UNASSIGNED: Complete bundle branch block in individuals without structural heart disease is known as isolated complete bundle branch block. Isolated complete left bundle branch block (CLBBB) is correlated with ventricular dysfunction secondary to dyssynchrony; however, few studies have investigated isolated complete right bundle branch block (CRBBB), which was previously considered benign but was recently found to be associated with adverse cardiovascular outcomes. This study aimed to evaluate cardiac mechanical synchrony, and systolic and diastolic function in patients with isolated CRBBB and compare cardiac synchrony and function to patients with isolated CLBBB.
UNASSIGNED: This cross-sectional study was conducted at The First Hospital of China Medical University in Shenyang, China, from 2020 to 2021. A total of 44 isolated CRBBB patients, 44 isolated CLBBB patients, and 42 healthy subjects were enrolled in the study. Transthoracic echocardiography was performed in all subjects. Synchrony parameters, including the mechanical dispersion of the right ventricle [the standard deviation of time to the peak longitudinal strain of six right ventricular (RV) segments] and atrioventricular dyssynchrony parameter [the ratio of left ventricular (LV) diastolic filling time to the time interval between two adjacent R waves (RR interval) measured by tissue Doppler imaging]. RV and LV function were assessed by the global longitudinal strain (GLS) of six RV segments and 18 LV segments, and the ratio of the peak early diastolic flow velocity to annular velocity (E/e\') of the tricuspid valve and mitral valve. Statistical analyses were performed, including an analysis of variance, Pearson correlation analysis, and linear regression analysis.
UNASSIGNED: Compared with the healthy subjects, the mechanical dispersion of the right ventricle was significantly increased, and ventricular function was impaired as evidenced by the decreased RV GLS and LV GLS, and the increased E/e\' of the tricuspid valve and mitral valve in the isolated CRBBB patients (all P<0.001). Moreover, compared with the isolated CLBBB patients, the mechanical dispersion of the right ventricle and E/e\' of the tricuspid valve were increased, and RV GLS was significantly reduced in the isolated CRBBB patients (all P<0.001). Mechanical dispersion of the right ventricle was independently associated with RV GLS [coefficient, 0.13; 95% confidence interval (CI): 0.004-0.26; P=0.04] in the isolated CRBBB patients. RV GLS (coefficient, 0.10; 95% CI: 0.01-0.20; P=0.03) and the ratio of the LV diastolic filling time to the RR interval measured (coefficient, -0.30; 95% CI: -0.53 to -0.07; P=0.01) were independent factors of LV GLS.
UNASSIGNED: The isolated CRBBB patients had impaired cardiac mechanical synchrony and ventricular function, and more decreased RV synchrony and function than the isolated CLBBB patients. Right intraventricular synchrony was independently associated with RV systolic dysfunction in patients with isolated CRBBB. Atrioventricular synchrony and RV systolic function were independently associated with the LV systolic function. Therefore, comprehensive evaluations of echocardiography results and close monitoring is required for isolated CRBBB patients.

Left ventricular (LV) longitudinal function is mechanically coupled to the elasticity of the ascending aorta (AA). The pathophysiologic link between a stiff AA and reduced longitudinal strain and the subsequent deterioration in longitudinal LV systolic function is likely relevant in heart failure with preserved ejection fraction (HFpEF). The proposed therapeutic effect of freeing the LV apex and allowing for LV inverse longitudinal shortening was studied in silico utilizing the Living Left Heart Human Model (Dassault Systémes Simulia Corporation). LV function was evaluated in a model with (A) an elastic AA, (B) a stiff AA, and (C) a stiff AA with a free LV apex. The cardiac model simulation demonstrated that freeing the apex caused inverse LV longitudinal shortening that could abolish the deleterious mechanical effect of a stiff AA on LV function. A stiff AA and impairment of the LV longitudinal strain are common in patients with HFpEF. The hypothesis-generating model strongly suggests that freeing the apex and inverse longitudinal shortening may improve LV function in HFpEF patients with a stiff AA.

Pulmonary hypertension (PH) is rarely a cause of syncope. We highlight an unusual presentation of pulmonary hypertension where management was a veritable challenge. We present a case report of a 35-year-old female with a history of stage 2 hypertension, polycystic ovarian syndrome, and obesity who presented to the hospital with a six-month history of progressive shortness of breath, lower extremity swelling, and recurrent syncope. Further evaluation with transthoracic echocardiography showed features consistent with severe pulmonary hypertension. This untreated severe pulmonary hypertension culminated in cardiogenic shock due to right ventricular (RV) failure. Successful care in this patient population entails preventing the acute downward spiral of decompensated right ventricular failure.

