Cardiac Hemodynamics Research Articles

Immediate and Short-Term Variations in the Echocardiographic Cardiac Hemodynamic Parameters after the Transcatheter Atrial Septal Defect Device Closure and its Procedural Success.

Background and Aims:Transcatheter closure of the secundum atrial septal defect (ASD) has become an accepted alternative to surgical repair. We aimed to analyze and compare the changes in cardiac hemodynamics with transthoracic echocardiography (TTE) before, within 48 hours, and after 3 months of ASD closure.
 Methods: This was a prospective, single-centered study of 43 patients who underwent ASD device closure in the Manmohan Cardiothoracic Vascular and Transplant Center during June 2020 to June 2021 with Amplatzer Septal Occluder under transesophageal and fluoroscopic guidance. The patients were evaluated with TTE before, at 48 hours, and 3 months after the procedure.
 Results: At 48 hours and 3 months of device closure, the right atrial major dimension, the maximum blood flow velocity at the pulmonary valve orifice, mean flow velocity, velocity time integral, and E peak and A peak blood flow velocity at the tricuspid valve orifice were significantly reduced (P < 0.001). At 3 months, the dimensions and ejection fraction of the left ventricle showed significant increment (P < 0.001). Likewise, the right atrial minor dimension and area, right ventricular basal, mid, and longitudinal dimensions, tricuspid annular plane systolic excursion, right ventricular Tei Index, and fractional area change were significantly reduced (P < 0.001). The main pulmonary artery diameter, pulmonary artery systolic and mean pressure, and the pulmonary vascular resistance and index were significantly reduced (p <0.001). The procedural success rate was 97.6%.
 Conclusion: Echocardiographic evaluation demonstrated that cardiac hemodynamics and loading conditions improved significantly at 3 months after percutaneous closure of ASD. The transcatheter closure of ASD was safe with good short-term outcomes.

Silencing of Long Noncoding RNA MIAT Contributes to Relieving Sepsis-Induced Myocardial Depression via the NF-κB Axis

IntroductionSepsis represents a life-threatening disease caused by a series of infections, which may be complicated with severe myocardial depression (MD). Long noncoding RNAs (lncRNAs) are closely related to sepsis-induced myocardial depression (SIMD). This study aimed to seek out the mechanism of lncRNA myocardial infarction-associated transcript (MIAT) in the growth of SIMD. MethodsVenous blood samples were collected from 62 patients with sepsis; the sepsis rat model was established with 15 mg/kg lipopolysaccharide (LPS), and the H9C2 cardiomyocyte injury model was established with 1 μg/mL LPS. In the rat and cardiomyocyte models, MIAT was inhibited. The expression of MIAT in normal tissues and SIMD tissues was detected. Then, the functional assays of MIAT were performed in rats and H9C2 cells for detection of cardiac function, hemodynamics, inflammation response, myocardial function, oxidative stress, tissue stainings, and cardiomyocyte viability and apoptosis. Western blot analysis was used to measure the levels of apoptosis-related proteins and the nuclear factor kappa B (NF-κB) axis-related proteins. ResultsMIAT was highly expressed in SIMD patients. Silencing MIAT alleviated inflammation and apoptosis and improved myocardial function in SIMD rats by downregulating the NF-κB axis. In LPS-induced H9C2 cardiomyocytes, silencing MIAT alleviated inflammation and oxidative stress and inhibited apoptosis by downregulating the NF-κB axis, thus mitigating cardiomyocyte injury. ConclusionsMIAT could assist the diagnosis of SIMD and might affect the progression of SIMD by regulating the NF-κB pathway.

A Lumped Two-Compartment Model for Simulation of Ventricular Pump and Tissue Mechanics in Ischemic Heart Disease.

