Increase In Cardiac Output Research Articles

Levosimendan Versus Milrinone in the Management of Impaired Left Ventricular Function in Patients Undergoing Coronary Artery Bypass Graft Surgery

Background: Patients undergoing cardiac surgery are at risk of postcardiotomy myocardial dysfunction. This condition causes delayed recovery, organ failure, prolonged intensive care unit and hospital stays, and an increased risk of mortality; these patients often require inotropic agent support. Levosimendan is a calcium sensitizer with a unique mechanism of action, binding to cardiac troponin C and enhancing myofilament responsiveness to calcium, increasing myocardial contraction without increasing myocardial oxygen consumption. Phosphodiesterase III inhibitors such as milrinone provide an alternative means of inotropic support by increasing the concentration of cyclic AMP and intracellular calcium. They also have vasodilatory effects. Objective: The aim of this study was the comparison between levosimendan versus milrinone regarding their effects on the hemodynamics, need for additional mechanical (intra aortic balloon pump) or pharmacological support to the heart, weaning from mechanical ventilation and duration of intensive care unit stay for patients after Off-Pump Coronary Artery Bypass Graft (OPCABG) surgery suffering from impaired left ventricular function (preoperative ejection fraction ≤ 40%). Methods: 60 patients between 40 and 70 years of both sexes with impaired left ventricular function (ejection fraction ≤ 40%), New York Heart Association (NYHA III & IV), undergoing elective Off-Pump Coronary Artery Bypass Graft (OPCABG) surgery were selected for this study. After induction of anesthesia, patients were randomly assigned to one of two equal groups each containing 30 patients: Group L (Levosimendan group) included patients who received levosimendan 0.1- 0.2 µg/kg/min. Started immediately with the induction of anesthesia. Group M (Milrinone group) included patients who received milrinone 0.4-0.6 µg/kg/min. Started immediately with the induction of anesthesia. In both groups, norepinephrine was titrated (8 mg norepinephrine in 50 ml saline) to keep mean arterial pressure MAP ≥ 70 mmHg. Hemodynamic findings included Preoperative and post ICU discharge ejection fraction, systemic and pulmonary artery pressures, systemic and pulmonary vascular resistance, cardiac output and stroke volume. Also laboratory findings included Serum lactate and Troponin I., in addition, to post operative findings were: Need for intra aortic balloon pump, time of weaning from the ventilator, days of ICU stay and appearance of drug allergy compared in both groups. Results: There was a significant increase in the ejection fraction in both groups that was greater in the levosimendan group. The decrease in pulmonary pressure in the levosimendan group was more significant than milrinone group. There was a gradual decrease in pulmonary and systemic vascular resistance in both groups with a more significant decrease in the levosimendan group. There was a gradual increase in cardiac output and stroke volume in both groups that was greater in the levosimendan group. Serum lactate gradually decreased in both groups with an insignificant difference; there was an increase in serum troponin I level in both groups which was more significant in the milrinone group. Weaning from mechanical ventilation and length of ICU stay was shown to be significantly shorter in time in the levosimendan group. Conclusion: Both levosimendan and milrinone caused a significant increase in cardiac output, stroke volume and ejection fraction, with a decrease in pulmonary and systemic vascular resistance. These effects improved cardiac performance by decreasing afterload and increasing cardiac inotropism. It was noticed that these effects were more significant with levosimendan than milrinone. Also, there was a decrease in ICU stay, mechanical ventilation timing and hospital stay with levosimendan than milrinone which decreased the costs of treatment for the patients.

Preeminent role of the cardiorenal axis in the antihypertensive response to an arteriovenous fistula: an in silico analysis.

