Improvement In Myocardial Function Research Articles

Therapeutic benefits of incretin hormones beyond glycemic control from a primary care perspective: A Narrative Review

The parallel rise in the prevalence of obesity and T2DM is a global health challenge. One of the pathogenesis involved in development and progression of type-2 diabetes mellitus is beta cell dysfunction. Until now, diabetes treatments could not restore the reduced function of pancreatic β cell, necessitating the need for advanced treatment options. This led to discovery of incretin hormones in the small intestine, which stimulates insulin secretion in response to glucose. Glucagon-like peptide 1 (GLP-1) and glucosedependent insulinotropic polypeptide (GIP) are two such incretin hormones, secreted by the small intestine in response to food ingestion. Important physiological effects of GLP-1 include enhancement of the insulinotropic response of beta cells to intake of nutrients, reduced gastrointestinal secretion and motility, as well as induction of satiety and ensuing reduction of food intake. Recent evidence suggests that in addition to its established glucose-lowering actions, GLP-1 RAs may also exert several beneficial actions extending beyond glycemic control. The recent finding that GIP/GLP-1 receptor co-agonists like tirzepatide have superior efficacy compared to selective GLP-1 receptor agonists with respect to glycaemic control as well as body weight has renewed interest in GIP, which previously was thought to lack therapeutic potential. This is a narrative review examining some of the ‘beyond-glycemic” benefits of incretin hormones, focusing predominantly on GLP-1 RAs including blood pressure lowering, improvements in the lipid profile, improvements in myocardial and endothelial function. We explore how those effects may help reduce the cardiovascular burden in patients with diabetes. The aim is to encourage use of GLP-1 RA early in patients with established CVD risk factors to prevent CVD related complications and mortality. Keywords: glucagon-like peptide-1 receptor agonist, cardiovascular diseases, major adverse cardiovascular events, type 2 diabetes mellitus, obesity, GIP receptor.

Citrus reticulata Olive Oil: Production and Nutraceutical Effects on the Cardiovascular System in an In Vivo Rat Model of Metabolic Disorder.

Recently, there has been significant exploration into the utilization of food by-products as natural reservoirs of bioactive substances, particularly in the creation of functional foods naturally enriched with antioxidants. Citrus peels represent a viable option for formulating enhanced olive oils that contribute to a healthier diet, due to their bioactive compound content. This study aimed to (i) ascertain the compositional characteristics of Citrus reticulata olive oil (CrOO) and (ii) assess its nutraceutical properties in rats with metabolic disorder induced by 3 weeks of feeding with a high-fat diet (HFD). The results showed a peculiar phytochemical composition, thanks to the contribution of citrus peels, which are excellent bio-products. In addition, it demonstrated HFD-induced weight gain (18 ± 2% for HFD vs. 13 ± 0.9% for CrOO) and showed protective effects on fasting blood glucose levels (90.2 ± 3.8 mg/dL for HFD vs. 72.3 ± 2.6 for CrOO). Furthermore, a reduction in cardiovascular risk (total cholesterol/HDL cholesterol = 5.0 ± 0.3 for HFD vs. 3.8 ± 0.3 for CrOO) and an improvement in myocardial tissue function were observed, as well as a significant reduction in inflammatory mediators such as iNOS, COX-2, and mPGES-1 in aortic vessel tissues, thus preserving endothelial function at the vascular level.

Oroxylin A alleviates myocardial ischemia-reperfusion injury by quelling ferroptosis via activating the DUSP10/MAPK-Nrf2 pathway.

Reperfusion therapy is the primary treatment strategy for acute myocardial infarction (AMI). Paradoxically, it can lead to myocardial damage, namely myocardial ischemia/reperfusion injury (MIRI). This study explored whether oroxylin A (OA) protects the myocardium after MIRI by inhibiting ferroptosis and the underlying mechanism. In vivo, we established an MIRI model to investigate the protective effect of OA. In vitro, H9C2 cells were used to explore the regulation of ferroptosis by OA through immunofluorescence staining, western blotting, assay kits, etc. Additionally, RNA sequencing analysis (RNA-seq) and network pharmacology analyses were conducted to elucidate the molecular mechanisms. Our results showed that MIRI caused cardiac structural and functional damage in rats. MIRI promoted ferroptosis, which was consistently observed in vitro. However, pretreatment with OA reversed these effects. The mitogen-activated protein kinases (MAPK) signaling pathway participated in the MIRI process, with dual-specificity phosphatase 10 (DUSP10) found to regulate it. Further confirmation was provided by knocking down DUSP10 using small interfering RNA (siRNA), demonstrating the activation of the DUSP10/MAPK-Nrf2 pathway by OA to protect H9C2 cells from ferroptosis. Our research has demonstrated the mitigating effect of OA on MIRI and the improvement of myocardial function for the first time. The inhibition of ferroptosis has been identified as one of the mechanisms through which OA exerts its myocardial protective effects. Moreover, we have first unveiled that DUSP10 serves as an upstream target involved in mediating ferroptosis, and the regulation of the DUSP10/MAPK-Nrf2 pathway by OA is crucial in inhibiting ferroptosis to protect the myocardium.

