Search Results (552)

An atrial septal defect (ASD) is the most common congenital heart defect (CHD) diagnosed in adulthood. It is characterized by significant anatomical heterogeneity and complications that evolve over time. While often asymptomatic in children, the signs of adverse effects of ASD increase with age, including a greater risk of heart failure, stroke, atrial fibrillation (AF), and reduced life expectancy. ASD is traditionally considered a right-heart lesion due to long-term complications such as arrhythmias, right-sided heart failure, thromboembolism, and, in a subset of patients, pulmonary arterial hypertension (PAH). The pathophysiology of atrial shunts also affects the left heart due to volume overload and adverse ventriculo-ventricular interaction. Early diagnosis of interatrial septal anomalies is essential to prevent hemodynamic consequences and/or thromboembolic events. Electrocardiographic (ECG) findings play a crucial role in this early diagnosis. This narrative review aims to update clinicians on the latest evidence regarding the pathophysiological link between ASD and cardiac rhythm disorders, the nuances of optimal diagnostics, treatment options (surgical, interventional, pharmacological), and the need for long-term follow-up for patients with ASD. The review will determine the risk of conduction disorders compared to a healthy population and to compare the prevalences of conduction disorders, mortality, and pacemaker use in patients with closed ASDs versus those with open ASDs. Full article

Hypertension is a major risk factor for heart failure. Acetylation of p53 is known to regulate its activities. We have previously identified that p53 acetylation is required for cardiac remodeling in a mouse model of pressure overload-induced heart failure. Acetylation mutant p53 (p53aceKO) mice have been shown to have the ability to regulate SIRT3 KO-induced cardiac fibrosis. In the present study, we hypothesized that p53aceKO mice would exhibit cardiac protection and blunt cardiac fibrosis when subjected to Ang-II-induced hypertension. Control and p53aceKO mice received either a micro-osmotic pump implant administering Ang-II for 28 days or a sham procedure. Blood pressure was measured weekly, and echocardiography was performed every two weeks. Mice were euthanized and hearts were processed for histological analysis. While both control and p53aceKO mice receiving Ang-II exhibit increased systolic and diastolic blood pressures, control mice also demonstrate increases in ejection fraction and fractional shortening compared to the sham, while p53aceKO mice do not. Furthermore, control mice receiving Ang-II exhibit decreased left ventricular diameter and volume at end-systole and end-diastole, as well as thickening of both the anterior and posterior walls, while p53aceKO mice exhibit no significant changes in any of these parameters. Additionally, p53aceKO mice do not exhibit the Ang-II infusion-induced cardiac fibrosis seen in control mice treated with Ang-II. Mutation of p53 acetylation is protective against Ang-II infusion-induced cardiac fibrosis and dysfunction in mice. Acetylated p53 may, therefore, be a novel therapeutic target to address complications in the heart associated with hypertension. Full article

Left ventricular (LV) hypertrabeculation is increasingly recognized as a phenotype that may reflect physiological adaptation, particularly in athletes exposed to chronic overload, although its functional relevance remains uncertain. This study evaluated the prevalence of excessive trabeculation and its physiological correlation with LV remodeling. We conducted a single-center, cross-sectional study involving 320 Olympic-level athletes without cardiovascular disease. All underwent cardiac magnetic resonance (CMR). Hypertrabeculation was defined by the Petersen criteria. Athletes meeting these criteria were classified as hypertrabeculated and compared with non-hypertrabeculated matched for age, sex, and sport category. LV morphology, function, strain parameters, and hemodynamic forces (HDFs) were analyzed. Hypertrabeculation was identified in 9% of the cohort. No significant differences were observed between groups for training exposure (p = 0.262), body surface area (p = 0.762), LV volumes (end-diastolic volume indexed p = 0.397 end-systolic volume indexed p = 0.118), ejection fraction (p = 0.101), mass (p = 0.919), sphericity index (p = 0.419), myocardial wall thickness (p = 0.394), tissue characterization (T1 mapping p = 0.366, T2 mapping p = 0.833), global longitudinal strain (GLS p = 0.898), global circumferential strain (GCS p = 0.219), or HDFs. All values were within the normal range. In our cohort, LV hypertrabeculation, evaluated by CMR, was relatively common but not associated with structural or functional abnormalities, supporting its interpretation as a benign variant in asymptomatic athletes with normal cardiac function. Full article

