Valvular heart disease (VHD) is traditionally assessed through gradients, regurgitant volumes, and ejection fraction-but these valve-centric indices miss the earliest and most decisive signal: myocardial injury. Contemporary evidence shows that VHD is a myocardial disease, where outcomes are driven far more by the ventricle's biological response than by the valve lesion itself. This state-of-the-art review redefines VHD through a myocardium-first lens, highlighting tools that expose dysfunction long before conventional thresholds fail. A focused triad-LV global longitudinal strain (LV-GLS), RV strain with RV-PA coupling, and LA reservoir strain-detects injury at its inception and sharply improves prognostic precision. Cardiac magnetic resonance adds mechanistic depth through native T1, extracellular volume, and late gadolinium enhancement, identifying diffuse and focal fibrosis that dictate timing and reversibility of remodelling. Next-generation technologies extend this paradigm: CT-derived ECV as a scalable fibrosis surrogate, molecular imaging revealing active calcification and fibro-inflammation, and AI-driven models that fuse imaging, biomarkers, and clinical variables into personalized risk trajectories. We propose a serial, multiparametric, AI-enhanced strategy centred on myocardial protection-using LV-GLS tracking, RV-PA coupling, atrial mechanics, and fibrosis imaging to intervene during the true therapeutic window. This review positions a simple but transformative concept: managing VHD means managing the myocardium. Adopting this shift is essential for preserving cardiac health-not merely correcting valve anatomy.

This study aimed to evaluate the risk of doxorubicin-induced cardiotoxicity in newly diagnosed breast cancer patients with type 2 diabetes receiving dapagliflozin in addition to metformin, using echocardiographic methods, and to investigate the potential cardioprotective effects of dapagliflozin. In this prospective observational study, a total of 60 newly diagnosed breast cancer patients with type 2 diabetes were enrolled. Thirty patients who had been treated with metformin and subsequently received dapagliflozin in addition to metformin during doxorubicin therapy constituted the dapagliflozin group. The non-dapagliflozin group consisted of 30 patients who, while continuing metformin, were initiated on another oral antidiabetic agent (excluding dapagliflozin) alongside doxorubicin therapy. N-terminal pro-B type natriuretic peptide (NT-proBNP), left ventricular ejection fraction (LVEF), and left ventricular global longitudinal strain (LVGLS) were measured at baseline and at the 3rd month of treatment. Between-group baseline characteristics were compared using the independent samples t-test for continuous variables. Within-group changes from baseline to 3 months were analyzed with paired t-tests. Between-group comparisons of 3-month outcomes and changes (ΔLVEF, ΔLVGLS, ΔNT-proBNP) were also conducted using independent samples t-tests. To evaluate the independent effect of dapagliflozin on LVGLS, multivariable linear regression analysis was performed. Model fit was reported with adjusted R², F-statistics and 95% confidence intervals. In the non-dapagliflozin group, LVEF and NT-proBNP levels showed no significant differences between baseline and post-treatment; however, LVGLS values significantly deteriorated. In contrast, the dapagliflozin group demonstrated a significant increase in LVEF (- 2.000 [95% CI - 2.392, - 1.608]) and LVGLS (+ 1.367 [95% CI + 1.159, + 1.574]), as well as a marked reduction in NT-proBNP levels (+ 64.933 [95% CI + 57.902, + 71.964]) after 3 months of treatment (p < 0.001). At the third month, the dapagliflozin group exhibited significantly better LVGLS (+ 2.133 [95% CI + 1.346, + 2.921]) and lower NT-proBNP levels (+ 57.000 [95% CI + 28.302, + 85.698]) compared with the non-dapagliflozin group (p < 0.001). Multivariable linear regression analysis confirmed that dapagliflozin use was independently associated with significant improvement in LVGLS at 3 months. In conclusion, dapagliflozin was associated with more favorable short-term surrogate changes in LVGLS and NT-proBNP during doxorubicin therapy. The favorable changes observed in LVEF, LVGLS, and NT-proBNP parameters suggest that dapagliflozin may be considered a potential cardioprotective agent and incorporated into preventive strategies against chemotherapy-related cardiotoxicity in diabetic patients. These hypothesis-generating findings require confirmation in larger randomized trials powered for clinical endpoints with longer follow-up. Not applicable.

