Enlarged Left Ventricle Research Articles

Revisiting echocardiographic ranges of left ventricular end-diastolic volume index: an analysis of the discrepancies between the 2006 and the 2015 recommendation for chamber quantification guidelines

Abstract Background Indexed left ventricular end-diastolic volume (LVEDVi) and indexed left ventricular end-diastolic diameter (LVEDDi) serve as crucial parameters indicative of left ventricle (LV) size. The "Recommendations for Chamber Quantification" guideline was published in 2006 and updated in 2015. While the previous guideline maintained uniform cut-off points for both men and women, the latest revision introduced new thresholds that vary between genders. Purpose The study's primary aim is to evaluate the extent of change in labeled indexed LV diastolic volumes in men and women following the adoption of the 2015 guidelines and identify potential contributing factors to this change. Methods In this cross-sectional study, we analyzed echocardiography data extracted from a web-based registry from March 2020 to October 2022. LV volume variables were categorized based on the indexed ranges specified in the 2006 and 2015 guidelines. Statistical analysis was performed using SPSS version 25. Results Among the 7598 individuals, the classification of LVEDDi according to the 2006 and 2015 guidelines differed in 456 (6.1%) subjects. The classification of LVEDVi differed in 910 (12.0%) individuals. In 213 (5.5%) female subjects initially categorized as having normal or mild LV enlargement according to the 2006 guideline, there was substantial reclassification following the application of the 2015 recommendation (i.e., transitioned from a normal classification to moderate LV enlargement and from mild to severe LV enlargement). All females classified as having moderately abnormal LVEDVi according to the 2006 guideline were reclassified as having severely abnormal LVEDVi according to the 2015 guideline. Conclusion The significant disparities observed in the classification of indexed LV volumes between the 2006 and 2015 guidelines underscore the importance of ongoing dedicated research to reassess the range of indexed echocardiographic parameters, considering various outcomes and differences in countries and races.

A Case of A Middle-Aged Woman with Cor Triatriatum Dexter and Sick Sinus Syndrome: Comprehensive Cardiovascular Evaluation

This case study discusses a 51-year-old woman with a complex cardiovascular condition, cor triatriatum dexter, complicated by sick sinus syndrome. The patient presented with a history of bradycardia, dizziness, and amaurosis, and was admitted to the emergency department due to numbness in her right limb. Diagnostic examinations, including computed tomography (CT) and cardiac color-ultrasound screening, revealed cor triatriatum dexter along with an enlarged left atrium and ventricle. Additional findings included the absence of the inferior vena cava and polysplenic syndrome. Based on these results, double-chamber pacemaker surgery was recommended, supported by cardiac and thoracic-abdominal CT angiography and three-dimensional vascular reconstruction. This case underscores the importance of comprehensive examinations in identifying associated cardiovascular abnormalities.

Remodeling of adult rat heart subjected to pressure overload from the neonatal period is dependent on the sex

Abstract Background Congenital heart diseases (CHD) represents the most common birth defect. Despite progress in their treatment improving acute survival, there is a paucity of data concerning the long-term consequences of CHD in adults. Purpose Here, we investigate the remodeling in adult rat hearts subjected to pressure overload from the early postnatal period. Methods We used the neonatal abdominal aortic constriction (AAC) model to analyze morphological, functional (by echocardiography), and electrophysiological long-term outcomes. Given the known differences in cardiac pathologies between males (M) and females (F), we focused on the role of sex in cardiac remodeling. Results Our data showed that both sexes exhibited a similar left ventricular weight/body weight ratio at the age of 12 weeks, indicating comparable left ventricle (LV) enlargement as a response to AAC (increase by 103 ± 9 % in M AAC and 99 ± 10 % in F AAC vs. sham-operated animals). However, the right ventricular weight/body weight and lung/ body weight ratios, indicative of LV failing, differed significantly between sexes with better values in F AAC. The favorable cardiac remodeling in F AAC was corroborated by significantly smaller LV systolic and diastolic diameters, along with a lower amount of myocardial fibrosis. Using optical mapping, we revealed preserved longitudinal and transversal conduction velocities (CVL; CVT) in females (CVL 104 ± 8 vs. 109 ± 8 cm/s and CVT 66 ± 7 vs. 59 ± 6 cm/s in F AAC and F Sham, respectively). However, compared to M Sham, the conduction velocities in M AAC showed a significant decrease (CVL 80 ± 3 vs. 92 ± 3 cm/s and CVT 35 ± 2 vs. 54 ± 3 cm/s). Similarly, the amount of connexion 43 (Cx43) and its phosphorylated state (Cx43Ser368) was preserved in F AAC while exhibiting a decrease in M AAC compared to the sham-operated controls. Thus, electrophysiological findings implicate that while the adult M AAC underwent pro-arrhythmogenic remodeling due to the elevated workload, the adult F AAC preserved physiological conduction properties. Conclusion Our data showed different consequences of the increased pressure load exposed from early after birth to the adult M and F heart. These findings highlighted the involvement of both sexes in cardiac studies.