Introduction: Computational modeling of cardiac mechanics and hemodynamics in ischemic heart disease (IHD) is important for a better understanding of the complex relations between ischemia-induced heterogeneity of myocardial tissue properties, regional tissue mechanics, and hemodynamic pump function. We validated and applied a lumped two-compartment modeling approach for IHD integrated into the CircAdapt model of the human heart and circulation. Methods: Ischemic contractile dysfunction was simulated by subdividing a left ventricular (LV) wall segment into a hypothetical contractile and noncontractile compartment, and dysfunction severity was determined by the noncontractile volume fraction (). Myocardial stiffness was determined by the zero-passive stress length ( and nonlinearity () of the passive stress-sarcomere length relation of the noncontractile compartment. Simulated end-systolic pressure volume relations (ESPVRs) for 20% acute ischemia were qualitatively compared between a two- and one-compartment simulation, and parameters of the two-compartment model were tuned to previously published canine data of regional myocardial deformation during acute and prolonged ischemia and reperfusion. In six patients with myocardial infarction (MI), the was automatically estimated using the echocardiographic LV strain and volume measurements obtained acutely and 6 months after MI. Estimated segmental values at the baseline and 6-month follow-up were compared with percentage late gadolinium enhancement (LGE) at 6-month follow-up. Results: Simulation of 20% of shifted the ESPVR rightward while moderately reducing the slope, while a one-compartment simulation caused a leftward shift with severe reduction in the slope. Through tuning of the , , and , it was found that manipulation of the alone reproduced the deformation during acute ischemia and reperfusion, while additional manipulations of and were required to reproduce deformation during prolonged ischemia and reperfusion. Out of all segments with LGE>25% at the follow-up, the majority (68%) had higher estimated at the baseline than at the follow-up. Furthermore, the baseline correlated better with percentage LGE than did at the follow-up. Conclusion: We successfully used a two-compartment model for simulation of the ventricular pump and tissue mechanics in IHD. Patient-specific optimizations using regional myocardial deformation estimated the in a small cohort of MI patients in the acute and chronic phase after MI, while estimated values closely approximated the extent of the myocardial scar at the follow-up. In future studies, this approach can facilitate deformation imaging–based estimation of myocardial tissue properties in patients with cardiovascular diseases.

Insulin reduces pyroptosis-induced inflammation by PDHA1 dephosphorylation-mediated NLRP3 activation during myocardial ischemia-reperfusion injury.

Previous studies proved that pyrin domain-containing protein 3 (NLRP3)-induced pyroptosis plays an important role in Myocardial ischemia-reperfusion injury (MIRI). Insulin can inhibit the activation of NLRP3 inflammasome, although the exact mechanism remains unclear. The aim of this study was to determine whether insulin reduces NLRP3-induced pyroptosis by regulating pyruvate dehydrogenase E1alpha subunit (PDHA1) dephosphorylation during MIRI. Rat hearts were subject to 30 min global ischemia followed by 60 min reperfusion, with or without 0.5 IU/L insulin. Myocardial ischemia-reperfusion injury was evaluated by measuring myocardial enzymes release, Cardiac hemodynamics, pathological changes, infarct size, and apoptosis rate. Cardiac aerobic glycolysis was evaluated by measuring ATP, lactic acid content, and pyruvate dehydrogenase complex (PDHc) activity in myocardial tissue. Recombinant adenoviral vectors for PDHA1 knockdown were constructed. Pyroptosis-related proteins were measured by Western blotting analysis, immunohistochemistry staining, and ELISA assay, respectively. It was found that insulin significantly reduced the area of myocardial infarction, apoptosis rate, and improved cardiac hemodynamics, pathological changes, energy metabolism. Insulin inhibits pyroptosis-induced inflammation during MIRI. Subsequently, Adeno-associated virus was used to knock down cardiac PDHA1 expression. Knockdown PDHA1 not only promoted the expression of NLRP3 but also blocked the inhibitory effect of insulin on NLRP3-mediated pyroptosis in MIRI. Results suggest that insulin protects against MIRI by regulating PDHA1 dephosphorylation, its mechanism is not only to improve myocardial energy metabolism but also to reduce the NLRP3-induced pyroptosis.