The role of nitric oxide in hypertensive target organ damage in patients without renal impairment: insights from left ventricular global longitudinal strain and albuminuria.

Left ventricular myocardial work (MW) has emerged as a valuable echocardiographic parameter for evaluating cardiac function and predicting clinical outcomes. Unlike conventional indices such as left ventricular ejection fraction and global longitudinal strain, MW integrates myocardial deformation with left ventricular pressure, providing a load-adjusted and physiologically meaningful assessment of myocardial performance. Growing evidence demonstrates that impaired MW is consistently associated with adverse outcomes, including heart failure hospitalization, mortality, and functional deterioration, across a wide spectrum of cardiovascular conditions such as ischemic heart disease, valvular heart disease, and cardiomyopathies. The noninvasive estimation of MW using commercially available echocardiographic software has enhanced its feasibility in routine clinical practice, enabling improved risk stratification and early identification of high-risk patients. This review summarizes current evidence supporting the prognostic value of MW, highlights its incremental role beyond conventional echocardiographic parameters, and discusses future perspectives for its integration into everyday clinical decision-making.

The interplay between systolic and diastolic dysfunction in heart failure with preserved ejection fraction (HFpEF) progression is unclear. First-phase ejection fraction (EF1), a sensitive marker of early systolic function, aids in assessing systolic-diastolic relationships in human hypertension and aortic stenosis. This study examines temporal changes in these relationships in mouse models of HFpEF and elevated afterload. Mouse models of abdominal aortic banding (AAB) and HFpEF (induced by hypertension and high fat feeding) underwent comprehensive serial echocardiography. In AAB, EF1 significantly decreased at week 1 post-surgery (18.8 ± 1.2 vs 24.3 ± 0.8%, p<0.001) compared to controls, with further reduction at week 3 (16.8 ± 0.6%) and week 6 (13.9 ± 0.9%, both p<0.001). EF, global longitudinal strain (GLS) and longitudinal strain rate (LSR) remained unchanged until week 3. Isovolumic relaxation time (IVRT) was the only abnormal index of diastolic function at week 1. In the HFpEF model, EF1 significantly decreased at week 2 (19.1 ± 1.1 vs 25.8 ± 1.0%, p<0.001) compared to controls, while EF, GLS, and LSR were unaltered. At week 3, EF1 decreased further (18.1 ± 0.7%) alongside a significant reduction in GLS (p<0.01), while EF and LSR remained unchanged. IVRT increased early in the HFpEF model, followed by later left atrial (LA) enlargement. EF1, an early marker of systolic impairment, decreases early in HFpEF and afterload-induced dysfunction, accompanied by IVRT prolongation. LA dilatation appears later. These findings highlight the interplay between systolic and diastolic dysfunction in HFpEF progression.

To evaluate coronary microvascular function using 13N-ammonia positron emission tomography/ computed tomography in individuals with pathogenic transthyretin (TTR) gene mutations, with and without cardiac involvement. This study is the first to assess coronary flow reserve (CFR) in this population before overt cardiac amyloidosis (CA) is detectable by conventional imaging. We evaluated microvascular impairment by measuring CFR in 20 patients with and 20 patients without cardiac involvement due to TTR amyloidosis (ATTR), all presumed to be free from epicardial coronary artery disease and carrying TTR gene mutations. The study revealed a significantly reduced mean global CFR in the cardiac involvement group (1.849 ± 0.379 vs. 2.952 ± 0.7, P < 0.001). Global CFR inversely correlated with age, functional class, troponin, and B-type natriuretic peptide while positively correlating with the 6-minute walk test distance, mean blood pressure, and global longitudinal strain. Receiver operating characteristic curve analysis identified an optimal cutoff value of global CFR < 2.58, yielding a sensitivity of 100% and a specificity of 75% for detecting cardiac involvement. In patients with ATTR CA, coronary microvascular dysfunction emerges as a clinically relevant marker of cardiac involvement, even in the absence of structural abnormalities or obstructive coronary disease. CFR assessment may aid in diagnostic suspicion, risk stratification, and understanding of angina symptoms in this population.