8081 Case report of sympathetic paraganglioma presenting as chronic catecholamine induced cardiomyopathy

Abstract Disclosure: Z. Tan: None. A. Taiwo: None. Background: Sympathetic paragangliomas are rare neuroendocrine tumors (<1/100,000) arising from extra-adrenal autonomic paraganglia, generally in the thorax, abdomen, and pelvis. They secrete catecholamines predominantly norepinephrine, which can cause a rare complication of catecholamine-induced cardiomyopathy. Clinical Case: A 33-year-old male, with history of obesity and borderline hypertension not on medication, presented with dyspnea on exertion, worsening paroxysmal nocturia dyspnea of 1 month duration and sudden onset of severe right flank pain. Work up for his chronic shortness of breath revealed: Troponin negative. EKG showed sinus tachycardia. Echocardiogram revealed enlarged left ventricle, severely decreased LV systolic function of 25-30%. Given the absence of angina symptoms, negative troponin, and EKG findings, his new-onset cardiomyopathy was presumed to be non-ischemic. CT chest, abdomen and pelvis was performed for the new onset right flank pain, which revealed a 4.1 cm x 4.0 cm centrally necrotic aortocaval soft tissue mass. This raise a concern about malignancy. A CT-guided Fine-Needle Aspiration of the retroperitoneal mass suggested paraganglioma. Further investigation showed plasma normetanephrine at 5.56 nmol/L (Reference range: 0-0.89 nmol/L), 24 hour urine normetanephrine at 2411 ug/d (Reference range: 114-865 ug/d), and 24 hour urine norepinephrine at 179 ug/d (Reference range: 14-20 ug/d). Plasma metanephrines and plasma dopamine were within the normal range. A gallium DOTATE PET/CT revealed a necrotic aortocaval mass with peripheral uptake, consistent with the known paraganglioma. He was diagnosed with sympathetic paraganglioma complicated with chronic catecholamine-induced cardiomyopathy and had exploratory laparotomy excision of his paraganglioma. Preoperatively, he was treated with phenoxybenzamine and carvedilol. However, his post-surgical course was complicated by acute on chronic heart failure and pneumonia, and he subsequently passed away from a pulseless electrical activity arrest. Conclusion: Although sympathetic paragangliomas rarely presents as catecholamine-induced cardiomyopathy, this case emphasizes the importance of considering hormonal abnormalities in patients who present with non-ischemic cardiomyopathy without high risk factors. Reference: 1. Alessandra Giavarini, Antoine Chedid et al. Acute catecholamine cardiomyopathy in patients with phaechromocytoma or functional paraganglioma. Heart 2013; 99: 1438-1444. Presentation: 6/2/2024

Revisiting Echocardiographic Ranges of Left Ventricular End-Diastolic Volume Index: An Analysis of the Discrepancies Between the 2006 and the 2015 Recommendation for Chamber Quantification Guidelines.

Indexed left ventricular end-diastolic volume (LVEDVi) is a left ventricle (LV) size marker. The "Recommendations for Chamber Quantification" guideline was published in 2006 and updated in 2015. Although the previous guideline maintained uniform cutoff points for both men and women, the latest revision introduced new thresholds that vary between genders. We evaluated the extent of change in labeled indexed LV diastolic volumes in men and women following the adoption of the 2015 guideline. Data were extracted from a web-based registry from March 2020 to October 2022. LV indexed volume variables were categorized on the basis of the 2006 and 2015 guidelines. Among the 7598 individuals, the classification of LVEDVi differed in 910 (12.0%) individuals. In 213 (5.5%) female subjects, substantial reclassification (i.e., transitioning from normal to moderate LV enlargement to mild to severe LV enlargement) occurred on the basis of the 2015 guideline. All females classified as having moderately abnormal LVEDVi according to the 2006 guideline were reclassified as having severely abnormal LVEDVi according to the 2015 guideline. Age, LV ejection fraction (LVEF), and significant aortic regurgitation (AR) were common factors contributing to the observed discrepancy in both men and women. Significant mitral regurgitation (MR) and regional or global motion abnormality were correlated with the reclassification of LVEDVi to higher abnormal partitions only in women. The observed disparities underscore the importance of ongoing dedicated research to reassess the range of indexed echocardiographic parameters, considering various outcomes and differences in countries.