During systole, longitudinal shortening of the left ventricle (LV) displaces the aortic root toward the apex of the heart and stretches the ascending aorta (AA). An in silico study (Living Left Heart Human Model, Dassault Systèmes Simulia Corporation) demonstrated that stiffening of the AA affects myocardial stress and LV strain patterns. With AA stiffening, myofiber stress increased overall in the LV, with particularly high-stress areas at the septum. The most pronounced reduction in strain was noted along the septal longitudinal region. The pressure-volume loops showed that AA stiffening caused a deterioration in LV function, with increased end-systolic volume, reduced systolic LV pressure, decreased stroke volume and effective stroke work, but elevated end-diastolic pressure. An increase in myofiber contractility indicated that stroke volume and effective stroke work could be recovered, with an increase in LV end-systolic pressure and a decrease in end-diastolic pressure. Longitudinal and radial strains remained reduced, but circumferential strains increased over baseline, compensating for lost longitudinal LV function. Myofiber stress increased overall, with the most dramatic increase in the septal region and the LV apex. We demonstrate a direct mechanical pathophysiologic link between stiff AA and reduced longitudinal left ventricular strain which are common in patients with HFpEF.

BACKGROUND: Robust risk assessment is crucial for the growing repaired tetralogy of Fallot population at risk of major adverse clinical outcomes; however, current tools are hindered by lack of validation. This study aims to develop and validate a risk prediction model for death in the repaired tetralogy of Fallot population.
RESULTS: Patients with repaired tetralogy of Fallot enrolled in the INDICATOR (International Multicenter Tetralogy of Fallot Registry) cohort with clinical, arrhythmia, cardiac magnetic resonance, and outcome data were included. Patients from London, Amsterdam, and Boston sites were placed in the development cohort; patients from the Toronto site were used for external validation. Multivariable Cox regression was used to evaluate factors associated with time from cardiac magnetic resonance until the primary outcome: all-cause death. Of 1552 eligible patients (n=1221 in development, n=331 in validation; median age at cardiac magnetic resonance 23.4 [interquartile range, 15.6-35.6] years; median follow up 9.5 years), 102 (6.6%) experienced the primary outcome. The multivariable Cox model performed similarly during development (concordance index, 0.83 [95% CI, 0.78-0.88]) and external validation (concordance index, 0.80 [95% CI, 0.71-0.90]) and identified older age at cardiac magnetic resonance, obesity, type of tetralogy of Fallot repair, higher right ventricular end-systolic volume index, and lower biventricular global function index as independent predictors of death. A risk-scoring algorithm dividing patients into low-risk (score ≤4) versus high-risk (score >4) groups was validated to effectively discriminate risk of death (15-year survival of 95% versus 74%, respectively; P<0.001).
CONCLUSIONS: This externally validated mortality risk prediction algorithm can help identify vulnerable patients with repaired tetralogy of Fallot who may benefit from targeted interventions.

Therapy with glucagon-like peptide 1 (GLP1) receptor agonists has raised great interest for its beneficial cardiovascular effects in preventing atherosclerosis and heart failure-related outcomes. However, while evidence about atherosclerosis consistently suggests a cardioprotective potential with class effect, controversies remain on its impact on heart failure. GLP1 receptor agonists appear to prevent hospitalization for new-onset heart failure and reduce symptoms in heart failure with preserved ejection fraction (as demonstrated by the recent STEP-HFpEF Trial). Still, GLP1 agonism has resulted in neutral or even harmful effects in patients with established heart failure with reduced ejection fraction (the LIVE trial). GLP1 receptor agonists benefit the cardiovascular system indirectly through their marked metabolic effects (improved weight management, glycemic control, blood pressure, systemic and tissue inflammation), while direct effects on the heart have been questioned. Nonetheless, weight loss alone achieved through GLP1 receptor agonists has failed in improving left ventricular functions. Tirzepatide is a dual agonist of GLP1 and glucose-dependent insulinotropic polypeptide, representing an innovative treatment option in diabetes with a major impact on weight loss and promising cardiovascular benefits. Whether this class of therapies is going to change the history of heart failure is an ongoing debate.