Pediatric epilepsy may adversely affect cardiac function. This study examined cardiac outcomes in children with controlled and drug-resistant epilepsy (DRE). Sixty children with epilepsy (30 DRE, 30 drug-responsive) and 30 healthy controls underwent 12-lead ECG, M-mode echocardiography, and speckle tracking echocardiography (STE) to assess cardiac electrical activity, left ventricular (LV) volumes, ejection fraction (EF), fractional shortening (FS), and global longitudinal strain (GLS). ECG findings were comparable among the three groups. LV end-diastolic (LVEDV) and end-systolic volumes (LVESV), FS, and EF were significantly lower in DRE vs. controls (p < 0.05). LVEDV and EF were significantly lower in DRE vs. drug-responsive epilepsy (p < 0.05), while drug-responsive cases had lower LVEDV vs. controls (p = 0.015). LV GLS was significantly lower in DRE (-19.34 ± 1.80) vs. drug-responsive epilepsy (-20.33 ± 1.45) (p = 0.023) and controls (-20.58 ± 0.91) (p = 0.003). LV GLS correlated positively with time since last seizure (p = 0.007) and negatively with the number of antiseizure medications (p = 0.007). Children with DRE exhibit significant cardiac dysfunction. STE enables early detection of subclinical cardiac abnormalities in DRE, advocating for its integration into routine monitoring. Compares cardiac function in pediatric drug-resistant epilepsy (DRE) and drug-responsive epilepsy, identifying impaired systolic function and global longitudinal strain (GLS) in DRE. Correlates GLS abnormalities with antiseizure medication burden and time since last seizure, linking cardiac dysfunction to treatment intensity and epilepsy disease course. Advocates STE for early cardiac monitoring in DRE and urges longitudinal studies to disentangle epilepsy-related cardiovascular risks from drug-driven effects.

Current clinical risk tools in type 1 diabetes do not include left ventricular dysfunction or inflammation, potentially limiting early risk detection. We aimed to evaluate the associations and predictive value of combining echocardiography with inflammatory biomarkers for mortality and major adverse cardiovascular events (MACE). In a prospective cohort of individuals with type 1 diabetes without known cardiovascular disease, we evaluated whether subclinical left ventricular dysfunction, defined by an elevated ratio of early mitral inflow velocity to early diastolic mitral annular velocity (E/e') or impaired global longitudinal strain (GLS), combined with elevated levels of an inflammatory biomarker (interleukin-6 [IL-6], soluble urokinase-plasminogen-activator-receptor [suPAR], or high-sensitivity C-reactive-protein [hsCRP]), was associated with all-cause mortality and MACE. Cox models were adjusted for all 10 variables included in the Steno T1 Risk Engine variables: age, sex, systolic blood pressure, duration of diabetes, HbA1c, low-density lipoprotein, estimated glomerular filtration rate, albuminuria status, smoking, and physical activity. C-statistics and net reclassification improvement were assessed. Among 876 participants (51% male, median age 50 years), 114 deaths occurred over 14.5 years of follow-up. Elevated E/e' combined with IL-6 or suPAR, but not hsCRP, was independently associated with mortality. Compared with individuals with E/e' <8 and non-elevated IL-6, the hazard ratio (HR) for E/e' 8-13 with elevated IL-6 was 2.5 (95% CI 1.4 to 4.6, P < 0.01), and for E/e' ≥13 with elevated IL-6 was 3.4 (1.5-7.6; P < 0.01). Corresponding HRs for suPAR were 2.4 (1.2 to 4.7, P < 0.01) and 3.9 (1.8 to 8.5, P < 0.01). Adding E/e' and an inflammatory biomarker increased the C-statistic from 0.839 (Steno T1 Risk Engine alone) to 0.887 (E/e' and IL6) and 0.868 (E/e' and suPAR). Findings were similar for GLS and with MACE as the outcome. Echocardiography combined with inflammatory biomarkers synergistically identifies individuals with type 1 diabetes, without known cardiovascular disease, who are at high risk of mortality and MACE.