MO604: Determinants of an Aerobic Threshold in Chronic Kidney Disease

Abstract BACKGROUND AND AIMS Anaerobic threshold (AT) is a widely used cardiopulmonary exercise test (CPX) parameter in the field of preoperative assessment in general population where it is used as a surrogate marker of cardiovascular fitness. There is growing interest in the application of AT in the evaluation of fitness for kidney transplantation. However, the determinants of anaerobic threshold in CKD have not been well studied. In the present study, we evaluated the hemodynamic, biochemical and anthropometric determinants of AT in CKD. Furthermore, we evaluated the association between AT and objectively measured index of cardiac functional reserve in CKD. METHOD In this cross-sectional study, 70 male CKD patients (stages 2–5) without any cardiac diseases or diabetes underwent a specialised CPX to measure exercise capacity, AT, peak cardiac hemodynamics and cardiac power output (CPO).1 Cardiac functional reserve was calculated as ∆CPOpeak—CPOrest. Blood samples were assayed for standard renal biochemistry. Univariate and multivariate regression were employed. Results were presented as mean ± SD. P < 0.05 is considered significant. RESULTS The study subjects had a mean age of 48.4 ± 12.6 years and a mean eGFR of 33.9 ± 23.5 mL/min. All subjects performed high intensity CPX to volitional exhaustion with a mean RER of 1.16 ± 0.09 and a mean peak aerobic capacity (VO2peak) of 2.51 ± 0.53 L/min. Table 1 shows the univariate and multivariate predictors of AT in CKD. Figure 1 shows the association between AT and objectively measured cardiac functional reserve. CONCLUSION The results demonstrate that AT only has a modest association with cardiac functional reserve in CKD. Noncardiac factors such as haemoglobin and peripheral O2 extraction are also significant determinants of AT in addition to cardiac factors. Therefore, AT should be interpreted with caution if employed as a surrogate marker of cardiovascular fitness in CKD. 1Chinnappa S et al. JASN July 2021, 32 (7): 1813–1822

C-9 | The Relation between Cardiac Hemodynamics and Cardiac Biomarkers in Patients with Submassive Pulmonary Embolism

The relation between cardiac biomarkers and cardiac hemodynamics in patients with submassive pulmonary embolism (PE) is not well studied. We aim to investigate the cardiac biomarkers and right ventricle (RV) dysfunction in patients with submassive PE and low or normal cardiac index (CI).

PO-628-01 CARDIAC RESYNCHRONISATION THERAPY ACUTELY ALTERS METABOLIC SUBSTRATE UPTAKE, CORRELATING WITH IMPROVEMENTS IN CARDIAC SYSTOLIC FUNCTION

The failing heart is thought to be metabolically inflexible, and oxygen limited, shifting from free fatty acid (FFA) towards glucose oxidation. CRT acutely improves cardiac haemodynamics in patients with severe heart failure and a LBBB, however whether CRT alters metabolic substrate usage is unknown.

Potential cardioprotective effect of octreotide via NOXs mitigation, mitochondrial biogenesis and MAPK/Erk1/2/STAT3/NF-kβ pathway attenuation in isoproterenol-induced myocardial infarction in rats

Myocardial infarction (MI) is a global health care problem, which instigates irreversible cardiac tissue damage and sudden death, necessitating new prevention and management strategies. Hence, the cardioprotective effect of octreotide in MI was scrutinized by tackling the possible underlying trajectories involved. Isoproterenol (ISO)-induced acute MI model was adopted using ISO (85 mg/kg/day, S.C.) for 2 days. Rats in octreotide groups were pretreated with 20 or 40 μg/kg/day S.C. for 8 days and ISO was given on the 7th and 8th days. Octreotide showed a restoration of ECG changes, cardiac hemodynamics abnormalities, serum cardiac markers elevation (creatine kinase MB, troponin I, lactate dehydrogenase, and aspartate aminotransferase), and cardiac histoarchitecture abnormalities. In addition, octreotide pretreatment showed a significant increase in the cardiac and serum level of the diagnostic microRNA-133a. Octreotide attenuates oxidative stress indices (MDA, GSH, SOD, TAC, and HIF-1α), besides a better adjustment of NOX-1/-2/-4 expression and protein levels. Mitochondrial morphology and mtDNA copy number were preserved following the pre-treatment of Octreotide. The inflammatory pathway p38 MAPK/Erk-1/-2/p-STAT3/NF-κB pathway and the proinflammatory cytokines (TNF- α, IL-6, and IL- 1β) were attenuated. The proapoptotic markers (cyt c, caspase-3/-9, and Bax) were also attenuated and the antiapoptotic Bcl2 marker was increased by the preadministration of octreotide. In almost all parameters, Octreotide 40 μg/kg/day was more prominent than its lower dose. Octreotide possesses dose-dependent cardioprotective properties via its antioxidant, anti-inflammatory, and anti-apoptotic capabilities.

Admission rate-pressure product as an early predictor for in-hospital mortality after aneurysmal subarachnoid hemorrhage.

