Ventricular Systolic Function Research Articles

B-type natriuretic peptide levels predict long-term mortality in a large cohort of adults with congenital heart disease.

Many adult patients with congenital heart disease (ACHD) are still afflicted by premature death. Previous reports suggested natriuretic peptides may identify ACHD patients with adverse outcome. The study investigated prognostic power of B-type natriuretic peptide (BNP) across the spectrum of ACHD in a large contemporary cohort. The cohort included 3392 consecutive ACHD patients under long-term follow-up at a tertiary ACHD centre between 2006 and 2019. The primary study endpoint was all-cause mortality. A total of 11 974 BNP measurements were analysed. The median BNP at baseline was 47 (24-107) ng/L. During a median follow-up of 8.6 years (29 115 patient-years), 615 (18.1%) patients died. On univariable and multivariable analysis, baseline BNP [hazard ratio (HR) 1.16, 95% confidence interval (CI) 1.15-1.18 and HR 1.13, 95% CI 1.08-1.18, respectively] and temporal changes in BNP levels (HR 1.22, 95% CI 1.19-1.26 and HR 1.19, 95% CI 1.12-1.26, respectively) were predictive of mortality (P < .001 for both) independently of congenital heart disease diagnosis, complexity, anatomic/haemodynamic features, and/or systolic systemic ventricular function. Patients within the highest quartile of baseline BNP (>107 ng/L) and those within the highest quartile of temporal BNP change (>35 ng/L) had significantly increased risk of death (HR 5.8, 95% CI 4.91-6.79, P < .001, and HR 3.6, 95% CI 2.93-4.40, P < .001, respectively). Baseline BNP and temporal BNP changes are both significantly associated with all-cause mortality in ACHD independent of congenital heart disease diagnosis, complexity, anatomic/haemodynamic features, and/or systolic systemic ventricular function. B-type natriuretic peptide levels represent an easy to obtain and inexpensive marker conveying prognostic information and should be used for the routine surveillance of patients with ACHD.

Injectable Self-Oxygenating Cardio-Protective and Tissue Adhesive Silk-Based Hydrogel for Alleviating Ischemia After Mi Injury.

Myocardial infarction (MI) is a significant cardiovascular disease that restricts blood flow, resulting in massive cell death and leading to stiff and noncontractile fibrotic scar tissue formation. Recently, sustained oxygen release in the MI area has shown regeneration ability; however, improving its therapeutic efficiency for regenerative medicine remains challenging. Here, a combinatorial strategy for cardiac repair by developing cardioprotective and oxygenating hybrid hydrogels that locally sustain the release of stromal cell-derived factor-1 alpha (SDF) and oxygen for simultaneous activation of neovascularization at the infarct area is presented. A sustained release of oxygen and SDF from injectable, mechanically robust, and tissue-adhesive silk-based hybrid hydrogels is achieved. Enhanced endothelialization under normoxia and anoxia is observed. Furthermore, there is a marked improvement in vascularization that leads to an increment in cardiomyocyte survival by ≈30% and a reduction of the fibrotic scar formation in an MI animal rodent model. Improved left ventricular systolic and diastolic functions by ≈10% and 20%, respectively, with a ≈25% higher ejection fraction on day 7 are also observed. Therefore, local delivery of therapeutic oxygenating and cardioprotective hydrogels demonstrates beneficial effects on cardiac functional recovery for reparative therapy.

Recovery of left ventricular systolic function in peripartum cardiomyopathy: an observational study from rural Tanzania

BackgroundThe aim of this study was to evaluate the recovery rate of the left ventricular systolic function of women diagnosed with peripartum cardiomyopathy receiving specialized care in rural Tanzania.MethodsIn this observational study, women diagnosed with peripartum cardiomyopathy at a referral center in rural Tanzania between December 2015 and September 2021 were included. Women diagnosed between February and September 2021 were followed prospectively, those diagnosed between December 2015 and January 2021 were tracked back for a follow-up echocardiography. All participants received a clinical examination, a comprehensive echocardiogram, and a prescription of guideline-directed medical therapy. The primary outcome was recovery of the left ventricular systolic function (left ventricular ejection fraction > 50%).ResultsMedian age of the 110 participants was 28.5 years (range 17–45). At enrolment, 49 (45%) participants were already on cardiac medication, 50 (45%) had severe eccentric hypertrophy of the left ventricle, and the median left ventricular ejection fraction was 30% (range 15–46). After a median follow-up of 8.98 months (IQR 5.72–29.37), 61 (55%) participants were still on cardiac medication. Full recovery of the left ventricular systolic function was diagnosed in 76 (69%, 95% CI 59.6–77.6%) participants. In the multivariate analysis, a higher left ventricular ejection fraction at baseline was positively associated with full recovery (each 5% increase; OR 1.7, 95% CI 1.10–2.62, p = 0.012), while higher age was inversely associated (each 10 years increase; OR 0.40, 95% CI 0.19–0.82, p = 0.012).ConclusionLeft ventricular systolic function recovered completely in 69% of study participants with peripartum cardiomyopathy from rural Tanzania under specialized care.

