End-diastolic Left Ventricular Research Articles

99mTc-HFAPi SPECT imaging predicts left ventricular remodeling after acute myocardial infarction

BackgroundDespite improved treatments for acute myocardial infarction (AMI), myocardial fibrosis remains a key driver of adverse left ventricular (LV) remodeling and increased mortality. Fibroblast activation and proliferation significantly contribute to this process by enhancing cardiac fibrosis, which can lead to detrimental changes in LV structure. This study evaluates the effectiveness of 99mTc-labeled fibroblast activation protein inhibitor (99mTc-HFAPi) SPECT imaging in predicting LV remodeling over 12 months in post-AMI patients. MethodsA cohort of 58 AMI patients (46 males, median age 61 [53, 67] years) underwent baseline 99mTc-HFAPi imaging (5 ± 2 days post-MI), perfusion imaging (6 ± 2 days post-MI), and echocardiography (2 ± 2 days post-MI). Additionally, 15 patients had follow-up 99mTc-HFAPi and perfusion imaging, while 30 patients had follow-up echocardiography. Myocardial 99mTc-HFAPi activity was assessed at the patient level. LV remodeling was defined as a ≥10% increase in LV end-diastolic diameter (LVEDD) or LV end-systolic diameter (LVESD) from baseline to follow-up echocardiography. ResultsAMI patients displayed localized but non-uniform 99mTc-HFAPi uptake, exceeding perfusion defects. Baseline 99mTc-HFAPi activity exhibited significant correlations with BNPmax, LDHmax, cTNImax, and WBCmax, inversely correlating with LVEF. After 12 months, 11 patients (36.66%) experienced LV remodeling. Univariate regression analysis demonstrated an association between baseline 99mTc-HFAPi uptake extent and LV remodeling (OR = 2.14, 95%CI, 1.04, 4.39, P = 0.038). Conclusions99mTc-HFAPi SPECT imaging holds promise in predicting LV remodeling post-MI, providing valuable insights for patient management and prognosis.

Central Obesity is Associated with Increased Left Ventricular Maximal Wall Thickness and Intrathoracic Adipose Tissue Measured with Cardiac Magnetic Resonance.

Central obesity (CO), characterized by an increased waist circumference increases the risk of cardiovascular disease (CVD) and morbidity, yet the underlying mechanisms are not fully understood. CO is often associated with general obesity, hypertension, and abnormal glucose tolerance, confounding the independent contribution of CO to CVD. We investigated the relationship of CO (without associated disorders) with left ventricular (LV) characteristics and intrathoracic adipose tissue (IAT) by cardiac magnetic resonance. LV characteristics, epicardial (EAT), and mediastinal adipose tissue (MAT) were measured from 29 normoglycemic, normotensive males with CO but without general obesity (waist circumference >100 cm, body mass index (BMI) <30 kg/m2) and 18 non-obese male controls. LV maximal wall thickness (LVMWT) and IAT but not LV mass or volumes were increased in CO subjects compared to controls (LVMWT, 12.3±1.2 vs. 10.7±1.5 mm, p < 0.001; EAT, 5.5±3.0 vs. 2.2±2.0 cm2, p = 0.001; MAT, 31.0±12.8 vs. 15.4±10.7 cm2, p < 0.001). The LVMWT was ≥12 mm in 69% of subjects with CO and 22% of controls (p = 0.002). In CO suspects, EAT correlated inversely with LV end-diastolic volume index (r = -0.403, p = 0.037) and LV stroke volume (SV) (r = -0.425, p = 0.027). MAT correlated inversely with SV (r = -0.427, p=0.026) and positively with LVMWT (r = 0.399, p = 0.035). Among CO subjects, the waist-to-hip ratio (WHR) was an independent predictor of LVMWT (B = 22.4, β = 0.617, p < 0.001). The optimal cut-off with Youden's index for LV hypertrophy was identified at WHR 0.98 (sensitivity 85%, specificity 89%). CO independent of BMI is associated with LV hypertrophy and intrathoracic adipose tissue contributing to cardiovascular burden.

Eicosapentaenoic acid and Arachidonic acid Protection Against Left Ventricle Pathology: the Multi-Ethnic Study of Atherosclerosis.

