Cardiac Contractile Parameters Research Articles

Cardiac cycle timing intervals in university varsity athletes

Cardiac cycle timing events in varsity athletes serve an important function for baseline assessment but are not reported in the literature. The purpose of this study was to characterize the cardiac cycle timing intervals and contractility parameters in university-level varsity athletes. 152 males and 93 females were assessed using a non-invasive seismocardiography cardiac sensor attached to the sternum for 1-minute. Shorter isovolumic relaxation time (IVRT), systolic time, mitral valve open to E-wave (MVO to E) time, rapid ejection period (REP), atrial systole to mitral valve closure (AS to MVC) time, and diastolic performance index (IVRT/systolic time) were found in females, while heart rate was lower in males. Varying differences in timing intervals were found between sports. Systolic times were longer in male and female basketball players, while diastole was shortest in male football players, who also had higher heart rates than the other male sport athletes. These results add reference cardiac cycle timing data to the literature and imply that male and female athletes show different cardiac characteristics. Team differences suggest that different training for different sports can result in unique cardiac function changes, however, these appear to be related to the sex of the participants. The addition of these cardiac cycle timing intervals adds a valuable comparative tool to better understand cardiac physiology in the varsity athletic population.

Investigating the sarcolemma-sarcomere connection and force transmission in the heart.

External mechanical signals are communicated through cardiac muscle cells by converting them to internal biochemical signals during mechanotransduction. In the heart, altered transmission of these signals can affect myocardial structure and function. This study examines the impact of sarcospan deletion, a sarcolemma protein, on cardiac muscle mechanics. Sarcospan is an integral member of the dystrophin-glycoprotein complex (DGC) and we are interested in investigating how it influences sarcomere contractile function. Measurements of cardiac contractile parameters were conducted using permeabilized left ventricular papillary muscle bundles obtained from wild-type and SSPN-deficient (SSPN-/-) mouse hearts. Myofilament Ca2+-sensitivity and cooperativity of thin filament activation was similar between WT and SSPN-/- cardiac muscle preparations. However, SSPN-/- muscle bundles exhibited a significantly faster rate of tension redevelopment (kTR) at submaximal activation conditions (pCa 5.8) but no significant changes in maximal kTR (recorded at maximal Ca2+ activation, pCa 4.5). Maximal steady-state isometric force and sinusoidal stiffness were proportionally increased in SSPN-/- cardiac muscle preparations during Ca2+ activation. These intriguing observations suggest that SSPN may play an inherent role in balancing pathways involved in force transmission and its deletion may cause compensatory remodeling of sarcomeric proteins (e.g. isoform switching or protein modification) changing mechanical properties of cardiac muscle. Mouse hearts lacking SSPN-/- exhibit increased sarcolemmal expression of integrin-linked kinase (ILK) and vinculin. ILK is an important biomechanical sensor shown to regulate cardiac contractility and ventricular hypertrophy whereas increasing vinculin expression has been shown to improve heart function and impact myofilament organization. Further examination of the WT and SSPN-/- myofibrils will allow us to assess sarcomere protein alterations that contribute to increased force at submax and max levels of Ca2+ activation. Therefore, the concentric enlargement observed in SSPN-/- mouse hearts could be explained by remodeling of the sarcomere itself.

Mitigating Cardiotoxicity of Dendrimers: Angiotensin-(1-7) via Its Mas Receptor Ameliorates PAMAM-Induced Cardiac Dysfunction in the Isolated Mammalian Heart.