Percutaneous creation of a small central arteriovenous (AV) fistula is currently being evaluated for the treatment of uncontrolled hypertension (HT). Although the mechanisms that contribute to the antihypertensive effects of the fistula are unclear, investigators have speculated that chronic blood pressure (BP) lowering may be due to 1) reduced total peripheral resistance (TPR), 2) increased secretion of atrial natriuretic peptide (ANP), and/or 3) suppression of renal sympathetic nerve activity (RSNA). We used an established integrative mathematical model of human physiology to investigate these possibilities from baseline conditions that mimic sympathetic overactivity and impaired renal function in patients with resistant HT. After a small fistula was stimulated, there were sustained increases in cardiac output, atrial pressures, and plasma ANP concentration (3-fold), without suppression of RSNA; at 8 wk, BP was reduced 14 mmHg along with a 32% fall in TPR. In contrast, when this simulation was repeated while clamping ANP at baseline BP decreased only 4 mmHg, despite a comparable fall in TPR. Furthermore, when chronic resetting of atrial mechanoreceptors was prevented during the fistula, RSNA decreased 7%, and along with the same threefold increase in ANP, BP fell 19 mmHg. This exaggerated fall in BP occurred with a similar decrease in TPR when compared with the above simulations. These findings suggest that ANP, but not TPR, is a key determinant of long-term BP lowering after the creation of an AV fistula and support a contribution of suppressed RSNA if resetting of the atrial-renal reflex is truly incomplete.NEW & NOTEWORTHY The mechanisms that contribute to the antihypertensive effects of a small arteriovenous (AV) fistula comparable to the size used by the ROX coupler currently in clinical trials are unclear and not readily testable in clinical or experimental studies. The integrative mathematical model of human physiology used in the current study provides a tool for understanding key causal relationships that account for blood pressure (BP) lowering and for testing competing hypotheses. The findings from the simulations suggest that after creation of a small AV fistula increased ANP secretion plays a critical role in mediating long-term reductions in BP. Measurement of natriuretic peptide levels in hypertensive patients implanted with the ROX coupler would provide one critical test of this hypothesis.

Cavopulmonary assist: Long-term reversal of the Fontan paradox

ObjectiveFontan circulatory inefficiency can be addressed by replacing the missing subpulmonary power source to reverse the Fontan paradox. An implantable cavopulmonary assist device is described that will simultaneously reduce systemic venous pressure and increase pulmonary arterial pressure, improving preload and cardiac output, in a univentricular Fontan circulation on a long-term basis. MethodsA rotary blood pump that was based on the von Karman viscous pump was designed for implantation into the total cavopulmonary connection (TCPC). It will impart modest pressure energy to augment Fontan flow without risk of obstruction. In the event of rotational failure, it is designed to default to a passive flow diverter. Pressure-flow performance was characterized in vitro in a Fontan mock circulatory loop with blood analog. ResultsThe pump performed through the fully specified operating range, augmenting flow in all 4 directions of the TCPC. Pressure rise of 6 to 8 mm Hg was readily achieved, ranging to 14 mm Hg at highest speed (5600 rpm). Performance was consistent across a wide range of cardiac outputs. In stalled condition (0 rpm), there was no discernible pressure loss across the TCPC. ConclusionsA blood pump technology is described that can reverse the Fontan paradox and may permit a surgical strategy of long-term biventricular maintenance of a univentricular Fontan circulation. The technology is intended for Fontan failure in which right-sided circulatory inefficiencies predominate and ventricular systolic function is preserved. It may also apply before clinical Fontan failure as health maintenance to preempt the progression of Fontan disease.

Safety, hemodynamic effects, and detection of acute xenon inhalation: rationale for banning xenon from sport.