Discordance interpretation of left ventricular size between echocardiography and cardiac magnetic resonance in pediatric patients with aortic/mitral regurgitation

PurposeThis study investigated discordance between echocardiography (echo) and cardiac magnetic resonance (CMR) measurements of the left ventricle (LV) in pediatric patients with aortic and/or mitral regurgitation (AR/MR).MethodsRetrospective cohort study of pediatric patients. The cohorts were comprised of patients with AR/MR vs. non-AR/MR. Left ventricular end diastolic volume (LVEDV) by CMR and left ventricular internal diameter diastolic (LVIDd) by echo were obtained from clinical reports then echo images were reviewed to remeasure LVEDV by bullet method. Left ventricular internal diameter systolic (LVIDs) and left ventricular ejection fraction (LVEF) measurements by echo and LVEF by CMR were obtained from clinical reports. Fractional shortening (FS%) was recalculated. Z-scores were calculated using normative data. Correlation between echo and CMR LV measurements was assessed using correlation coefficients. Bland-Altman plots assessed bias between imaging modalities. Receiver operator characteristic (ROC) analysis was performed for detection of LV enlargement and LV dysfunction.ResultsAR/MR patients had greater discrepancy in LV size interpretation by Z-score compared to non-AR/MR patients. This discrepancy persisted when the bullet method short axis measurements were incorporated. There was negative bias in echo-based measurements compared to CMR. The diagnostic performance of echo in identifying moderate LV enlargement was worse for AR/MR pediatrics patients.ConclusionThe discordant interpretation of LV size by echo compared to CMR is worse in pediatric patients with AR/MR when compared to patients without AR/MR even when short axis measurements are incorporated. This finding suggests non-uniform geometrical changes in the LV as it enlarges due to AR/MR.

Massive Restrictive Aortic Regurgitation Caused by Aortic Chordae Tendineae Strands: Unusual Links

Determination of the etiology of a valvular heart disease is one of the major steps of every echocardiogram. Sometimes very unusual and rare etiologies can be found. In this article we report a case of very rare cause of aortic regurgitation, caused by the presence of aortic chordae tendineae strands leading to aortic cusps restriction in young asymptomatic athlete. In this case, we discuss two major problems. The first is the challenging diagnosis of this chordae tendineae strands, the second is the evaluation of an asymptomatic severe aortic regurgitation in a competitive athlete with an enlarged left ventricle.

Left Ventricular Hypertrophy in Male and Female Judo Athletes.

Changes in cardiac geometry develop after intense and prolonged training. Left ventricular enlargement, increased relative wall thickness, and growing mass of the left ventricle occur after strenuous exercise. Combat sports such as judo can lead to left ventricular hypertrophy. Previous studies have found that there are differences in left ventricular chamber size and thickness between the sexes, with female athletes having smaller wall diameters and less hypertrophy than male athletes. The research aims to examine heart muscle adaptations and remodeling of cardiac geometry among elite judo athletes and to evaluate differences between males and females. A cross-sectional study included a group of 19 (males n=10, females n=9) professional judokas between 20 and 30 years. Demographic and anthropometric data were collected. Cardiac geometry was determined by two-dimensional transthoracic echocardiography. In terms of left ventricular mass and the left ventricular mass index significant differences were found between male and female judokas (233.44±68.75 g vs. 164.11±16.59 g, p=0.009), (105.16±24.89 vs. 84.66±15.06, p=0.044), respectively. A greater enlargement of the heart muscle is observed in male athletes compared to the female group. Left ventricle enlargement is likely to occur among elite-level judokas.

Echocardiographic assessment of morphofunctional and hemodynamic changes of rheumatic mitral valve dysfunction in the young. Morphological changes in rheumatic valve lesions