Purpose: While peak oxygen uptake ($\stackrel{.}{\mathrm{V}}$O_2peak) is the gold standard method for assessing exercise tolerance, there is a tendency for underestimation. Several other cardiopulmonary exercise testing (CPET) variables may provide additive prognostic value beyond $\stackrel{.}{\mathrm{V}}$O_2peak alone. The aim of this study was to examine if alternative CPET indices of exercise tolerance are (a) impaired in people with T2D and (b) independently associated with measures of cardiovascular structure and function measured via echocardiography and cardiac MRI. Methods: Participants with type 2 diabetes (T2D) and healthy controls underwent cardiac magnetic resonance imaging, transthoracic echocardiography, and a CPET. Multiple linear regression was used to determine the relationship between indices of exercise tolerance and markers of cardiovascular structure and function. Results: A total of 84 people with T2D and 36 healthy volunteers were included in the analysis. All CPET outcomes were worse in those with T2D vs. the controls. Three CPET outcomes were associated with markers of cardiovascular structure and function: $\stackrel{.}{\mathrm{V}}$O₂ recovery with mean aortic distensibility (β = 0.218, p = 0.049); heart rate recovery with early filling velocity on transmitral Doppler/early relaxation velocity (β = −0.270, p = 0.024), left ventricular mass/volume ratio (β = −0.248, p = 0.030) and mean aortic distensibility (β = 0.222, p = 0.029); and $\stackrel{.}{\mathrm{V}}$O₂ at the ventilatory threshold with myocardial perfusion reserve (β = 0.273, p = 0.018). Perspective: These lesser-used CPET indices could be used to identify which people with T2D are at elevated risk of progression to symptomatic heart failure. However, larger longitudinal studies are required to confirm these findings and their potential clinical application. Full article

Myocardial hypoxia is a major cause of cardiac dysfunction, triggering cellular injury and apoptosis. This study aims to investigate the effects of subacute hypoxia on cardiac remodeling and mitochondrial oxygen consumption. This study is based on a rabbit experimental model. Hypoxia was induced using a rabbit tracheal stenosis model. Endotracheal intubation with a 1.5 cm segmented tube wrapped with an absorbable hemostat was used to generate tracheal stenosis in six rabbits. Sham controls (n = 3) underwent tracheotomy, with the tracheal exposure site being sutured immediately. After 1 week, the tube was removed. Echocardiography and mitochondrial function from both groups were morphologically and functionally analyzed at 2 weeks after endoscopic confirmation of tracheal stenosis. Compared to sham group, tracheal stenosis group showed significantly reduced interventricular septal wall thickness (2.3 ± 0.1 mm vs. 2.7 ± 0.2 mm, p = 0.08) and enlarged left ventricular end-diastolic volume (5.86 ± 0.58 mL vs. 5.39 ± 0.18 mL, p = 0.46) with reduced left ventricular ejection fraction (54.5 ± 5.3% vs. 66.9 ± 4.0%, p = 0.005). The tracheal stenosis group showed significantly reduced mitochondrial oxygen consumption at state 3 with reduced respiratory control ratio. Caspase activities (caspase-9 and caspase-3) were increased in the tracheal stenosis group than in the sham group. Subacute hypoxia induced by the tracheal stenosis model causes cardiac remodeling and mitochondrial dysfunction through apoptotic pathways. This study suggests that management of hypoxia could prevent cellular apoptosis and cardiac dysfunction. Full article

