Increase In Ejection Fraction Research Articles

Factors Associated With the Improvement of Left Ventricular Systolic Function by Continuous Positive Airway Pressure Therapy in Patients With Heart Failure With Reduced Ejection Fraction and Obstructive Sleep Apnea

BackgroundObstructive sleep apnea (OSA) is a potential risk factor in cardiovascular diseases, including arrhythmia, coronary artery disease, and heart failure (HF). Continuous positive airway pressure (CPAP) therapy is an effective therapy for OSA and the underlying HF, partly through a 5–9% increase in the left ventricular ejection fraction (LVEF). However, the data on the factors associated with the efficacy of CPAP on LVEF in patients with HF complicated by OSA are scarce. This study aimed to investigate whether LVEF improves in patients with OSA and HF after 1 month of CPAP therapy, and to clarify which factors are associated with the degree of LVEF improvement.MethodThis was a prospective, single-arm, open-label study. We enrolled moderate-to-severe patients with OSA and HF who were being followed up at the cardiovascular center of Toranomon Hospital (Tokyo, Japan). The parameters of sleep study and LVEF were assessed at the baseline and after 1 month of CPAP. The multivariate regression analyses, with changes in LVEF as a dependent variable, were performed to determine the factors that were associated with the degree of LVEF improvement.ResultsWe analyzed 55 consecutive patients with OSA and HF (mean age: 60.7 ± 12.2 years, mean LVEF value: 37.2 ± 9.8%). One month of CPAP treatment decreased the apnea-hypopnea index (AHI) from 45.3 ± 16.1 to 5.4 ± 4.1 per hour, and the LVEF improved from 37.2 ± 9.8 to 43.2 ± 11.7%. The multivariate regression analyses demonstrated that age and body mass index (BMI) were significant determinants of LVEF improvement.ConclusionThe LVEF improved significantly after 1 month of CPAP therapy in Japanese patients with OSA and HF. Multivariate regression analyses indicated that an improvement in LVEF was likely to be observed in young patients with obesity.

Parallel improvement of systolic function with surgical weight loss in patients with heart failure and reduced ejection fraction: a systematic review and patient-level meta-analysis.

Morbid obesity (MO) is an increasingly common condition in patients with heart failure with reduced ejection fraction (HFrEF). Although substantial weight loss in morbidly obese patients has proved to slow the progression of heart failure, parallel alteration of ejection fraction (EF) and New York Heart Association (NYHA) functional class along with post-bariatric surgery weight loss is yet to be determined. This systematic review aimed to measure the effect of bariatric weight loss on EF and NYHA functional class in patients with HFrEF. A systematic literature review was performed in Medline/PubMed to identify studies in patients with MO and pre-existing HFrEF, who underwent bariatric surgery. A total of 11 studies encompassing 136 patients with HFrEF undergoing bariatric surgery for MO were included. Six studies provided patient-level data on 37 cases. Patients lost an average body mass index (BMI) of 12.9 ± 4.2 kg/m2 (5.1 to 23 kg/m2) after an average follow up of 22.43 ± 18.6 months (2-89 mo). There was a direct correlation between BMI loss and EF improvement (r = 0.61, P < .0001), but not between BMI loss and NYHA functional class changes (r = 0.17, P = .4). Weight loss induced by bariatric surgery results in parallel EF increase in patients with MO and HFrEF. However, current data does not indicate a parallel improvement of clinical symptoms (NYHA functional class) along with such an increase in EF in this population of patients.

EP165: Improvement in left ventricular ejection fraction in patients treated with triheptanoin for Long-chain Fatty Acid Oxidation Disorders (LC-FAOD)

In situations of energy crises or fasting, the inability to convert long-chain fats into energy can cause unpredictable, life-threatening, cardiomyopathic events in people with long-chain fatty acid oxidation disorders (LC-FAOD). Triheptanoin, a seven carbon, medium-chain triglyceride (MCT) approved in the United States, Canada and Brazil as a source of calories and fatty acids for the treatment of LC-FAOD, demonstrated increases in left ventricular ejection fraction (LVEF) in a double-blind, randomized clinical trial (RCT).

Does left ventricular reverse remodeling influence long-term outcomes in patients with Chagas cardiomyopathy?