Left ventricular (LV) mechanical dyssynchrony results from nonuniform myocardial activation, leading to inefficient LV contraction and worse clinical outcomes. Synchromax® is a noninvasive system that performs real-time spatial variance analysis of QRS complexes from a standard electrocardiogram, generating an electrical synchrony index (ESI) that may be a potential marker of LV mechanical dyssynchrony. This study evaluated the efficacy of the ESI in predicting LV mechanical dyssynchrony compared to the gold standard: LV mechanical dispersion (LVMD)>60ms as measured by speckle-tracking strain echocardiography. A cross-sectional study was conducted with consecutive adult patients undergoing echocardiography in San Salvador, El Salvador. Clinical, electrocardiographic (rhythm, QRS duration, ESI), and echocardiographic (LVMD, LV ejection fraction, global longitudinal strain) data were collected. Eighty-four studies from 83 patients were analyzed. Mean ESI was 0.36±0.31 and mean LVMD was 58.4±27.1ms. The ESI showed a sensitivity of 70.0% and a specificity of 88.9%, with negative and positive predictive values of 84.2% and 77.8%, respectively. Agreement with the gold standard was moderate (kappa=0.60; p<0.001). ROC curve analysis demonstrated good discriminative performance (area under the curve=0.81), superior to QRS duration (area under the curve=0.71) for identifying LV mechanical dyssynchrony. The optimal ESI cutoff was 0.42. ESI correlated consistently and significantly with LVMD, indicating that it may be a more sensitive functional marker than QRS duration, especially in cases without evident dyssynchrony. The ESI is a simple, accessible tool for complementary assessment of ventricular electromechanical synchrony.

Objective The long-term effects of childhood asthma on cardiac functions remain unclear. This study evaluates the relationship between asthma severity and cardiac function in pediatric asthma patients. Methods Children aged 10–18 years with at least five years of asthma follow-up and no known cardiac disease were included. A control group of healthy children with no chronic diseases participated. Both groups underwent electrocardiography, conventional echocardiography, tissue Doppler examination (TDI), and 2D speckle tracking echocardiography (2D-STE). Results A total of 113 asthma patients (59 mild, 54 moderate-severe) and 59 controls were assessed. Compared to controls, the asthma group had increased right ventricular area (RVA) (p = 0.04), while interventricular septal and left ventricular S’ velocity (IVSS’, LVS’) and right ventricular late diastolic velocity (RVA’) were lower (p = 0.04, p = 0.04, p = 0.02, respectively). Conventional and TDI parameters showed no other significant differences. In 2D-STE measurements, left ventricular global longitudinal and circumferential strain (LVGLS, LVGCS), right ventricular global longitudinal strain (RVGLS), and right atrial reservoir strain (RARS) were lower (p = 0.01, p = 0.03, p = 0.01, p = 0.01, respectively), while left ventricular global longitudinal and circumferential strain rate (LVGLSR, LVGCSR), right ventricular global longitudinal strain rate (RVGLSR), and right atrial reservoir strain rate (RARSR) were higher (p = 0.04, p = 0.04, p = 0.03, p = 0.04, respectively) in the asthma group, with more pronounced differences in the moderate-severe asthma group. Conclusion Our study shows a decrease in both systolic and diastolic functions in both ventricles and right atrium in relation to the severity of childhood asthma, and 2D-STE can be useful in identifying early changes.

Myocardial work indexes in elite athletes: An emerging echocardiographic tool to confirm physiologic cardiac remodeling in elite athletes with mildly reduced systolic function.

Prognostic value of speckle-tracking imaging score for patients with childhood-onset systemic lupus erythematosus.

Safety and Tolerability of Tocilizumab in a Case Series of Heart Transplant Recipients With Chronic Antibody-Mediated Rejection.

Heart failure with preserved ejection fraction (HFpEF) has a high prevalence and a low quality of life, and there are limited medications for the treatment of this disease. In recent years, disulfiram (DSF), an FDA-approved drug for the treatment of chronic alcohol addiction, has been found to have anti-inflammatory properties. The present study was designed to investigate the cardioprotective effects of DSF on patients with HFpEF and its mechanism using a model of HFpEF induced in mice fed a high-fat diet (HFD, 60% of calories from fat) and Nω-nitro-L-arginine methyl ester (L-NAME, 0.5 g/L in drinking water). The results showed that DSF effectively reversed the HFD + L-NAME-induced increases in left ventricular end-diastolic diameter (LVEDD), left ventricular end-systolic diameter (LVESD), interventricular septal thickness, left ventricular mass, the ratio of peak early mitral diastolic velocity to peak late mitral diastolic velocity, the ratio of early mitral diastolic velocity to early diastolic velocity, as well as the reductions in the absolute value of global longitudinal strain (GLS), without affecting the left ventricular ejection fraction (LVEF). In addition, DSF notably attenuated the HFD + L-NAME-induced increase in blood pressure, exercise intolerance, cardiac hypertrophy, pulmonary edema, and elevated N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels. Mechanistically, we found that DSF inhibited myocardial PANoptosis-like cell death, mainly by inhibiting the release of myocardial interleukin 1β (IL-1β), which inhibited transforming growth factor-β-activated kinase 1(TAK1)-mediated PANoptosis. Given the cardioprotective effects of DSF, its clinical use would be a novel strategy for the protection and treatment of cardiac injury in patients with HFpEF.

