was visualized by immunofluorescence staining to detect the co-localization of GTPase-activating protein SH3 domain binding protein 1 (G3BP1) and T cell-restricted intracellular antigen 1 (TIA-1). Eukaryotic translation initiation factor alpha (eIF2α) phosphorylation, an indicator of SG formation, was assessed by western blotting. Tumor necrosis factor alpha (TNF-α) production was assessed by PCR and enzyme-linked immunosorbent assays. CMs function was evaluated by intracellular cyclic adenosine monophosphate (cAMP) levels in response to dobutamine. Pharmacological inhibition (ISRIB), a G3BP1 CRISPR activation plasmid, and a G3BP1 KO plasmid were employed to modulate SG activation. The fluorescence intensity of JC-1 was used to evaluate mitochondrial membrane potential. Results: LPS challenge in CMs induced SG activation and resulted in eIF2α phosphorylation, increased TNF-α production, and decreased intracellular cAMP in response to dobutamine. The pharmacological inhibition of SG (ISRIB) increased TNF-α expression and decreased intracellular cAMP levels in CMs treated with LPS. The overexpression of G3BP1 increased SG activation, attenuated the LPS-induced increase in TNF-α expression, and improved CMs contractility (as evidenced by increased intracellular cAMP). Furthermore, SG prevented LPS-induced mitochondrial membrane potential dissipation in CMs. Conclusion: SG formation plays a protective role in CMs function in sepsis and is a candidate therapeutic target. [ABSTRACT FROM AUTHOR]

Sepsis‐induced myocardial dysfunction (SIMD) is the leading cause of death in patients with sepsis in the intensive care units. The main manifestations of SIMD are systolic and diastolic dysfunctions of the myocardium. Despite our initial understanding of the SIMD over the past three decades, the incidence and mortality of SIMD remain high. This may be attributed to the large degree of heterogeneity among the initiating factors, disease processes, and host states involved in SIMD. Previously, organ dysfunction caused by sepsis was thought to be an impairment brought about by an excessive inflammatory response. However, many recent studies have shown that SIMD is a consequence of a combination of factors shaped by the inflammatory responses between the pathogen and the host. In this article, we review the mechanisms of the inflammatory responses and potential novel therapeutic strategies in SIMD. [ABSTRACT FROM AUTHOR]

Purpose of Review: Cancer patients are at risk for treatment-related myocardial dysfunction and heart failure during or after treatment. Risk prediction models have the potential to play an important role in identifying patients at high or low risk in order to take appropriate measures. Here, we review their current role. Recent Findings: More and more risk prediction models are currently being developed. Unfortunately, they vary widely in their ability to identify patients and survivors at risk for myocardial dysfunction or heart failure, from very poor to strong. Part of this variation might be explained by methodological limitations of the models, but due to a lack of reporting it is not possible to completely assess this. Summary: There lies great potential in the improvement of the quality and the use of risk prediction models to inform patients and clinicians on the absolute risk of cardiac events in order to guide care. [ABSTRACT FROM AUTHOR]

The outcome of cardiac arrest is worse when there is fever after spontaneous circulation is restored (ROSC). The purpose of this study was to investigate the mechanism of post-ROSC cardiac dysfunction after hyperthermia treatment and the effects of temperature control. Twenty-four male Bama minipigs were randomized into 3 groups (8 per group): CPR + controlled normothermia (CN), CPR + hyperthermia (HT), and CPR + therapeutic mild hypothermia (TMH). Defibrillation was given to pigs with ventricular fibrillation after 8 min of untreated fibrillation. Subsequently, these animals received the post-ROSC treatments of hyperthermia (38 °C), controlled normothermia (37 °C) or hypothermia (33 °C) according to the groups. Hemodynamic parameters, left ventricular ejection fraction, blood samples and myocardial tissues were assessed. At 24 h after the post-ROSC treatments, the pigs treated with hyperthermia showed increments in heart rate and plasma cardiac troponin I, and decreases in mean arterial pressure, cardiac index, and left ventricular ejection fraction, compared to those with the controlled normothermia pigs. However, the deterioration of the above parameters can be attenuated by TMH. The pigs in the TMH group also had a reduced percentage of apoptotic cardiomyocytes, an increased anti-apoptotic Bcl-2/Bax ratio and a decreased caspase-3 activity in myocardium, as compared with both controlled normothermia and hyperthermia pigs. In conclusion, hyperthermia is associated with a worse myocardial dysfunction. TMH improves hyperthermia-induced myocardial dysfunction by attenuating apoptosis in a porcine model of cardiac arrest. [ABSTRACT FROM AUTHOR]

Background: Sepsis-induced myocardial dysfunction is associated with worse clinical outcomes and high mortality, but no effective therapeutic intervention has been explored, reinforcing the urgent need to develop innovative strategies. Mitochondrial dysfunction underlies the pathogenesis of sepsis-induced myocardial dysfunction. Herein, we assessed the effect of mitochondrial transplantation on sepsis-induced myocardial dysfunction in a rat model of cecal ligation and puncture (CLP)-induced sepsis. Methods: Male Wistar rats (n = 80, 12 weeks old, 250-300 g) were divided into groups with/without CLP-induced sepsis receiving mitochondrial transplantation in single or two repetitive injections (1 h or 1 and 7 h post-CLP, respectively). Mitochondria were isolated from donor rats and injected intravenously (400 µl of mitochondrial suspension containing 7.5 × 106 mitochondria/ml of respiration buffer) in recipient groups. Twenty-four hours post-operation, LDH and cTn-I levels, mitochondrial functional endpoints, expression of mitochondrial biogenesis (SIRT-1 and PGC-1α) and fission/fusion (Drp1/Mfn1 and Mfn2) genes, and inflammatory cytokines (TNF-α, IL-1β, and IL-6) levels were evaluated. Survival was tested over 72 h post-operation. Results: Mitotherapy significantly improved 72-hours survival (P <.05) and decreased LDH and cTn-I levels (P <.01). It also restored mitochondrial function and expression of mitochondrial biogenesis and fusion genes, and decreased the expression of mitochondrial fission gene and the levels of inflammatory cytokines (P <.05 to P <.01). Mitotherapy with repetitive injections at 1 and 7 h post-CLP provided noticeable mitoprotection in comparison with the group receiving mitotherapy at single injection. Conclusion: Mitotherapy improved mitochondrial function, biogenesis, and dynamic associated with SIRT-1/PGC-1α network and suppressed inflammatory response in CLP-induced sepsis model, therefore, offers a promising strategy to overcome life-threatening sepsis challenge. [ABSTRACT FROM AUTHOR]