Isoliquiritigenin attenuates myocardial ischemia reperfusion through autophagy activation mediated by AMPK/mTOR/ULK1 signaling

BackgroundIschemia reperfusion (IR) causes impaired myocardial function, and autophagy activation ameliorates myocardial IR injury. Isoliquiritigenin (ISO) has been found to protect myocardial tissues via AMPK, with exerting anti-tumor property through autophagy activation. This study aims to investigate ISO capacity to attenuate myocardial IR through autophagy activation mediated by AMPK/mTOR/ULK1 signaling.MethodsISO effects were explored by SD rats and H9c2 cells. IR rats and IR-induced H9c2 cell models were established by ligating left anterior descending (LAD) coronary artery and hypoxia/re-oxygenation, respectively, followed by low, medium and high dosages of ISO intervention (Rats: 10, 20, and 40 mg/kg; H9c2 cells: 1, 10, and 100 μmol/L). Myocardial tissue injury in rats was assessed by myocardial function-related index, HE staining, Masson trichrome staining, TTC staining, and ELISA. Autophagy of H9c2 cells was detected by transmission electron microscopy (TEM) and immunofluorescence. Autophagy-related and AMPK/mTOR/ULK1 pathway-related protein expressions were detected with western blot.ResultsISO treatment caused myocardial function improvement, and inhibition of myocardial inflammatory infiltration, fibrosis, infarct area, oxidative stress, CK-MB, cTnI, and cTnT expression in IR rats. In IR-modeled H9c2 cells, ISO treatment lowered apoptosis rate and activated autophagy and LC3 fluorescence expression. In vivo and in vitro, ISO intervention exhibited enhanced Beclin1, LC3II/LC3I, and p-AMPK/AMPK levels, whereas inhibited P62, p-mTOR/mTOR and p-ULK1(S757)/ULK1 protein expression, activating autophagy and protecting myocardial tissues from IR injury.ConclusionISO treatment may induce autophagy by regulating AMPK/mTOR/ULK1 signaling, thereby improving myocardial IR injury, as a potential candidate for treatment of myocardial IR injury.

Deletion of Irisin Mitigates HDAC4 Inhibitor-Elicited Protective Effect in Hemorrhage

Introduction: Histone deacetylate inhibition contributes critically to modulating insulin resistance and cardiovascular function. It remains unknown whether inhibition of specific HDAC isoform 4 could improve cardiac function and attenuates inflammatory response and whether HDAC4 inhibition-induced protection is related to irisin. The objective of this study is to investigate whether HDAC4 inhibition induced protective effect against hemorrhage-induced detrimental effects would be diminished by deletion of irisin. Method: Irisin knockout (irisin−/−) mice was generated by using the CRISPR/Cas-9 genome-editing system. Hemorrhage was induced in mice by achieving a mean arterial blood pressure of 35-45 mmHg for one hour, followed by two hours of resuscitation. Experimental groups were divided as followings: I) Wild type (WT)+Hemorrhage (control) (N=7): WT mice were subjected to hemorrhage for 60 minutes followed by resuscitation; II) NVS-HD-1+Hemorrhage (n=7): The same as the group I except that NVS-HD1, a selective HDAC inhibitor (3mg/kg) was infused during resuscitation; III) Irisin −/− +Hemorrhage (n=6): Irisin −/− mice underwent hemorrhage and resuscitation; IV) NVS-HD-1 + Irisin−/−+Hemorrhage (n=6): The same as the groups III except that NVS-HD-1 was given to Irisin −/− during resuscitation. Myocardial function and hemodynamics were assessed using echocardiography and femoral artery catheterization, respectively. Cytokine releases from serum were measured using Enzyme-linked immunosorbent assay (ELISA). Histological assessment was performed to determine tissue damage in both myocardium and skeletal muscles. TUNEL was carried out to assess apoptotic signal in tissues. Results: As compared to control group, HDAC4 inhibitor significantly improved the cardiac function and recovery of hemodynamics, which was associated with the decreased release of IL6 and TNF-α in hemorrhage. The infiltration of inflammatory cells and TUNEL positive apoptosis in muscles were mitigated by inhibition of HDAC4. However, HDAC4 inhibitor-induced myocardial protection and suppression of inflammation against hemorrhage was lost by genetic deletion of irisin. Conclusion: Selective inhibition of HDAC4 produced protective effects with an improvement in myocardial function and attenuation of inflammation against hemorrhage, which is dependent on irisin. The work is supported by the National Institute of General Medical Sciences (R01GM 141339), United States; the National Heart, Lung, and Blood Institute Grants (R01 HL089405), United States. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