Abstract Background In healthy subjects, women have smaller cardiac chambers than men even after indexation by body surface area (BSA), as well as higher left ventricular (LV) ejection fraction (EF) and global longitudinal strain (GLS). The current guidelines for management of severe degenerative mitral regurgitation (MR) do not take these differences into account when referring patients to surgery. Purpose To assess the sex-specific pre- and postoperative LV remodeling and function in patients with mitral valve prolapse (MVP). Methods Patients with MVP undergoing mitral valve repair between 2007-2024 at two Heart Valve Centers were included. We excluded patients with previous cardiac surgery, coronary artery disease, other concomitant procedures than tricuspid valve repair, non-sinus rhythm at baseline and those with significant post-surgical MR (≥2+). Cutoffs for defining normal LV chamber size and function were based on current guidelines. Results 174 patients (36 % women) were assessed before and at a median of 14 [11-23] months after surgery. At baseline, women were older, had more often dyspnoea and palpitations (all p &amp;lt;0.05), and smaller non-indexed LV diameters and volumes compared to men (Figure 1). Using sex-specific cutoffs and indexation by BSA, women had more often dilated LVs by both LV end-systolic diameter and volume, but LV dilatation by volume was a more sensitive marker in both sexes (Figure 2). At follow-up, women were more likely to have persistent LV dilatation (Figure 2). In logistic regression analysis, women had 7.2 (95 % CI 2.8-18.2) times higher probability of having persistently enlarged LV end-systolic volume indexed by BSA after surgery, after adjustment for age, MVP phenotype, LV EF, systolic pulmonary artery pressure and baseline LV end-systolic volume indexed by BSA. LV EF was similar between sexes at baseline, while LV GLS was higher in women than in men (Figure 2). Whereas LV dysfunction was a rare finding before surgery, low LV EF and GLS were significantly more frequent in women after surgery (Figure 2). Women also had 3.2 (95 % CI 1.4-7.1) times higher probability of having low LV GLS after surgery, after adjustment for age, baseline LV GLS, LV end-systolic diameter indexed by BSA, left atrial reservoir strain and TAPSE. Conclusions In patients with MVP referred to mitral valve repair, LV volumes indexed by BSA are more sensitive markers of LV dilatation than LV diameters in both sexes, and show that women have more often dilated LVs than men before and after surgery. Though significant reverse remodeling is present in both sexes after mitral valve repair, women have more frequently low LV EF and GLS than men after surgery. These findings call for use of sex-specific thresholds in the assessment of LV size and function when timing surgery in patients with MVP.Figure 1.LV size and function Figure 2.LV dilatation and dysfunction