The influence of the physiochemical properties of dendrimer nanoparticles on cardiac contractility and hemodynamics are not known. Herein, we investigated (a) the effect of polyamidoamine (PAMAM) dendrimer generation (G7, G6, G5, G4 and G3) and surface chemistry (-NH2, -COOH and -OH) on cardiac function in mammalian hearts following ischemia-reperfusion (I/R) injury, and (b) determined if any PAMAM-induced cardiotoxicity could be mitigated by Angiotensin-(1-7) (Ang-(1-7), a cardioprotective agent. Hearts isolated from male Wistar rats underwent regional I/R and/or treatment with different PAMAM dendrimers, Ang-(1-7) or its MAS receptors antagonists. Thirty minutes of regional ischemia through ligation of the left anterior descending coronary artery was followed by 30 min of reperfusion. All treatments were initiated 5 min prior to reperfusion and maintained during the first 10 min of reperfusion. Cardiac function parameters for left ventricular contractility, hemodynamics and vascular dynamics data were acquired digitally, whereas cardiac enzymes and infarct size were used as measures of cardiac injury. Treatment of isolated hearts with increasing doses of G7 PAMAM dendrimer progressively exacerbated recovery of cardiac contractility and hemodynamic parameters post-I/R injury. Impairment of cardiac function was progressively less on decreasing dendrimer generation with G3 exhibiting little or no cardiotoxicity. Cationic PAMAMs (-NH2) were more toxic than anionic (-COOH), with neutral PAMAMs (-OH) exhibiting the least cardiotoxicity. Cationic G7 PAMAM-induced cardiac dysfunction was significantly reversed by Ang-(1-7) administration. These cardioprotective effects of Ang-(1-7) were significantly revoked by administration of the MAS receptor antagonists, A779 and D-Pro7-Ang-(1-7). PAMAM dendrimers can impair the recovery of hearts from I/R injury in a dose-, dendrimer-generation-(size) and surface-charge dependent manner. Importantly, PAMAM-induced cardiotoxicity could be mitigated by Ang-(1-7) acting through its MAS receptor. Thus, this study highlights the activation of Ang-(1-7)/Mas receptor axis as a novel strategy to overcome dendrimer-induced cardiotoxicity.

Cardiac and vascular effects of low-dose steroids during the early phase of septic shock: An echocardiographic study.

BackgroundLow-dose steroids are known to increase arterial pressure during septic shock through restoration of vasopressor response to norepinephrine. However, their effects on cardiac performance and ventriculo-arterial coupling (VAC) have never been scrutinized during human septic shock. The aim of this study was to perform a comprehensive description of the cardiovascular effects of low-dose steroids using modern echocardiographic tools (including speckle tracking imaging).MethodsThis prospective study was conducted in the intensive care unit (ICU) of a university hospital in France. Consecutive adult patients admitted for septic shock and requiring low-dose steroid therapy were prospectively enrolled within 24 h of septic shock onset. We recorded hemodynamic and echocardiographic data to explore left ventricle (LV) contractility, loading conditions and VAC just before the initiation of low-dose steroids (50 mg intravenous hydrocortisone plus 50 μg enteral fludrocortisone) and 2–4 h after.ResultsFifty patients [65 (55–73) years; 33 men] were enrolled. Arterial pressure, heart rate, almost all LV afterload parameters, and most cardiac contractility parameters significantly improved after steroids. VAC improved with steroid therapy and less patients had uncoupled VAC (> 1.36) after (24%) than before (44%) treatment.ConclusionIn this comprehensive echocardiographic study, we confirmed an improvement of LV afterload after initiation of low-dose steroids. We also observed an increase in LV contractility with improved cardiovascular efficiency (less uncoupling with decreased VAC).

Cardiac cycle timing and contractility following acute sport-related concussion

ABSTRACT Cardiac sequelae following sport-related concussion are not well understood. This study describes changes in the cardiac cycle timing intervals and contractility parameters during the acute phase of concussion. Twelve athletes (21 ± 2 years, height = 182 ± 9 cm, mass = 86 ± 15 kg, BMI = 26 ± 3 kg/m2) were assessed within 5 days of sustaining a diagnosed concussion against their own pre-season baseline. A non-invasive cardiac sensor (LLA RecordisTM) was used to record the cardiac cycle parameters of the heart for 1 minute during supine rest. Cardiac cycle timing intervals (Isovolumic relaxation and contraction time, Mitral valve open to E wave, Rapid ejection period, Atrial systole to mitral valve closure, Systole, and Diastole) and contractile forces (Twist force and Atrial systole: AS) were compared. Systolic time significantly decreased during acute concussion (p = 0.034). Magnitude of AS significantly increased during acute concussion (p = 0.013). These results imply that concussion can result in altered systolic function.