We have shown that ω3 polyunsaturated fatty acids (PUFAs) reduce risk for heart failure, regardless of ejection fraction status. Ventricular remodeling and reduced ventricular performance precede overt hear failure, however there is little insight into how PUFAs contribute to maladaptive signaling over time. PUFAs are agonists for regulatory activity at g-protein coupled receptors such as Ffar4, and downstream as substrates for monooxygenases (e.g lipoxygenase, cytochrome p450, or cyclooxygenase (COX)) which mediate intracellular adaptive signaling. Plasma phospholipid PUFA abundance at Exam 1 as mass percent EPA, DHA, and arachidonic acid (AA) from the Multi-Ethnic Study of Atherosclerosis (MESA) were evaluated using pathway modeling to determine the association with time-dependent changes in left ventricular (LV) mass (LVM), end-diastolic LV volume (EDV), and end-systolic volume (ESV) measured by cardiac MRI at Exams 1 and 5. Ejection fraction (EF) and mass:volume (MV) were calculated posteriorly from the first three. 2,877 subjects had available MRI data. Participants with low AA and EPA had accelerated age-dependent declines in LVM. Males with low AA and EPA also had accelerated declines in EDV, but among females there was no PUFA association with EDV declines and exam 5 EDV status was positively associated with AA. Both sexes had nearly the same positive association of AA with changes in ESV. Plasma phospholipid AA and EPA are prospectively associated with indices of heart remodeling, including ventricular remodeling and performance. Combined AA and EPA scarcity was associated with the most accelerated age-related changes and exam 5 status, while the greatest benefits were found among participants with both PUFAs. This suggests that both PUFAs are required for optimal slowing of age-related declines in ventricular function.

Association Between Major Adverse Cardiovascular Events and Left Ventricular Mass Index in Patients Who Have Undergone Coronary Computed Tomography Angiography: From the FU-CCTA Registry.

Left ventricular mass (LVM) is a predictor of future cardiovascular risk. We determined the association between LVM measured by coronary computed tomography angiography (CCTA) and the prognosis in patients who have undergone CCTA for screening of coronary artery disease (CAD). We performed a prospective cohort study. Five hundred twenty consecutive patients who underwent CCTA at Fukuoka University Hospital (FU-CCTA registry) were enrolled. They were clinically suspected of having CAD or had at least one cardiovascular risk factor, and were a follow-up of up to 5 years. Equal to more than 50% of coronary stenosis as assessed by CCTA was diagnosed as CAD. Using CCTA, LVM index (LVMI), LV ejection fraction (LVEF), LV end-diastolic volume (LVEDV) and LV end-systolic volume were measured. The primary endpoint was major adverse cardiovascular events (MACEs: including all causes of death, ischemic stroke, acute myocardial infarction and coronary revascularization). The patients were divided into non-MACEs and MACEs groups. The non-MACEs and MACEs groups consisted of 478 and 42 patients, respectively. Percent of CAD in the MACEs group was significantly higher than that in the non-MACEs group. The MACEs group showed significantly higher LVMI and tended to have a lower LVEF and LVEDV than the non-MACEs group. Although LVMI was not associated with MACEs in all patients, LVMI was independently associated with MACEs in males (odd ratio: 1.018, 95% confidence interval: 1.002 - 1.035, P = 0.030), but not females. Evaluation of LVMI by CCTA may be useful for predicting MACEs in males.

Predicting the response to cardiac resynchronization therapy using in silico heart models: pilot study of comparison between in silico and real cardiac resynchronization therapy outcomes

Abstract Background Cardiac resynchronization therapy (CRT) is treatment for patients with heart failure and left ventricular (LV) dyssynchrony. The objective of this study is to evaluate the feasibility of an in silico electromechanical heart model to predict CRT outcomes. Methods The three-dimensional heart geometries of 11 patients (age, 64.0±10.7 years, 4 men) with CRT were constructed from cardiac computed tomography images. We coupled cardiac electrical excitation and mechanical contraction with vascular hemodynamics using a lumped parameter model. We predicted the LV end-diastolic and end-systolic volumes and LV ejection fraction (LVEF) after CRT implantation using the in silico CRT simulation model. We compared the in silico CRT outcomes with the real CRT outcomes. Results Two patients were in silico CRT responders, and those 2 patients were also real CRT responders. Nine patients were in silico CRT non-responders, 8 who were real CRT non-responders, and 1 who was a real CRT responder. The in silico CRT outcomes agreed with the real CRT outcomes in 10 of 11 patients. The positive and negative predictive values and accuracy of the in silico CRT model were 100%, 88.9%, and 90.9%, respectively. Conclusion The in silico CRT simulation model is feasible for predicting real CRT outcomes.In silico CRT simulation model generatioAn example (patient No. 2) of LV (black

Incremental Prognostic Value of Left Atrial Strain in Patients With Suspected Myocarditis and Preserved Left Ventricular Ejection Fraction.