(156) - Myocardial Functional Improvement is Associated with Improved HF-Related Outcomes in Patients While on Durable LVAD: An STS INTERMACS Analysis

(156) - Myocardial Functional Improvement is Associated with Improved HF-Related Outcomes in Patients While on Durable LVAD: An STS INTERMACS Analysis

SIRT3 MEDIATES THE CARDIOPROTECTIVE EFFECT OF THERAPEUTIC HYPOTHERMIA AFTER CARDIAC ARREST AND RESUSCITATION BY RESTORING AUTOPHAGIC FLUX VIA THE PI3K/AKT/MTOR PATHWAY.

Background : Postresuscitation cardiac dysfunction is a significant contributor to early death following cardiopulmonary resuscitation (CPR). Therapeutic hypothermia (TH) mitigates myocardial dysfunction due to cardiac arrest (CA); however, the underlying mechanism remains unclear. Sirtuin 3 (Sirt3) was found to affect autophagic activity in recent research, motivating us to investigate its role in the cardioprotective effects of TH in the treatment of CA. Methods : Sprague-Dawley rats were used to establish an in vivo CA/CPR model and treated with a selective Sirt3 inhibitor or vehicle. Survival rate, myocardial function, autophagic flux, and Sirt3 expression and activity were evaluated. H9C2 cells were subjected to oxygen-glucose deprivation/reoxygenation (OGD/R) injury in vitro . The cells were transfected with Sirt3-siRNA and treated with the autophagy inhibitor chloroquine or the PI3K inhibitor LY294002, and cell viability and autophagic flux were assessed. Results : Rats exhibited decreased survival and impaired cardiac function after CA/CPR, which were alleviated by TH. Mechanistically, TH restored Sirt3 expression and autophagic flux, which were impaired by CA/CPR. Sirt3 inactivation diminished the capacity of TH to restore autophagic flux and partially abolished the improvements in myocardial function and survival. An in vitro study further showed that TH-induced restoration of disrupted autophagic flux by OGD/R was attenuated by pretreatment with Sirt3-siRNA, and this attenuation was partially rescued by the inhibition of PI3K/Akt/mTOR signaling cascades. Conclusions : Sirt3 mediates the cardioprotective effect of TH by restoring autophagic flux via the PI3K/Akt/mTOR pathway. These findings suggest the potential of Sirt3 as a therapeutic target for CA.

The effect of vitamin D levels on clinical outcomes after pediatric open-heart surgery

Objectives: Congenital heart disease is a massive structural abnormality in the heart or large vessels inside the chest that is potentially important. Vitamin D is essential for the recovery of organs. This study aimed to evaluate the effect of serum vitamin D levels on clinical outcomes after pediatric open-heart surgery. Recent studies in infants have shown that vitamin D deficiency and hypocalcemia are associated with heart shock.
 Methods: The following descriptive cross-sectional study was conducted in the Cardiology Unit of Shahid Faghihi Hospital in Shiraz from April 2021 to October 2022, involving 115 patients aged one to seven years old. Serum levels of vitamin D were measured to evaluate the correlation between vitamin D levels and postoperative clinical outcomes. Data was gathered using SPSS.v16 software and analyzed through statistical tests.
 Results: The mean age of the patients in this study was 29.20± 53.10 months. The average vitamin D level of the patients was 24.52± 10.3 ng/ml. The study's findings indicated that infants eligible for heart surgery with normal vitamin D levels had significantly shorter durations of Inotropes, ventilators, chest tubes, and Intensive Care Unit (ICU) stay (P<0.001).
 Conclusions: Decreased vitamin D levels in children with abnormal vitamin D can delay the improvement of heart and myocardial function and increase the use of inotropes, ventilators, and chest tubes. It also increases the number of days hospitalized in the ICU after Cardio Pulmonary Bypass (CPB) surgery.