Background: In arterial hypertension (AH), adverse hemodynamic consequences in the left atrium (LA) are often observed. The prognostic significance of functional vs. structural LA abnormalities among high-risk AH patients (with heart failure with preserved ejection fraction [HFpEF]) are not clearly defined. Objective: to compare the prognostic significance of structural vs. functional LA indices in hypertensive patients with HFpEF. Methods: We retrospectively selected 274 hypertensive patients with AH, HFpEF, and sinus rhythm. The primary outcome was a composite of all-cause mortality and HF hospitalization; the median follow-up was 4.3 (2.5–6.5) years. Results: The composite endpoint occurred in 133 patients (49%). Kaplan–Meier analysis revealed significantly lower event-free survival rates in patients with lower functional LA reservoir strain [LASr] (≤median) compared to patients with higher LASr (p < 0.001). Patients with higher structural LA volume index (LAVI) as well as with higher LV filling pressure (E/e′ ratio) or more severe left ventricular (LV) hypertrophy (higher LV mass index) had a similar prognosis to patients with lower values. In multivariable analysis, decreased LASr and paroxysmal atrial fibrillation (AF) were independently associated with adverse outcomes after accounting for potential confounders (for both p < 0.05). Conclusions: Among patients with AH and HFpEF, the functional LA parameter LASr seems to be more effective than the structural LA parameter LAVI, or traditional indexes of LV hypertrophy and filling pressure, in predicting prognosis. Full article

Extracellular volume fraction (ECV) analysis on computed tomography (CT) is now available. The purpose of this study was to assess the usefulness of CT-derived ECV analysis for predicting outcomes in patients with hypertrophic cardiomyopathy (HCM). One hundred and one HCM patients (67 males, 66 ± 11 years old) who received cardiac CT between January 2009 and December 2021 were included. We measured left ventricular (LV) ECV (LV-ECV) on CT and investigated the relationship between LV-ECV and the major adverse cardiac events (MACE) after CT. Fifteen patients (15%) experienced MACE. The patients with MACE had a significantly higher LV-ECV, left atrial diameter, LV end-systolic diameter, and lower LVEF than those without MACE. The proportion of dilated phase HCM was significantly higher in the patients with MACE than those without MACE. LV-ECV and LVEF were significant predictors of MACE based on the multivariate analysis by Cox proportional hazards model. The optimal threshold of LV-ECV to predict MACE was 37.6% based on the receiver operating characteristic analysis. The patients with LV-ECV ≥ 37.6% (30 patients) experienced significantly higher MACE than those with LV-ECV < 37.6% (p < 0.001). CT-derived ECV analysis suggested potential usefulness for predicting MACE in patients with HCM. Full article

Background/Objectives: Telomeres and the enzyme telomerase play essential roles in cellular aging and cardiovascular health. Physical activity is thought to influence telomere dynamics via upregulation of the hTERT gene, which encodes the catalytic subunit of telomerase. However, data on this relationship in middle-aged endurance athletes remain limited. This study aimed to investigate the association between long-term endurance training, cardiac structural adaptations, and hTERT gene expression in middle-aged elite athletes. Methods: A total of 38 middle-aged elite runners and 37 age-matched sedentary controls were enrolled. Echocardiographic assessments, VO₂peak measurements, and hTERT gene expression analysis using RT-PCR were conducted. Left ventricular mass (LVM), wall thicknesses, and cardiac volumes were compared, and correlations with hTERT expression were analyzed. Results: Athletes demonstrated significantly higher VO₂peak and echocardiographic parameters including LVEDD, LV mass, and wall thicknesses (p < 0.05). hTERT gene expression was 2.06-fold higher in athletes compared to controls. Significant positive correlations were observed between hTERT expression and VO₂peak, LVM, LV wall thicknesses, and right ventricular parameters. Conclusions: These findings suggest that regular aerobic exercise may contribute to both improved cardiovascular performance and cellular longevity by enhancing telomerase-related mechanisms. Full article