Background- Rheumatic fever and its sequel rheumatic heart disease remain a major health problem across the globe. This investigation aims to analyse the mitral valve morphofunctional changes, stratified by severity, and the magnitude of the mitral regurgitation and stenosis through a simplified echocardiographic scoring system in patients with rheumatic heart disease. Methods- As cross-sectional echocardiographic study was carried out in 98 consecutive patients with confirmed rheumatic heart disease. Patients undergoing outpatient clinical care over an 18-month period (mean follow-up period of 9,7±2,9 years) were selected for echocardiographic investigation. After a double-blind echocardiograms review, the inter-rater reliability was calculated (Kappa=0.875 (0.775- 0.974; CI 95%). The morphofunctional data of mitral apparatus were scored on a rating scale from one to fifteen, encompassing three categories (1-5: mild; 6-10: moderate; 10-15: severe) to quantify the degrees of severity. Pearson's Chi-squared test with Yates' continuity correction were performed for comparative analysis and the Wilcoxon test and the Cliff's Delta effect size was calculated to examine differences related to morphological features. Results- The majority of patients had rheumatic heart disease with clinical evidence and twenty patients (20,4%) had subclinical disease.The thickening of both mitral valve leaflets and the restrictive motion of the posterior leaflet were most frequently found in contrast with the low percentage of chordal and/or commissural fusion. The degree of the anterior mitral valve leaflet thickening was proportional to the magnitude of the mitral valve regurgitation (p=0.021). The higher degrees of mitral valve dysfunction were associated with more severe carditis (mitral valve regurgitation, p: 0.000; mitral valve stenosis, p: 0.031). No association was found between the severity of valvular lesions and patient age or length of the disease (p=0.320). The presence of beading was only observed in the acute phase (p=0,000); coaptation defect of the mitral valve was associated with significant left ventricle enlargement (p=0.000). The morphofunctional score of mitral apparatus, stratified by severity, was associated with the magnitude of mitral valve regurgitation (p=0,000) and of mitral valve stenosis (p=0,031) also quantified by severity. The highest scores were observed in patients with the most severe degrees of carditis (p=0,000); however, no association was found with either, the patients’ age (p=0.373) or the duration of the disease (p=0.361). Conclusions- In the analysis of severity of the mitral apparatus deformities and the resulting valve dysfunction, the morphofunctional score stratification was highly associated with the magnitude of mitral regurgitation and stenosis. In this young cohort, the higher scores were associated to severe carditis, but not to the patients’ age or the duration of the disease. Taking into account the low prevalence of severe valve dysfunctions, these results highlight the importance of early intervention and adequate prevention.

High prevalence and distinctive clinical features of LMNA-associated atrioventricular block in young patients

Atrioventricular block (AVB) is a degenerative disease and more commonly encountered in elderly patients, but unusual and often of unknown etiology in young patients. This study aimed to investigate the potential contributions of genetic variations to AVB of unknown reasons in young patients. We enrolled 41 patients aged <55 years with high-degree AVB of unknown etiology whose clinical and genetic data were collected. Genetic variants were identified in 20 (20/41, 48.8%) patients, 11 (11/20, 55%) of whom had LMNA variants including 3 pathogenic (c.961C > T, c.936+1G > T and c.646C > T), 4 likely pathogenic (c.1489-1G > C, c.265C > A, c.1609-2A > G and c.1129C > T) and 3 of uncertain significance (c.1158-3C > G, c.776A > G and c.674G > T). Compared to those without LMNA variants, patients with LMNA variants demonstrated a later age at onset of AVB (41.45 ± 9.89 years vs 32.93 ± 12.07 years, P = .043), had more prevalent family history of cardiac events (81.8% vs 16.7%, P < .000), suffered more frequently atrial (81.8% vs 10.0%, P < .000) and ventricular (72.7% vs 10.0%, P < .000) arrhythmias, and were more significantly associated with enlargement of left atrium (39.91 ± 7.83 mm vs 34.30 ± 7.54 mm, P = .043) and left ventricle (53.27 ± 8.53 mm vs 47.77 ± 6.66 mm, P = .036). Our findings provide insights into the genetic etiology of AVB in young patients. LMNA variants are predominant in genotype positive patients and relevant to distinctive phenotypic properties.

Artificial intelligence-enabled electrocardiogram in the detection of patients at risk of atrial functional mitral regurgitation