Analysis of left atrial (LA) strain and left atrioventricular coupling index (LACI) have prognostic value in cardiovascular diseases. However, the prognostic value of LA strain and LACI in patients with suspected myocarditis and preserved left ventricular ejection fraction (LVEF) is unclear. To investigate the prognostic value of LA strain and LACI in patients with suspected myocarditis and preserved LVEF in comparison with conventional MRI outcome predictors. Retrospective. One hundred sixty-five patients with clinically suspected myocarditis and preserved LVEF with available follow-up data. Steady-state free precession cine and phase-sensitive inversion recovery segmented gradient echo late gadolinium enhancement sequences at 3.0 T. Left ventricular (LV) and LA strain were evaluated using feature tracking. LACI was calculated as the ratio of LA and LV volumes at LV end-diastole. Patients were followed-up with the primary endpoint being major adverse cardiovascular events (MACE). Independent-samples t-test and Mann-Whitney U test to compare patients with and without MACE, receiver operating characteristic (ROC) curve analysis to define high/low risk groups, Kaplan-Meier survival analysis and Cox proportional hazards regression to assess prognosis. A P value of <0.05 was considered statistically significant. The associations of LV strain parameters (including global radial, circumferential, and longitudinal strain) and LACI with MACE were not significant (P = 0.511, 0.108, 0.148, and 0.847, respectively). An optimal LA conduit strain (Ԑe) cutoff value of 10.4% was identified to best classify patients into low- and high-risk groups. Only Ԑe was significantly associated with MACE in both univariable (hazards ratio [HR] 0.936, 95% confidence interval [CI] 0.884-0.991) and multivariable Cox survival analyses (HR 0.937, 95% CI 0.884-0.994). LA conduit strain has prognostic value in patients with suspected myocarditis and preserved LVEF, incremental to conventional MRI outcome predictors, whereas LACI was not associated with MACE occurrence. 3 TECHNICAL EFFICACY: Stage 2.

Diagnosis and treatment of feline persistent ductus arteriosus: a retrospective evaluation of 17 cats

The objective of this study was to evaluate the signalement, clinical features, and echocardiographic findings of cats diagnosed with patent ductus arteriosus (PDA) as well as short- and medium-term outcome after successful ligation of the PDA. Over a 10-year period 17 cats were diagnosed with PDA by transthoracic echocardiography. Thirteen cats were surgically treated by thoracotomy and ligation of the PDA. In all cats, a heart murmur was detected. In 88.2% of the cases, this presented as grade 4 out of 6 murmur (15/17 cats). A continuous murmur was more common (10/17 cats; 58.9%) than a systolic murmur (7/17 cats; 41.1%). Echocardiography showed that left ventricular internal diameter end diastole (LVIDd) and left ventricular internal diameter end systole (LVIDs) were significantly above reference values in the majority of cats. Mean diameter of the PDA measured at the widest point of the vessel was 3.4 mm (± 1.08 mm) and mean maximum flow velocity amounted to 5,06 m/sec (2,6m/sec-6,4m/sec). Surgery was successfully performed in all cats treated by surgical ligation and all of these patients were discharged after postoperative inpatient therapy. One cat experienced perioperative bleeding from the PDA, which was stopped efficaciously. This cat exhibited a residual shunt directly postoperatively; this could no longer be visualized in a re-check echocardiography 3 months later. Six cats were followed over a longer period of time. The surgical prognosis in this case study is very good with a postoperative survival rate of 100%. Surgical treatment of PDA is curative in animals not displaying advanced cardiac lesions. The auscultation of a heart murmur can provide initial findings indicative of PDA. Therefore, cardiac auscultation is warranted at every first presentation of a kitten. It must however be taken into consideration that not every cat with PDA necessarily has a continuous murmur but may display a systolic heart murmur. Therefore, it is important give utmost attention to the patients' clinical signs.

Sacubitril/valsartan reversal of left ventricular remodeling is associated with improved hemodynamics in resistant hypertension

BackgroundSacubitril/valsartan (S/V) has been shown to be an effective antihypertensive drug combination. However, its therapeutic effects on blood pressure (BP), hemodynamics, and left ventricular (LV) remodeling in resistant hypertension (RHTN) remain unclear. MethodsEighty-six patients completed this self-control study, during which olmesartan was administered within the first 8 weeks (phase 1), followed by S/V within the second 8 weeks (phase 2), with nifedipine and hydrochlorothiazide taken as background medications. Office BP, echocardiography, and hemodynamics assessment using impedance cardiography were performed at baseline and at the eighth and sixteenth weeks. ResultsThe reduction in office BP was larger in phase 2 than in phase 1 (19.59/11.66 mmHg vs. 2.88/1.15 mmHg). Furthermore, the treatment in phase 2 provided greater reductions in systemic vascular resistance index (SVRI) and thoracic blood saturation ratio (TBR), with differences between the two phases of −226.59 (−1212.80 to 509.55) dyn·s/cm5/m2 and −0.02 (−0.04 to 0.02). Switching from olmesartan to S/V also significantly reduced E/E′, LV mass index, LV end-diastolic volume index, and LV end-systolic volume index (all P < 0.05). Decreases in arterial stiffness, SVRI, and TBR were correlated with changes in indicators of LV remodeling (all P < 0.05). This correlation persisted even after adjusting for confounders including changes in BP. ConclusionsSwitching from olmesartan to S/V effectively lowered BP and reversed ventricular remodeling in RHTN. In addition, hemodynamic improvement was also observed. Changes in hemodynamics played an important role in reversing LV remodeling of S/V, and were independent of its antihypertensive effect.