Subcutaneous anakinra in the management of refractory MIS-C in France.

Multisystemic inflammatory syndrome in children (MIS-C) is a therapeutic emergency and can lead to myocardial dysfunction (17%-75%) and heart failure (52%-53%). Intravenous immunoglobulins (IVIG) and corticosteroids (CST) have been validated for the management of this condition. Recent reports suggest that an interleukin-1(IL-1) receptor antagonist, namely anakinra, may be a valuable add-on to the 2019 novel coronavirus disease (COVID-19) treatment for refractory patients. The purpose of this study was to describe the clinico-biological characteristics of patients treated with anakinra as well as the efficacy and safety of subcutaneous anakinra therapy in this condition. The prospective multicentre study of children hospitalized for MIS-C between March 2020 and September 2022, including 23 international paediatric centres, followed for a mean duration of 3.072 ± 3.508 months. The patient data were extracted from the Juvenile Inflammatory Rheumatism (JIR) cohort. The clinico-pathological characteristics, cardiac ultrasound data, and adverse events were reported in patients receiving anakinra. Of the 470 children admitted with MIS-C, 18 French patients (50% girls) with a mean age of 10.06 ± 3.9 years were treated with subcutaneous anakinra. Anakinra was used in two situations, macrophage activation syndrome (MAS) (4 patients) and heart failure (14 patients) with a median left ventricular ejection fraction (LVEF) of 39.5% (30%-45%). The average dose of anakinra received was 2.53 ± 1.3 mg/kg/day for a median duration of 3 days. Prior to introduction, 78% (n = 14/18) of the patients had received CST and 56% (n = 10/18) had received IVIG. Only two patients received IVIG alone and six received CST alone plus anakinra. In 10% of cases, IVIG was poorly tolerated from a cardiovascular point of view and was discontinued. Transient elevations in serum transaminases were noted in four patients on anakinra without the need for treatment or dose modification. In all patients, rapid (48 h) improvement in myocardial function was observed (LVEF > 55%) with a concomitant significant decrease in myocardial enzymes (p < 0.05). All patients survived with complete recovery of cardiac function without sequelae. Subcutaneous anakinra appears to be a safe and effective treatment for the management of heart failure or MAS in MIS-C patients. The value of IVIG in these two situations remains to be reviewed.

The Effect of HIF1-α/NF-κB/MMP2 Signaling Pathways Mediated by ALDH2 on Chronic Intermittent Hypoxia Induced Myocardial Injury in Rats

(1) Objective: To investigate the effect of HIF1-α/NF-κB/MMP2 signaling pathways mediated by ALDH2 on chronic intermittent hypoxia induced myocardial injury in rats. (2) Methods: Thirty SD rats were randomly assigned to three groups (10 rats in each group): control group (CONTROL), chronic intermittent hypoxia group (CIH), and CIH + ALDH2 group. Rats in the CIH + ALDH2 group were established by an intraperitoneal injection of the ALDH2 activator, Alda-1 (20 mg/kg), once a day for three consecutive days. After three months, changes in ventricular function were determined by ultrasound. The expressions of HIF1-α, NF-κB, and MMP2 proteins were detected by protein blotting, and the concentration of 4-HNE in myocardial tissue was measured. (3) Results: Compared with the control group, echocardiography showed that rats in the CIH group had significantly reduced myocardial function, elevated protein levels of HIF1-α, NF-κB, and MMP2 in myocardial tissues, and increased the expression of 4-HNE in myocardial tissues (P&lt;0.01); Compared with the CIH group, rats in the CIH + ALDH2 group showed significant improvement in myocardial function, decreased protein levels of HIF1-α, NF-κB, and MMP2 in myocardial tissue, and decreased the expression of 4-HNE in myocardial tissue (P&lt;0.01). (4) Conclusion: Chronic intermittent hypoxia increases the expression of HIF1-α to damage the myocardium and affect cardiac function, and ALDH2 inhibits the expression of HIF1-α to protect the myocardium.

Determination of viable myocardium through delayed enhancement cardiac magnetic resonance imaging combined with 18F-FDG PET myocardial perfusion/metabolic imaging before CABG.