Abstract Background Atrial functional mitral regurgitation (AFMR) is an increasingly recognized cause of functional MR thought to result from left atrial enlargement and myopathy in the setting of preserved left ventricular geometry and function. AFMR mostly occurs in patients with atrial fibrillation (AF) and/or heart failure with preserved ejection fraction. Purpose We investigated whether the use of an artificial intelligence-based electrocardiogram (AI-ECG) can identify patients with new-onset AF and sinus rhythm (SR) who are at highest risk of developing AFMR. Methods Adults with a new diagnosis of AF between 2010 and 2021 who had a transthoracic echocardiogram (TTE) within 1 month after AF diagnosis were identified. Similarly, adults in SR who never had AF diagnosis and had a TTE during the same period were identified. Exclusion criteria from both groups included &amp;gt;mild MR at baseline, primary mitral valve disease, cardiomyopathy, ≥moderate aortic valve disease, current or previous low ejection fraction, enlarged left ventricle, cardiac devices, previous cardiac surgeries, and the absence of follow-up TTE ≥6 months from baseline. Only patients who had ECG within 10 days of the TTE were included. When multiple ECGs were available, the closest was considered. A previously trained AI-ECG algorithm to detect the probability of AF was utilized. Incident AFMR was defined as &amp;gt;mild functional MR in the absence of &amp;gt;mild left ventricle enlargement or dysfunction. Diastolic dysfunction was defined according to ASE/EACVI guidelines. Results Overall, 1,570 patients with new-onset AF (median age 67 years; 34% females) and 16,802 patients in SR (median age 59 years; 46% females) were included. The median AI ECG probability for AF was 43% (IQR 26%-59%) in the new-onset AF group and 2% (0.5%-7%) in the SR group, Figure 1. Incident AFMR occurred in 152 patients in the AF group over median 3.06 (IQR 1.5-5.2) years of follow-up and in 482 patients in the SR group over median 3.0 (1.5-5.6) years of follow-up. The probability of silent AF by the AI-ECG was associated with incident AFMR in the new-onset AF group [hazard ratio 1.19 (95% CI 1.11-1.28) per 10%, p &amp;lt;.001] and the SR group [hazard ratio 1.19 (95% CI 1.12-1.25) per 10%, p &amp;lt;.001]. The AI ECG-derived AF probability remained as an independent risk factor for AFMR in multivariable analysis in both AF and SR, Table 1. Conclusion The AI ECG for AF might be able to reflect the degree of left atrial myopathy and thus the risk of incident AFMR in patients with AF and SR.Distribution of AI ECG probability of AFMultivariable risk factors for AFMR

Abstract 18718: A Deep Learning Model for Classifying Left Ventricular Enlargement Using Transthoracic and Point-of-Care Echocardiograms

Background: Enlargement or dilation of the left ventricle (LV) is associated with increased cardiovascular morbidity and mortality, and is an established precursor of ventricular dysfunction and heart failure in almost all major cardiovascular conditions. Although there are existing artificial intelligence frameworks that make use of deep learning to detect LV enlargement, many entail LV segmentation, which can be error-prone especially for point-of-care ultrasound (POCUS) images. Goal: To develop a fully end-to-end deep learning framework that takes as input either transthoracic echocardiographic (TTE) or POCUS 2D image clips, and classifies directly (i.e., without first segmenting the LV) whether a patient has an enlarged LV. Methods: Using a sample of retrospective TTE data enriched for LV enlargement (out of 13,868 patients total, 3,351 had an enlarged LV defined using sex-specific guideline-directed criteria), we trained a classifier that takes as input apical 2-chamber and parasternal long axis videos, and provides as output a binary label denoting whether a patient has an enlarged LV. Then, we evaluated the trained model using a holdout testing dataset of retrospective TTE data (2,087 patients) as well as data from a prospective cohort of 428 patients from whom TTE and POCUS were collected simultaneously. Results: For the retrospective TTE testing dataset, the AUC was 0.851 (95% confidence interval (CI) of 0.830-871). For the prospective cohort, the model performed comparably for both TTE and POCUS video clips (TTE: AUC of 0.865, 95% CI of 0.823-0.906; POCUS: AUC of 0.840, 95% CI of 0.797-0.883). Conclusions: The current deep learning model performed comparably well for both TTE and POCUS echocardiograms. We regard these results as a proof-of-concept of the potential utility of this model in helping point-of-care clinicians make decisions regarding whether patients should receive further evaluation for LV enlargement and associated conditions.

Abstract 14699: Effects of Papillary Muscle Approximation and Annuloplasty Ring Sizing for Functional Mitral Regurgitation Repair in Enlarged Ventricles

Introduction: Our recent large animal study showed that papillary muscle approximation (PMA) repairs functional mitral regurgitation (FMR) and increases valve coaptation in enlarged left ventricles without negatively affecting ventricular function. However, since PMA does not reduce mitral annular dilation, addition of annuloplasty ring might be beneficial for such repair. In this study, we used computational modeling to investigate the benefit of the addition of annuloplasty to PMA and the effects of ring sizing on FMR repair in enlarged ventricles. Methods: 3D echo images were obtained in 3 pigs with heart failure, enlarged ventricles, and FMR. Each echo dataset was segmented, and computational model of the mitral valve was developed. To mimic PMA repair, the papillary muscles were drawn together in diastole. A true-sized annuloplasty ring of 40 mm and two downsized-rings of 38 mm and 36 mm were then added to each model. Leaflet closure was simulated and mitral valve geometry and biomechanics in peak systole were evaluated ( Fig A-B ). Results: On average, compared to pre-repair, PMA increased coaptation area by 30.6%, while the addition of annuloplasty increased this area by 85.1% with 40 mm, 138.1% with 38 mm, and 190.6% with 36 mm ring. Tenting area was reduced by 45.8% after PMA, 64.1% with the addition of 40 mm ring, 70.6% with 38 mm, and 76.5% with 36 mm ring. PMA reduced tension forces in chordae by 19.8%, while adding true-sized ring reduced forces by 16.4%. Annular downsizing allowed to reduce chordal forces by 31.2% with 38 mm, and 43.0% with 36 mm ring. Peak leaflet stress was observed on the P2 cusp, and PMA reduced it by 26.9%. True-sized ring reduced peak stress by only 10.7%, while 38 mm ring by 29.9%, and 36 mm by 43.7% ( Fig C ). Conclusions: Addition of true-sized ring to PMA further improved systolic valve geometry but not biomechanical parameters. Annular downsizing added to PMA was more beneficial for FMR repair, as it improved both mitral valve geometry and biomechanics.