Effects of Hyperthyroidism on Contractility and Na+/Ca2+ Exchanger Activity in the Isolated Papillary Muscle of Rats

Background: Hyperthyroidism (Hy) is an endocrine disorder, in which the thyroid hormones markedly alter the cardiac function. Increased myocardial contractility and cardiac output, improvement in diastolic relaxation, changes in electrical activity, increments in ventricular mass, and arrhythmias have been reported. However, the influences of thyroid hormones upon molecular mechanisms of cardiac functions have not yet been fully understood. Objectives: To evaluate changes in cardiac contractile parameters and the Na+/Ca2+ exchanger (NCX) function in induced hyperthyroid rats. Methods: Hy was [...]

Beta-adrenergic receptors gene polymorphisms are associated with cardiac contractility and blood pressure variability.

Beta-adrenergic receptors (beta-ARs) play a pivotal role in the cardiovascular regulation. In the human heart beta1- and beta2-ARs dominate in atria as well as in ventricle influencing heart rate and myocardial contractility. Some single nucleotide polymorphisms (SNPs) of beta-ARs might influence cardiovascular function. However, the influence of beta-AR genes SNPs on hemodynamic parameters at rest and their reactivity under stress is still not well known. We aimed to explore the associations between four selected beta-ARs gene polymorphisms and selected cardiovascular measures in eighty-seven young healthy subjects. While in beta1-AR polymorphism rs1801252 no significant association was observed, second beta1-AR polymorphism rs1801253 was associated with decreased cardiac output and cardiac index during all phases and with decreased flow time corrected and ejection time index at rest and during mental arithmetics. Polymorphism rs1042713 in beta2-AR was associated with alterations in blood pressure variability at rest and during head-up-tilt, while rs1042714 was associated predominantly with decreased parameters of cardiac contractility at rest and during mental arithmetics. We conclude that complex analysis of various cardiovascular characteristics related to the strength of cardiac contraction and blood pressure variability can reveal subtle differences in cardiovascular sympathetic nervous control associated with beta-ARs polymorphisms.

Improvement of cardiac ventricular function by magnesium treatment in chronic streptozotocin-induced diabetic rat heart.

Chronic diabetes mellitus is associated with detrimental cardiovascular complications and electrolyte imbalances such as hypomagnesaemia. We investigated the effect of magnesium (Mg2+) on cardiac function and the possible role of histological and electrical alterations in chronic, streptozotocin-induced diabetic rats. Wistar rats were treated once intraperitoneally with streptozotocin or citrate, and then daily with MgSO4 or saline for four weeks. Cardiac contractile and electrocardiographic parameters were measured on Langendorff-perfused hearts. Other hearts were histologically stained or immunoblotted for the mitochondrial ATP synthase (ATP5A). In diabetic hearts, Mg2+ prevented a diabetes-induced decrease in left ventricular developed pressure and improved contractility indices, as well as attenuated the reduction in heart rate and prolongation of QT interval, but not the QT interval corrected for heart rate (QTc). Histologically, there were neither differences in cardiomyocyte width nor interstitial collagen. The expression of ATP5A was not different among the treatment groups. Mg2+ supplementation improved cardiac contractile activity in chronic diabetic hearts via mechanisms unrelated to electrocardiographic or histologically detectable myocardial alterations.

Does chest shape influence exercise stress echocardiographic results in patients with suspected coronary artery disease?

Despite the good specificity of exercise stress echocardiography (ESE) for the detection of coronary artery disease (CAD), false positive (FP) results may occur. We have previously reported that chest abnormalities may affect parameters of cardiac contractility. The influence of chest shape on ESE results has never been previously investigated. We retrospectively analyzed 160 consecutive patients (64.4 ± 13.0-year old, 91 women) who had undergone coronary angiography at our Institution because of positive ESE, between June 2014 and May 2020. Modified Haller index (MHI; chest transverse diameter over the distance between sternum and spine) was assessed in all patients. Obstructive CAD was diagnosed by ≥ 70% stenosis in any epicardial coronary artery. Outcome was false-positivity at ESE. 80.6% of patients were diagnosed with obstructive CAD, while 19.4% had no CAD (FP). We separately analyzed patients with normal chest shape (MHI ≤ 2.5) and those with concave-shaped chest wall (MHI > 2.5). These latter were mostly women with small cardiac chambers, mitral valve prolapse (MVP) and exercise-induced ST-segment changes. Likelihood of false-positivity was significantly higher in subjects with MHI > 2.5 than those with MHI ≤ 2.5 (30.7% vs 9.4%, p = 0.001). By multivariate logistic regression analysis, MHI > 2.5 (OR 4.04, 95%CI 1.45-11.2, p = 0.007), MVP (OR 3.47, 95%CI 1.32-9-12, p = 0.01) and dyssynergy in the left circumflex territory (OR = 3.35, 95%CI 1.26-8.93, p = 0.01) were independently associated with false-positivity. Concave-shaped chest wall (MHI > 2.5) may be associated with false-positive stress echocardiographic result. Mechanisms underpinning this finding need to be further explored.