Early prediction of in-hospital mortality in aneurysmal subarachnoid hemorrhage (aSAH) is essential for the optimal management of these patients. Recently, a retrospective cohort observation has reported that the rate-pressure product (RPP, the product of systolic blood pressure and heart rate), an objective and easily calculated bedside index of cardiac hemodynamics, was predictively associated with in-hospital mortality following traumatic brain injury. We thus wondered whether this finding could also be generalized to aSAH patients. The current study aimed to examine the association of RPP at the time of emergency room (ER) admission with in-hospital mortality and its predictive performance among aSAH patients. We retrospectively included 515 aSAH patients who had been admitted to our ER between 2016 and 2020. Their baseline heart rate and systolic blood pressure at ER presentation were extracted for the calculation of the admission RPP. Meanwhile, we collected relevant clinical, laboratory, and neuroimaging data. Then, these data including the admission RPP were examined by univariate and multivariate analyses to identify independent predictors of hospital mortality. Eventually, continuous and ordinal variables were selected from those independent predictors, and the performance of these selected predictors was further evaluated and compared based on receiver operating characteristic (ROC) curve analyzes. We identified both low (< 10,000; adjusted odds ratio (OR) 3.49, 95% CI 1.93-6.29, p < 0.001) and high (> 15,000; adjusted OR 8.42, 95% CI 4.16-17.06, p < 0.001) RPP on ER admission to be independently associated with in-hospital mortality after aSAH. Furthermore, after centering the admission RPP by its median, the area under its ROC curve (0.761, 95% CI 0.722-0.798, p < 0.001) was found to be statistically superior to any of the other independent predictors included in the ROC analyzes (all p < 0.01). In light of the predictive superiority of the admission RPP, as well as its objectivity and easy accessibility, it is indeed a potentially more applicable predictor for in-hospital death in aSAH patients.

Dapagliflozin protects against doxorubicin-induced cardiotoxicity by restoring STAT3.

Doxorubicin (Dox), an effective therapy in different types of cancer, is known to exhibit cardiotoxic effects. Despite previous studies indicating the benefits of dapagliflozin (DAPA) in patients experiencing heart failure, it remains uncertain whether DAPA exerts a protective effect on Dox-induced cardiac dysfunction. Signal transducer and activator of transcription 3 (STAT3) participates in various mechanisms of cardioprotection. Herein, we aimed to investigate the effects of DAPA on Dox-induced cardiotoxicity and the role of STAT3. Sprague-Dawley rats were pretreated with oral DAPA for 6weeks followed by Dox for 4weeks. Sequential echocardiography was applied to assess cardiac function. For in vitro analysis, cardiomyocytes were treated with 10μM DAPA and subsequently exposed to 1μM Dox. The expression of reactive oxygen species- and apoptosis-related proteins was measured. Using STAT3 siRNA, we further examined the effects of STAT3 effect on DAPA-associated protection against Dox-induced apoptosis. In rats treated with Dox, DAPA significantly reduced cardiac fibrosis and improved cardiac function and hemodynamics. Additionally, DAPA effectively inhibited Dox-induced apoptosis and reactive oxygen species (ROS) in cardiomyocytes. Mechanistically, we showed that DAPA decreased cardiac expression of Bax and cleaved caspase 3 but increased Bcl-2 expression. DAPA also significantly rescued Dox-suppressed STAT3 expression. Conversely, knocking down STAT3 in cardiomyocytes reversed the DAPA-related protective effects on Dox-induced cell apoptosis and ROS. Collectively, our findings indicate that DAPA could be useful for preventing Dox-induced cardiotoxicity by restoring STAT3.

New Evidence About Aortic Valve Stenosis and Cardiovascular Hemodynamics.

Aortic stenosis (AS) is the most common degenerative valvular disease in western word. In patients with severe AS, small changes in aortic valve area can lead to large changes in hemodynamics. The correct understanding of cardiac hemodynamics and its interaction with vascular function is of paramount importance for correct identification of severe AS and to plan effective strategies for its treatment. In the current review with highlight the importance of pressure recovery phenomenon and valvular arterial impedance as novel tools in the evaluation of patients with aortic stenosis.

Investigation of Beraprost Sodium on Cardiac Function and Hemodynamics in Canine Models of Chronic Pulmonary Hypertension.