Study aims to investigate the consistency of delayed enhancement cardiac magnetic resonance imaging (DE-CMR) and 18F-FDG PET myocardial imaging in evaluating myocardial viability before CABG. The study analyzed data from 100 patients who were examined with DE-CMR, PET imaging, and echocardiography before and after CABG. All subjects were followed up for 6-12 month post- CABG. DE-CMR and PET imaging have high consistency (90.1%; Kappa value = 0.71, p < 0.01) in determining myocardial viability. The degree of delayed enhancement was negatively correlated with the improvement in myocardial contractile function in this segment after revascularization (P < 0.001). The ratio of scarred myocardial segments and total DE score was significantly lower in the improvement group than non-improvement group. Multivariate regression identified that hibernating myocardium (OR = 1.229, 95%CI: 1.053-1.433, p = 0.009) was influencing factor of LVEF improvement after CABG. Both imaging techniques are consistent in evaluating myocardial viability. Detecting the number of hibernating myocardium by PET is also important to predict the left heart function improvement after CABG.

Left ventricular myocardial work improves in response to treatment and is associated with survival among patients with light chain cardiac amyloidosis.

Complete haematologic response to treatment for light chain cardiac amyloidosis (AL-CA) may lead to improvement of myocardial function and better outcomes. We sought to evaluate the effect of response to treatment for AL-CA on echocardiographic indices of myocardial deformation and work and their prognostic significance. Sixty-one patients treated for AL were enrolled and underwent echocardiographic assessment at baseline and at 1 year. Patients were stratified according to haematologic response as complete or not complete responders. A significant reduction in median N-terminal pro-brain natriuretic peptide (NT-proBNP) (2771-1486 pg/mL; P < 0.001) and posterior wall thickness (13-12 mm; P = 0.002) and an increase in global work index (GWI) (1115-1356 mmHg%; P = 0.018) was observed at 1 year. Patients with complete response (CR) had a more pronounced decrease in intraventricular septum thickness (14.2-12.0 mm; P = 0.006), improved global longitudinal strain (GLS) (-11.6 to -13.1%; P for interaction = 0.045), increased global constructive work (1245-1436 mmHg%; P = 0.008), and GWI (926-1250 mmHg%, P = 0.002) compared with non-CR. Furthermore, deltaGLS (ρspearman = 0.35; P < 0.001) and deltaGWI (ρspearman = -0.32; P = 0.02) correlated with delta NT-proBNP. Importantly, patients with GLS and GWI response had a better prognosis (log-rank P = 0.048 and log-rank P = 0.007, respectively). After adjustment for Mayo stage, gender, and response status, deltaGLS [hazard ratio (HR) = 1.404, P = 0.046 per 1% increase] and deltaGWI (HR = 0.996, P = 0.042 per 1mmHg% increase) were independent predictors of survival. Complete haematologic response to treatment is associated with improved left ventricular myocardial work indices, and their change is associated with improved survival in AL-CA.

Improvement in myocardial energetics and perfusion with Liraglutide in patients with type 2 diabetes- A randomised, single centre, open label, cross-over drug trial

Abstract Background Both the insulin secretion and insulin resistance in Type 2 diabetes (T2D) are amenable to pharmacological intervention. In a single center, open-label, randomized, cross-over design trial we sought to compare two distinct glycaemic control strategies of targeting beta-cell dysfunction and promoting insulin secretion using Glucagon-like peptide-1 receptor agonists (GLP-1RA) -liraglutide and targeting peripheral insulin resistance using a peroxisome proliferator activated receptor-gamma agonist (PPAR-g)-pioglitazone to see which results in greater improvements in myocardial perfusion, energetics and function in patients with T2D. Methods Fifty-two T2D patients were screened. Eligible patients with no known prior cardiovascular disease were randomized in a 1:1 ratio to be administered one of the study drugs for a 16-week treatment period followed by an 8-week washout and a further 16-week treatment period for the second drug. Thirty-three eligible participants completed both treatment periods. Participants have undergone 31phosphorus magnetic resonance spectroscopy (31P-MRS) at rest and dobutamine stress followed by the cardiac magnetic resonance (CMR) scans. The CMR protocol consisted of rest and dobutamine stress cine imaging, perfusion imaging (motion corrected, automated in-line perfusion mapping), velocity-encoded mitral in-flow imaging and late gadolinium enhanced imaging at 3T immediately before commencement and after completion of each treatment arm (four scans per participant). Results Clinical and biochemical characteristics, and CMR/31P-MRS results are provided in Tables 1&amp;2 respectively. Liraglutide therapy resulted in a significant reductions in the body mass index and significant improvements in glycemic control. Both drugs reduced insulin resistance indicated by a reduction in the mean triglyceride index. There were no significant changes in NTproBNP or troponin levels with either drug. Therapy with either drug did not result in a significant change in the LV end-diastolic volume, ejection fraction or global longitudinal shortening. Pioglitazone led to a significant increment in mean LV mass and LV mass index, while no significant effect in myocardial mass or mass index were detected with liraglutide. Liraglutide therapy resulted in increased rest and dobutamine stress energetics, global stress myocardial blood flow and myocardial perfusion reserve index. While pioglitazone treatment showed no significant effect in these parameters, an isolated improvement in the rest diastolic function was detected in this arm. Conclusions In this randomised cross-over design trial we showed for the first time that four months treatment with glucagon like protein 1 receptor agonist liraglutide results in significant improvements in myocardial stress perfusion and energetics. Pioglitazone results in an isolated improvement in rest diastolic funct