Abstract Background/Introduction In patients with hypertrophic cardiomyopathy (HCM), sudden cardiac death (SCD) risk stratification is challenging, especially in those with low to intermediate risk according to currently recommended SCD scores. The ESC HCM Risk-SCD score uses left atrial (LA) diameter but does not consider LA dysfunction, which may precede LA dilatation; additionally, it does not include a left ventricular (LV) function measure. LA reservoir strain (LARS) and LV global longitudinal strain (LVGLS) are often impaired in HCM patients and have been associated with worse outcomes, but not specifically with SCD. Purpose To assess the incremental predictive value of LARS and LVGLS for arrhythmic outcomes in HCM patients with low to intermediate SCD risk. Methods We analyzed consecutive HCM patients from three centers and excluded patients with a history of aborted SCD or sustained VT/VF, and those with no follow-up. The ESC HCM Risk-SCD score was calculated at baseline, and those who had a score &amp;lt;6% were included. Patients were followed up for the composite endpoint of arrhythmic events, including SCD, aborted SCD, and appropriate implantable cardiac device (ICD) therapy. Results A total of 989 patients were included (mean age 55±15; 55% male). The median SCD risk score was 2.27 (1.39-3.15). LARS and LVGLS mean values were 24.3±10.3% and -15.5±4.6%, respectively. During a median follow-up of 61 (35-117) months, a total of 71 (7.2%) patients reached the composite endpoint, including 18 (1.8%) cases of SCD, 9 (0.9%) cases of aborted SCD, and 18 (1.8%) appropriate ICD therapies. From the ROC analysis, optimal cut-off values of LARS and LVGLS for the specific arrhythmic endpoints were derived: LARS ≤23.3% and LVGLS ≥−14.1%. In univariate analysis, the ESC HCM-risk score, LARS ≤23.3% and LVGLS ≥−14.1% were significantly associated with the outcome (Figure 1). After adjusting for relevant clinical and echocardiographic variables, LVGLS ≥−14.1% and LARS ≤23.3% remained associated with the outcome (HR 1.72, 95% CI 1.02–2.91, p=0.043 and HR 1.85, 95% CI 1.08–3.18, p=0.025, respectively) together with the ESC HCM-risk score. Accordingly, Kaplan–Meier analysis showed significantly lower event-free survival in patients with impaired LARS and LVGLS (log rank test p&amp;lt;0.001 for both) (Figure 2). The addition of LARS and LVGLS to the ESC HCM-risk score led to a significant increase in the ability of the model to predict the composite endpoint (Chi-square difference = 9.2, p&amp;lt;0.001; C-statistic = 0.78, Net Reclassification Index= 0.403). Conclusion LARS and LVGLS provide an incremental value to the ESC HCM Risk-SCD score in predicting arrhythmic events among HCM patients with low to intermediate SCD risk. Therefore, incorporating LARS and LVGLS may improve risk stratification and guide decision-making for ICD implantation in these challenging patient groups.Figure 1 Figure 2

Abstract Background Sepsis and septic shock, and the sequelae of septic cardiomyopathy (SCM), are a common yet major concern in the intensive care unit and are associated with high mortality (Zakynthinos, 2025). Traditionally, echocardiography using two-dimensional ejection fraction (2DEF) is used to diagnose SCM. However, these measurements may be affected by other confounding factors (Berman, 2022). Different methods of detecting cardiac dysfunction such as global longitudinal strain (GLS) or biomarkers (NT-ProBNP or Troponin T) are not routinely used. Furthermore, 2DEF measurements are subject to poor sensitivity and specificity, with documented inter-operator errors (Kim, 2022). Purpose To evaluate relationship between LVEF, GLS and biomarkers across 90 days in patients with sepsis/septic shock on ICU. Method A single UK site, prospective cohort study of patients on ICU meeting criteria for sepsis/septic shock. Simpson’s biplane 2DEF and GLS performed by single operator. Biomarker samples taken within 24hrs of echo. Data collection took place at days 1, 3 (no biomarker), 30 and 90 as inpatient or returning outpatient. Normal values were defined by British Society Echocardiography and National Institute Clinical Excellence guidelines respectively. Statistical significance was determined using Pearson Correlation and Principal Component Analysis (PCA). Results From 118 patients enrolled, 105 met inclusion criteria at time of echo, all were on inotropes or vasopressors. Mean age 60yrs, 61% male, 38% female. Days 1, 3, 30 and 90 results shown in table 1. Loss to follow up over the study was 33%. At day 1 there was no significant correlation between 2DEF and any biomarker (NT-ProBNP r =0.15,p =0.55, Troponin T, r =0.25 ,p=0.27). Nor any significant relationship between GLS and Troponin T (r = 0.20, p =0.390). Conversely there was a borderline relationship between GLS and NT-pro-BNP, (r =0.49, p=0.05) at day 1. Over 90 days,despite a normal 2DEF in many cases, GLS and biomarkers were frequently abnormal and persisted beyond recovery (see figure 1). PCA mimic these findings with no 2DEF and GLS relationship but some degree of inter-relationship between GLS and NT ProBNP. Conclusion Generally, 2DEF is the chosen method for the diagnosis of SCM. Given that many patients have normal 2DEF despite abnormal GLS and biomarkers, this study raises the question of ‘what is a normal LVEF’ for ICU patients with sepsis. Perhaps given the fluid loading, sepsis-driven vasodilatation, and inotropic support, an otherwise normal 2DEF of 50-60% may be impaired in this cohort. As such, GLS and biomarkers may identifying subtle (potentially subclinical) dysfunction in sepsis or septic shock. These changes persist to day 90, despite clinical recovery. While 2DEF is the primary factor influencing decision-making in the ICU, the relationship between GLS and NT ProBNP post day 3 requires further investigation with regards to genuine persisting myocardial dysfunctionTable 1 Figure 1