Abstract 14766: Acute Impact of Transapical Ventricular Reshaping Device on Dilated Left Ventricle With Functional Mitral Regurgitation in Swine Model

Introduction: Functional mitral regurgitation (FMR) after myocardial infarction (MI) exacerbates morbidity and mortality. Correcting FMR plays a critical role in mitigating or reversing ventricular remodeling in MI patients with FMR. However, the COAPT trial demonstrated that FMR correction yields favorable results in smaller left ventricles (LVs) but not in severely dilated LVs. In this study, we evaluated the efficacy of a transapical device in MI swine model with FMR, which can perform papillary muscle approximation (PMA) and simultaneous reduction of LV volume. Methods: Yorkshire pig (n=15) were used in this study. MI was induced by percutaneous occlusion of the left circumflex artery, which caused LV dilatation and FMR by 3 months. The device was implanted through the LV apex to achieve PMA and LV reshaping until FMR was eliminated (Figure A). The immediate effects of the device implantation on the mitral valve and the LV were assessed using echocardiography and pressure-volume loops. Results: The device implantation decreased inter-papillary muscle distance from 24.5±3.8mm to 16.7±3.8mm (p&lt;0.0001), and significantly reduced FMR. Coaptation length significantly increased from 3.4±0.7mm to 5.5±1.2mm (p&lt;0.0001). End-diastolic volume decreased from 153±48ml to 117±33ml, a 23.5% reduction (p=0.0004). The end-systolic pressure-volume relationship and preload adjusted dP/dt max significantly increased after the device implant, indicating an improvement of LV contractility. There were no differences observed in Tau and end-diastolic pressure-volume relationship, depicting minimal acute impact on diastolic ventricular function after device implantation (Figure B and C). Conclusions: This transapical reshaping device effectively corrects FMR in very enlarged LVs, but also reduces systolic chamber wall stress by reducing the LV volume. An acute improvement in LV systolic function was observed, potentially indicating a therapeutic effect.

Multi-valve Libman-Sacks's endocarditis-related multiple, massive and fatal systemic embolization. A case report and a review of diagnostic work-up.

We reported a case of non-bacterial thrombotic endocarditis (NBTE) in a 37-year-old woman who presented with signs and symptoms of cardio-embolic cerebral stroke caused by a prothrombotic state due to underlying advanced uterine cancer. Multimodal imaging, including 3D-ecocardiography, as well as laboratory and cultural tests, were critical in making the diagnosis. After starting anticoagulation therapy with low molecular weight heparin (LMWH), the patient underwent surgical aortic valve replacement due to worsening aortic valve function, initial left ventricle enlargement, increasing dimensions, and mobility of vegetations. Unfortunately, vegetations relapsed on the aortic valve bio-prosthesis as well as the mitral leaflets, resulting in a final picture of multi-valve NBTE. The fatal outcome was due to a massive multiple limb embolism, which resulted in leg amputations and septical complications. Starting with the case, we present a brief overview of the pathology's presentation, treatment, management, and prognosis, as well as the diagnostic work-up.

Evaluation of Left Ventricular Mass in Different Cardiac Geometry Using Three-Dimensional Contrast-Enhanced Echocardiography.