ASSESSMENT OF LEFT VENTRICULAR FUNCTION AFTER CORONARY ARTERY BYPASS GRAFTING

Coronary artery bypass grafting (CABG) is a commonly performed surgical intervention for coronary artery disease (CAD), aiming to restore blood flow to the myocardium and improve cardiac function. Left ventricular (LV) systolic function is a crucial determinant of postoperative outcomes in CABG patients, yet the predictors of adverse outcomes remain incompletely understood. Objective: This study aimed to evaluate left ventricular function outcomes following CABG and identify predictors of mortality among CABG patients. Methods: A prospective cohort study was conducted at, Ch. Pervaiz Elahi Institute Of Cardiology (CPEIC), Multan, Pakistan, from December 2022 to December 2023. The study included 96 patients undergoing CABG surgery. Preoperative data collection encompassed demographic information, medical history, and baseline clinical characteristics. Left ventricular function was assessed using echocardiography preoperatively and postoperatively. Statistical analysis involved descriptive statistics, univariate analysis, and univariate regression. Results: The study cohort comprised 96 participants, with a mean age of 56.1 years (±12.2) and a male predominance (67.7%). Prevalent comorbidities included diabetes mellitus (78.1%) and hypertension (79.2%). LV systolic dysfunction (30.2%) and old ischemic heart disease (72.9%) were common preexisting conditions. Intraoperative variables included perioperative inotropes (5.2%) and emergent surgeries (3.1%). Postoperative complications included reoperation for bleeding (5.2%) and deterioration of LV ejection fraction (34.4%). The mortality rate was 5.2%. Postoperatively, the mean LVEF increased significantly from 32.00% (±5.219) to 37.00% (±9.801) in isolated CABG patients. Conclusion: This study confirms the significant improvement in LV systolic function following CABG and underscores the high benefit of CABG in patients with reduced EF. However, diabetes mellitus, advanced diastolic dysfunction, and the insertion of IABP were identified as significant predictors of adverse outcomes. Identifying patients with these risk predictors could provide complementary prognostic information and help optimise care, monitoring, and follow-up to improve their expected poor outcomes.

Left ventricular systolic function in patients with acute coronary syndrome-risk profile

Abstract Funding Acknowledgements None. Introductions and objectives Left ventricular (LV) systolic dysfunction is one of the most important determinants of long-term outcome in acute coronary syndrome (ACS). Aim To determine the impact of the patient’s risk profile on the LV systolic function. Methods A single-center cross-sectional cohort study that included 3093 patients with ACS without pre-existing LV dysfunction. The comparison was performed between patients who did or did not develop a reduction in LV systolic function during the index event (&amp;lt;50%/≥50%), analyzing patients’ demographic, clinical, biochemical data, LV functional data, and anatomical distribution of the coronary artery disease (CAD). Result 1369 patients out of 3093 developed LV systolic dysfunction (44.3%). They were predominantly males 75.1% (1028), p=0.002; older (63.39±11.04 vs 61.21±11.12, p&amp;lt;0.00000); had higher level of cardiac troponin (p=0.00002), higher stress glycemia (9.2±5.3; p=0.0000001), HbA1c (6.9±1.8, p=0.000003), WBC (11.7±4.1, p=0.00001), blood urea nitrogen (BUN) (6.8±3.7, p=0.000003), and creatinine (93.2±45.1 p=0.000167), and had anemia (OR 0.35 (CI 0.29–41, p=0.000012). They had more severe CAD (SINTAX score 16.8±8.4 p=0.000012). Patients with preserved LV systolic function were predominantly females (29.7%, OR 1.1 95% CI 1.0-1.2), p = 0.002), younger (p&amp;lt;0.00000), and severely metabolically burdened (hypothyreosis (2.7%, OR 1.28 95% CI 0.93-1.76, p=0.052), higher levels of triglycerides (2.2±1.7 vs 1.9±1.5, p = 0.001), cholesterol (5.3±1.4 vs 5.2±1.4, p = 0.002), non-HDL-C (4.1±1.5 vs 3.9±1.3, p=0.006), however less likely to have pre-existing DM (OR 0.8 (CI 0.78–0.92), p=0.000094). They were more often NSTEMI [851 (49.4%), p = 0.000012]. Independent variables associated with a reduction in LV function were: advanced age, male gender, previous DM and anemia, stress glycemia, WBC, creatinine, and BUN. Conclusion Patients who developed reduced LV function had a very specific risk profile with bigger neuro-hormonal activation and inflammation, higher degree of myocardial damage, and worse renal function, whereas those with preserved LV systolic function after ACS were younger, predominantly females, more severely metabolically burdened, more often with NSTEMI and without LAD involvement.