BackgroundThe impact of left ventricular reverse remodeling (LVRR) on the prognosis of Chagas cardiomyopathy is unknown. The aim of this study was to determine whether the presence of LVRR can predict mortality in these patients.MethodsFrom January 2000 to December 2010, the medical charts of 159 patients were reviewed. LVRR was defined as an increase of left ventricular ejection fraction (LVEF) and a decrease of left ventricular end-diastolic diameter (LVDD) by two-dimensional echocardiography. No patient underwent cardiac resynchronization therapy or required mechanical ventricular assistance.ResultsAt baseline, median (25th–75th) LVDD was 64 mm (59–70), and median LVEF was 33.2% (26.4–40.1). LVRR was detected in 24.5% of patients in a 40-month (26–64) median follow-up. In the LVRR group, LVDD decreased from 64 mm (59–68) to 60 mm (56–65; p < 0.001), and LVEF increased from 31.3% (24.1–39.0) to 42.5% (32.2–47.7; p < 0.001). However, LVRR was not associated with heart failure hospitalization, cardiogenic shock, heart transplantation, or mortality (p > 0.05 for all comparisons). The Cox proportional hazard model analysis identified only cardiogenic shock (hazard ratio [HR]: 2.41; 95% confidence interval [CI]: 1.51–3.85; p < 0.001) and serum sodium level (HR: 0.91; 95% CI: 0.86–0.96; p < 0.001) as independent predictors of all-cause mortality.ConclusionsLeft ventricular reverse remodeling occurs in one quarter of patients with Chagas cardiomyopathy and have no impact on the outcomes of patients with this condition.

Ten-year follow-up of cardiac resynchronization therapy patients with non-ischemic dilated cardiomyopathy assessed by radionuclide angiography: a single-center cohort study.

Relatively few data are available on long-term survival and incidence of ventricular arrhythmias in cardiac resynchronization therapy (CRT) patients. We investigated long-term outcomes of CRT patients with non-ischemic dilated cardiomyopathy stratified as responders or non-responders according to radionuclide angiography. Fifty patients with non-ischemic dilated cardiomyopathy undergoing CRT were assessed by equilibrium Tc99 radionuclide angiography with bicycle exercise at baseline and after 3months. Intra- and interventricular dyssynchrony were derived by Fourier phase analysis. Patient clinical outcome was assessed after 10years. At 3months, 50% of patients were identified as CRT responders according to an increase in LV ejection fraction ≥ 5%. During a follow-up of 109 ± 48months, 30% of patients died and 6% underwent heart transplantation. Age and history of paroxysmal atrial fibrillation were found to be predictors of all-cause mortality. CRT responders showed lower risk of death from cardiac causes than non-responders. At follow-up, 38% of patients presented at least one episode of sustained ventricular tachycardia, with a similar percentage between responders and non-responders. At long-term follow-up, non-ischemic CRT recipients identified as responders by radionuclide angiography were found to be at lower risk of worsening heart failure death than non-responders. Long-term risk for sustained ventricular arrhythmia was similar between CRT responders and non-responders.

Cardiomyocyte BRAF and type 1 RAF inhibitors promote cardiomyocyte and cardiac hypertrophy in mice in vivo.

The extracellular signal-regulated kinase 1/2 (ERK1/2) cascade promotes cardiomyocyte hypertrophy and is cardioprotective, with the three RAF kinases forming a node for signal integration. Our aims were to determine if BRAF is relevant for human heart failure, whether BRAF promotes cardiomyocyte hypertrophy, and if Type 1 RAF inhibitors developed for cancer (that paradoxically activate ERK1/2 at low concentrations: the ‘RAF paradox') may have the same effect. BRAF was up-regulated in heart samples from patients with heart failure compared with normal controls. We assessed the effects of activated BRAF in the heart using mice with tamoxifen-activated Cre for cardiomyocyte-specific knock-in of the activating V600E mutation into the endogenous gene. We used echocardiography to measure cardiac dimensions/function. Cardiomyocyte BRAFV600E induced cardiac hypertrophy within 10 d, resulting in increased ejection fraction and fractional shortening over 6 weeks. This was associated with increased cardiomyocyte size without significant fibrosis, consistent with compensated hypertrophy. The experimental Type 1 RAF inhibitor, SB590885, and/or encorafenib (a RAF inhibitor used clinically) increased ERK1/2 phosphorylation in cardiomyocytes, and promoted hypertrophy, consistent with a ‘RAF paradox' effect. Both promoted cardiac hypertrophy in mouse hearts in vivo, with increased cardiomyocyte size and no overt fibrosis. In conclusion, BRAF potentially plays an important role in human failing hearts, activation of BRAF is sufficient to induce hypertrophy, and Type 1 RAF inhibitors promote hypertrophy via the ‘RAF paradox'. Cardiac hypertrophy resulting from these interventions was not associated with pathological features, suggesting that Type 1 RAF inhibitors may be useful to boost cardiomyocyte function.