A total of 69 patients were enrolled in the study, including 23 patients with hypertrophic cardiomyopathy (HCM), 26 patients with Left Ventricle (LV) enlargement comprising 16 dilated cardiomyopathy (DCM) patients and 10 ischemic cardiomyopathy (ICM) patients, and 20 control subjects. All patients underwent 2DE, contrast-enhanced 2DE (Contrast-2DE), 3DE, Contrast-3DE, and single photon emission computed tomography (SPECT) examinations. The 2DE-AL and 3DE methods measured the left ventricular mass (LVM). The results were compared with those measured by SPECT. The measured LVM of the 69 patients was systematically overestimated by 2DE-AL (177.4 ± 56.2 g), Contrast-2DE-AL (174.5 ± 55.5 g), 3DE (167.3 ± 59.2 g), and Contrast-3DE (154.2 ± 46.7 g) when compared with SPECT (148.5 ± 52.4 g) (P < 0.05), while Contrast-3DE provided the best agreement with SPECT in LVM measurement (r = 0.898, P < 0.001) and had the smallest deviation (5.7 ± 23.1 g). 3DE overestimated LVM more compared to Contrast-3DE in LV hypertrophy group (165.5 ± 37.9 g versus 153.5 ± 27.6 g, P = 0.003) and LV enlargement group (204.5 ± 69.3 g versus 183.5 ± 53.5 g, P = 0.006). For 2DE methods, there was no significant difference between the LVM obtained with or without contrast enhancement in control group (132.3 ± 23.6 g versus 128.4 ± 23.3 g), LV hypertrophy group (177.7 ± 38.6 versus 178.3 ± 30.9 g, P = 0.889), and LV enlargement group (211.9 ± 63.2 g versus 206.5 ± 66.0 g, P = 0.386). The difference between LVM measured by 2DE-AL and SPECT was the greatest (27.9 ± 34.0 g), especially in LV hypertrophy group and LV enlargement group (LV hypertrophy group 39.7 ± 26.0 g; LV enlargement group 24.2 ± 42.8 g). To conclude, Contrast-3DE and SPECT show greater consistency in LVM measurement, especially in cardiomyopathy, when compared with 2DE. Administering contrast can effectively reduce the overestimation of LVM by non-contrast DE.

Alpha-lipoic Acid Protects Against Chronic Alcohol Consumption-induced Cardiac Damage by the Aldehyde Dehydrogenase 2-associated PINK/Parkin Pathway.

Chronic alcohol intake contributes to high mortality rates due to ethanol-induced cardiac hypertrophy and contractile dysfunction, which are accompanied by increased oxidative stress and disrupted mitophagy. Alpha-lipoic acid (α-LA), a well-known antioxidant, has been shown to protect against cardiac hypertrophy and inflammation. However, little is known about its role and mechanism in the treatment of alcoholic cardiomyopathy. Here, we evaluated the role of α-LA in alcohol-induced cardiac damage by feeding mice a 4.8% (v/v) alcohol diet with or without α-LA for 6 w. Our results suggested that chronic alcohol consumption increased mortality, blood alcohol concentrations, and serum aldehyde levels, but a-LA attenuated the elevations in mortality and aldehydes. Chronic alcohol intake also induced cardiac dysfunction, including enlarged left ventricles, reduced left ventricular ejection fraction, enhanced cardiomyocyte size, and increased serum levels of brain natriuretic peptide, lactate dehydrogenase, and creatine kinase myocardial isoenzyme. Moreover, alcohol intake led to the accumulation of collagen fiber and mitochondrial dysfunction, the effects of which were alleviated by α-LA. In addition, α-LA intake also prevented the increase in reactive oxygen species production and the decrease in mitochondrial number that were observed after alcohol consumption. Chronic alcohol exposure activated PINK1/Parkin-mediated mitophagy. These effects were diminished by α-LA intake by the activation of aldehyde dehydrogenase 2. Our data indicated that α-LA helps protect cardiac cells against the effects of chronic alcohol intake, likely by inhibiting PINK1/Parkin-related mitophagy through the activation of aldehyde dehydrogenase 2.

The Role of Extracellular Signal-Regulated Kinase Pathways in Different Models of Cardiac Hypertrophy in Rats.

Cardiac hypertrophy develops following different triggers of pressure or volume overload. In several previous studies, different hypertrophy types were demonstrated following alterations in extracellular signal-regulated kinase (ERK) pathway activation. In the current study, we studied two types of cardiac hypertrophy models in rats: eccentric and concentric hypertrophy. For the eccentric hypertrophy model, iron deficiency anemia caused by a low-iron diet was implemented, while surgical aortic constriction was used to induce aortic stenosis (AS) and concentric cardiac hypertrophy. The hearts were evaluated using echocardiography, histological sections, and scanning electron microscopy. The expression of ERK1/2 was analyzed using Western blot. During the study period, anemic rats developed eccentric hypertrophy characterized by an enlarged left ventricle (LV) cavity cross-sectional area (CSA) (59.9 ± 5.1 mm2 vs. 47 ± 8.1 mm2, p = 0.002), thinner septum (2.1 ± 0.3 mm vs. 2.5 ± 0.2 mm, p < 0.05), and reduced left ventricular ejection fraction (LVEF) (52.6% + 4.7 vs. 60.3% + 2.8, p < 0.05). Rats with AS developed concentric hypertrophy with a thicker septum (2.8 ± 0.6 vs. 2.4 ± 0.1 p < 0.05), increased LV muscle cross-sectional area (79.5 ± 9.33 mm2 vs. 57.9 ± 5.0 mm2, p < 0.001), and increased LVEF (70.3% + 2.8 vs. 60.0% + 2.1, p < 0.05). ERK1/2 expression decreased in the anemic rats and increased in the rats with AS. Nevertheless, the p-ERK and the p-MEK did not change significantly in all the examined models. We concluded that ERK1/2 expression was altered by the type of hypertrophy and the change in LVEF.