The biological equivalent and prognostic relevance of c-reactive protein (CRP) velocity in ST segment elevation myocardial infarction

Abstract Funding Acknowledgements None. Background The rate of increase, i.e. the velocity, of circulating C-reactive protein (CRP) concentrations during myocardial infarction has been associated with left ventricular dysfunction. However, the prognostic yield of this biomarker as well as the underlying biological process that links high CRP velocity (CRPv) with increased myocardial injury are not clear. Therefore, we sought to determine the associations between CRPv early during STEMI with short- and long-term mortality and its correlation to myocardial necrosis. Methods We retrospectively examined 1,155 patients with the diagnosis of acute STEMI, who had at least two successive CRP measurements (up to 48 hours apart) and at least one echocardiographic evaluation, all within the first 96 hours of admission. We calculated CRPv and examined its correlation with myocardial injury, measured by cardiac troponin and overall mortality over a median follow-up period of 5.2 years [IQR 3.7-6.5]. Results Patients with high CRPv values (above 90th percentile, &amp;gt; 1 mg/L/h) had higher concentrations of cardiac troponin upon presentation regardless of their left ventricular systolic function (EF above or below 40%; Figure 1). Patients with high CRPv had increased 30-day and long-term mortality rates; OR= 4.6, 95% CI 2.3-9.2, p&amp;lt;0.001 for 30-day mortality and HR= 2.2, 95% CI 1.5-3.2, p&amp;lt;0.001 for long-term mortality. Furthermore, CRPv was associated with increased 30 –day and long term mortality rates even among patients with similar systolic function (EF above or below 40%; Figure 2). Conclusions High levels of CRPv early during STEMI are associated with increased mortality rates and elevated cardiac troponin release across all levels of left ventricular function. The higher mortality risk might be explained by an aggravated systemic inflammatory response to STEMI.CRP velocity and troponinCRP velocity and mortality

How COVID-19 Can Damage the Heart? – Association of Cardiac Injury with COVID-19: A Narrative Review

Abstract Severe acute respiratory syndrome coronavirus 2 and its resulting disease, COVID-19, remain a significant public health concern. Cardiovascular injury is the second most common complication, following respiratory disease, encompassing conditions such as myocarditis, acute myocardial injury, acute coronary syndrome, arrhythmia, and heart failure. It presents with high-troponin levels, reduced left ventricular systolic function, and/or electrocardiographic abnormalities. Cardiac involvement is an independent risk factor for worse clinical outcomes and higher mortality, particularly in the elderly patients. The debate continues regarding whether the cardiac manifestations of COVID-19 result from direct viral infection or indirect cellular injuries. The virus attaches directly to angiotensin-converting enzyme 2 receptor, which is extensively expressed in the heart, invades myocardial tissue, and triggers an excessive inflammatory response. Indirect mechanisms stem from endothelial damage, hypercoagulability and micro-thrombosis, cytokine storm, respiratory failure and hypoxia, and autoimmunity. The pathophysiology of cardiac injury in COVID-19 patients is important to frame the main pathways and biomarkers to encourage new therapeutic trials to improve the disease prognosis and to understand the course of the disease.

In-hospital trimethylamine N-oxide (TMAO) variation predicts major adverse cardiovascular events in myocardial infarction survivors