The effect of remote ischemic post-conditioning on left ventricular ejection fraction in STEMI patients undergoing primary percutaneous coronary intervention

Abstract Funding Acknowledgements Type of funding sources: None. Background/Introduction Primary Percutaneous Coronary Intervention (PPCI) in ST-Segment Elevation Myocardial Infarction (STEMI) is an effective method to limit the infarct area, reduce clinical symptoms, and improve clinical prognosis. However, it has the potential to creates an acute reperfusion injury which will result in worsening of left ventricular ejection fraction and eventually worsen the prognosis. Remote ischemic post-conditioning (RIPostC) is an additional, non-invasive, and inexpensive protective strategy that has been proved to play an important role in preventing worsening of reperfusion injury and left ventricular ejection fraction. Purpose The aim of this study was to evaluate whether PPCI combined with RIPostC improves the left ventricular ejection fraction of STEMI patients Methods This study used a post test only approach with control group design with an experimental research design. From June 2019 to June 2020, Fifty STEMI patients who underwent PPCI were randomized into PPCI with RIPostC (n = 24) and PPCI-only group (n = 26). After crossing wire or crossing balloon, RIPostC group was given 5 minutes inflating and 5 minutes deflating of cuff for 4 cycles. Furthermore, both groups were subjected to echocardiography follow up at 1 day and 6 months after PPCI. A bivariate analysis was performed to determine the effect of RIPostC on left ventricular ejection fraction in both groups. Results Based on baseline characteristics, beta-blocker therapy was found to be statistically more significant in PPCI with RIPostC than the control group (18 vs 7; p = 0.001). There was no statistically significant increase in left ventricular ejection fraction after 1 month and 6 months after PPCI in RIPostC group (p&amp;gt; 0.05) and the control group (p&amp;gt; 0.05). There was no significant difference in the changes of LVEDV, LVESV, and LVEF between 1 day and 6 months after PPCI between both groups. However, there was a different result in delta LVEF between RIPostC and without RIPostC, 6.21 ± 9.316 and 2.81 ± 8.079 respectively. Conclusion(s) The effect of RIPostC on echocardiography results in 1 day and 6 months after PPCI, as well as changes in echocardiography values in 1 day and 6 months did not appear to be statistically significant between the two groups. Abstract Figure. Baseline characteristics

Immunomodulator FTY720 improves glucose homeostasis and diabetic complications by rejuvenation of β-cell function in nonhuman primate model of diabetes.

Inadequate β‐cell mass is essential for the pathogenesis of type 2 diabetes (T2D). Previous report showed that an immunomodulator FTY720, a sphingosine 1‐phosphate (S1P) receptor modulator, sustainably normalized hyperglycemia by stimulating β‐cell in vivo regeneration in db/db mice. We further examined the effects of FTY720 on glucose homeostasis and diabetic complications in a translational nonhuman primate (NHP) model of spontaneously developed diabetes. The male diabetic cynomolgus macaques of 18–19 year old were randomly divided into Vehicle (Purified water, n = 5) and FTY720 (5 mg/kg, n = 7) groups with oral gavage once daily for 10 weeks followed by 10 weeks drug free period. Compared with the Vehicle group, FTY720 effectively lowered HbA1c, blood concentrations of fasting glucose (FBG) and insulin, hence, decreased homeostatic model assessment of insulin resistance (HOMA‐IR); ameliorated glucose intolerance and restored glucose‐stimulated insulin release, indicating rejuvenation of β‐cell function in diabetic NHPs. Importantly, after withdrawal of FTY720, FBG, and HbA1c remained at low level in the drug free period. Echocardiography revealed that FTY720 significantly reduced proteinuria and improved cardiac left ventricular systolic function measured by increased ejection fraction and fractional shortening in the diabetic NHPs. Finally, flow cytometry analysis (FACS) detected that FTY720 significantly reduced CD4 + and CD8 + T lymphocytes as well as increased DC cells in the circulation. Immunomodulator FTY720 improves glucose homeostasis via rejuvenation of β‐cell function, which can be mediated by suppression of cytotoxic CD8 + T lymphocytes to β‐cells, thus, may be a novel immunotherapy to reverse T2D progression and ameliorate the diabetic complications.