Sepsis is a life-threatening disease state characterized by organ dysfunction and a dysregulated response to infection. The heart is one of the many organs affected by sepsis, in an entity termed sepsis-induced cardiomyopathy. This was initially used to describe a reversible depression in ejection fraction with ventricular dilation but advances in echocardiography and introduction of new techniques such as speckle tracking have led to descriptions of other common abnormalities in cardiac function associated with sepsis. This includes not only depression of systolic function, but also supranormal ejection fraction, diastolic dysfunction, and right ventricular dysfunction. These reports have led to inconsistent definitions of sepsis-induced cardiomyopathy. Just as there is heterogeneity among patients with sepsis, there is heterogeneity in the cardiac response; thus resuscitating these patients with a single approach is likely suboptimal. Many factors affect the heart in sepsis including inflammatory mediators, catecholamine responsiveness, and pathogen related toxins. This review will discuss different functional effects characterized by echocardiographic changes in sepsis and their prognostic and management implications.

Myocardial ischemia caused by coronary artery disease (CAD) and the presence of metabolic abnormalities and microvascular impairments detected in patients with diabetes mellitus (DM) are a common cause of left ventricular (LV) dysfunction. Transthoracic echocardiography is the most-used, non-invasive imaging method for the assessment of myocardial contractility. The accurate evaluation of LV function is crucial for identifying patients who are at high risk or may have worse outcomes. Myocardial work (MW) is emerging as an alternative tool for the evaluation of LV systolic function, providing additional information on cardiac performance when compared to conventional parameters such as left ventricular ejection fraction (LVEF) and global longitudinal strain (GLS) because it incorporates deformation and load into its analysis. The potential of MW in various conditions is promising and it has gained increased attention. However, larger studies are necessary to further investigate its role and application before giving an answer to the question of whether it can have widespread implementation into clinical practice. The aim of this review is to summarize the actual knowledge of MW for the analysis of LV dysfunction caused by myocardial ischemia and hyperglycemia.

Abstract Sepsis‐induced myocardial dysfunction (SIMD) is the leading cause of death in patients with sepsis in the intensive care units. The main manifestations of SIMD are systolic and diastolic dysfunctions of the myocardium. Despite our initial understanding of the SIMD over the past three decades, the incidence and mortality of SIMD remain high. This may be attributed to the large degree of heterogeneity among the initiating factors, disease processes, and host states involved in SIMD. Previously, organ dysfunction caused by sepsis was thought to be an impairment brought about by an excessive inflammatory response. However, many recent studies have shown that SIMD is a consequence of a combination of factors shaped by the inflammatory responses between the pathogen and the host. In this article, we review the mechanisms of the inflammatory responses and potential novel therapeutic strategies in SIMD.

Introduction: ivabraddine is a pure heart rate lowering medication that its usage is beneficial in SIRS and MODS as it can reduce heart rate and decrease oxygen consumption especially at low ejection fraction where other medications cannot undergo their potential cardioprotective effect. Aim of work: The aim of this case study was to report the use of Ivabradine in patients who developed SIRS and compare this group with patients who developed SIRS without Ivabradine use for incidence of changes in systolic and diastolic indices, ejection fraction EF and cardiac index CI and effects on hemodynamics, organ perfusion parameters, and outcome of SIRS and MODS. Patients and methods: Patients who presented to emergency department with SIRS and admitted to ICU. The study population will include 40 patients who developed SIRS and admitted to ICU. A total of 40 patients were divided into two groups: Group I: SIRS patients with ivabradine treatment. Group II: SIRS patients without Ivabradine treatment. Results; Comparative study between the 2 groups revealed, highly significant increase in follow up SvO2, EF and CI, at end of Ivabradine treatment, compared to control group without Ivabradine treatment (p < 0.05 respectively). Conclusion: By comparative study between two groups of sepsis there was a significant improvement in cardiac indices in Ivabradine group at the end of the study (high cardiac index and ejection fraction), In addition to improvement of petfusion parameters. [ABSTRACT FROM AUTHOR]

The authors reported a rare case of ectopic atrial tachycardia (EAT) with reversible myocardial dysfunction associated with enterovirus 71 (EV71) infection. A previously healthy 11-year-old boy presented with progressive heart failure. An initial ECG revealed a regular narrow QRS tachycardia with abnormal P wave morphology. Echocardiography showed severely impaired left ventricular function (LVEF 20%). Viral study (PCR) in stool was positive for EV71. Treatment with inotropic support, amiodarone, and carvedilol resulted in gradual restoration of sinus rhythm over 10 days. Cardiac function returned to normal within three months. EV71 can cause EAT along with other complications and should be considered in patients with persistent tachycardia and cardiac dysfunction. Recognizing this arrhythmia led to proper management to control ventricular rate, then termination of the tachycardia and gradual restoration of ventricular function to normal. [ABSTRACT FROM AUTHOR]