BACKGROUND: Long-term exposure to a high altitude environment with low pressure and low oxygen could cause abnormalities in the structure and function of the heart. Myocardial strain is a sensitive indicator for assessing myocardial dysfunction, monitoring myocardial strain is of great significance for the early diagnosis and treatment of high altitude heart-related diseases. This study applies cardiac magnetic resonance tissue tracking technology (CMR-TT) to evaluate the changes in left ventricular myocardial function and structure in rats in high altitude environment.
METHODS: 6-week-old male rats were randomized into plateau hypoxia rats (plateau group, n = 21) as the experimental group and plain rats (plain group, n = 10) as the control group. plateau group rats were transported from Chengdu (altitude: 360 m), a city in a plateau located in southwestern China, to the Qinghai-Tibet Plateau (altitude: 3850 m), Yushu, China, and then fed for 12 weeks there, while plain group rats were fed in Chengdu(altitude: 360 m), China. Using 7.0 T cardiac magnetic resonance (CMR) to evaluate the left ventricular ejection fraction (EF), end-diastolic volume (EDV), end-systolic volume (ESV) and stroke volume (SV), as well as myocardial strain parameters including the peak global longitudinal (GLS), radial (GRS), and circumferential strain (GCS). The rats were euthanized and a myocardial biopsy was obtained after the magnetic resonance imaging scan.
RESULTS: The plateau rats showed more lower left ventricular GLS and GRS (P < 0.05) than the plain rats. However, there was no statistically significant difference in left ventricular EDV, ESV, SV, EF and GCS compared to the plain rats (P > 0.05).
CONCLUSIONS: After 12 weeks of exposure to high altitude low-pressure hypoxia environment, the left ventricular global strain was partially decreased and myocardium is damaged, while the whole heart ejection fraction was still preserved, the myocardial strain was more sensitive than the ejection fraction in monitoring cardiac function.

Investigating ventricular diastolic properties is crucial for understanding the physiological cardiac functions in organisms and unraveling the pathological mechanisms of cardiovascular disorders. Ventricular stiffness, a fundamental parameter that defines ventricular diastolic functions in chordates, is typically analyzed using the end-diastolic pressure-volume relationship (EDPVR). However, comparing ventricular stiffness accurately across chambers of varying maximum volume capacities has been a long-standing challenge. As one of the solutions to this problem, we propose calculating a relative ventricular stiffness index by applying an exponential approximation formula to the EDPVR plot data of the relationship between ventricular pressure and values of normalized ventricular volume by the ventricular weight. This article reviews the potential, utility, and limitations of using normalized EDPVR analysis in recent studies. Herein, we measured and ranked ventricular stiffness in differently sized and shaped chambers using ex vivo ventricular pressure-volume analysis data from four animals: Wistar rats, red-eared slider turtles, masu salmon, and cherry salmon. Furthermore, we have discussed the mechanical effects of intracellular and extracellular viscoelastic components, Titin (Connectin) filaments, collagens, physiological sarcomere length, and other factors that govern ventricular stiffness. Our review provides insights into the comparison of ventricular stiffness in different-sized ventricles between heterologous and homologous species, including non-model organisms.

BACKGROUND: Point-of-care ultrasound has become a universal practice, employed by physicians across various disciplines, contributing to diagnostic processes and decision-making.
OBJECTIVE: To assess the association of reduced (<50%) left-ventricular ejection fraction (LVEF) based on prospective point-of-care ultrasound operated by medical students using an artificial intelligence (AI) tool and 1-year primary composite outcome, including mortality and readmission for cardiovascular-related causes.
METHODS: Eight trained medical students used a hand-held ultrasound device (HUD) equipped with an AI-based tool for automatic evaluation of the LVEF of non-selected patients hospitalized in a cardiology department from March 2019 through March 2020.
RESULTS: The study included 82 patients (72 males aged 58.5 ± 16.8 years), of whom 34 (41.5%) were diagnosed with AI-based reduced LVEF. The rates of the composite outcome were higher among patients with reduced systolic function compared to those with preserved LVEF (41.2% vs. 16.7%, p = 0.014). Adjusting for pertinent variables, reduced LVEF independently predicted the composite outcome (HR 2.717, 95% CI 1.083-6.817, p = 0.033). As compared to those with LVEF ≥ 50%, patients with reduced LVEF had a longer length of stay and higher rates of the secondary composite outcome, including in-hospital death, advanced ventilatory support, shock, and acute decompensated heart failure.
CONCLUSIONS: AI-based assessment of reduced systolic function in the hands of medical students, independently predicted 1-year mortality and cardiovascular-related readmission and was associated with unfavorable in-hospital outcomes. AI utilization by novice users may be an important tool for risk stratification for hospitalized patients.

This cohort study characterizes heterogeneity in cardiac function prior to sepsis and describes associations with hospitalization outcomes and mortality.