Long noncoding RNA H19 suppresses cardiac hypertrophy through the MicroRNA-145-3p/SMAD4 axis

ABSTRACT Sustained cardiac hypertrophy (CH) contributes to many heart diseases. Long noncoding RNAs (lncRNAs) collectively play critical roles in cardiovascular diseases (CVDs). However, the roles of lncRNA H19 in CH are still unclear. A CH model was constructed utilizing isoproterenol (ISO). We demonstrated H19 could participate in regulating ISO-induced CH development both in vivo and in vitro. The online databases DIANA and TargetScan were used to predict the targets of H19 and MicroRNA-145-3p (miR-145-3p), respectively. Luciferase reporter assay was used to verify the downstream targets. The results showed that H19 was decreased under ISO stimulation. The H19 overexpression resulted in significant decrease in mouse heart size and weight, left ventricular systolic dysfunction, left ventricular posterior wall thickness and cardiac hypertrophic growth, while promoted the increase of left ventricular ejection fraction and left ventricle fraction shortening. H19 also inhibited protein expression levels of CH markers, such as atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and MYH7. Luciferase assays results showed that miR-145-3p was a target of H19 and SMAD4 was a target of miR-145-3p. We found that H19 regulated SMAD4 by sponging miR-145-3p. Knockout of miR-145-3p or overexpression of SMAD4 facilitated H19-induced decreases in ANP, BNP, and MYH7. Collectively, our findings have indicated that the H19/miR-145-3p/SMAD4 axis should be a negative regulator involved in CH progression.

Left ventricle reverse remodeling in chronic aortic regurgitation patients with dilated ventricle after aortic valve replacement

BackgroundAortic valve replacement (AVR) for chronic aortic regurgitation (AR) with a severe dilated left ventricle and dysfunction leads to left ventricle remodeling. But there are rarely reports on the left ventricle reverse remodeling (LVRR) after AVR. This study aimed to investigate the LVRR and outcomes in chronic AR patients with severe dilated left ventricle and dysfunction after AVR.MethodsWe retrospectively analyzed the clinical datum of chronic aortic regurgitation patients who underwent isolated AVR. The LVRR was defined as an increase in left ventricular ejection fraction (LVEF) at least 10 points or a follow-up LVEF ≥ 50%, and a decrease in the indexed left ventricular end-diastolic diameter of at least 10%, or an indexed left ventricular end-diastolic diameter ≤ 33 mm/m2. The changes in echocardiographic parameters after AVR, survival analysis, the predictors of major adverse cardiac events (MACE), the association between LVRR and MACE were analyzed.ResultsSixty-nine patients with severe dilated left ventricle and dysfunction underwent isolated AVR. LV remodeling in 54 patients and no LV remodeling in 15 patients at 6–12 months follow-up. The preoperative left ventricular dimensions and volumes were larger, and the EF was lower in the LV no remodeling group than those in the LV remodeling group (all p < 0.05). The adverse LVRR was the predictor for MACE at follow-up. The mean follow-up period was 47.29 months (range 6 to 173 months). The rate of freedom from MACE was 94.44% at 5 years and 92.59% at 10 years in the remodeling group, 60% at 5 years, and 46.67% at 10 years in the no remodeling group.ConclusionsThe left ventricle remodeling after AVR was the important predictor for MACE. LV no remodeling may not be associated with benefits from AVR for chronic aortic regurgitation patients with severe dilated LV and dysfunction.

Effect of vitamin D on myocardial remodeling and inflammatory status in children with congenital heart disease.