MID-TERM ECHOCARDIOGRAPHIC OUTCOMES OF AORTIC VALVE REPLACEMENT USING AUTOLOGOUS PERICARDIUM

Highlights:The mid-term echocardiographic outcomes of aortic valve replacement with autologous pericardium presented in the literature are limited to the basic parameters related to transvalvular hemodynamics;This study is the first in the world to conduct a comprehensive detailed analysis of echocardiographic parameters after neocuspidization using autologous pericardium, both in comparison with standard replacement and between different age populations;Aortic valve neocuspidization using autologous pericardium adult patients of any age group in comparison with mechanical replacement in the mid-term period is characterized by a higher effective orifice area, significant dynamics of left ventricular myocardial mass regression, low potential for the preservation of significant mitral regurgitation. AbstractAim. To analyze echocardiographic parameters after aortic valve replacement using autologous pericardium in various age groups of the adult population.Methods. The multicenter prospective non-randomized cross-controlled study included 71 patients evaluated after surgical correction of aortic valve (AV) stenosis in the mid-term. The population (n = 71) is divided into the following populations: 1 – AVNeo Y (n = 24) – patients aged 19 to 50 years who underwent neocuspidization using autologous pericardium; 2 – AVNeo A (n = 23) – patients aged 51 to 79 years who underwent neocuspidization using autologous pericardium; Group 3 – AVR (n = 24) are patients aged 26 to 50 years who have undergone mechanical replacement. The end points were as follows: index of effective orifice area (EOA), left ventricular mass index (LVMI), peak gradient on AV, peak velocity on AV, pulmonary hypertension (PH), frequency of significant mitral regurgitation (MR), end-diastolic LV volume, LV ejection fraction.Results. In the group 3 (AVR), the lowest EOA index was noted in comparison with the group 1 (AVNeo Y) (p &lt; 0.01) and the group 2 (AVNeo A) (p = 0.02). Significant dynamics of LVMI decrease was observed in groups 1 (AVNeo Y) (p &lt; 0.01) and 2 (AVNeo A) (p &lt; 0.01). In the group 3 (AVR), there was also a decrease in the LVMI in the mid-term, but it went beyond the limits of reliability (p = 0.07). The peak gradient between the groups in the mid-term period was 8.5±2.7 mmHg in the group 1 (AVNeo Y), 8.5±2.6 mmHg in the group 2 (AVNeo A) and 15.6±4.1 mmHg in the group 3 (AVR) (p &lt; 0.01). With respect to significant MR, there was a significant increase in its frequency in the group 3 (AVR) in comparison with other groups (p &lt; 0.01). Moreover, in the group 3 (AVR), a more frequent occurrence of PH was noted in comparison with the group 1 (AVNeo Y) (p &lt; 0.01).Conclusions. AV mechanical replacement in young patients in comparison with neocuspidization using autologous pericardium in adult patients of any age in the mid-term period is characterized by a lower EOA index, the absence of significant dynamics of LVMI regression, a higher peak transvalvular gradient, and a high potential to preserve significant MR and PH.

Cardiac magnetic resonance patterns of left ventricular remodeling in patients with severe aortic stenosis referred to surgical aortic valve replacement

Left ventricular (LV) hypertrophy is a common finding in patients with severe aortic stenosis (AS). Cardiac magnetic resonance (CMR) is the gold-standard technique to evaluate LV remodeling. Our aim was to assess the prevalence and describe the patterns of LV adaptation in AS patients before and after surgical aortic valve replacement (AVR). Prospective study of 130 consecutive patients (71y [IQR 68–77y], 48% men) with severe AS, referred for surgical AVR. Patterns of LV remodeling were assessed by CMR. Besides normal LV ventricular structure, four other patterns were considered: concentric remodeling, concentric hypertrophy, eccentric hypertrophy, and adverse remodeling. At baseline CMR study: mean LV indexed mass: 81.8 ± 26.7 g/m2; mean end-diastolic LV indexed volume: 85.7 ± 23.1 mL/m2 and median geometric remodeling ratio: 0.96 g/mL [IQR 0.82–1.08 g/mL]. LV hypertrophy occurred in 49% of subjects (concentric 44%; eccentric 5%). Both normal LV structure and concentric remodeling had a prevalence of 25% among the cohort; one patient had an adverse remodeling pattern. Asymmetric LV wall thickening was present in 55% of the patients, with predominant septal involvement. AVR was performed in 119 patients. At 3–6 months after AVR, LV remodeling changed to: normal ventricular geometry in 60%, concentric remodeling in 27%, concentric hypertrophy in 10%, eccentric hypertrophy in 3% and adverse remodeling (one patient). Indexes of AS severity, LV systolic and diastolic function and NT-proBNP were significantly different among the distinct patterns of remodeling. Several distinct patterns of LV remodelling beyond concentric hypertrophy occur in patients with classical severe AS. Asymmetric hypertrophy is a common finding and LV response after AVR is diverse.