Incident atrial functional mitral regurgitation in atrial fibrillation and sinus rhythm

Abstract Funding Acknowledgements Type of funding sources: None. Background Atrial functional mitral regurgitation (AFMR) has been associated with atrial fibrillation (AF) and heart failure with preserved ejection fraction. However, data on its incidence, risk factors, and clinical outcomes are scarce. Objective We aimed to study the incidence, risk factors and clinical significance of AFMR, defined as &amp;gt;mild functional MR in the absence of more than mild left ventricle enlargement or dysfunction, in AF and sinus rhythm (SR). Methods Adults with a new diagnosis of AF between 2010–2021 who had a transthoracic echocardiogram (TTE) were identified (n=57,109). Similarly, adults with no diagnosis of AF who had a TTE between 2010–2021 were identified for comparison (n= 364,767). Patients with &amp;gt;mild MR at baseline, primary mitral valve disease, cardiomyopathy, ≥moderate aortic valve disease, current or previous low ejection fraction, enlarged left ventricle, cardiac devices, previous cardiac surgeries, or with no follow up TTE ≥6 months from baseline were excluded. Furthermore, patients with AF had to have a TTE within 1 month of AF diagnosis. The presence of ≥2 of 4 abnormal diastolic function parameters [mitral septal e’ &amp;lt;0.07 m/sec, mitral septal E/e’ &amp;gt;15 in SR and &amp;gt;11 in AF, TR velocity &amp;gt;2.80 m/sec, left atrial volume index &amp;gt;34 ml/m2] was determined. Cox proportional hazards regression was used to determine risk factors associated with incident AFMR and all-cause death. Patients without the event of interest were censored at last follow up. Patients who developed &amp;gt;mild MR of other types (primary or functional ventricular) were censored at that time. Results Overall, 1,747 (median age 67 years; 34% females) patients with AF and 29,623 (median age 59; 51% females) in SR were included. Incident AFMR occurred in 167 patients with AF over median 3.1 (IQR 1.6–5.1) years [incidence rate of 2.6 per 100-person year] and in 780 patients in SR over median 3.1 (IQR 1.5–5.8) years [incidence rate 0.7 per 100-person year] (Figure 1). AF remained associated with AFMR after adjusting to confounding factors [age ≥65, female sex, ≥2 abnormal diastolic function parameters, and low hemoglobin; adjusted HR 3.23 (2.71–3.85)]. Independent risk factors associated with incident AFMR in AF were age ≥65, female sex, persistent AF, and ≥2 abnormal diastolic function parameters, whereas successful rhythm control without recurrence was a protective factor (Figure 2a). Risk factors for AFMR in SR were age ≥65 years, female sex, presence of ≥2 abnormal diastolic function parameters, and low hemoglobin (Figure 2a). Incident AFMR was independently associated with all-cause death in both AF and SR (Figure 2b). Conclusions AF confers more than 3-fold increase in the risk of AFMR. Diastolic dysfunction, older age, and female sex were independent risk factors for incident AFMR in both SR and AF. Paroxysmal AF and successful rhythm control were protective factors against AFMR in AF. AFMR is universally associated with worse mortality.

Effects of cardiac growth on electrical dyssynchrony in the single ventricle patient

Single ventricle patients, including those with hypoplastic left heart syndrome (HLHS), typically undergo three palliative heart surgeries culminating in the Fontan procedure. HLHS is associated with high rates of morbidity and mortality, and many patients develop arrhythmias, electrical dyssynchrony, and eventually ventricular failure. However, the correlation between ventricular enlargement and electrical dysfunction in HLHS physiology remains poorly understood. Here we characterize the relationship between growth and electrophysiology in HLHS using computational modeling. We integrate a personalized finite element model, a volumetric growth model, and a personalized electrophysiology model to perform controlled in silico experiments. We show that right ventricle enlargement negatively affects QRS duration and interventricular dyssynchrony. Conversely, left ventricle enlargement can partially compensate for this dyssynchrony. These findings have potential implications on our understanding of the origins of electrical dyssynchrony and, ultimately, the treatment of HLHS patients.