Vitamin D insufficiency is a common public health problem that is often unrecognized in children with congenital heart disease, and is not generally evaluated at congenital heart disease (CHD) follow-up. Recent studies have suggested that inadequate vitamin D status may have an adverse effect on cardiovascular health. This study investigates the relationship between vitamin D levels and hemodynamic parameters in children with CHD. Included in the study 40 patients (25 females, 15 males) with CHD, who were evaluated for Ross heart failure score, vitamin D, parathyroid hormone (PTH), calcium, phosphorus, alkaline phosphatase (ALP), whole blood count (WBC) and echocardiographic measurements, and all measurements were repeated in the third month of the therapy. The mean vitamin D level was 16.4 ± 6.6 ug/L before and 27.5 ± 9.9 μg/L in the third month of therapy, while the mean PTH level was 53.3 ± 34.9 pg/mL before and 43.8 ± 21.4 pg/mL in the third month of therapy. The mean WBC was 8084 ± 2324/µL before and 7378±1893/µL in the third month of the therapy, and the mean platelet (PLT) count was 280,897 ± 80,119/µL before and 307,179 ± 60,202/µL in the third month of the therapy. The mean ejection fraction (EF) was 64% ± 7.2% before and 66.7% ± 6.2% in the third month of therapy, while the right ventricle (RV) myocardial performance index (MPI) was 32.1% ± 6.7% before and 28.9% ± 6.5% in the third month of the therapy. IL10 level was increased in four patients in the third month of therapy. A statistically significant decrease in PTH level and WBC, and an increase in PLT number and IL-10 level were detected by the therapy. Furthermore, echocardiographic findings revealed a statistically significant increase in EF and a decrease in RVMPI attributable to the therapy. The decreased levels of PTH, which is a proinflammatory marker, the increases in IL-10, which is an antiinflammatory cytokine, and the decreases in the number of WBC resulting from vitamin D treatment demonstrate the antiinflammatory effects of vitamin D. An improvement in EF means improvement in left ventricular contractility, while a decrease in RV MPI has been shown to improve the systolic and diastolic function of the right ventricle. These results suggest that vitamin D therapy has a positive effect on the heart, and so vitamin D levels should be evaluated during the routine follow-up of congenital heart disease.

Exogenous H2S Protects against Septic Cardiomyopathy by Inhibiting Autophagy through the AMPK/mTOR Pathway

Background Given the cardioprotective role of autophagy, this study aimed to investigate the protective effect of exogenous H2S (NaHS) on infectious cardiomyopathy through the inhibition of the AMPK/mTOR pathway. Methods In this study, sepsis models were established by cecal ligation and puncture (CLP) induction in vivo and intraperitoneal injection of NaHS was performed. Autophagy- and apoptosis-related proteins were observed by western blot, isolated myocardial tissue morphology was observed by hematoxylin-eosin (H&E) staining, and myocardial apoptosis was evaluated by the tunnel method. The ultrastructure of autophagy was observed by using an electron transmission electron microscope. Results In an SD rat model of cecum ligation puncture-induced sepsis, the level of autophagy-related proteins was significantly increased, and hematoxylin and eosin staining showed irregular myocardial bands and swollen cardiomyocytes. Following NaHS treatment, the level of autophagy-related proteins decreased, and electron transmission microscopy revealed decreased autophagosomes. Echocardiography suggested an increase in ejection fraction and significant relief of myocardial inhibition. Conclusions Our results suggest that NaHS treatment can attenuate the cellular damage caused by excessive autophagy through the AMPK/mTOR pathway.

Transendocardial CD34+ Cell Therapy Improves Local Mechanical Dyssynchrony in Patients With Nonischemic Dilated Cardiomyopathy

We investigated the effects of cell therapy on local mechanical dyssynchrony (LMD) in patients with nonischemic dilated cardiomyopathy (NICM). We analyzed electromechanical data of 30 NICM patients undergoing CD34+ cell transplantation. All patients underwent bone marrow stimulation; CD34+ cells were collected by apheresis and injected transendocardially. At baseline and at 6 months after therapy, we performed electromechanical mapping and measured unipolar voltage (UV) and LMD at cell injection sites. LMD was defined as a temporal difference between global and segmental peak systolic displacement normalized to the average duration of the RR interval. Favorable clinical response was defined as increase in the left ventricular ejection fraction (LVEF) ≥5% between baseline and 6 months. Using paired electromechanical point-by-point analysis, we were able to identify 233 sites of CD34+ cell injections in 30 patients. We found no overall differences in local UV between baseline and 6 months (10.7 ± 4.1 mV vs 10.0 ± 3.6 mV, P = 0.42). In contrast, LMD decreased significantly (17 ± 17% at baseline vs 13 ± 12% at 6 months, P = 0.00007). Favorable clinical response at 6 months was found in 19 (63%) patients (group A), and 11 (37%) patients did not respond to cell therapy (group B). At baseline, the two groups did not differ in age, gender, LVEF, or N terminal-pro brain natriuretic peptide (NT-proBNP) levels. Similarly, we found no differences in baseline UV (9.5 ± 2.9 mV in group A vs 8.6 ± 2.4 mV in group B, P = 0.41) or LMD at cell injection sites (17 ± 19% vs 16 ± 14%, P = 0.64). In contrast, at 6 months, we found higher UV in group A (10.0 ± 3.1 mV vs 7.4 ± 1.9 mV in group B, P = 0.04). Furthermore, when compared with group B, patients in group A displayed a significantly lower LMD (11 ± 12% vs 16 ± 10%, P = 0.002). Thus, it appears that favorable clinical effects of cell therapy in NICM patients may be associated with a decrease of LMD at cell injection sites.