High induction doses of propofol (PPF) may cause adverse effects. Co-induction protocols can reduce doses and enhance the beneficial profile of each drug. This study compared the induction quality, clinical, and echocardiographic effects of two rapid co-inductions in healthy, unpremedicated dogs. Baseline cardiorespiratory and echocardiographic variables were recorded. Dogs randomly received rapid intravenous PPF (2.2 mg/kg) with either dexmedetomidine (3 µg/kg) (PROPODEX; n = 12) or butorphanol (0.4 mg/kg) (PROPOBUT; n = 12). Induction quality, additional PPF dose, intubation time, cardiorespiratory parameters (2, 5, 10, 15, 20 min), and recovery quality were recorded. A second echocardiography was performed 5 min after induction. Induction quality was significantly higher in PROPODEX, with significantly lower additional PPF requirements and shorter intubation time. In PROPODEX, heart rate significantly decreased from baseline and was significantly lower than PROPOBUT, while arterial blood pressures significantly increased in PROPODEX and decreased in PROPOBUT from baseline. PROPOBUT significantly reduced left ventricular (LV) diastolic volumes and increased E/A ratio, while PROPODEX significantly increased LV systolic diameter and volumes, and significantly decreased fractional shortening. Recovery was significantly faster and better in PROPODEX. PROPOBUT preserved cardiac function but caused hypotension. PROPODEX provided superior induction and recovery quality, and cardiorespiratory stability, with only mild systolic function depression. Full article

Objectives: Our aim was to determine imaging-derived parameters from echocardiography associated with the presence of atrial fibrosis in a cohort of atrial fibrillation (AF) patients. Methods: Initially, 123 participants were included in this prospective cross-sectional observational study (clinicaltrials.gov: NCT03584126); after exclusion criteria, 112 full datasets were analyzed. All participants underwent clinical evaluation, echocardiography, and cardiac MRI. Overall, 29 patients with AF and left atrial (LA) fibrosis at MRI, 37 with AF and without LA fibrosis at MRI, and 46 healthy controls were included in the final database. Results: The cardiac structural parameters as assessed by MRI were not significantly different between AF patients with and without fibrosis, apart from LA volume. The area under the curve (AUC) reached a value of 0.69 when using body-surface-area-indexed LA volume (LAVi) determined by echocardiography as a factor associated with LA fibrosis in AF patients. Moreover, when detecting LA fibrosis using LAVi, an optimal cut-off value of 42.7 mL/m² was obtained, resulting in 41.67% specificity and 88.46% sensitivity with a total accuracy of 65.06%. Testing BSA-indexed left ventricular mass (LVMi) as a factor associated with LA fibrosis, the optimal cut-off value was 140.2 g/m², with 76.92% sensitivity, 58.33% specificity and 67.62% total accuracy for the discrimination between AF patients with and without LA fibrosis. A strong association between body-surface-area-indexed left atrial volume (LAVi) and the presence of atrial fibrillation was identified (54.5 mL/m² vs. 29.8 mL/m² in controls, p-value < 0.0001). Conclusion: LA volume indexed to BSA could be a promising tool for the identification of cardiac fibrosis in AF patients. Full article

Background: There is no information on how the dose of exercise training prior to myocardial infarction (MI) affects cardioprotection. Objective: This study aimed to evaluate the cardioprotective role of different volumes of exercise training prior to MI. Methods: Wistar female rats were allocated to one of the following groups: SHAM (not trained and undergoing simulated MI surgery), NT+MI (untrained and undergoing MI surgery), T60+MI (trained 60 min per session and undergoing MI surgery), T90+MI (trained 90 min per session and undergoing MI surgery), and T180+MI (trained 180 min per session and undergoing MI surgery). The training protocol was performed in a swimming pool for eight weeks. On the seventh day after MI, the animals underwent left ventricular (LV) structural and functional evaluation and were euthanized for molecular analyses. Results: Exercise training groups had greater VO₂peak and LV mass than did the SHAM group. The MI size did not differ statistically among the experimental groups. Compared with the SHAM group, all the MI groups presented a lower LV shortening fraction. LV systolic pressure was significantly lower in the T60+MI group than in the SHAM and T180+MI groups. The +dP/dt of the LV was significantly lower in the NT+MI, T60+MI, and T90+MI groups than in the SHAM group. We did not find significant changes in the inflammatory mediators and oxidative stress markers as well as proteins involved in calcium handling. Conclusions: Exercise training prior to MI enhanced cardiorespiratory fitness and induced LV hypertrophy, however, regardless of volume, was unable to counteract the detrimental effects of MI. Full article