This study aimed to quantify the sedative effects, detection rates, and cardiovascular responses to xenon. On 3 occasions, participants breathed xenon (FiXe 30% for 20 min; FiXe 50% for 5 min; FiXe 70% for 2 min) in a nonblinded design. Sedation was monitored by a board-certified anesthesiologist. During 70% xenon, participants were also verbally instructed to operate a manual value with time-to-task failure being recorded. Beat-by-beat hemodynamics were measured continuously by ECG, photoplethysmography, and transcranial Doppler. Over 48 h postadministration, xenon was measured in blood and urine by gas chromatography-mass spectrometry. Xenon caused variable levels of sedation and restlessness. Task failure of the self-operating value occurred at 60-90 s in most individuals. Over the first minute, 50% and 70% xenon caused a substantial reduction in total peripheral resistance (P < 0.05). All dosages caused an increase in cardiac output (P < 0.05). By the end of xenon inhalation, slight hypertension was observed after all three doses (P < 0.05), with an increase in middle cerebral artery velocity (P < 0.05). Xenon was consistently detected, albeit in trace amounts, up to 3 h after all three doses of xenon inhalation in blood and urine with variable results thereafter. Xenon inhalation caused sedation incompatible with self-operation of a breathing apparatus, thus causing a potential life-threatening condition in the absence of an anesthesiologist. Yet, xenon can only be reliably detected in blood and urine up to 3 h postacute dosing.NEW & NOTEWORTHY Breathing xenon in dosages conceivable for doping purposes (FiXe 30% for 20 min; FiXe 50% for 5 min; FiXe 70% for 2 min) causes an initial rapid fall in total peripheral resistance with tachycardia and thereafter a mild hypertension with elevated middle cerebral artery velocity. These dose duration intervals cause sedation that is incompatible with operating a breathing apparatus and can only be detected in blood and urine samples with a high probability for up to ~3 h.

Correlation between V?O2max and systolic time interval in athletes

Correlation between V?O2max and systolic time interval in athletes - IJPCA- Print ISSN No: - 2394-2789 Online ISSN No:- 2394-2797 Article DOI No:- 10.18231/j.ijpca.2019.009, International Journal of Pharmaceutical Chemistry and Analysis-Int J Pharm Chem Anal

Ex vivo assessment of bicuspidization repair in treating severe functional tricuspid regurgitation: a stereo-scopic PIV study

There has been a resurgence of interest in the treatment of severe functional tricuspid regurgitation (FTR) due to the awareness of its poor outcomes and potential percutaneous therapies. Kay bicuspidization has been adapted in percutaneous therapies but its clinical outcome remains uncertain. The present study evaluates the efficacy of Kay repair in a novel ex vivo pulsatile system. Porcine tricuspid valve (TV) (n = 3) was extracted and incorporated into a patient-specific silicon right ventricle (RV) emulating severe FTR, on which Kay repair was subsequently performed. TV area metrics and RV hemodynamic assessment by means of stereo-scopic particle image velocimetry were quantified in both FTR and post-repair conditions. Bicuspidization led to significant increase in cardiac output although the overall increment due to this approach alone was generally small, possibly due to existence of residual TR and the large reduction in TV opening area. Kinetic energy and viscous loss levels were increased post-repair, especially during diastolic filling. Main vortex structures generally maintained post-procedural. However, there was enhanced swirling motion in larger RV domain. Although this might reduce mural-thrombus risk, the relatively more complex vortex phenomenon likely resulted in elevated viscous loss observed and may potentially impact long-term adaptation. The RV hemodynamic alteration after tricuspid repair could be used to predict the success of these future transcatheter solutions.

End Tidal Carbon dioxide can track cardiac output changes during fluid challenge in Shocked Mechanically Ventilated Patients

Background: In this study, we investigated the ability of end tidal carbon dioxide pressure (PETCO2) to monitor the changes in cardiac output (CO) induced by fluid challenge and to predict fluid responsiveness. Patients and Methods: We conducted our study upon 38 shocked patients requiring fluid challenge (FC). Hemodynamic variables, central venous pressure (CVP), End-tidal CO2, arterial and venous blood gas analysis and cardiac output were recorded before and after fluid challenges. Fluid responders were identified when cardiac output increased more than 15% after fluid challenge, cardiac output (CO) was estimated by measuring left ventricular outflow tract velocity-time integral (LVOT VTI) by transthoracic doppler echocardiography. Results: Twenty-one (55.3%) patients were fluid responders. Fluid challenge induced increase in CO and PETCO2 was moderately correlated (r = 0.5; P 0.002). The area under receiver operating characteristic (ROC) curve of Δ PETCO2 was 0.89±0.05 CI (81- 98) with an increase ≥ 3.13% in PETCO2 can predict fluid responsiveness with 85.7% sensitivity and 88.3% specificity. No other clinical or hemodynamic variables can predict fluid responsiveness. The area under ROC curve of ΔCVP was 0.48±0.1 CI (32- 64) with an increase ≥ 2cmH2O in CVP can predict fluid responsiveness with 38% sensitivity and 76.5% specificity. Conclusions: Our findings indicate that induced changes in PETCO2 during fluid challenge could be used to monitor changes in cardiac output (CO) for prediction of fluid responsiveness in mechanically ventilated shocked patients, under stationary minute ventilation and steady CO2 production