THE CLINICAL EXPERIENCE OF THE EFFECTIVE USE OF DAPAGLIFLOZIN IN COMORBID CARDIAC PATIENTS WITH CONCOMITANT TYPE 2 DIABETES MELLITUS AND ARTERIAL HYPERTENSION ON THE BACKGROUND OF OVERWEIGHT IN OUTPATIENT SETTING.

The aim: To assess the efficacy and safety of dapagliflozin in the treatment of comorbid cardiac patients with type 2 diabetes mellitus (T2DM) in combination with arterial hypertension (AH) and overweight in outpatient setting. Materials and methods: Under observation were 19 patients who were treated in outpatient setting during 2019-2021 for AH and had T2DM, overweight or obesity. As part of complex treatment, patients received dapagliflozin 10 mg once a day for 12 months. Results: The normalization of blood pressure, elimination of heart failure symptoms on the background of increased ejection fraction, improved indicators of the functional capacity of the kidneys, and a decrease in the degree of proteinuria/albuminuria were noted after treatment. The patients had an easier time losing weight (body mass index and waist circumference decreased; p<0.05) and decreased levels of total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C). None of the monitored patients had cases of hypoglycemia or urinary tract infection. The number and/or doses of antihypertensive, hypouricemic and diuretic drugs were gradually reduced. Conclusions: Using dapagliflozin in a standard dose of 10 mg/day in the complex therapy of patients with T2DM in combination with arterial hypertension and overweight contributes not only to the normalization of blood pressure, but also to a reduction in body weight and waist circumference. The proposed therapy can be an alternative for the treatment of patients with T2DM with concomitant overweight or obesity, arterial hypertension, with or without heart and/or renal failure as a first-line antidiabetic drug.

Circulating Chromogranin B Is Associated With Left Ventricular Functional Recovery After Successful Recanalization of Chronic Total Occlusion.

Background: Chromogranin B (CgB) is increased in heart failure and proportionate to disease severity. We investigated whether circulating CgB level is associated with left ventricular (LV) functional recovery potential after successful recanalization of chronic total occlusion (CTO).Methods: Serum levels of CgB were assayed in 53 patients with stable angina with LV functional recovery [an absolute increase in LV ejection fraction (EF) of ≥5%] and 53 age- and sex-matched non-recovery controls after successful recanalization of CTO during 12-month follow-up.Results: We found that CgB level was significantly lower in the recovery group than in the non-recovery group (593 [IQR 454–934] vs. 1,108 [IQR 696–2020] pg/ml, P < 0.001), and that it was inversely correlated with changes in LVEF (Spearman's r = −0.31, P = 0.001). Receiver operating characteristic (ROC) analysis showed that the area under the curve of CgB for predicting LVEF improvement was 0.76 (95% CI 0.664–0.856), and that the optimal cutoff value was 972.5 pg/ml. In multivariate analyses, after adjusting for confounding factors, high CgB level remained an independent determinant of impaired LV functional recovery after CTO recanalization. LV functional improvement appeared to be more responsive to CgB in patients with poor than with good coronary collaterals.Conclusions: Elevated circulating CgB level confers an increased risk of impaired LV functional recovery after successful recanalization of CTO in patients with stable coronary artery disease.

Ribosomal protein S6 kinase beta-1 gene variants cause hypertrophic cardiomyopathy

BackgroundHypertrophic cardiomyopathy (HCM) is a genetic heart muscle disease with preserved or increased ejection fraction in the absence of secondary causes. Mutations in the sarcomeric protein-encoding genes predominantly cause HCM....