Implementation and Calibration of a Deep Neural Network to Predict Parameters of Left Ventricular Systolic Function Based on Pulmonary and Systemic Arterial Pressure Signals.

The evaluation of cardiac contractility by the assessment of the ventricular systolic elastance function is clinically challenging and cannot be easily obtained at the bedside. In this work, we present a framework characterizing left ventricular systolic function from clinically readily available data, including systemic and pulmonary arterial pressure signals. We implemented and calibrated a deep neural network (DNN) consisting of a multi-layer perceptron with 4 fully connected hidden layers and with 16 neurons per layer, which was trained with data obtained from a lumped model of the cardiovascular system modeling different levels of cardiac function. The lumped model included a function of circulatory autoregulation from carotid baroreceptors in pulsatile conditions. Inputs for the DNN were systemic and pulmonary arterial pressure curves. Outputs from the DNN were parameters of the lumped model characterizing left ventricular systolic function, especially end-systolic elastance. The DNN adequately performed and accurately recovered the relevant hemodynamic parameters with a mean relative error of less than 2%. Therefore, our framework can easily provide complex physiological parameters of cardiac contractility, which could lead to the development of invaluable tools for the clinical evaluation of patients with severe cardiac dysfunction.

Transcriptional signatures regulated by TRPC1/C4-mediated Background Ca2+ entry after pressure-overload induced cardiac remodelling

AimsAfter summarizing current concepts for the role of TRPC cation channels in cardiac cells and in processes triggered by mechanical stimuli arising e.g. during pressure overload, we analysed the role of TRPC1 and TRPC4 for background Ca2+ entry (BGCE) and for cardiac pressure overload induced transcriptional remodelling. Methods and resultsMn2+-quench analysis in cardiomyocytes from several Trpc-deficient mice revealed that both TRPC1 and TRPC4 are required for BGCE. Electrically-evoked cell shortening of cardiomyocytes from TRPC1/C4-DKO mice was reduced, whereas parameters of cardiac contractility and relaxation assessed in vivo were unaltered. As pathological cardiac remodelling in mice depends on their genetic background, and the development of cardiac remodelling was found to be reduced in TRPC1/C4-DKO mice on a mixed genetic background, we studied TRPC1/C4-DKO mice on a C57BL6/N genetic background. Cardiac hypertrophy was reduced in those mice after chronic isoproterenol infusion (−51.4%) or after one week of transverse aortic constriction (TAC; −73.0%). This last manoeuvre was preceded by changes in the pressure overload induced transcriptional program as analysed by RNA sequencing. Genes encoding specific collagens, the Mef2 target myomaxin and the gene encoding the mechanosensitive channel Piezo2 were up-regulated after TAC in wild type but not in TRPC1/C4-DKO hearts. ConclusionsDeletion of the TRPC1 and TRPC4 channel proteins protects against development of pathological cardiac hypertrophy independently of the genetic background. To determine if the TRPC1/C4-dependent changes in the pressure overload induced alterations in the transcriptional program causally contribute to cardio-protection needs to be elaborated in future studies.