Abstract 177: Hemodynamic Status From Photoplethysmography, Signs of Successful Pregnancy

The key physiological condition for successful pregnancy is a critical issue in reproductive science. Many studies have shown that the pregnancy process requires a lot of subtle cardiovascular adaptation, including a decrease in systemic vascular resistance, an increase in maternal heart rate, stroke volume, and cardiac output. Those adaptation will also lead to changes in the arterial pulse spectrum. Since pregnancy requires the mother's competency to change the hemodynamic state, an interesting question is if the pre-pregnancy hemodynamics of the cardiovascular system affect the clinical pregnancy rate of each embryo transfer. Therefore, we initiated an observational study to validate our conjecture. We recruited 116 women of childbearing age(range 22 to 41 years) who planned to carry out in vitro fertilization(IVF). Each subject underwent photoplethysmography(PPG) before embryo implantation. We calculated the first ten harmonic amplitudes (C1~C10) and phases (P1~P10) from the pulse data of PPG using the Fourier transform method, and tracked these women to 42 days after implantation to confirm the successful pregnancy. The results showed that the subjects with successful IVF had higher C4 and C7(P=0.006; P=0.018), compared with those who failed the IVF. We then classified the enrolled patients into quartile groups of C4 and C7 respectively. Log rank test further proved that the cumulative rates of successful pregnancy were significant higher for those with the higher C4 and C7, taking groups with smaller values as reference(Figure 1). In conclusion, maternal hemodynamic state before implantation have an impact on the successful pregnancy rate during IVF.

Abstract 333: Cardiomyocyte Hypercontractility is an Adaptational Response to Stiffness in High-Fat Diet Mice

Diabetic heart disease typically features a restrictive/ hypertrophic cardiac phenotype characterised by diastolic dysfunction with preserved systolic performance. Little is known about the early adaptational mechanisms that underpin maintenance of systolic performance in diabetic diastolic dysfunction and how this may contribute to disease progression. This study aimed to evaluate cardiomyocyte contractility in a high-fat diet (HFD) mouse model of diastolic dysfunction. Echocardiography (GE Vivid 9) was performed in 33 wk old male C57Bl/6 mice fed a high-fat diet (HFD, 43% kcal fat, 24 wks duration). Isolated cardiomyocytes (paced 2Hz, 2.0mM Ca 2+ , 37C) were subjected to progressive axial stretch. Sarcomere length/ shortening, tension and intracellular calcium transients (Fura-2AM, 5μM) were simultaneously measured (Myostretcher, Ionoptix). HFD hearts displayed in vivo (22.2±1.4 vs 16.7±1.0 E/E’; p&lt;0.05) and in vitro diastolic dysfunction (0.244±0.039 vs 0.075±0.017 nN/pl/ %cell stretch; p&lt;0.05). HFD cardiomyocytes exhibited length-dependent hypercontractility with augmented developed tension amplitude at maximal stretch (4.891±0.942 vs 2.484±0.677 nN/pl; p&lt;0.05), but not basal stretch. Hypercontractility could not be attributed to a difference in Ca 2+ transient amplitude but was correlated with length dependence of Ca 2+ sensitivity (n=17 cells, R 2 =0.4039 p&lt;0.05). During progressive cardiomyocyte stretch, systolic tension slopes were strongly correlated with diastolic tension slopes (cardiomyocyte stiffness) (n=30 cells; R 2 =0.8442, p&lt;0.05) while there was no difference in the ratio of systolic/diastolic tension slopes indicating maintained length-dependent activation. These findings provide the first evidence that cardiomyocyte hypercontractility and stiffness are strongly linked. High-fat diet cardiomyocytes may operate near maximal contractile capacity to maintain basal cardiac output, potentially limiting capacity for cardiac output increase in response to physiological stressors. An aberrant myofilament post-translational modification profile represents a potential mechanism through which cardiac dysfunction arises during the development of diabetes.