Optimal periods for coronary artery bypass surgery on working heart in patients with stenosis of left main coronary artery and acute coronary syndrome

Introduction: The treatment strategies of patients with stenosis of the left main coronary artery (LMCA) and acute coronary syndrome (ACS) is being debated. One of the key problems is the selection of the optimal time for coronary artery bypass surgery (CABS) in these patients.&#x0D; Aim: To analyze different periods of revascularization of the myocardium by CABS on a working heart in patients with LMCA stenosis and ACS.&#x0D; Materials and methods: A prospective analysis of treatment of 112 patients with LMCA stenosis ( 50%) and ACS was performed. Patients were divided to three groups depending on the time of surgical treatment: upto 7 days after occurrence of ACS, 18 (16.1%, group1) patients; 814 days, 38 (33.9%, group2) patients; 14 days, 56 (50%, group3) patients. The average time of ACS-CABS in all patients was 15 days. The groups were comparable in terms of the main preoperative parameters, except for EuroSCORE II and GRACE scale that were predominant in the early periods of CABS.&#x0D; Results: LMCA subocclusion (stenosis 90%) with coexistence of anginal syndrome at rest was observed in more than half of patients with surgery upto 7 days (56%, p=0.019). The surgery duration, blood loss through drains, number of days in the resuscitation unit, duration of artificial lung ventilation, and use of vasopressor support were not significantly different. The revascularization index was higher in surgeries conducted within 7 days than in surgeries performed within 814 days (2.33 0.59 versus 1.89 0.65, p=0.02). The evaluation of the dynamics of the functional parameters of the myocardium showed a greater increase in ejection fraction in group1 when compared with group3 after surgery (p=0.036). In the evaluation of the end-diastolic volume of the left ventricle, the average reductions were 16 mL, 14 mL, and 8.5 mL, respectively, without any significant differences among the groups. The rate of intrahospital lethality was highest in group3 (.4%), followed by group2 (2.6%). No fatal outcomes were noted in surgeries conducted in upto 7 days (p 0.050).&#x0D; Conclusion: Early CABS performed upto 7 days have similar immediate results to delayed ones and considerably improves the contractile ability of the myocardium in patients with ACS and LMCA stenosis.

Machine Learning Prediction of Cardiac Resynchronisation Therapy Response From Combination of Clinical and Model-Driven Data.

Background: Up to 30–50% of chronic heart failure patients who underwent cardiac resynchronization therapy (CRT) do not respond to the treatment. Therefore, patient stratification for CRT and optimization of CRT device settings remain a challenge.Objective: The main goal of our study is to develop a predictive model of CRT outcome using a combination of clinical data recorded in patients before CRT and simulations of the response to biventricular (BiV) pacing in personalized computational models of the cardiac electrophysiology.Materials and Methods: Retrospective data from 57 patients who underwent CRT device implantation was utilized. Positive response to CRT was defined by a 10% increase in the left ventricular ejection fraction in a year after implantation. For each patient, an anatomical model of the heart and torso was reconstructed from MRI and CT images and tailored to ECG recorded in the participant. The models were used to compute ventricular activation time, ECG duration and electrical dyssynchrony indices during intrinsic rhythm and BiV pacing from the sites of implanted leads. For building a predictive model of CRT response, we used clinical data recorded before CRT device implantation together with model-derived biomarkers of ventricular excitation in the left bundle branch block mode of activation and under BiV stimulation. Several Machine Learning (ML) classifiers and feature selection algorithms were tested on the hybrid dataset, and the quality of predictors was assessed using the area under receiver operating curve (ROC AUC). The classifiers on the hybrid data were compared with ML models built on clinical data only.Results: The best ML classifier utilizing a hybrid set of clinical and model-driven data demonstrated ROC AUC of 0.82, an accuracy of 0.82, sensitivity of 0.85, and specificity of 0.78, improving quality over that of ML predictors built on clinical data from much larger datasets by more than 0.1. Distance from the LV pacing site to the post-infarction zone and ventricular activation characteristics under BiV pacing were shown as the most relevant model-driven features for CRT response classification.Conclusion: Our results suggest that combination of clinical and model-driven data increases the accuracy of classification models for CRT outcomes.

Ejection Fraction Recovery after Coronary Artery Bypass Grafting for Ischemic Cardiomyopathy.