Pulmonary hypertension (PH) is a life-threatening disease in dogs characterized by increased pulmonary arterial pressure (PAP) and/or pulmonary vascular resistance. No study has evaluated the utility of Beraprost sodium (BPS) in dogs with PH. This study aimed to evaluate the effect of BPS on cardiac function and hemodynamics and examine the optimal dose of BPS in canine models of chronic embolic PH. In this prospective crossover study, three doses of BPS (5, 15, and 25 μg/kg, twice a day) were examined in eight canine models of chronic embolic PH. All model dogs underwent invasive PAP measurement, echocardiography, and non-invasive systemic blood pressure measurement before and after continuous administration of oral BPS for 1 week. No side effects of BPS were observed in any dog during the study. All doses of BPS significantly decreased systolic PAP and pulmonary vascular impedance. Additionally, systemic vascular impedance significantly decreased with 15 and 25 μg/kg of BPS. The right ventricular stroke volume and longitudinal strain significantly decreased with all doses of BPS. The left ventricular stroke volume and circumferential strain decreased with 15 μg/kg BPS. BPS was well-tolerated in this study. A dose-dependent vasodilating effect on pulmonary vessels was observed in canine models of chronic PH. Additionally, 15 μg/kg BPS showed a balanced vasodilating effect on systemic and pulmonary vessels. Furthermore, with a decrease in systemic and pulmonary vascular impedance, the left and right ventricular functions were significantly improved. Our results suggest that BPS may be useful in the treatment of canine PH.

Evolution of Kidney Disease in Single Ventricle Patients After Cardiac Transplantation

<h3>Purpose</h3> Unlike Fontan-associated liver disease, the impact of heart transplant (HT) on Fontan associated kidney disease has not been well described. In this single center study, we sought to characterize the natural history of chronic kidney disease in a small cohort of Fontan patients from listing to follow up after HT. <h3>Methods</h3> We conducted a retrospective review of pediatric patients at our institution with prior Fontan palliation that underwent HT between 2000-2020. We collected demographic information, data regarding baseline renal function/anatomic abnormalities, presence of protein losing enteropathy/liver disease/renal insufficiency/diabetes, and cardiac hemodynamics. Estimated glomerular filtration rate (eGFR) was calculated based on serum creatinine (Cr) using the Cr-based "Bedside Schwartz" formula which was used to determine the stage of kidney disease. We trended data at listing, at transplant, and then at post-transplant follow-up visits (90 days, 180 days, then annually). <h3>Results</h3> Fourteen patients with prior Fontan palliation who underwent HT were identified. At listing, 10 out of 14 patients were noted to have a normal eGFR (GFR ≥ 90). By transplant, four of these patients declined to Stage 2 kidney disease (GFR 60 - 90, not inclusive). All four normalized by 1 year follow-up. The <b>4</b> patients with eGFR < 90 at listing all had further decline in renal function by the time of HT. Post-transplant, 2 normalized, 1 remained with eGFR <90, and 1 required dialysis. The progression of eGFR of all the patients is summarized in the figure below. <h3>Conclusion</h3> In this small single center series, Cr based eGFR at listing and at transplant appear to be risk factors for progressive renal insufficiency in Fontan patients undergoing HT. The predictive value of other pre-transplant variables is limited by our population size. Cr-based eGFR calculations may help identify Fontan patients at increased risk for a decline in renal function post HT who may benefit from enhanced longitudinal renal surveillance.

Noninvasive Assessment Of Cardiovascular Hemodynamics During Exercise Using Systolic Time Intervals

Noninvasive Assessment Of Cardiovascular Hemodynamics During Exercise Using Systolic Time Intervals

Comparison of fibrosing mediastinitis patients with vs. without markedly increased systolic pulmonary arterial pressure: a single-center retrospective study

IntroductionFibrosing mediastinitis (FM) complicated with pulmonary hypertension (PH) has been considered as an important cause of morbidity and mortality. This study was designed to observe the possible effects of abnormal hemodynamics on patients by conducting a between-group comparison according to the presence of markedly increased systolic pulmonary arterial pressure (SPAP), so as to provide more information for clinical management.Materials and methodsFifty-one patients with clinically diagnosed FM were divided in two groups (SPAP < 50 mmHg group; SPAP ≥ 50 mmHg group) and retrospectively included in the study. Data mainly including demographic factors, echocardiographic data, results of right heart catheter and computed tomography (CT) examination were retrieved from the medical database. Echocardiographic parameters pre- and post- balloon pulmonary angioplasty (BPA) treatment were also collected in 8 patients.ResultsSignificant changes in cardiac structure, hemodynamics and cardiac function were detected in patients complicated with markedly increased SPAP. Patients in the SPAP ≥ 50 mmHg group had increased right heart diameter, right heart ratio and velocity of tricuspid regurgitation (VTR) (p < 0.05). Deteriorated right heart function was also observed. There was no significant difference in CT findings between the two groups, except that more patients in the SPAP ≥ 50 mmHg group had pleural effusion (p < 0.05). After primary BPA in 8 patients, improvement in the right atrium proportion was observed.ConclusionsChanges due to significantly increased SPAP in patients with FM include adverse structure and function of the right heart, but differences in CT findings were not significant. Echocardiography has advantages as a noninvasive tool for the evaluation of cardiac structure, function and hemodynamics in patients with FM.