Maternal Fontan procedure is a predictor of a small-for-gestational-age neonate: a 10-year retrospective study

Women with single ventricle cardiac physiologic condition who have undergone Fontan procedures are surviving well into reproductive age and historically have been discouraged from pregnancy, despite the paucity of data regarding maternal and neonatal outcomes. Our primary objective was to investigate, in a large cohort, the maternal and neonatal outcomes of pregnant women who have undergone the Fontan procedure and to understand maternal and neonatal sequelae of their pregnancies. This single-center retrospective cohort study involves pregnant women with a Fontan palliation who delivered at UCLA Medical Center over a 10-year period (2007-2017). All pregnancies were evaluated for differences in maternal and neonatal characteristics. We identified 37 distinct pregnancies in 24 women with a Fontan procedure. The physiologic pregnancy-related increase in cardiac output is blunted substantially in Fontan circulation. Third-trimester cardiac index positively correlated to birthweight z-score (R2=0.48; P=.038) but not to small for gestational age (R2=0.13; P=.339). The most common cardiac complications in pregnancies of >24 weeks gestation were sustained arrhythmia (37.5%) and decompensated heart failure (21%). The 37 pregnancies comprised 25 live births (67.6%), 1 fetal death (2.7%), 9 spontaneous abortions (24%), and 2 pregnancy terminations (5.4%). Of the live births, 60% were preterm at an average gestational age of 34.9±3.7 weeks. Newborn infants were delivered via cesarean in 53%, operative vaginal delivery in 28%, and spontaneous vaginal delivery in 20%. Forty percent of neonates were born small (<10th percentile) for gestational age; 44.0% of all neonates were admitted to the neonatal intensive care unit. Women with a single ventricle and Fontan circulation can have a successful pregnancy, although they are at increased risk for arrhythmias and heart failure. The decreased cardiac reserve in these pregnancies blunts the normal increase in maternal cardiac output, which is associated with preterm delivery and small-for-gestational-age neonates. Further studies are needed to determine to what extent the impaired rise in maternal cardiac output reduces uteroplacental perfusion, placental exchange, fetal growth, and onset of parturition.

Predictors of Hemodynamic Response to Intra-Aortic Balloon Pump Therapy in Patients with Acute Decompensated Heart Failure and Cardiogenic Shock

Introduction There is renewed interest in the utility of the intra-aortic balloon pump (IABP) for short-term and durable support in patients with chronic systolic heart failure (HF) who present with acute decompensation and cardiogenic shock (CS). However, the clinical characteristics of IABP-responders and non-responders remain incompletely defined. We sought to identify predictors of early IABP response to guide optimal use of IABP therapy in this population. Methods We retrospectively analyzed the records of chronic systolic HF patients who presented at our institution between 2011-2018 with acute decompensated HF with hemodynamic evidence of CS and underwent IABP placement. IABP-responder was defined as having an immediate increase in cardiac output (CO) and an immediate decrease in mean pulmonary artery pressure (MPAP) above the median values of the cohort. Logistic regression was used to identify predictors of hemodynamic response. Results During the study period, 218 chronic systolic HF patients underwent IABP insertion for acute decompensation with CS. The mean age was 59.4 ±13.4 years, 79.8% were men, and 38.5% had ischemic cardiomyopathy (ICM). The average hemodynamic response to IABP in the whole cohort was a CO increase of 0.57 ±0.85L/min and a MPAP reduction of 5.1 ±7.6mmHg; IABP-responders had a CO increase of 1.21 ±0.87L/min and a MPAP reduction of 12.1 ±5.9mmHg (figure). Univariable predictors of IABP-response were ICM, presence of severe mitral regurgitation, baseline heart rate, elevated MPAP, and elevated systemic vascular resistance (SVR). Following multivariable logistic regression, independent predictors of IABP-response were elevated baseline SVR (OR 2.05, 95% CI 1.01 - 4.17; p=0.047) and elevated MPAP (OR 2.47, 95% CI 1.23 - 5.00; p=0.01). MPAP reduction decreased the odds of death or need for escalation to another short-term circulatory support device while CO increase did not [OR 0.52 (0.28 - 0.97; p=0.04) vs. 0.83 (0.45 - 1.54; p=0.56)]. Conclusions A subset of chronic systolic HF patients had a robust hemodynamic response to IABP insertion with CO augmentation and MPAP reduction. Elevated baseline SVR and MPAP are predictors of robust response following device insertion. These parameters may be used to identify patients who may respond favorably to IABP counterpulsation therapy.