Abstract Funding Acknowledgements None. Background Trimethylamine N-oxide (TMAO), a gut microbiota result of the fermentation of animal foods rich in choline, L-carnitine and phosphatidylcholine (red meat, egg yolk, dairy food), is associated with alterations in lipid metabolism, increased foam cell formation, promotion of inflammation, oxidative stress, platelet aggregation and thrombosis. To date the data evaluating TMAO as a predictor of mortality and ischemic events in patients with acute myocardial infarction (AMI) based on one-time measurement of TMAO levels lead to conflicting results. TMAO levels are fluctuating and in addition to diet, genetic factors, general condition and some co-morbidities affect its circulating levels. Purpose Since, there is a need for better risk stratification of AMI patients before the hospital discharge for more personalised treatment, we evaluated in-hospital variation in TMAO levels and its impact on outcome. Methods Blood samples from 149 consecutive AMI patients were collected on admission and on discharge. The endpoint was a three-point major adverse cardiovascular events (MACE) composed as all-cause mortality, reinfarction and development of heart failure. Results The majority of AMI patients were male (77%), hospitalized for first coronary event, with mean age 64(11) years. Median circulating TMAO level was significantly higher on admission than on discharge, (7.81 [3.47 –19.98] vs 3.45 [2.3 – 4.78] μM, respectively, p&amp;lt;0.001). In order to evaluate the impact of TMAO variation during the hospital stay on outcome, we estimated TMAO cut-off value by continuous hazard ratio analysis; values above the 3.45 μM were associated with incident of MACE in a linear fashion (Fig. 1a). Subsequently, we stratified AMI patients in 2 groups: 1) LL/HL (low-low/high-low) that included 75 (50.3%) patients whose TMAO levels remained low or were high and decreased during hospitalization and 2) HH/LH (high-high/low-high) including 74 patients (49.7%) patients whose TMAO levels remained elevated or were initially low, but rose above the estimated threshold during hospitalisation (Fig. 1b). Thirty-two (21.5%) patients reached the combined endpoint during the median follow-up of 30 months. The Kaplan-Meier analysis demonstrated that patients from the HH/LH group had a higher likelihood of experiencing MACE (p=0.05) (Fig. 2a). The multivariate Cox analysis revealed that patients in the HH/LH group had over twice the risk of MACE compared to those in the LL/HL group. Furthermore, older age and worse left ventricular systolic function were identified as independent predictors of MACE during long-term follow-up (Fig. 2b). Conclusions AMI patients with permanently elevated or increasing levels of TMAO have a worse outcome. The novelty and the strength of our study is the fact that the direction of variation of TMAO during the index hospitalisation identifies patients at higher risk of MACE during 30 months follow-up.

Incremented Amyloid-beta values predict mortality during long-term follow-up in patients with acute myocardial infarction, both STEMI and NSTEMI

Abstract Funding Acknowledgements None. Background Both the amyloid-β (Aβ) isoforms, namely Aβ1-40 and Aβ1-42 are implicated in the pathogenesis of Alzheimer’s disease through different mechanisms. While Aβ42 easily forms oligomers in brain, Aβ1-40 is more abundant in circulation where it exerts a pro-inflammatory role. Recently, Aβ1-40 has raised interest in the cardiovascular field for its contribution to atherosclerosis, more specifically through plaque formation and destabilization. However, to date, the prognostic role of Aβ1-40 in patients with acute myocardial infarction (AMI) is limited to NSTEMI. Purpose Since there is a need for better risk stratification of AMI patients, we analyzed the impact of plasma Aβ1-40 on long-term mortality in a cohort of real-world patients with AMI, including STEMI and NSTEMI. Further, we sought to identify predictors for elevated Aβ1-40 levels. Methods Blood samples were obtained from patients hospitalized for AMI and Aβ1-40 levels were evaluated with Human Aβ40 ELISA Kit. The endpoint was all-cause mortality. Results Our population included 1119 consecutive patients, with a mean age of 67 years, 72% male, 2/3 of them had a first ischemic event and 68.4% had STEMI diagnosis. The median plasma Aβ1-40 concentration on admission was 86.9 [54.5-128.9] pg/ml and there was no difference in Aβ1-40 levels between NSTEMI and STEMI (93.6 [61.2-130.9] Vs. 85.3 [52.9-128.7] pg/ml, respectively, p=0.1). At logistic regression multivariate analysis, higher Aβ1-40 levels were predicted by older age, worse left ventricular systolic function, HbA1C &amp;gt; 39 mmol/mol and GFR&amp;lt;60ml/min/m 2 (Fig.1a). From the final multivariable model, a nomogram for prediction of high levels of Aβ1-40 was computed (Fig.1b). One hundred ninety-three patients (17.2%) died, during the median follow-up of 57 [30 - 80] months. Patients who died had significantly higher levels of Aβ1-40 compared to alive patients (113.1 [67.9 – 159.5] Vs. 83.9 [52.5 – 122.6] pg/ml, p&amp;lt;0.01). Higher plasma Aβ1-40 values were associated with increased mortality risk, in both STEMI and NSTEMI (p&amp;lt;0.01) (Fig.2a). Further, at Cox multivariate analysis including the whole population, Aβ1-40 levels were predictive of mortality (HR 1.03, p=0.02), together with older age, higher Il-1β, GFR&amp;lt;60ml/min/m 2 and worse left ventricular systolic function (Fig.2b). The predictive value of our final model was superior to GRACE score for up to 60 months (AUC 0.830 (0.793 – 0.868) Vs 0.797 (0.756 – 0.837), respectively, p=0.03, Fig.2c), after which they were comparable. Conclusions Elevated levels of Aβ1-40 values are independent predictors of long-term mortality in a real-world cohort including both STEMI and NSTEMI patients.