Abstract Background Cancer therapy–related cardiac dysfunction (CTRCD) has become an increasingly common clinical concern due to the growing use and effectiveness of cancer treatments that may adversely affect cardiac function. Transthoracic echocardiography (TTE) remains the primary and most widely utilized non-invasive imaging modality for the routine screening and assessment of CTRCD. The primary objective in clinical practice is to facilitate the early identification of subclinical cardiac dysfunction. Early detection is critical, as it enables timely intervention to prevent the progression of cardiac damage and supports the continuation of potentially life-saving cancer therapies with minimal cardiovascular compromise. Purpose Evaluate the role of risk stratification, imaging and biomarkers in cardio-oncology patients. Methods A total of eighty-eight cancer patients scheduled to receive Anthracycline and/or Trastuzumab (AC/TZB) therapy were prospectively enrolled. Baseline cardiovascular evaluation included two-dimensional transthoracic echocardiography (2D TTE), global longitudinal strain (GLS), and measurement of cardiac biomarkers—troponin I and N-terminal pro-B-type natriuretic peptide (NT-proBNP)—prior to initiation of cancer therapy. Follow-up assessments were conducted at three and six months intervals using the same imaging and biomarkers. The aim was to facilitate the early detection of CTRCD and to initiate cardioprotective therapy (CPT) at the earliest signs of cardiac impairment. Results Out of the 88 patients, 26 of them (29.5%) developed cancer therapy–related cardiac dysfunction (CTRCD). Among them, 18 patients exhibited mild asymptomatic dysfunction, while 8 developed moderate asymptomatic CTRCD, defined by relative reductions in global longitudinal strain (GLS) and left ventricular ejection fraction (LVEF). The relative percentage change in GLS from the baseline was a reliable marker for early detection of CTRCD. At 3 months, a GLS reduction greater than 16.6% was significantly associated with the development of CTRCD (P &amp;lt; 0.001; 95% CI: 0.783–0.934). At 6 months, a reduction exceeding 10.1% maintained its predictive value (P &amp;lt; 0.001; 95% CI: 0.765–0.935). Patients with mild asymptomatic CTRCD demonstrated approximately twofold higher NT-proBNP levels compared to those without dysfunction, with a median value of 99.50 pg/mL at the 3-month follow-up (P = 0.037). These levels returned to the baseline by 6 months. Conclusions Baseline GLS alone was insufficient to predict CTRCD. A combined approach using serial imaging, cardiac biomarkers, and baseline risk factors improves early detection and risk stratification. In patients receiving Anthracycline therapy, a relative GLS reduction alongside elevated NT-proBNP effectively identified subclinical CTRCD. Early cardioprotective therapy (CPT) allowed continuation of chemotherapy and prevented progression to significant left ventricular dysfunction.Patients selection flowchart GLS estimation using 2D STE