Effect of knockout of the ASIC3 on cardiovascular reflexes arising from hindlimb muscle in decerebrated rats.

The exercise pressor reflex is initiated by the contraction-induced activation of group III and IV muscle afferents. The reflex is manifested by increases in arterial blood pressure and cardiac output, which, in turn, are generated by increases in the sympathetic outflow to the heart and vasculature and decreases in the vagal outflow to the heart. In previous experiments, we used a pharmacological approach to assess the role played by the acid-sensing ion channel 3 (ASIC3) on group III and IV afferents in evoking the exercise pressor reflex. In the present experiments, we used an alternative approach, namely functional knockout (KO) of the ASIC3 gene, to confirm and extend our previous finding that pharmacological blockade of the ASIC3 had only a small impact on the expression of the exercise pressor reflex when the arterial supply to the contracting hindlimb muscles of rats was patent. Using this alternative approach, we compared the magnitude of the exercise pressor reflex evoked in ASIC3 KO rats with that evoked in their wild-type (WT) counterparts. We found both WT and ASIC3 KO rats displayed similar pressor responses to static contraction (WT, n = 10, +12 ± 2 mmHg; KO, n = 9, +11 ± 2 mmHg) and calcaneal tendon stretch (WT, n = 9, +13 ± 2 mmHg; KO, n = 7, +11 ± 2 mmHg). Likewise, both WT and ASIC3 KO displayed similar pressor responses to intra-arterial injection of 12 mM lactic acid (WT, n = 9, +14 ± 3 mmHg; KO, n = 8, +18 ± 5 mmHg), 24 mM lactic acid (WT, n = 9,+24 ± 2 mmHg; KO, n = 8, +20 ± 5 mmHg), capsaicin (WT, n = 9,+27 ± 5 mmHg; KO, n = 10, +29 ± 5 mmHg), and diprotonated phosphate ([Formula: see text]; WT, n = 6,+22 ± 3 mmHg; KO, n = 6, +32 ± 6 mmHg). We conclude that redundant receptors are responsible for evoking the pressor reflexes arising from group III and IV afferents.

PH Grand Rounds: A Case of Pulmonary Hypertension Associated With High Cardiac Output State from Arteriovenous Fistula–Or Is It?

PH Grand Rounds: A Case of Pulmonary Hypertension Associated With High Cardiac Output State from Arteriovenous Fistula–Or Is It?

PRECISION MEDICINE

Objective:For decades, it has been widely accepted that initiation of salt-induced hypertension involves a type of kidney dysfunction (natriuretic handicap) which causes salt-sensitive subjects to excrete less of a sodium load than normal subjects and to undergo abnormal increases in cardiac output,

Pulmonary capillary surface area in supine exercising humans: demonstration of vascular recruitment.

In exercising humans, cardiac output (CO) increases, with minor increases in pulmonary artery pressure (PAP). It is unknown if the CO is accommodated via distention of already perfused capillaries or via recruitment of nonconcomitantly perfused pulmonary capillaries. Ten subjects (9 female) performed symptom-limited exercise. Six had resting mean PAP (PAPm) <20 mmHg, and four had PAPm between 21 and 24 mmHg. The first-pass pulmonary circulatory metabolism of [3H]benzoyl-Phe-Ala-Pro (BPAP) was measured at rest and at peak exercise, and functional capillary surface area (FCSA) was calculated. Data are means ± SD. Mean pulmonary arterial pressure rose from 18.8 ± 3.3 SD mmHg to 28.5 ± 4.6 SD mmHg, CO from 6.4 ± 1.6 to 13.4 ± 2.9 L/min, and pulmonary artery wedge pressure from 14 ± 3.3 to 19.5 ± 5 mmHg (all P ≤ 0.001). Percent BPAP metabolism fell from 74.7 ± 0.1% to 67.1 ± 0.1%, and FCSA/body surface area (BSA) rose from 2,939 ± 640 to 5,018 ± 1,032 mL·min-1·m-2 (all P < 0.001). In nine subjects, the FCSA/BSA-to-CO relationship suggested principally capillary recruitment and not distention. In subject 10, a marathon runner, resting CO and FCSA/BSA were high, and increases with exercise suggested distention. Exercising humans demonstrate pulmonary capillary recruitment and distention. At moderate resting CO, increasing blood flow causes principally recruitment while, based on one subject, when exercise begins at high CO, further increases appear to cause distention. Our findings clarify an important physiologic question. The technique may provide a means for further understanding exercise physiology, its limitation in pulmonary hypertension, and responses to therapy.