P561Acute effects of dronedarone and amiodarone on functional, morphological and oxidative stress parameters in isolated rat heart with hypertension

Abstract Introduction Amiodarone represents the most widely used antiarrhythmic drug, even though it has been shown that it has negative inotropic and lusitropic effect in healthy hears. On the other hand, dronedarone reduces the risk of recurrent atrial fibrillation, but with increased early mortality related to the worsening of heart failure. However, the mechanisms responsible for these fatal outcomes remain unclear and require further examinations. Purpose To investigate acute, direct effects of Dronedarone and Amiodarone on cardiac contractility, coronary flow and oxidative stress parameters in isolated rat heart with hypertension. Methods The present study was carried out on 18 isolated hearts of spontaneously hypertensive Wistar Kyoto male rats (6 weeks old, bodyweight 200 ± 10 g). After isolation, all hearts were retrogradely perfused according to Langendorff technique with a gradually increment of coronary perfusion pressure (CPP from 40 to 120 cm H2O) and randomly divided into 3 groups: Control (n = 6), Amiodarone (n = 6, isolated hearts perfused with Amiodarone in dose of 3 umol), Dronedarone (n = 6, isolated hearts perfused with Dronedarone in dose of 1.8 umol). During ex vivo protocol continuously were registered cardiac contractility parameters and coronary flow, while from collected coronary venous effluent markers of oxidative stress were measured. All hearts were then fixated and stained with Hematoxylin/eosin. Results Dronedarone severely depressed the function of all cardiodynamic parameters of the heart compared with Amiodarone or Control while Amiodarone intensified the function of the isolated rat heart with hypertension compared to Control (dp/dt max mmHg/s at coronary perfusion pressure 120cmH2O Dronedarone vs. Amiodarone vs. Control 579.733 ± 202.27 vs. 3063.65 ± 467.93 vs. 2682.88 ± 368.75; p < 0.001. dp/dt min mmHg/s 120cmH2O -352.13 ± 204.65 vs. 1960 ± 242.21 vs. -1858.83 ± 118.23; p < 0.001. SLVP mmHg at CPP 120cmH20 27.8 ± 3.46 vs. 98.95 ± 11.78 vs. 71.45 ± 7.56; p < 0.001. DLVP mmHg at CPP 120cmH2O 6.32 ± 0.49 vs. 4.83 ± 0.54 vs. 0.85 ± 0.35; p < 0.001). Acute administration of Dronedarone decreased the level of NO2- and increased the level of H2O2 , while Amiodarone heightens O2- levels (O2- nmol/min g wt at coronary perfusion pressure 120cmH2O Dronedarone vs. Amiodarone vs. Control 28.62 ± 2.54 vs. 77.3 ± 8.86 vs. 31.72 ± 4.56; p < 0.001. H2O2 nmol/min g wt at CPP 120cmH2O 92.56 ± 11.65 vs. 48.63 ± 10.11 vs. 42.84 ± 84; p < 0.001. NO2- nmol/min g wt at CPP 120cmH2O 38.61 ± 4.94 vs. 82.28 ± 5.76 vs. 64.71 ± 3.51; p < 0.001). Pathohistological, structural changes were observed in both, experimental groups. Conclusions Acute administration of Dronedarone depresses cardiac function in isolated, working rat heart with hypertension, with decreasing the NO2- levels, increasing the level of H2O2 and enhanced structural changes when compared to Amiodarone.

Mecanism and inotropic actions of the water exracts of the leaves and seeds of Datura metel (solanaceae) on isolated frogs heart

Datura metel leaves are used by athletes to enhance their performances. The water extract of the leaves and seeds was tested for their cardiotonic effect. Langherdoff’s model for the measurement of the mechanical activity of isolated amphibian heart in ventricular perfusion was used to evaluate some parameters of cardiac contractility. The effect of the extracts was also compared to sympathetic agonist and antagonist. The leaves and seed extracts induced significant (p

Management with Guidance of Minimally Invasive Cardiac Output Monitoring (PiCCO<sup>®</sup>) in Coronary Artery Bypass Surgery and Postoperative Results