Relationship between G protein level with left ventricular systolic function in children with acyanotic heart disease

Heart failure is a pediatric emergency caused by the heart's inability to adequately meet the body metabolic needs and the most common cause is congenital heart disease (CHD). The G protein is the most prominent family of membrane-bound protein known to act in major regulatory events of the cardiovascular system, one of which is heart failure. The aim of this study was to determine the level of G protein and its relationship with left ventricular systolic function in children with acyanotic CHD. A cross-sectional study was conducted in Dr. Zaionel Abidin Hospital, Banda Aceh, Indonesia. The patients aged 0 to 18 years and had acyanotic CHD diagnosis by echocardiography were included. Anthropometry measurement was performed according to standard WHO procedures and G protein level was measured using the ELISA method. The Chi-squared test was used to measure the relationship between G protein level and left ventricular systolic function. Out of a total of 38 children with acyanotic CHD, the mean level of G protein was 36.25 ng/mL and the mean of left ventricular systolic function was 73.1%. There was no relationship between G protein and left ventricular systolic function in children with acyanotic CHD. However, further study with a larger sample size and considering other variables are needed to confirm this finding.

Empagliflozin to prevent progressive adverse remodelling after myocardial infarction (EMPRESS-MI): rationale and design.

Patients with a reduced left ventricular ejection fraction (LVEF) following an acute myocardial infarction (MI) are at risk of progressive adverse cardiac remodelling that can lead to the development of heart failure and death. The early addition of a sodium-glucose cotransporter 2 (SGLT2) inhibitor to standard treatment may delay or prevent progressive adverse remodelling in these patients. EMpagliflozin to PREvent worSening of left ventricular volumes and Systolic function after Myocardial Infarction (EMPRESS-MI) is a randomized, double-blind, placebo-controlled, multi-centre trial designed to assess the effect of empagliflozin on cardiac remodelling evaluated using cardiovascular magnetic resonance (CMR) in 100 patients with left ventricular systolic dysfunction following MI. Eligible patients were those ≥12h and ≤14days following acute MI, with an LVEF <45% by CMR. Patients were randomized to empagliflozin 10mg once a day or matching placebo. The primary outcome will be change in left ventricular end-systolic volume indexed to body surface area over 24weeks from randomization. Secondary endpoints include measures of left ventricular and atrial volumes, left ventricular mass, LVEF, and circulating cardiac biomarkers. EMPRESS-MI will assess the effect of the SGLT2 inhibitor empagliflozin on cardiac remodelling in patients with left ventricular systolic dysfunction after an acute MI.

Assessment of left ventricular systolic function in obesity

Assessment of left ventricular systolic function in obesity

Investigation of left atrial mechanical function and left ventricular systolic and diastolic parameters in athletes performing resistance exercise and combined exercise

Some individuals who go to fitness centers for various purposes perform resistance exercise (RE) alone, while others engage in combined exercise (CE) by including cardio exercises along with RE. Studying the effects of these two different training methods on left ventricular (LV) systolic and diastolic parameters and left atrial mechanical function is an important step toward understanding the effects of different types of exercise on cardiac function. This knowledge has significant implications for public health, as it can inform the development of targeted and effective exercise programs that prioritize cardiovascular health and reduce the risk of adverse outcomes. Therefore, the primary aim of this study is to comprehensively investigate the LV systolic and diastolic parameters of athletes who engage in RE and CE using ECHO, to contribute to the growing body of literature on the cardiovascular effects of different types of exercise. Forty-two amateur athletes aged between 17 and 52 were included in our study. The participants consisted of the RE (n = 26) group who did only resistance exercise during the weekly exercise period, and the CE group (n = 16) who also did cardio exercise with resistance exercises. After determining sports age (year), weekly exercise frequency (day), and training volume (min) in addition to demographic information of RE and CE groups, left ventricular systolic and diastolic parameters and left atrial functions were determined by ECHO. Findings from our study revealed that parameters including the left ventricular end-diastolic diameter (LVEDD) (p = .008), left ventricular end-diastolic volume (LVEDV) (p = .020), stroke volume index (SV-I) (p = .048), conduit volume (CV-I) (p = .001), and aortic strain (AS) (p = .017) were notably higher in the RE group compared to the CE group. Also left atrial active emptying volüme (LAAEV) of CE was higher than the RE group (p = .031). In conclusion, the cardiac parameters of the RE group showed more athlete’s heart characteristics than the CE group. These results may help to optimize the cardiovascular benefits of exercise routines while minimizing the potential risks associated with improper training.

Atrial Septal Defect Closure: Not Always Straightforward.