Thyroid dysfunction and its relation to myocardial performance among patients with acute myocardial infarction

Background: The cardiovascular system is one of the most important targets on which thyroid hormones act, thyroid hormone has a major role in the cardiovascu­lar system function and cardiac hemodynamics. Objectives: The primary aim of our study was to evaluate the prevalence of thyroid dysfunction in patients with acute myocardial infarction and to study the impact of these dysfunctions on in-hospital morbidity and mortality among those subjects. Patients and Methods: This study was conducted on one hundred critically ill patients admitted to the critical care department with the diagnosis of acute myocardial infarction in the period from April 2017 to January 2019. Results: According to thyroid profile, 78 patients (78%) had euthyroid status and the remaining 22 patients (22%) had thyroid dysfunctions which include: 12 patients (54.54%) were euthyroid sick syndrome, 7 patients (13.81%) had subclinical hypothyroidism, 3 patients (13.63%) had subclinical hyperthyroidism. Conclusion: Thyroid dysfunction in association with acute myocardial infarction affect the myocardial performance and this was evident in our study by lower ejection fraction, higher initial killip class, higher wall motion score index, and increased myocardial performance index compared to those with normal thyroid status but it has no impact on the in-hospital mortality.

High Density Lipoprotein Reduces Blood Pressure and Protects Spontaneously Hypertensive Rats Against Myocardial Ischemia-Reperfusion Injury in an SR-BI Dependent Manner.

BackgroundHypertension is a key risk factor in the development of cardiovascular diseases. Elevation in blood pressure alters high density lipoprotein (HDL) function and composition. The exact role of HDL in cardiovascular complications observed in hypertension is however not clearly understood. HDL protected against myocardial ischemia/reperfusion (I/R) injury in normotensive rats. Nonetheless, it's not clear if restoration of HDL function and/or composition protects against myocardial I/R injury in spontaneously hypertensive rats (SHR).ObjectivesIn this study we tested the effect of HDL treatment on I/R injury in Wistar Kyoto rats (WKY) and SHR and investigated the possible underlying mechanism(s).MethodsHDL (900 ng/kg/min) or vehicle were continuously administered to 11-week old WKY and SHR for 1 week (chronic treatment). Blood pressure was measured before and after treatment. Hearts were subjected to I/R injury using a modified Langendorff system. Another set of rats were treated with HDL administered at reperfusion (acute treatment) in the presence or absence of scavenger receptor class B type-I (SR-BI) blocking antibody. Cardiac hemodynamics were computed and cardiac enzyme release and infarct size were measured. Total cholesterol (TC) and HDL-cholesterol (HDL-C) were enzymatically assayed. Markers of autophagy and inflammation were detected by immunoblotting and ELISA, respectively.ResultsHDL treatment did not increase TC or HDL-C levels in SHR or WKY, yet it significantly (P < 0.01) reduced systolic and diastolic blood pressure in SHR. Chronic and acute HDL treatment significantly (P < 0.05) protected WKY and SHR against myocardial I/R injury. Chronic HDL treatment was significantly (P < 0.05) more protective in SHR whereas acute HDL treatment induced significantly (P < 0.05) greater protection in WKY. The extent of HDL induced protection was proportional to the expression levels of cardiac SR-BI and blockage of SR-BI completely abolished HDL mediated protection in SHR. Chronic HDL treatment significantly (P < 0.05) reduced markers of autophagy and inflammation in hypertensive rats.ConclusionsWe demonstrate a novel anti-hypertensive and a cardioprotective effect of HDL against myocardial I/R injury in SHR, the magnitude of which is directly related to the expression levels of cardiac SR-BI. Mechanistically, chronic HDL treatment protected SHR hearts by reducing autophagy and inflammation.