Effects of treatment response on echocardiographic features among patients with light-chain cardiac amyloidosis

Abstract Background Complete response to treatment for light chain cardiac amyloidosis (AL-CA) may lead to improvement of myocardial function. The aim of this study was to evaluate the effect of treatment for AL-CA on echocardiographic characteristics of patients, and the prognostic impact of changes in longitudinal strain and myocardial work. Methods The study population comprised of sixty-one patients treated for AL between 2020 and 2022. All patients underwent comprehensive echocardiographic assessment including longitudinal strain and myocardial work imaging at baseline and at 1-year follow-up. Patients were stratified according to the depth of hematologic response to treatment for AL-CA as complete or not complete responders. The relationship between echocardiographic parameters and all-cause mortality was assessed by Kaplan Meir curves and cut-off points were selected using ROC analysis. Results A significant reduction in median NT-proBNP (from 2,771 to 1,486 pg/mL; p&amp;lt;0.001), posterior wall thickness (PWT) (from 13 to 12mm; p=0.002), and an increase in global work index (GWI) (from 1,115 to 1,356 mmHg%; p=0.018) was observed in all patients at 1-year follow up. After stratifying patients based on hematologic response to treatment, patients with complete response (CR) had a more pronounced decrease in intraventricular septum thickness (14.2 to 12.0mm; p=0.006), a trend towards improved global longitudinal strain (GLS) (-11.6 to -13.1%; p=0.064) and increased global constructive work (1,245 to 1,436 mmHg%; p=0.008), in addition to significant improvements in NT-proBNP, posterior wall thickness and global work index. Furthermore, the delta GLS (ρspearman=0.35; p&amp;lt;0.001) and delta GWI (ρspearman=-0.32; p=0.02) significantly correlated with delta NT-proBNP. Patients with GWI response, either any response or ROC-curve derived cut-off, had a better prognosis compared with patients without GWI response (log-rank p=0.043 and log-rank p=0.035, respectively). Conclusions Among patients treated for AL-CA, those with hematologic CR exhibited significant improvement in GWI and GWW. Additionally, our results indicate that GLS and GWI may have prognostic value in predicting survival among AL-CA patients and their changes correlate to NTproBNP decrease.

Cardiological Challenges Related to Long-Term Mechanical Circulatory Support for Advanced Heart Failure in Patients with Chronic Non-Ischemic Cardiomyopathy.

Long-term mechanical circulatory support by a left ventricular assist device (LVAD), with or without an additional temporary or long-term right ventricular (RV) support, is a life-saving therapy for advanced heart failure (HF) refractory to pharmacological treatment, as well as for both device and surgical optimization therapies. In patients with chronic non-ischemic cardiomyopathy (NICM), timely prediction of HF's transition into its end stage, necessitating life-saving heart transplantation or long-term VAD support (as a bridge-to-transplantation or destination therapy), remains particularly challenging, given the wide range of possible etiologies, pathophysiological features, and clinical presentations of NICM. Decision-making between the necessity of an LVAD or a biventricular assist device (BVAD) is crucial because both unnecessary use of a BVAD and irreversible right ventricular (RV) failure after LVAD implantation can seriously impair patient outcomes. The pre-operative or, at the latest, intraoperative prediction of RV function after LVAD implantation is reliably possible, but necessitates integrative evaluations of many different echocardiographic, hemodynamic, clinical, and laboratory parameters. VADs create favorable conditions for the reversal of structural and functional cardiac alterations not only in acute forms of HF, but also in chronic HF. Although full cardiac recovery is rather unusual in VAD recipients with pre-implant chronic HF, the search for myocardial reverse remodelling and functional improvement is worthwhile because, for sufficiently recovered patients, weaning from VADs has proved to be feasible and capable of providing survival benefits and better quality of life even if recovery remains incomplete. This review article aimed to provide an updated theoretical and practical background for those engaged in this highly demanding and still current topic due to the continuous technical progress in the optimization of long-term VADs, as well as due to the new challenges which have emerged in conjunction with the proof of a possible myocardial recovery during long-term ventricular support up to levels which allow successful device explantation.