The effect of long-term soccer training on left ventricular structure and function in elite male youth soccer players.

Cardiac adaptations in elite, male adolescent youth soccer players have been demonstrated in relation to training status. The time course of these adaptations and the delineation of the influence of volatile growth phases from the training effect on these adaptations remain unclear. Consequently, the aims of the study were to evaluate the impact of 3 years of elite-level soccer training on changes in left ventricular (LV) structure and function in a group of highly trained elite youth male soccer players (SP) as they transitioned through the pre-to-adolescent phase of their growth. Twenty-two male youth SP from the highest Level of English Premier League Academy U-12 teams were evaluated once a year for three soccer seasons as the players progressed from the U-12 to U-14 teams. Fifteen recreationally active control participants (CON) were also evaluated over the same 3-year period. Two-dimensional transthoracic echocardiography was used to quantify LV structure and function. After adjusting for the influence of growth and maturation, training-induced increases in Years 2 and 3 were noted for: LV end diastolic volume (LVEDV; p = 0.02) and LV end systolic volume (LVESV; p = 0.02) in the SP compared to CON. Training-induced decrements were noted for LV ejection fraction (LVEF; p = 0.006) and TDI-S' (p < 0.001). An increase in training volume (Years 2 and 3) were aligned with LV volumetric adaptations and decrements in systolic function in the SP that were independent from the influence of rapid somatic growth. Decrements in systolic function were suggestive of a functional reserve for exercise.

MSC exosomes attenuate sterile inflammation and necroptosis associated with TAK1-pJNK-NFKB mediated cardiomyopathy in diabetic ApoE KO mice.

Diabetes is a debilitating disease that leads to complications like cardiac dysfunction and heart failure. In this study, we investigated the pathophysiology of diabetes-induced cardiac dysfunction in mice with dyslipidemia. We hypothesize diabetes in ApoE knockout (ApoE-/-) mice induces cardiac dysfunction by increasing inflammation and necroptosis. ApoE-/- mice were divided into experimental groups: Control, Streptozotocin (STZ), STZ + MSC-Exo (mesenchymal stem cell-derived exosomes), and STZ+MEF-Exo (Mouse embryonic fibroblast derived exosomes). At Day 42, we assessed cardiac function, collected blood and heart tissues. Heart tissue samples were analyzed for inflammation, necroptosis, signaling mechanism, hypertrophy and adverse structural remodeling using histology, immunohistochemistry, western blotting, RT-PCR, cytokine array and TF array. STZ treated ApoE-/- mice developed diabetes, with significantly (p<0.05) increased blood glucose and body weight loss. These mice developed cardiac dysfunction with significantly (p<0.05) increased left ventricular internal diameter end diastole and end systole, and decreased ejection fraction, and fractional shortening. We found significant (p<0.05) increased expression of inflammatory cytokines TNF- a, IL-6, IL-1a, IL-33 and decreased IL-10 expression. Diabetic mice also exhibited significantly (p<0.05) increased necroptosis marker expression and infiltration of inflammatory monocytes and macrophages. MSC-Exos treated mice showed recovery of diabetes associated pathologies with significantly reduced blood glucose, recovered body weight, increased IL-10 secretion and M2 polarized macrophages in the heart. These mice showed reduced TAK1-pJNK-NFKB inflammation associated expression and improved cardiac function with significantly reduced cardiac hypertrophy and fibrosis compared to diabetic mice. Treatment with MEF-Exos did not play a significant role in attenuating diabetes-induced cardiomyopathy as these treatment mice presented with cardiac dysfunction and underlying pathologies observed in STZ mice. Thus, we conclude that cardiac dysfunction develops in diabetic ApoE-/- mice, arising from inflammation, necroptosis, and adverse tissue remodeling, which is ameliorated by MSC-Exos, a potential therapeutic for diabetes-induced cardiomyopathy.

The Clinical Effects of Pharmacotherapy Combined with Blood Flow Restriction and Isometric Exercise Training in Rehabilitating Patients with Heart Failure with Reduced Ejection Fraction.