Background and Objectives: Atrial fibrillation (AF) is a common arrhythmia in patients with mitral valve prolapse (MVP) after mitral valve repair surgery and is associated with adverse cardiac outcomes. Early identification of patients at high risk for AF development after repair surgery is crucial for early treatment and follow-up of these patients. This study aimed to identify ECG predictors of AF in patients with MVP following mitral valve repair surgery. Materials and Methods: This retrospective, non-randomized study included 62 patients who underwent mitral valve repair for MVP. The patients’ ECGs were analyzed preoperatively and at 1, 3, and 6 months post-surgery to identify patients who developed AF. AF was diagnosed based on ECG findings or Holter monitoring. The P wave dispersion, P wave peak time (PWPT), P wave duration, PR interval, P wave terminal force in lead V1 (PWTF), interatrial block, P wave axis, biphasic P waves in inferior leads, QRS duration, corrected QT interval (QTc), fragmented QRS (fQRS), and ST segment-T wave abnormalities were analyzed on baseline ECG as AF predictors. Results: The PWPT, P wave dispersion, and maximum P wave duration were significantly longer on preoperative ECG in patients who developed AF postoperatively compared to those who did not. Biphasic P waves were more frequently observed in patients who developed AF postoperatively. Univariate analysis identified biphasic P waves, P wave dispersion, maximum P wave duration, PWPT, and left ventricular ejection fraction (LVEF) as potential predictors of postoperative AF. However, multivariate analysis revealed that P wave dispersion, PWPT, and left atrial volume index (LAVI) were independent predictors of AF in six months after mitral valve repair. No significant changes were observed in QRS duration, QT interval, or the fQRS. Conclusions: The P wave dispersion, PWPT, and LAVI are significant ECG predictors of AF following mitral valve repair surgery in MVP patients. These ECG markers may help identify individuals at higher risk for postoperative AF, allowing for targeted monitoring and management strategies. Full article

Background: Non-ischemic dilated cardiomyopathy (DCM) is a heterogeneous myocardial disease associated with variable progression and an increased risk of major adverse cardiovascular events (MACEs). Cardiovascular magnetic resonance (CMR) allows the comprehensive evaluation of myocardial structure, function, and fibrosis. This prospective study aimed to assess the prognostic value of CMR-derived global longitudinal strain (GLS) and left ventricular (LV) torsion in patients with DCM. Methods: We prospectively enrolled 150 patients with newly diagnosed non-ischemic DCM and 100 age- and sex-matched healthy controls. All participants underwent standardized CMR protocols including cine imaging, late gadolinium enhancement (LGE), and feature-tracking analysis for myocardial deformation. LV volumes, ejection fraction (LVEF), GLS, and LV torsion were quantified. The primary endpoint was the first occurrence of MACE, defined as cardiac death, sustained ventricular arrhythmia, or heart failure hospitalization. The median follow-up was 33 months. Results: Compared to controls, DCM patients had significantly impaired LV function and myocardial mechanics: lower LVEF (35.1% vs. 65.2%, p < 0.001), reduced GLS (−9.2% vs. −19.7%, p < 0.001), and diminished LV torsion (1.04 vs. 1.95 °/cm, p < 0.001). GLS ≤ −8.6% was independently associated with increased MACE risk (adjusted hazard ratio [HR]: 1.09; 95% confidence interval [CI]: 1.01–1.61; p < 0.01). Similarly, reduced LV torsion predicted adverse events (adjusted HR: 1.37; 95% CI: 1.03–1.81; p < 0.01). The presence of LGE (42% of patients) further stratified risk (HR: 2.86; 95% CI: 1.48–12.52; p < 0.001). Conclusions: CMR-derived GLS and LV torsion are strong, independent predictors of adverse outcomes in DCM. Their integration into routine imaging protocols enhances risk stratification beyond conventional metrics such as LVEF and LGE. These findings support the use of myocardial deformation analysis in the comprehensive evaluation of patients with DCM. Full article