A nine-year old boy presented following a chest x-ray for COVID-19 infection that showed cardiomegaly. Transthoracic echocardiogram revealed a large atrial septal defect, dilated right heart, and normal function. Surgical repair was performed eight weeks after his COVID diagnosis. After weaning from cardiopulmonary bypass, pulmonary artery pressures were 2/3 systemic and ectopy was seen, requiring inotropes, nitric oxide, lidocaine, and amiodarone. He was discharged on postoperative day (POD) 5. On POD 6, he presented with acute right foot ischemia. Computed tomography showed a large aortic thrombus, requiring emergent thrombectomy. Coagulopathy workup was negative. Cardiac magnetic resonance imaging (CMR) and catheterization showed reduced biventricular function and diastolic dysfunction. Diuretics and β blockers were started, with gradual improvement in left ventricular systolic function.

Association of attenuated leptin signaling pathways with impaired cardiac function under prolonged high-altitude hypoxia

Cardiovascular function and adipose metabolism were markedly influenced under high altitudes. However, the interplay between adipokines and heart under hypoxia remains to be elucidated. We aim to explore alterations of adipokines and underlying mechanisms in regulating cardiac function under high altitudes. We investigated the cardiopulmonary function and five adipokines in Antarctic expeditioners at Kunlun Station (4,087 m) for 20 days and established rats exposed to hypobaric hypoxia (5,000 m), simulating Kunlun Station. Antarctic expeditioners exhibited elevated heart rate, blood pressure, systemic vascular resistance, and decreased cardiac pumping function. Plasma creatine phosphokinase-MB (CK-MB) and platelet-endothelial cell adhesion molecule-1 (sPecam-1) increased, and leptin, resistin, and lipocalin-2 decreased. Plasma leptin significantly correlated with altered cardiac function indicators. Additionally, hypoxic rats manifested impaired left ventricular systolic and diastolic function, elevated plasma CK-MB and sPecam-1, and decreased plasma leptin. Chronic hypoxia for 14 days led to increased myocyte hypertrophy, fibrosis, apoptosis, and mitochondrial dysfunction, coupled with reduced protein levels of leptin signaling pathways in myocardial tissues. Cardiac transcriptome analysis revealed leptin was associated with downregulated genes involved in rhythm, Na+/K+ transport, and cell skeleton. In conclusion, chronic hypoxia significantly reduced leptin signaling pathways in cardiac tissues along with significant pathological changes, thus highlighting the pivotal role of leptin in regulation of cardiac function under high altitudes.

Diltiazem reduces levels of NT-proBNP and improves symptoms compared with metoprolol in patients with permanent atrial fibrillation.

Short-term treatment with calcium channel blockers lowers levels of N-terminal pro B-type natriuretic peptide (NT-proBNP) and reduces rhythm-related symptoms compared to treatment with beta-blockers. The aim of this study was to compare the longer-term effects of metoprolol and diltiazem for rate control in patients with permanent atrial fibrillation after six months. Men and women with permanent atrial fibrillation and preserved left ventricular systolic function were randomised to receive either diltiazem 360 mg or metoprolol 100 mg once daily. The primary endpoint was the level of NT-proBNP after a six-month treatment period. Secondary endpoints included heart rate, rhythm-related symptoms and exercise capacity. A total of 93 patients (mean age 71 ±7 years, 28 women) were randomised. After six months' treatment, mean levels of NT-proBNP decreased in the diltiazem group and increased in the metoprolol group, with a significant between-group difference (409.8 pg/mL, 95% CI: 230.6 - 589.1, P<0.001). Treatment with diltiazem significantly reduced rhythm-related symptoms compared to baseline, but no change was observed in the metoprolol group. Diltiazem and metoprolol had similar effects on heart rate and exercise capacity. Diltiazem reduced NT-proBNP levels and improved rhythm-related symptoms. Metoprolol increased peptide levels but had no impact on symptoms despite similar heart rate reduction. Non-dihydropyridine calcium channel blockers should be considered more often for rate control in permanent atrial fibrillation.

Left and Right Ventricular Longitudinal Systolic Function Following Aortic Valve Replacement in the PARTNER 2 Trial And Registry.