The benefits of a challenge approach on match day: Investigating cardiovascular reactivity in professional academy soccer players

This study assessed physiological (cardiovascular) and psychological (confidence, control, and approach focus) data in professional academy soccer players prior to performance in competitive matches. A challenge state is characterised by an increase in cardiac output (CO), and a decrease in total peripheral vascular resistance (TPR). Data were collected from 37 participants, with 19 of these providing data on two separate occasions. Performance was measured using coach and player self-ratings. Challenge reactivity was positively, and significantly, associated with performance. Participants who demonstrated blunted cardiovascular (CV) responses performed significantly worse than participants who displayed either challenge or threat reactivity. There was mixed consistency in CV reactivity for those participants whose data were collected on more than one occasion, suggesting that some participants responded differently across the competitive matches. The association between self-report data and CV responses was weak. This study supports previous research demonstrating that challenge reactivity is associated with superior performance.

Sex differences in blood pressure regulation during ischemic isometric exercise: the role of the β-adrenergic receptors.

We sought to investigate whether the β-adrenergic receptors play a pivotal role in sex-related differences in arterial blood pressure (BP) regulation during isometric exercise. Sixteen volunteers (8 women) performed 2 min of ischemic isometric handgrip exercise (IHE) and 2 min of postexercise circulatory occlusion (PECO). Heart rate (HR) and beat-to-beat arterial BP were continuously measured. Beat-to-beat estimates of stroke volume (ModelFlow) were obtained and matched with HR to calculate cardiac output (Q̇) and total peripheral resistance (TPR). Two trials were randomly conducted between placebo and nonselective β-adrenergic blockade (40 mg propranolol). Under the placebo condition, the magnitude of the BP response in IHE was lower in women compared with men. During PECO, the BP remained elevated and the sex differences persisted. The β-blockade attenuated the BP response during IHE in men (∆57 ± 4 vs. ∆45 ± 7 mmHg, P = 0.025) due to a reduction in Q̇ (∆3.7 ± 0.5 vs. ∆1.8 ± 0.2 L/min, P = 0.012) while TPR was not affected. In women, however, the BP response during IHE was unchanged (∆27 ± 3 vs. ∆28 ± 3 mmHg, P = 0.889), despite attenuated Q̇ (∆2.7 ± 0.4 vs. ∆1.3 ± 0.2 L/min, P = 0.012). These responses were mediated by a robust increase in TPR under β-blockade (∆-0.2 ± 0.4 vs. ∆2.2 ± 0.7 mmHg·L-1·min, P = 0.012). These findings demonstrate that the sex differences in arterial BP regulation during ischemic IHE are mediated by β-adrenergic receptors.NEW & NOTEWORTHY We found that the blood pressure response during isometric exercise in women is mediated by increases in cardiac output, whereas in men it is mediated by increases in both cardiac output and total peripheral resistance. In addition, women showed a robust increase in total peripheral resistance under β-blockade during isometric exercise and muscle metaboreflex activation. These findings demonstrate that sex differences in blood pressure regulation during isometric exercise are mediated by β-adrenergic receptors.

Hypotension in Cirrhosis.