Impact of perinatal management on neurodevelopmental outcomes in congenital heart disease

With advancements in cardiopulmonary bypass technique and perioperative care, there has been a progressive decline in mortality associated with neonatal surgical correction of congenital heart disease (CHD). Thus, there is now increased focus on improving neurodevelopmental outcomes in CHD survivors. While the cause of these neurodevelopmental impairments is multifactorial, there is increasing evidence that structural and functional cerebral abnormalities are present before cardiac corrective repair. This suggests that in addition to patient specific risk factors, underlying cardiac physiology and clinical hemodynamics are critical to brain health and development. Prenatal diagnosis of CHD and subsequent optimization of perinatal care may therefore be important modifiable factors for long-term neurodevelopmental outcome.This article reviews the impact that prenatal diagnosis of CHD has on perinatal care and the preoperative clinical status of a neonate, as well as the potential influence this may have on lessening the degree of cerebral injury and long-term neurodevelopmental impairments.

Effects of a New Form of Resistance-Type High-Intensity Interval Training on Cardiac Structure, Hemodynamics, and Physiological and Performance Adaptations in Well-Trained Kayak Sprint Athletes.

This study examined the effects of a resistance-type high-intensity interval training (RHIIT) matched with the lowest velocity that elicited O2peak (100% vO2peak) in well-trained kayak sprint athletes. Responses in cardiac structure and function, cardiorespiratory fitness, anaerobic power, exercise performance, muscular strength, and hormonal adaptations were examined. Male kayakers (n = 24, age: 27 ± 4 years) were randomly assigned to one of three 8-wk conditions (N = 8): (RHIIT) resistance training using one-armed cable row at 100% vO2peak; paddling-based HIIT (PHIIT) six sets of paddling at 100% vO2peak; or controls (CON) who performed six sessions including 1-h on-water paddling/sessions at 70–80% maximum HR per week. Significant increases (p < 0.05) in O2peak, vO2peak, maximal cardiac output, resting stroke volume, left ventricular end-systolic dimension, 500-m paddling performance were seen pre- to post-training in all groups. Change in O2peak in response to PHIIT was significantly greater (p = 0.03) compared to CON. Also, 500-m paddling performance changes in response to PHIIT and RHIIT were greater (p = 0.02, 0.05, respectively) than that of CON. Compared with pre-training, PHIIT and RHIIT resulted in significant increases in peak and average power output, maximal stroke volume, end-diastolic volume, ejection fraction, total testosterone, testosterone/cortisol ratio, and 1,000-m paddling performance. Also, the change in 1,000-m paddling performance in response to PHIIT was significantly greater (p = 0.02) compared to that of CON. Moreover, maximum strength was significantly enhanced in response to RHIIT pre- to post-training (p < 0.05). Overall, RHIIT and PHIIT similarly improve cardiac structure and hemodynamics, physiological adaptations, and performance of well-trained kayak sprint athletes. Also, RHIIT enhances cardiorespiratory fitness and muscular strength simultaneously.

LncRNA LINC00461 exacerbates myocardial ischemia\u2013reperfusion injury via microRNA-185-3p/Myd88

ObjectiveLong non-coding RNAs (lncRNAs) play critically in the pathogenesis of myocardial ischemia–reperfusion (I/R) injury. Thus, it was proposed to investigate the mechanism of LINC00461 in the disease through mediating microRNA-185-3p (miR-185-3p)/myeloid differentiation primary response gene 88 (Myd88) axis.MethodsmiR-185-3p, LINC00461 and Myd88 expression in mice with I/R injury was measured. Mice with I/R injury were injected with the gene expression-modified vectors, after which cardiac function, hemodynamics, myocardial enzyme, oxidative stress, and cardiomyocyte apoptosis were analyzed.ResultsI/R mice showed LINC00461 and Myd88 up-regulation and miR-185-3p down-regulation. Down-regulating LINC00461 or up-regulating miR-185-3p recovered cardiac function, reduced myocardial enzyme levels, and attenuated oxidative stress and cardiomyocyte apoptosis in mice with I/R. miR-185-3p overexpression rescued the promoting effect of LINC00461 upregulation on myocardial injury in I/R mice.ConclusionLINC00461 knockdown attenuates myocardial I/R injury via elevating miR-185-3p expression to suppress Myd88 expression.