Evaluation of left and right ventricular longitudinal systolic function may enhance risk stratification following aortic valve replacement (AVR). The study objective was to evaluate the changes in left and right ventricular longitudinal systolic function and RV-pulmonary artery (RV-PA) coupling from baseline to 30-days and 1-year after aortic valve replacement (AVR). LV longitudinal strain (LS), tricuspid annulus plane systolic excursion (TAPSE), and RV-PA coupling were evaluated in patients from the PARTNER-2A surgical AVR (SAVR) arm (n=985) and from the PARTNER-2 SAPIEN-3 registry (n=719). TAPSE and RV-PA coupling decreased significantly following SAVR, but remained stable following TAVR. Lower LV LS, TAPSE, or RV-PA coupling at baseline were associated with increased risk of the composite of death, hospitalization, and stroke at 5-years (Adjusted-HRs for LV LS<15%: 1.24 95%CI 1.05-1.45, p=0.001; TAPSE<14mm: 1.44 95%CI 1.21-1.73, p<0.001; RV/PA coupling<0.55mm/mmHg: 1.32 95% CI 1.07-1.63, p=0.011). Reduced TAPSE at baseline was the most powerful predictor of the composite endpoint at 5-years. Patients with LV ejection fraction <50% at baseline had increased risk of the primary endpoint with SAVR (HR: 1.34, 95%CI 1.08-1.68, p=0.009) but not with TAVR (HR: 1.12, 95%CI 0.88-1.42). Lower RV-PA coupling at 30-days showed the strongest association with cardiac mortality. SAVR but not TAVR was associated with a marked deterioration in RV longitudinal systolic function and RV-PA coupling. Lower TAPSE and RV-PA coupling at 30-days were associated with inferior clinical outcomes at 5-years. In patients with LVEF<50%, TAVR was associated with superior 5-year outcomes.

Abstract PO4-12-07: INSTITUTIONAL EXPERIENCE IN PATIENTS WITH EARLY BREAST CANCER WHO RECEIVED CARDIOTOXIC THERAPY IN CARDIONCOLOGY UNIT

Abstract Introduction: Early breast cancer (eBC) is the most frequent malignancy diagnosed in women worldwide; fortunately, survival is increasing related to early diagnosis and the incorporation of new drugs. In this scenario, preventing long-term toxicities become essential. Cardiac adverse events related to anthracyclines or trastuzumab such as reduction in left ventricular (LV) systolic function and clinical heart failure (HF), are well known and are the leading cause of morbidity in breast cancer survivors. Cardioprotective strategies and early diagnoses of asymptomatic cardiac dysfunction are essential to optimized management and prevention of overt cardiovascular (CV) disease. We made a specific cardiac assessment within an Oncocardiology multidisciplinary Unit in patients receiving anticancer therapies. We present the experience in patients with eBC treated with anthracyclines, trastuzumab or both in the past five years. Materials and Methods: We conducted an institutional, interventional, prospective study in patients who received anthracyclines, trastuzumab or both according to the standard of care (SoC) in eBC. Basal CV risk stratification included lipid profile, glycated haemoglobin, high-sensitive troponin T (hs-TnT) and N-terminal ProB-type natriuretic peptide (NT-ProBNP) was done. Image assessment was done by echocardiogram (echo), including myocardial deformation assessed by speckle tracking (STRAIN). Follow-up was done according to anthracycline or trastuzumab therapy with echo and cardiac biomarkers during the systemic therapy and at the end of anticancer treatment, 1, 2 and 5 years after. Patients with uncontrolled CV risks factors according to local protocol, asymptomatic cardiac dysfunction defined as decreased strain (&amp;gt;15% compared with baseline) or increased cardiac biomarkers (Hs-TnT &amp;gt;14 at baseline or x3 basal value during the follow-up; NT-ProBNP &amp;gt; 300 in patients with &amp;lt; 50y; &amp;gt; 600 in patients between 50-75-y or &amp;gt;900 in patients &amp;gt; 75 years or older) or patients who develop heart failure during the treatment or follow-up were referred to cardiologist. Results: between 2018 and 2022, 1125 patients were diagnosed with eBC in our institution, and 435 patients received systemic treatment with anthracyclines, trastuzumab or both. During the study period, 165 of these patients were referred to the cardio-oncologist. 60% received treatment with anthracyclines, 36% with trastuzumab and 4.1% with both. The median age was 58(±23.2), 60% had previous CV risk factors. The main reason to refer patients to the cardio-oncologist was asymptomatic cardiac dysfunction and uncontrolled CV risk factors. (Table 1). 60% of patients initiated angiotensin-converting-enzyme inhibitors or Beta-blockers, and only two patients stopped anticancer therapy due to severe cardiac dysfunction. The period of high risk of developing cardiotoxicity was the first year after the end of treatment. Conclusion: multidisciplinary evaluation within a cardio-oncology unit is useful to optimize CV risk factors and to detect asymptomatic cardiac dysfunction in patients receiving cardiotoxic drugs. Table 1. Main reasons to refer patients to cardiologist. Citation Format: Tamara Martos, Laia Carla Belarte-Tornero, Mireia Ble, Eva Gimeno, Laura Sanhauja, Felicidad Martines-Medina, Maria Martinez-García, Maria Castro-Henriques, Joan Albanell, Sonia Servitja. INSTITUTIONAL EXPERIENCE IN PATIENTS WITH EARLY BREAST CANCER WHO RECEIVED CARDIOTOXIC THERAPY IN CARDIONCOLOGY UNIT [abstract]. In: Proceedings of the 2023 San Antonio Breast Cancer Symposium; 2023 Dec 5-9; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2024;84(9 Suppl):Abstract nr PO4-12-07.