Abstract Background Peripartum cardiomyopathy (PPCM) is a rare complication occurring in the last weeks of pregnancy and in the peripartum period characterized by sign and symptoms of heart failure and left ventricular (LV) systolic dysfunction. While recovery is observed in about 50% of women, this condition is still associated with high morbidity and mortality. To date, little is known about clinical and echocardiographic factors related to LV function recovery, and no data are available on myocardial mechanics and performance. Methods We retrospectively selected 17 consecutive women (mean age 39.2 ±9.0 years) with confirmed diagnosis of PPCM enrolled in the Italian multicenter, observational registry of PPCM coordinated by our hospital. Demographics were collected and myocardial mechanics were assessed using speckle tracking-derived global longitudinal strain (GLS), global work index (GWI), global constructive work (GCW), global wasted work (GWW), and global work efficiency (GWE). Patients were categorized according to the subsequent LV ejection fraction (LVEF): group A, LVEF≤35%; group B, 35%&amp;lt;LVEF&amp;lt;50%;&amp;gt; Results LV recovery was observed in 8 women (47%, group C), with a mean LVEF of 55±2%. In 6 patients (35%) mild dysfunction was still observed (mean LVEF 44±3%, group B), while 3 patients had persistent severe LV dysfunction (mean LVEF 26±7%), requiring ICD implantation (group A). The three groups significantly differed for LV end-diastolic diameter (62.7 ± 9.5 vs 54.7 ± 5.0 vs 48.5 ±2.6 mm respectively in group A vs group B vs group C, p=0.002), LV volume (209.7 ± 110.6 vs 147.3 ±37.1 vs 101.1 ± 19.8 ml respectively, p=0.017), TAPSE (15.3 ± 5.8 vs 23.3 ± 1.9 vs 22.9 ± 2.3 mm respectively, p=). Speckle tracking analysis revealed a significant improvement in myocardial performance from group A to C: GLS (9.7 ±5.4 vs 14.6 ±3.2% vs 19.9 ±0.9% respectively, p&amp;lt;0.001), GWI (854±674 vs 1231±476 vs 1914±511mmHg%, p=0.021), GCW(1123±699 vs 1695±536 vs 2239 ± 540 mmHg%, p=0.032), GWW (166±81 vs 261±78 vs 104±34 mmHg%, p=0.002), GWE (84±10 vs 86±4 vs 95±2%, p=0.005). Also atrial strain improved across the different groups (17±11 vs 29±9 vs 42±4%, p=0.001), with no significant difference in left atrial volume. Also in patients with recovered LV systolic function, GLS was significantly reduced compared to controls (19.9 ±9 vs 21.7±1.3% respectively, p=0.007). Conclusion in patients with history of PPCM, GLS and myocardial work provide a better definition of myocardial performance in those with partially o complete systolic recovery. GLS remains impaired also in women with normalized LVEF suggesting that GLS is a more sensitive marker of continued LV dysfunction in recovered PPCM.LVEF&amp;lt;50%;&amp;gt;

Abstract Introduction Endomyocardial Fibrosis (EMF) is a restrictive cardiomyopathy of unknown etiology and poor prognosis, with higher prevalence in underdeveloped countries. It is characterized by deposits of fibrous tissue in the subendocardium and the underlying myocardium. Transthoracic echocardiography (TTE) is an important method for the diagnostic and prognostic evaluation of EMF. However, there are no studies concerning TTE with Global Longitudinal Strain (GLS) or myocardial work (MW) analysis by Speckle Tracking technique (STE) in patients with EMF. Purpose To analyze cardiac mechanics through biventricular GLS and left ventricular (LV) MW using STE in patients with EMF. Hypothesis: The analysis of cardiac mechanics through MW in patients with EMF can yield knowledge about cardiac physiology in patients with EMF. Methods Patients older than 18 years with a diagnosis of EMF underwent conventional TTE for morphological and functional cardiac analysis, as well as subsequent evaluation of biventricular GLS and LV MW by STE. Results Twenty-five patients with EMF were evaluated; demographic and echocardiographic parameters are detailed in Table 1. The average LV GLS was reduced (13.9 ± 1.6%) despite preserved LV ejection fraction (EF) by Simpson's method (57.3 ± 3.6%). Global work index (GWI: 1306 ± 250 mmHg%), global constructive work (GCW: 1730 ± 253 mmHg%), and global work efficiency (GWE: 84.2 ± 3.6 mmHg%) values were reduced, along with an increase in global wasted work (GWW: 282 ± 50 mmHg%). Regarding the right ventricular GLS, there was a reduction in global (16.8 ± 2.1%) and free wall values (18.7 ± 2.9%). These results show early systolic biventricular dysfunction, despite preserved LVEF, and reduction myocardial efficiency and increased wasted work, providing physiological bases for the underlying mechanisms of heart failure with preserved ejection fraction in patients with EMF. Conclusion Advanced methods of cardiac mechanics analysis, such as myocardial work and GLS by STE, are promising tools for the follow-up of patients with EMF, potentially serving as viable alternatives to predict early myocardial dysfunction.