Objective: Our study aimed to assess the correlation between the measured PiCCO® parameters and extubation time and intensive care unit length of stay in patients who underwent coronary artery bypass grafting (CABG) surgery and were managed by monitorization of cardiac output and cardiac performance parameters with PiCCO. Method: This study was conducted by retrospective analysis data of all 44 patients who underwent CABG surgery during December 2015-March 2016 and were managed through PiCCO® monitorization, having obtaining approval (17.03.2016-2016/449) of the Ethics Board of Health Sciences University, Istanbul Bagcýlar Training and Research Hospital. The patients’ demographic characteristics (age, sex, weight, height, body mass index), ASA (American Society of Anesthesiologists) physical conditions, comorbidities, ejection fractions, anesthetic management, operative details, hemodynamic data, PiCCO parameters, extubation times, cardiovascular surgery ICU lengths of stay, requirements for vasoactive agent and blood transfusion, mortality, and morbidity were recorded from patient records and evaluated the correlation between the measured PiCCO® parameters and extubation time and intensive care unit length of stay in patients. Results: A significant increase was detected in the parameters of cardiac contractility and performance monitored with PiCCO in the postoperative period (p

Chronic high-dose testosterone treatment: impact on rat cardiac contractile biology.

Androgen therapy provides cardiovascular benefits for hypogonadism. However, myocardial hypertrophy, fibrosis, and infarction have been reported in testosterone or androgenic anabolic steroid abuse. Therefore, better understanding of the factors leading to adverse results of androgen abuse is needed. The aim of the present study was to examine the impact of high dose of androgen treatment on cardiac biology, and whether exposure duration modulates this response. Male rats were treated with 10 mg/kg testosterone, three times a week, for either 4 or 12 weeks; vehicle injections served as controls. Four weeks of testosterone treatment induced an increase in ventricular wall thickness, indicative of concentric hypertrophy, as well as increased ejection fraction; in contrast, both parameters were blunted following 12 weeks of high‐dose testosterone treatment. Cardiac myocyte contractile parameters were assessed in isolated electrically stimulated myocytes (sarcomere and intracellular calcium dynamics), and in chemically permeabilized isolated myocardium (myofilament force development and tension‐cost). High‐dose testosterone treatment for 4 weeks was associated with increased myocyte contractile parameters, while 12 weeks treatment induced significant depression of these parameters, mirroring the cardiac pump function results. In conclusion, chronic administration of high‐dose testosterone initially induces increased cardiac function. However, this initial beneficial impact is followed by significant depression of cardiac pump function, myocyte contractility, and cardiac myofilament function. Our results indicate that chronic high‐testosterone usage is of limited use and may, instead, induce significant cardiac dysfunction.

Flow Pulsatility of Heart Pump: State Space Modeling and Control

In this work, a physiological control strategy using full state feedback (FSF) control method is developed to drive mechanical circulatory support (MCS). This strategy is utilized a validated state space pump model to implement the controller and to track the desired reference flow. The developing strategy is assessed using a software model of the hemodynamical cardiovascular system interacted with left ventricular assist device in different physiological conditions ranging from rest to exercise scenarios. During these scenarios, heart failure disease simulates by changing the hemodynamical parameters of total blood volume, heart rate, cardiac contractility, and systemic peripheral resistance. The results are numerically observed during postural changes. The rate of change in physiological variables showed that the control method can track the reference pump flow with minimal error within acceptable clinical range to prevent suction with lower pump flow (3.35 L/min) and over perfusion with higher pump flow (5.2 L/min).

Physiological studies of cardiac contractility of rabbit heart with experimental hyperthyroidism

Aim: The aim of this study was to evaluate physiological parameters of cardiac contractility in rabbit heart with experimental hyperthyroidism induced with Tyroxine (T4).

Neutrophil to lymphocyte ratio as a predictor of myocardial damage and cardiac dysfunction in acute coronary syndrome patients

BackgroundNeutrophil to lymphocyte ratio (NLR) in peripheral blood is established to correlate with the morbidity and mortality of heart disease patients. We aimed to define the severity of inflammation (NLR) by observing the association of NLR with cardiac functions or myocardial damage parameters in patients with acute myocardial infarction. MethodsData from 715 patients who underwent percutaneous coronary intervention (PCI) within 72hours of incidence in 2016 were analysed retrospectively. ResultsThe NLR ranges from 0.50 to 46 (medium±SD, 2.76±2.96) in 715 patients. NLR positively correlated with myocardial damage (NLR vs. CK-mB: p<0.0001) but negatively correlated with myocardial function (NLR vs. EF: p<0.0001; NLR vs. FS: p<0.0001). Myocardial damage markers (CK, CK-mB, ASL, LDH) were significantly increased, and cardiac contractile parameters (EF and FS) were reduced at NLR>2.76 compared to those of NLR<2.76. ELISA analysis has shown that IL-10 was significantly increased when NLR≥4.6 and TGF-β was increased at NLR>4. The correlation was diminished between NLR and CK-mB at NLR>2.76 or at NLR>4, but that of NLR and EF or FS was maintained in NLR>2.76 and at NLR>4. EF and FS were comparable between NLR>2.76 and NLR>4. But myocardial damage parameters increased significantly at NLR>4 compared to those of NLR>2.76. ConclusionNLR is a strong predictor of myocardial damage in acute myocardial patients. High NLR are associated with myocardial dysfunction in all the patients. Severe inflammation (NLR) can predict the consequence of the heart in patients with coronary syndrome.