Controversy exists about left ventricular systolic function recovery after coronary artery bypass grafting in patients with ischemic cardiomyopathy. The aim of this study is to evaluate the temporal evolvement of left ventricular systolic function after coronary artery bypass surgery in patients with ischemic cardiomyopathy. A total of 50 patients with coronary artery disease and left ventricular ejection fraction (LVEF) ≤35% underwent isolated coronary artery bypass grafting in a single center in the period 2017 to 2019. We performed a retrospective analysis of the echocardiographic and clinical follow-up data at 3 months and 1 year postoperatively. Median LVEF preoperatively was 25% (20-33%), mean patient age was 66 ± 8.2 years, 33 (66%) patients were operated off-pump, and 22 (44%) procedures were non-elective. There was no in-hospital myocardial infarction, stroke, and repeat revascularization. Three (6%) patients underwent re-exploration for bleeding or tamponade. In-hospital mortality was 8% and 1-year mortality was 12%. At 1 year postoperatively, there was no repeat revascularization, no myocardial infarction, 1 (2.6%) patient had a transient ischemic attack, and 10 (20%) patients required an implantable defibrillator. There was a statistically significant median ejection fraction increase at 3 months (15% [5-22%], p < 0.0001) and 1 year (23% [13-25%], p < 0.0001) postoperatively, with an absolute increase ≥10% in 32 (74.4%) and 30 (78.9%) patients at 3 months and 1 year, respectively. Patients with ischemic cardiomyopathy undergoing coronary artery bypass surgery show continuous recovery of left ventricular systolic function in the first postoperative year.

787 Ablation of the ventricular ectopic foci: a therapeutic option for dilated cardiomyopathy due to arrhythmic MVP

Abstract Aims A subset of patients with mitral valve prolapse (MVP) are affected by a still not well understood condition characterized by frequent ventricular arrhythmias (mostly originating from papillary muscles) and sudden cardiac death (SCD). It is called MVP malignant syndrome (MVP MS). In these patients, the high arrhythmic burden may lead to left ventricular (LV) dyssynchrony and dysfunction, determining a tachycardia-induced cardiomyopathy (TIC). Reduction in arrhythmic burden determines LV recovery and ejection fraction improvement and interrupts LV progressive dilatation. Methods and reports We report the case of a 52-year-old woman with MVP and family history of both MVP and SCD who was referred to our department for symptomatic extrasystoles and dyspnoea during exercise. Palpitations begun 11 years before: in that occasion she performed a 3-lead-ECG-Holter monitoring which documented 3457 ventricular extrasystoles. Transthoracic echocardiography (TTE) showed normal LV dimension and function and a myxomatous mitral valve with prolapse of both leaflets. At that time beta-blocker therapy was introduced, but soon suspended because of patient’s clinical intolerance (bradycardia and hypotension). Since then she was lost at follow-up for years, until symptoms worsened. When she came to our attention, TTE showed dilated and hypokinetic LV (ejection fraction was 38%, S2 wave at TDI was 6.4 cm/s and global longitudinal strain value was −13%). CMR was performed and confirmed TTE findings. Mitral-annulus disjunction was described in anterior, lateral, and posterior wall and late gadolinium enhancement analyses showed subendocardial fibrosis in correspondence of the posterior papillary muscle (PM) and in the mid-inferior wall. Holter monitoring enlightened a high arrhythmic burden with 24 065 premature ventricular complexes (PVCs) of two morphologies (right bundle branch block-like and −120° axis and right bundle branch block-like and −75° axis). During stress test, PVCs increased as the heart rate increased, resulting in bigeminism at peak exercise. Considering all these features, we hypothesized a case of MVP MS in which the high ventricular arrhythmic burden resulted in TIC. Any available pharmacological attempt to reduce arrhythmias failed. Transcatheter (TC) ablation of PVCs was then proposed. Electrophysiological study identified the inner part of the posterior papillary muscle implantation region and the antero-lateral basal wall as PVCs sites of origin. Radiofrequency ablation was performed in both sites. After the procedure, despite an incomplete suppression of the posterior PM focus, 12-lead 24-h Holter monitoring and TTE performed during the hospitalization showed a consistent arrhythmic burden reduction and LV function improvement. At 6 months from the procedure, symptoms improved and Holter monitoring showed 7515 PVCs with a 54% arrhythmic burden reduction compared with the presentation. TE showed lower LV end-diastolic volume and an increase in ejection fraction up to 47%; global longitudinal strain was −17% and TDI showed a S2 wave on lateral wall of 11 cm/s, confirming left ventricle improvement after the arrhythmic burden reduction. Conclusions Complete suppression of PMs PVCs with TC ablation is difficult to obtain, especially when the focus is in the inner part of the PM and TC ablation of ventricular arrhythmias in MVP patients has not yet demonstrated his efficacy in reducing SCD. Nevertheless, it should be taken into consideration to obtain at least PVCs reduction in patients with high arrhythmic burden leading to TIC.