Circulatory and cardiac compromise in cirrhosis has been well studied. The primary pathophysiology stems from portal hypertension, which is induced from an increased resistance to flow secondary to distorted sinusoidal architecture and is further sustained from an increase in portal venous flow.1 Portal hypertension induces both progressive splanchnic and systemic vasodilation mediated via nitric oxide and other vasoactive molecules secondary to endothelial stretching and sheer stress.2 A hyperdynamic state then ensues with an increase in cardiac output, increase in heart rate, and a low systemic vascular resistance secondary to systemic vasodilatation. The decreased effective arterial blood volume activates neurohormonal systems such as the renin‐angiotensin‐aldosterone system (RAAS), leading to further volume expansion via sodium and water retention. However, because of portosystemic shunting and splanchnic vasodilatation, effective central blood volume remains low and the hyperdynamic state continues, eventually leading to high‐output heart failure (Fig. ​(Fig.1).1). A lower mean arterial pressure (MAP) of 60 to 65 mm Hg is often tolerated in compensated and stable patients through these compensatory mechanisms, which allow end‐organ perfusion to be maintained.1, 2 Any degree of insult to this system can result in significant hypotension and decompensation. Open in a separate window Figure 1 Pathophysiology of hypotension in cirrhosis.

Exercise haemodynamics after restrictive mitral annuloplasty for functional mitral regurgitation.

Restrictive mitral annuloplasty (RMA) can provide a durable solution for functional mitral regurgitation (MR), but might result in obstruction to antegrade mitral flow. Aim of this study was to assess the magnitude of change in mitral valve area (MVA) during exercise after RMA, to relate the change in MVA to left ventricular (LV) geometry and function, and to assess its haemodynamic and clinical impact. Bicycle exercise echocardiography was performed in 32 patients after RMA. Echocardiographic data at rest and during exercise were compared with preoperative echocardiographic data. Clinical endpoints were collected following the study visit. MVA increased during exercise in 25 patients (1.6 ± 0.4 cm2 to 2.0 ± 0.6 cm2, P < 0.001), whereas MVA decreased in 7 patients (1.8 ± 0.5 cm2 to 1.5 ± 0.4 cm2, P = 0.020). Patients with an increased MVA showed a significant reduction in LV volumes at rest compared to preoperatively, and an increase in stroke volume and cardiac output (CO) during exercise. In patients with decreased MVA, LV reverse remodelling was absent and myocardial flow reserve limited. Patients with decreased exercise MVA had a higher increase in mean pulmonary artery pressure (PAP) with respect to CO and worse survival 36 months after the study visit (69±19% vs. 92±5%, P = 0.005). Both increased and decreased MVA were observed during exercise echocardiography after RMA for functional MR. Change in MVA was related to the extent of LV geometrical and functional changes. A decreased MVA during exercise was associated with a higher increase in mean PAP with respect to CO, and worse survival.

Influence of left ventricular assist device pressure-flow characteristic on exercise physiology: Assessment with a verified numerical model.

Current left ventricular assist devices are designed to reestablish patient's hemodynamics at rest but they lack the suitability to sustain the heart adequately during physical exercise. Aim of this work is to assess the performance during exercise of a left ventricular assist device with flatter pump pressure-flow characteristic and increased pressure sensitivity (left ventricular assist device 1) and to compare it to the performance of a left ventricular assist device with a steeper characteristic (left ventricular assist device 2). The two left ventricular assist devices were tested at constant rotational speed with a verified computational cardiorespiratory simulator reproducing an average left ventricular assist device patient response to exercise (EXE↑) and a left ventricular assist device patient with no chronotropic and inotropic response (EXE→). According to the results, left ventricular assist device 1 pumps a higher flow than left ventricular assist device 2 both at EXE↑ (6.3 vs 5.6 L/min) and at EXE→ (6.7 vs 6.1 L/min), thus it better unloads the left ventricle. Left ventricular assist device 1 increases the power delivered to the circulation from 0.63 W at rest to 0.67 W at EXE↑ and 0.82 W at EXE→, while left ventricular assist device 2 power shows even a minimal decrease. Left ventricular assist device 1 better sustains exercise hemodynamics and can provide benefits in terms of exercise performance, especially for patients with a poor residual left ventricular function, for whom the heart can hardly accommodate an increase of cardiac output.