Chronic activation of hypothalamic oxytocin neurons improves cardiac function during left ventricular hypertrophy-induced heart failure

A distinctive hallmark of heart failure (HF) is autonomic imbalance, consisting of increased sympathetic activity, and decreased parasympathetic tone. Recent work suggests that activation of hypothalamic oxytocin (OXT) neurons could improve autonomic balance during HF. We hypothesized that a novel method of chronic selective activation of hypothalamic OXT neurons will improve cardiac function and reduce inflammation and fibrosis in a rat model of HF. Two groups of male Sprague-Dawley rats underwent trans-ascending aortic constriction (TAC) to induce left ventricular (LV) hypertrophy that progresses to HF. In one TAC group, OXT neurons in the paraventricular nucleus of the hypothalamus were chronically activated by selective expression and activation of excitatory DREADDs receptors with daily injections of clozapine N-oxide (CNO) (TAC + OXT). Two additional age-matched groups received either saline injections (Control) or CNO injections for excitatory DREADDs activation (OXT NORM). Heart rate (HR), LV developed pressure (LVDP), and coronary flow rate were measured in isolated heart experiments. Isoproterenol (0.01 nM-1.0 µM) was administered to evaluate β-adrenergic sensitivity. We found that increases in cellular hypertrophy and myocardial collagen density in TAC were blunted in TAC + OXT animals. Inflammatory cytokine IL-1β expression was more than twice higher in TAC than all other hearts. LVDP, rate pressure product (RPP), contractility, and relaxation were depressed in TAC compared with all other groups. The response of TAC and TAC + OXT hearts to isoproterenol was blunted, with no significant increase in RPP, contractility, or relaxation. However, HR in TAC + OXT animals increased to match Control at higher doses of isoproterenol. Activation of hypothalamic OXT neurons to elevate parasympathetic tone reduced cellular hypertrophy, levels of IL-1β, and fibrosis during TAC-induced HF in rats. Cardiac contractility parameters were significantly higher in TAC + OXT compared with TAC animals. HR sensitivity, but not contractile sensitivity, to β-adrenergic stimulation was improved in TAC + OXT hearts.

Hemodynamic Analysis of Pediatric Septic Shock and Cardiogenic Shock Using Transpulmonary Thermodilution.

Septic shock and cardiogenic shock are the two most common types of shock in children admitted to pediatric intensive care units (PICUs). The aim of the study was to investigate which hemodynamic variables were associated with mortality in children with shock. We retrospectively analyzed 50 children with shock (37 septic shock cases and 13 cardiogenic shock cases) in the PICU and monitored their hemodynamics using transpulmonary thermodilution from 2003 to 2016. Clinical factors were analyzed between the patients with septic and cardiogenic shock. In addition, hemodynamic parameters associated with mortality were analyzed. The 28-day mortality was significantly higher in the septic group than in the cardiogenic group (p = 0.016). Initially, the parameters of cardiac output and cardiac contractility were higher in the septic group (p < 0.05) while the parameters of preload and afterload were all higher in the cardiogenic group (p < 0.05). Cardiac index was significantly lower in the nonsurvivors of cardiogenic shock at the time of initial admission and after the first 24 hours (both p < 0.05), while systemic vascular resistance index (SVRI) was significantly lower in the nonsurvivors of septic shock (p < 0.001). Therefore, during the first 24 hours after intensive care, SVRI and cardiac index are the most important hemodynamic parameters associated with mortality.