Heart failure with reduced ejection fraction (HFrEF) is associated with reduced cardiac function and impaired quality of life. Blood flow restriction (BFR) training is emerging as a potential adjunctive therapy. This study aimed at evaluating the efficacy of combination of BFR and isometric exercises on cardiac function, functional status, and quality of life in HFrEF patients. Totally 44 patients with HFrEF were equally divided into a control group and a combined treatment group. Both groups received standard pharmacotherapy and upper limb exercise, with the combined group also undergoing BFR and isometric exercise training. We assessed demographic and clinical characteristics, New York Heart Association (NYHA) functional classification, cardiac function parameters, serum Brain Natriuretic Peptide levels, physical capacity via the 6-minute walking test, and quality of life using the Heart Failure Questionnaire (Minnesota Living with Heart Failure Questionnaire). Post-treatment, the combined group significantly improved in NYHA classification (p = 0.012), with more patients shifting to a better class. Cardiac function improved in both groups, with the combined group showing a greater increase in mean left ventricular ejection fractions (p < 0.001), and reductions in left ventricular end-diastolic and end-systolic diameters (p < 0.05). The addition of BFR training to standard pharmacotherapy with upper limb exercise in HFrEF patients led to significant enhancements in cardiac function, functional status, and quality of life. These findings support the integration of BFR training into conventional HFrEF treatment regimens to maximize patient recovery outcomes.

Off-pump minimally invasive coronary artery bypass grafting in patients with left ventricular dysfunction: the lampang experience.

The minimally invasive cardiac surgery off-pump coronary artery bypass (MICSOPCAB) is technically difficult; therefore, previous studies have indicated that MICSOPCAB should be contraindicated in patients with impaired left ventricular (LV) function. In this study, we investigated the feasibility of MICSOPCAB in patients with impaired LV function. The 226 patients underwent MICSOPCAB between August 2017 and September 2022. Our study defined impaired LV function as ejection fraction (EF) in echocardiography 40% or less. The patients were divided into Low EF group (n = 39) and Normal EF group (n = 187). The Low EF group was in a more critical preoperative condition than Normal EF group (41.0% in the Low EF group vs. 14.4% in the Normal EF group; p < 0.001). For preoperative transthoracic echocardiography, LV end-diastolic diameter (5.5 ± 0.9 cm in the Low EF group vs. 5.0 ± 0.8 cm in the Normal EF group; p < 0.001) and LV end-systolic diameter (4.4 ± 1.0 cm in the Low EF group vs. 3.4 ± 1.0 cm in the Normal EF group; p < 0.001) were significantly larger in the Low EF group. No differences were found in the operative time (180 [160-240] min in the Low EF group vs. 205 [165-253] min in the Normal EF group; p = 0.231) and the median number of distal anastomoses (2 [1-2] in the Low EF group vs. 2 [1-3] in the Normal EF group; p = 0.073). Intensive care unit stay was longer in the Low EF group than in the Normal EF group (2 [1-2] in the Low EF group vs. 1 [1-2] in the Normal EF group; p = 0.010). Perioperative transfusion was more common in the Low EF group than in the Normal EF group (69.7% vs. 49.2%; p = 0.023). There were no differences in major complications, hospital stay, and 30-day mortality. The Kaplan-Meier curve showed no significant difference in postoperative major adverse cardiac or cerebrovascular events rates between the two groups (p = 0.185). In this study, MICSOPCAB can be performed in patients with low EF having short- and mid-term outcomes similar to patients with normal EF. Therefore, low EF should not be contraindicated in MICSOPCAB.

Low-flow in aortic valve stenosis patients with reduced ejection fraction does not depend on left ventricular function.

Patients with severe aortic stenosis (AS) and reduced left ventricular ejection fraction (LVEF) can be distinguished into high- (HG) and low-gradient (LG) subgroups. However, less is known about their characteristics and underlying (pathophysiological) hemodynamic mechanisms. 98 AS patients with reduced LVEF were included. Subgroup characteristics were analyzed by a multimodal approach using clinical and histological data, next-generation sequencing (NGS) and applying echocardiography as well as cardiovascular magnetic resonance (CMR) imaging. Biopsy samples were analyzed with respect to fibrosis and mRNA expression profiles. 40 patients were classified as HG-AS and 58 patients as LG-AS. Severity of AS was comparable between the subgroups. Comparison of both subgroups revealed no differences in LVEF (p = 0.1), LV mass (p = 0.6) or end-diastolic LV diameter (p = 0.12). Neither histological (HG: 23.2% vs. LG: 25.6%, p = 0.73) and circulating biomarker-based assessment (HG: 2.6 ± 2.2% vs. LG: 3.2 ± 3.1%; p = 0.46) of myocardial fibrosis nor global gene expression patterns differed between subgroups. Mitral regurgitation (MR), atrial fibrillation (AF) and impaired right ventricular function (MR: HG: 8% vs. LG: 24%; p < 0.001; AF: HG: 30% vs. LG: 51.7%; p = 0.03; RVSVi: HG 36.7 vs. LG 31.1ml/m2, p = 0.045; TAPSE: HG 20.2 vs. LG 17.3mm, p = 0.002) were more frequent in LG-AS patients compared to HG-AS. These pathologies could explain the higher mortality of LG vs. HG-AS patients. In patients with low-flow severe aortic stenosis, low transaortic gradient and cardiac output are not primarily due to LV dysfunction or global changes in gene expression, but may be attributed to other additional cardiac pathologies like mitral regurgitation, atrial fibrillation or right ventricular dysfunction. These factors should also be considered during planning of aortic valve replacement.