Can yoga show better vascular outcomes than regular exercise among office workers: a scoping review

Background: Isolated systolic hypertension (ISH) in the elderly is mostly brought on by arterial stiffness with ageing, which results in a lack of vascular compliance. The main cardiovascular (CV) hazards for elderly persons are arterial ageing and high blood pressure (BP). The aim of this study was to investigate if endothelial function in young, middle-aged, and older, healthy persons would be improved by Bikram yoga, a heated form of hatha yoga. Methods: Randomised control trials on yoga, vascular function, exercise, and office employees were used in the study, which was done in four databases (Scopus, PubMed, Ovid, and Science Direct). Results: 3 of 103 articles were included. We identified improvement of vascular function, FMD and arterial stiffness using yoga intervention. While exercise does not significantly affect ventricular function, yoga significantly reduces heart rate (p = 0.031) and increases pulse pressure (PD). Yoga also results in a mean increase in left ventricular ejection time (LVET), which was observed in the yoga group. The improvement in myocardial function was more pronounced in the yoga group than in the exercise group, according to the between-group analysis, which revealed a significant difference in post-intervention rate-pressure product (RPP) between the yoga and exercise groups. With a P value of 0.004, the mean% Mean Arterial Pressure (MAP) was significantly lower, demonstrating that yoga was effective in lowering MAP. However, older adults, but not younger ones, experienced a significant increase in brachial artery FMD (Flow Mediated Dilation) following the intervention. Conclusions: Yoga interventions may improve vascular function, arterial stiffness, flow-mediated dilation, heart rate, RRP and MAP, with older adults experiencing a significant increase in brachial artery FMD, suggesting the effectiveness of yoga in improving myocardial function and lowering MAP, particularly in older adults.

Baseline angina burden predicts quality of life and functional improvement in patients with viable myocardium treated for chronic total occlusion

Chronic total occlusion (CTO) is a common finding in patients with known or suspected coronary artery disease and has a distinctive role in these patients’ quality of life. However, there is still a lack of evidence of correct patient selection for percutaneous coronary intervention (PCI). From July 2017 to August 2020, 68 patients with successful PCI of a CTO and previous evidence of viability for PCI by cardiovascular magnetic resonance imaging (CMR) were prospectively included in this single-centre observational study. Of these patients, 62 underwent follow-up CMR, and 56 underwent surveys using the Seattle Angina Questionnaire before PCI and 3, 12 and 24 months after PCI. The CMR results were assessed for volumetric, functional and deformation parameters. From the baseline to the follow-up, there was a significant reduction in the left ventricular volumes (all p < 0.001) and an increase in the left ventricular ejection fraction (57.6 ± 11.6% vs. 60.3 ± 9.4%, p = 0.006). Among the deformation parameters, only the left ventricular radial strain showed significant improvement. The SAQ showed an early improvement that emphasised angina stability and frequency as well as a summary score, which persisted after 24 months. A low SAQ summary score before PCI was the best predictive factor of good clinical improvement thereafter. Improvements in myocardial function and quality of life can be achieved with PCI of a CTO. Patient selection for PCI should be performed primarily among relevantly symptomatic patients when evidence of viability for PCI is present. The SAQ can help guide such patient selection.Trial registration ISRCTN, identifier: ISRCTN33203221. Retrospectively registered on 01.04.2020. https://www.isrctn.com/ISRCTN33203221

Clinical and hemodynamic particularities of patients with acute ST-segment elevation myocardial infarction subjected to late interventional treatment

To save the viability of the ischemic myocardium in a patient with ST-segment elevation myocardial infarction and improve the survival, coronary blood flow must be restored as soon as possible, preferably within the first 12 hours after the onset of pain. The current dilemma of interventional cardiologists is the decision about the possibility of performing interventional myocardial reperfusion in the patients with delayed presentation (more than 12 hours from the onset) and establishing the predictive factors of the procedures performed in this category of patients. In ths study 63 patients with STEMI were included, divided into 2 groups: the first one included 33 patients presentetd at the emergency department within the first 12 hours after the onset of STEMI, and the second group consited of 30 subjects with STEMI in whom the first medical contact was more than 12 hours after the onset of symptoms. The groups were compared with each other according to the well-established criteria. The primary end points were the assessment of major cardiovascular events (MACE), as well of ventricular myocardium remodeling/reverse-remodeling and predictors of interventional procedures. The improvement of left ventricular myocardial contractile function (LVEF), seems to be associated with early myocardial revascularization. Early presentation in STEMI can be considered an independent predictor of the improvement of the regional kinetics affected by AMI. The contractile function of the LV myocardium represented by the ejection fraction is considered an independent predictor of long-term and short-term mortality in patients with STEMI. The preliminary results of the research highlight the applicative value of PCI procedures also for patients with delayed presentation - more than 12 hours from the onset of the disease and the first medical contact.