The interaction between the left ventricle (LV) and aorta is critical for cardiovascular performance, particularly under pathophysiological conditions. However, how changes in LV mechanics, including preload and afterload, affect aortic function via LV–aorta interactions remains poorly understood due to the challenges associated with varying loading conditions in vivo. To overcome these limitations, the effects of varying LV preload or afterload on LV and aortic functions via LV–aorta interactions are quantified using ex vivo beating rat heart experiments in this study. In five healthy rat hearts under retrograde Langendorff and antegrade working heart perfusion, LV pressure, volume, aortic pressure, and aortic blood flow were measured. Key findings include the following: (1) under Langendorff perfusion, aortic flow increased linearly with LV developed pressure (DP), with a slope of 4.04 mmHg·min/mL; under working heart constant-pressure perfusion (2) a 12.4% increase in afterload decreased aortic flow by 58.8%, indicating that elevated aortic pressure significantly impedes aortic flow; (3) a 10.4% increase in preload enhanced aortic flow by 44.2%, driven primarily by an increase in LV DP that promoted forward flow. These results suggest that aortic pressure predominantly influences aortic flow under varying afterload conditions, whereas LV DP plays the dominant role in regulating aortic flow under different preload conditions. These findings demonstrate that the heart’s loading conditions strongly impact aortic blood flow. Specifically, elevated LV afterload can severely limit forward blood flow, while increased LV filling with increased LV preload can enhance blood flow, highlighting the importance of managing both afterload and preload in conditions such as hypertension and heart failure with preserved ejection fraction. This pilot study also established the feasibility of experimental platforms for coronary and ventricular function analysis. Full article

Background/Objectives: Survivors of sepsis can develop left ventricular (LV) systolic function with focal myocardial fibrosis. The relationship between diffuse myocardial fibrosis or oedema and LV systolic function remains unknown in this patient cohort. This study sought to address this knowledge gap using cardiovascular magnetic resonance (CMR) parametric mapping methods. Methods: Sepsis survivors who underwent CMR at a UK cardiac centre were included. CMR images analysed include cines, native T1-mapping, native T2-mapping, and post-contrast T1-mapping. Synthetic extracellular volume (ECV) fraction was also estimated. Native myocardial T1 values, native myocardial T2 values, and ECV values were compared against LV ejection fraction (LVEF). Results: Of the 37 sepsis survivors (age 53 ± 16 years old; 57% males), the mean left ventricular ejection fraction (LVEF) was 55% (IQR 43–62), and 43% of the patients had LV systolic dysfunction (LVEF < 50%). Mean native myocardial T1 values were 1055 ± 65 ms (septal) and 1051 ± 60 ms (global). Mean synthetic ECV values were 0.30 ± 0.04. Mean native myocardial T2 values were 52 ± 7 ms (septal) and 53 ± 6 ms (global). Septal and global native myocardial T1 values were not significantly correlated with LVEF (rho = 0.080, p = 0.637; rho = 0.036, p = 0.831, respectively). Synthetic ECV was not significantly correlated to LVEF (rho = −0.082; p = 0.723). Septal and global native myocardial T2 values were weakly correlated with LVEF (rho = 0.261, p = 0.281; rho = 0.216, p = 0.375, respectively). On ROC analysis, the performance of native myocardial T1 values, ECV, and native myocardial T2 values for predicting LV dysfunction was modest (AUC: 0.53 ± 0.10, 0.54 ± 11, and 0.68 ± 0.14; all p > 0.05, respectively). Conclusions: CMR markers of diffuse myocardial fibrosis (native T1-mapping and ECV) and myocardial oedema (native T2-mapping) have weak relationships with left ventricular systolic function in this study cohort of sepsis survivors. Further work is needed to better assess the role of diffuse myocardial fibrosis and oedema in the pathophysiology of post-sepsis cardiomyopathy. Full article