Reverse left ventricular remodeling after aortic valve replacement for aortic stenosis: a systematic review and meta-analysis.

Reverse left ventricular (LV) remodeling after aortic valve replacement (AVR), in patients with aortic stenosis, is well-documented as an important prognostic factor. With this systematic review and meta-analysis, we aimed to characterize the response of the unloaded LV after AVR. We searched on MEDLINE/PubMed and Web of Science for studies reporting echocardiographic findings before and at least 1 month after AVR for the treatment of aortic stenosis. In total, 1,836 studies were identified and 1,098 were screened for inclusion. The main factors of interest were structural and dynamic measures of the LV and aortic valve. We performed a random-effects meta-analysis to compute standardized mean differences (SMD) between follow-up and baseline values for each outcome. Twenty-seven studies met the eligibility criteria, yielding 11,751 patients. AVR resulted in reduced mean aortic gradient (SMD: mmHg, 95% CI: to , ), LV mass (SMD: g, 95% CI: to , ), end-diastolic LV diameter (SMD: mm, 95% CI: to , ), end-diastolic LV volume (SMD: ml, 95% CI: to 3.51, ), increased effective aortic valve area (SMD: 1.10 cm2, 95% CI: 1.01 to 1.20, ), and LV ejection fraction (SMD: 2.35%, 95% CI: 1.31 to 3.40%, ). Our results characterize the extent to which reverse remodeling is expected to occur after AVR. Notably, in our study, reverse remodeling was documented as soon as 1 month after AVR.

Insights into the effects of Friedreich ataxia on the left ventricle using T1 mapping and late gadolinium enhancement.

The left ventricular (LV) changes which occur in Friedreich ataxia (FRDA) are incompletely understood. Cardiac magnetic resonance (CMR) imaging was performed using a 1.5T scanner in subjects with FRDA who are homozygous for an expansion of an intron 1 GAA repeat in the FXN gene. Standard measurements were performed of LV mass (LVM), LV end-diastolic volume (LVEDV) and LV ejection fraction (LVEF). Native T1 relaxation time and the extracellular volume fraction (ECV) were utilised as markers of left ventricular (LV) diffuse myocardial fibrosis and late gadolinium enhancement (LGE) was utilised as a marker of LV replacement fibrosis. FRDA genetic severity was assessed using the shorter FXN GAA repeat length (GAA1). There were 93 subjects with FRDA (63 adults, 30 children, 54% males), 9 of whom had a reduced LVEF (<55%). A LVEDV below the normal range was present in 39%, a LVM above the normal range in 22%, and an increased LVM/LVEDV ratio in 89% subjects. In adults with a normal LVEF, there was an independent positive correlation of LVM with GAA1, and a negative correlation with age, but no similar relationships were seen in children. GAA1 was positively correlated with native T1 time in both adults and children, and with ECV in adults, all these associations independent of LVM and LVEDV. LGE was present in 21% of subjects, including both adults and children, and subjects with and without a reduced LVEF. None of GAA1, LVM or LVEDV were predictors of LGE. An association between diffuse interstitial LV myocardial fibrosis and genetic severity in FRDA was present independently of FRDA-related LV structural changes. Localised replacement fibrosis was found in a minority of subjects with FRDA and was not associated with LV structural change or FRDA genetic severity in subjects with a normal LVEF.

Nicorandil Regulates Ferroptosis and Mitigates Septic Cardiomyopathy via TLR4/SLC7A11 Signaling Pathway