P69 SHORT–TERM EFFECT OF DAPAGLIFLOZIN ON LEFT VENTRICULAR LONGITUDINAL FUNCTION IN PATIENTS WITH HEART FAILURE WITH REDUCED LEFT VENTRICULAR EJECTION FRACTION

Abstract Background It is known that sodium–glucose cotransporter 2 (SGLT2) inhibitors have been shown to confer important clinical benefits in patients with congestive heart failure (HF). Several evidences show SGLT2 influence the longitudinal systolic function of the left ventricle after medium and long term follow–up (FUP) in patients with HF. The aim of this study is to demonstrate how dapagliflozin can modify the global longitudinal strain (GLS) in a population of patients with systolic congestive heart failure (HFrEF) evaluating possible correlations with the basal functional capacity. Methods Clinical and echocardiographic data were retrospectively analyzed in 60 HFrEF patients treated with dapagliflozin, within a dedicated outpatient HF clinic. Pre–treatment data were correlated with to clinical and instrumental FUP date that was generally performed after two months of treatment. The clinical and instrumental data consisted of the NYHA functional class, the left ventricular ejection fraction (LVEF) and the GLS. Results There was no significant change between baseline and FUP date on LVEF (25.2 ± 9.9% vs 25.6 ± 9.6% p.s.), while GLS showed significant improvement (13.1 ± 3.7% vs 14.3 ± 3.1% p &amp;lt; 0.03). GLS improvement in HFrEF patients with more impaired functional class (NYHA III/IV) was more significant from 10.9 ± 3.4% to 13.1 ± 2.2% (p &amp;lt; 0.01), compared to that in HFeEF patients with less compromised functional class (NYHA I–II) from 13.6 ± 2.4% to 14.1 ± 2.1% (p 0.07). Conclusions Dapagliflozin was associated with short term improvement in longitudinal left ventricular myocardial function in patients with chronic congestive systolic heart failure. This improvement is more evident in patients who start from a more impaired functional capacity than in clinically more stable patients.

Myocardial Function after Coronary Artery Bypass Grafting in Patients with Preoperative Preserved Left Ventricular Ejection Fraction-The Role of the Left Ventricular Longitudinal Strain.

Background and Objectives: The role of coronary artery bypass grafting (CABG) on postoperative left ventricular (LV) function in patients with preoperatively preserved left ventricular ejection fraction (LVEF) is still being discussed and only a few studies address this question. This study aimed to assess LV function after CABG in patients with preoperatively preserved LVEF using left ventricular longitudinal strain assessed by 2D speckle tracking imaging (STI). Materials and Methods: Fifty-nine consecutive adult patients with coronary artery disease (CAD) referred for a first-time elective CABG surgery were enrolled in the final analysis of this prospective single-center clinical study. Transthoracic echocardiography (TTE), with conventional measures and STI measures, was performed within 1 week before CABG as well as 4 months after surgery. Patients were divided into groups based on their preoperative global longitudinal strain (GLS) value. Differences in systolic and diastolic parameters between groups were analyzed. Results: Preoperative GLS was reduced (GLS < -17%) in 39% of the patients. Parameters of systolic LV function were significantly reduced in this group of patients compared to the patient group with GLS% ≥ -17%. In both groups, 4 months after CABG there was a decline in LVEF but statistically significant only in the group with GLS% ≥ -17% (p = 0.035). In patients with reduced GLS, there was a statistically significant postoperative improvement (p = 0.004). In patients with preoperative normal GLS, there was not a significant change in any strain parameters after CABG. There was an improvement in diastolic function parameters measured by Tissue Doppler Imaging (TDI) in both groups. Conclusions: There is improvement in LV systolic and diastolic function after CABG in patients with preserved preoperative LVEF measured by STI and TDI. GLS might be more sensitive and effective than LVEF for monitoring improvements in myocardial function after CABG surgery in patients with preserved LVEF.