Elevated plasma solMER concentrations link ambient PM2.5 and PAHs to myocardial injury and reduced left ventricular systolic function in children

Exposure to fine particulate matter (PM2.5) and polycyclic aromatic hydrocarbons (PAHs) is known to be associated with the polarization of pro-inflammatory macrophages and the development of various cardiovascular diseases. The pro-inflammatory polarization of resident cardiac macrophages (cMacs) enhances the cleavage of membrane-bound myeloid-epithelial-reproductive receptor tyrosine kinase (MerTK) and promotes the formation of soluble MerTK (solMER). This process influences the involvement of cMacs in cardiac repair, thus leading to an imbalance in cardiac homeostasis, myocardial injury, and reduced cardiac function. However, the relative impacts of PM2.5 and PAHs on human cMacs have yet to be elucidated. In this study, we aimed to investigate the effects of PM2.5 and PAH exposure on solMER in terms of myocardial injury and left ventricular (LV) systolic function in healthy children. A total of 258 children (aged three to six years) were recruited from Guiyu (an area exposed to e-waste) and Haojiang (a reference area). Mean daily PM2.5 concentration data were collected to calculate the individual chronic daily intake (CDI) of PM2.5. We determined concentrations of solMER and creatine kinase MB (CKMB) in plasma, and hydroxylated PAHs (OH-PAHs) in urine. LV systolic function was evaluated by stroke volume (SV). Higher CDI values and OH-PAH concentrations were detected in the exposed group. Plasma solMER and CKMB were higher in the exposed group and were associated with a reduced SV. Elevated CDI and 1-hydroxynaphthalene (1-OHNa) were associated with a higher solMER. Furthermore, increased solMER concentrations were associated with a lower SV and higher CKMB. CDI and 1-OHNa were positively associated with CKMB and mediated by solMER. In conclusion, exposure to PM2.5 and PAHs may lead to the pro-inflammatory polarization of cMacs and increase the risk of myocardial injury and systolic function impairment in children. Furthermore, the pro-inflammatory polarization of cMacs may mediate cardiotoxicity caused by PM2.5 and PAHs.

Doppler-derived pulmonary pulse transit time measurements in chronic obstructive pulmonary disease: Reproducibility and cardiopulmonary function.

Doppler-derived pulmonary pulse transit time (pPTT) is an auspicious hemodynamic marker in chronic pulmonary diseases. The aim is to compare four distinct pPTT measurements and its relation to right cardiac and pulmonary function. Prospectively, 25 chronic obstructive pulmonary disease (COPD) patients (four patients excluded) and 32 healthy subjects underwent repeated distinct pPTT measurements, standard echocardiography, and pulmonary function testing on the same day. pPTT was defined as the interval from the R or Q-wave in the electrocardiogram to the corresponding pulse wave Doppler peak late systolic (S) 2 or diastolic (D) pulmonary vein flow velocity (pPTT R-S, Q-S, R-D, Q-D). Reproducibility was assessed using Bland-Altman analysis, coefficient of variation (COV), intraclass correlation coefficient (ICC), and power calculations. Associations with right ventricular RV tissue and pulse wave Doppler velocities (RV E', RV S', RV A', RV E, RV A, RV E/E', RV E/A), TAPSE, right ventricular fractional area change, left ventricular systolic and diastolic function (LV ejection fraction, E, A, E/A, E/E', septal E', lateral E'), LA diameters, as well as forced expiratory volume in 1 s, forced vital capacity (FVC) predicted (%), and in liters were analyzed. There was no significant difference and no bias between pPTT measures (p range:.1-.9). COV was in COPD 1.2%-2.3%, in healthy subjects 1.0%-3.1%. ICC ranged from.92 (COPD) to.96 (healthy subjects). In COPD significant correlations were found for pPTT R-S, Q-S and R-D with RV E`, (all>ρ:.49,<p=.0364), pPTT R-S, Q-S with RV E/E` (both>ρ:.49,<p=.0291), pPTT Q-S with RV S´ (ρ:.58, p=.0134), RV A (ρ:.59, p=.0339) and heart rate>ρ: -.39,<p=.0297). pPTT R-S, R-D showed significant correlations with FVC predicted (%) (ρ:.48 p=.0224) and FVC (l) (ρ:.47 p=.0347). All pPTT measures exhibited high reproducibility. In COPD patients pPTT measures correlate with diastolic right ventricular function. Defining Q as starting point seems clinically advantageous considering electromechanical desynchrony in patients with conduction disorders.