This study mainly explored the role of nicorandil in regulating ferroptosis and alleviating septic cardiomyopathy through toll-like receptor (TLR) 4/solute carrier family 7 member 11 (SLC7A11) signaling pathway. Twenty-four male SD rats were randomly divided into control, Nic (nicorandil), LPS (lipopolysaccharide), and LPS + Nic groups and given echocardiography. A detection kit was applied to measure the levels of lactic dehydrogenase (LDH), cardiac troponin I (cTnI), and creatine kinase-MB (CK-MB); HE staining and the levels of glutathione (GSH), malondialdehyde (MDA), total iron, and Fe2+ of myocardial tissues were detected. Moreover, the expression of TLR4 and SLC7A11 were measured by qRT-PCR and the proteins regulating ferroptosis (TLR4, SLC7A11, GPX4, ACSL4, DMT1, Fpn, and TfR1) were checked by western blot. Myocardial cells (H9C2) were induced with lipopolysaccharide (LPS) and transfected with si-TLR4 or SLC7A11-OE. Then, the viability, ferroptosis, and TLR4/SLC7A11 signaling pathway of cells were examined. Nicorandil could significantly increase left ventricular (LV) ejection fraction (LVEF) while reduce LV end-diastolic volume (LVEDV) and LV end-systolic volume (LVESV). Also, it greatly reduced the levels of LDH, cTnI, and CK-MB; alleviated the pathological changes of myocardial injury; notably decreased MDA, total iron, and Fe2+ levels in myocardial tissues; and significantly increased GSH level. Besides, nicorandil obviously raised protein levels of GPX4, Fpn, and SLC7A11, and decreased protein levels of ACSL4, DMT1, TfR1, and TLR4. After knockdown of TLR4 or overexpression of SLC7A11, the inhibition effect of nicorandil on ferroptosis was strengthened in LPS-induced H9C2 cells. Therefore, nicorandil may regulate ferroptosis through TLR4/SLC7A11 signaling, thereby alleviating septic cardiomyopathy.

Senescent hearts from male Ts65Dn mice exhibit preserved function but altered size and nicotinamide adenine dinucleotide pathway signaling.

Down syndrome (DS) is associated with congenital heart defects at birth, but cardiac function has not been assessed at older ages. We used the Ts65Dn mouse, a model of DS, to quantify heart structure and function with echocardiography in 18-mo male Ts65Dn and wild-type (WT) mice. Heart weight, nicotinamide adenine dinucleotide (NAD) signaling, and mitochondrial (citrate synthase) activity were investigated, as these pathways may be implicated in the cardiac pathology of DS. The left ventricle was smaller in Ts65Dn versus WT, as well as the anterior wall thickness of the left ventricle during both diastole (LVAW_d; mm) and systole (LVAW_s; mm) as assessed by echocardiography. Other functional metrics were similar between groups including left ventricular area end systole (mm2), left ventricular area end diastole (mm2), left ventricular diameter end systole (mm), left ventricular diameter end diastole (mm), isovolumetric relaxation time (ms), mitral valve atrial peak velocity (mm/s), mitral valve early peak velocity (mm/s), ratio of atrial and early peak velocities (E/A), heart rate (beats/min), ejection fraction (%), and fractional shortening (%). Nicotinamide phosphoribosyltransferase (NAMPT) protein expression, NAD concentration, and tissue weight were lower in the left ventricle of Ts65Dn versus WT mice. Sirtuin 3 (SIRT3) protein expression and citrate synthase activity were not different between groups. Although cardiac function was generally preserved in male Ts65Dn, the altered heart size and bioenergetic disturbances may contribute to differences in aging for DS.

Cardiovascular Effects of Chronic Hormone Therapy: Study on Olympic Female Athletes

Female physiology is regulated after puberty by the menstrual cycle, whose hormonal fluctuations create a multitude of effects on several systems, including the cardiovascular one. The use of hormone therapy (HT) is quite common in female athletes and data on cardiovascular effects in this population are lacking. We sought to investigate the effects of HT in highly trained athletes to assess any difference associated with HT on cardiac remodelling, exercise capacity and clinical correlates. We studied 380 female elite athletes (mean age 25.5 ± 4.8) competing in endurance and mixed sports. 67 athletes (18%) were in chronic HT therapy. All athletes underwent baseline ECG, exercise ECG stress test, transthoracic echocardiogram, complete blood tests including lipid profile and inflammation indexes. The echocardiographic study showed a characteristic left ventricular (LV) remodelling, defined by lower LV mass index (86.2 vs. 92.5 g/m2, p<0.006), end-diastolic LV diameter (28.3 vs. 29.4 mm/m2, p<0.004) and end-diastolic LV volume (61.82 vs. 67.09 mL/m2, p<0.010) compared to controls, without changes in systolic function and diastolic relaxation/filling indexes. A lower burden of ventricular arrhythmias on exercise was observed in HT athletes (1.5% vs 8.6% in those without therapy, p=0.040). Linear regression analysis showed that HT had independent effect on LVEDDi (p=0.014), LVEDVi (p=0.030) and LVMi (p=0.020). In conclusion, chronic treatment with HT in female athletes is associated with less cardiac remodelling, including a lower LV cavity, volume and mass, with preserved systolic and diastolic function, and decreased burden of exercise-induced ventricular arrhythmias. HT, therefore, appears to be responsible for a more economic, but equally efficient, cardiac adaptation to intensive athletic conditioning.