Cardiac Output Research Articles

Space Travel: The Radiation and Microgravity Effects on the Cardiovascular System.

Space flight modulates the functions of the cardiovascular system. The exposure to space conditions can alter the cerebral blood flow, as well as the venous return. Anemia, cardiac output changes, and increased activity of the sympathetic nervous system can also be seen. Understanding cardiac changes prepares astronauts for both better in-flight adaptations and long-term protection against cardiovascular diseases. The heart could undergo radio-degenerative effects when exposed to space radiation, increasing the risk of cardiovascular diseases in the long run. A high frequency of arrhythmias, such as ventricular/atrial premature complexes, have been reported during the Gemini and Apollo missions. Additionally, microgravity can lead to progressive degeneration of the myocytes and muscle atrophy with altered gene expression and calcium handling, along with impaired contractility. This review summarizes the potential cardiovascular effects of spaceflight and prevention measures.

Accidental finding of ALCAPA in a child with severe mitral regurgitation: A case study.

A six-year-old child who had undergone cardiac surgery five years ago presented to us with severe mitral valve regurgitation. During her current surgery, the coronary artery was injured during the attempt to release extensive epicardial adhesion, resulting in very poor contractility that prompted a delay in the intended valve repair. The injured coronary vessels were successfully repaired, yet low cardiac output syndrome persisted during perioperative care, necessitating further investigation of the coronary problem. It was later discovered that the patient had anomalous left coronary artery from pulmonary artery (ALCAPA) syndrome. The presence of severe mitral regurgitation, pulmonary hypertension, and anatomical factors may have contributed to the delayed presentation and diagnosis in this case. The severity of mitral regurgitation and the most likely underlying mechanism indicates a low possibility of recovery following coronary repair alone, warranting the need for concomitant mitral surgery. Coronary and mitral repair were performed in this patient, resulting in a favorable outcome. The management of ALCAPA presents unique challenges, especially in cases with delayed diagnosis. Proper diagnosis and tailored surgical approaches are crucial for achieving favorable outcomes in patients with ALCAPA.

Electrophysiological tolerance - a new concept for understanding the electrical stability of the heart.

The coordinated electrical activity of ∼2 billion cardiac cells ensures stability of the heartbeat. Indeed, the remarkably low incidence (<1%) of ventricular arrhythmias in the healthy heart is only possible when the electrical event across this syncytium is closely controlled. In contrast, the diseased myocardium is associated with increased electrophysiological heterogeneity, unstable rhythm, and increased incidence of lethal arrhythmias. But what is the link between cellular and tissue level heterogeneity? Recent research has shown the existence of considerable cellular heterogeneity even in the healthy heart, suggesting that cell-to-cell variability in electrical (e.g. action potential duration) and mechanical performance (e.g. twitch amplitude) is a normal property. This observation has been previously unappreciated because the aggregated function in the form of QT-interval and cardiac output varies <1% on a beat-to-beat basis. This article describes the underlying cellular variability that is tolerated - and perhaps needed - by different regions of the heart for normal function and indicates why this variability is not apparent in function at the chamber and organ level. Thus, in contrast to the current dominant view, this article postulates that heterogeneity is normal and potentially endows various functional benefits. This new view of how the component parts of the heart come together to function also suggests novel mechanisms for cardiac pathologies, namely that dysfunction may emerge from changes in the extent and/or nature of heterogeneity. Once understood, restoring normal forms of heterogeneity could be a novel approach to treatment.

Cardiovascular responses to experimental weight gain in humans: a feasibility study.

Obesity and hypertension share a well known association. However, the mechanisms underlying their relationship are not well understood. Our goal was to assess the feasibility of a longitudinal, interventional weight gain study with detailed cardiovascular measurements in humans. Sixteen healthy, normotensive, young, male volunteers (28 ± 7 years) were enrolled. Body composition, biochemical and cardiovascular data were obtained at baseline, and after an 8-week period of overfeeding (800-1000 kcal/day). Blood pressure (BP), cardiac output (CO) and peripheral vascular resistance (PVR) were determined, as were the minimum forearm vascular resistance (MFVR), forearm blood flow (FBF) response to mental stress and heart rate variability (HRV) parameters. Overfeeding resulted in a median weight gain of 5.6 kg [interquartile range (IQR) 4.6-6.4 kg; P < 0.001]. Seated systolic and diastolic BP were significantly increased by 10 ± 9 and 4 ± 6 mmHg, respectively, after weight gain ( P < 0.001 and P = 0.011, respectively). CO also increased and PVR decreased significantly as a result of weight gain ( P = 0.032 and P = 0.044, respectively). MFVR was also significantly decreased after weight gain ( P = 0.023). The FBF response to mental stress was blunted significantly ( P = 0.002), and sympathovagal balance and responsiveness to orthostatic challenge altered moderately after weight gain. Our overfeeding regimen resulted in moderate weight gain and significant increases in BP. An increase in CO is likely to be the dominant mechanism underlying the observed BP changes, with decreases in PVR partially compensating for these effects. Experimental weight gain, coupled with detailed cardiovascular phenotyping, is a feasible model to examine potential mechanisms underlying obesity-associated hypertension in young adults.

Sodium-Glucose Cotransporter-2 Inhibition Normalizes Metabolic Derangements in the Ischemic Myocardium

IntroductionSodium-glucose cotransporter-2 inhibitors (SGLT2i) have shown efficacy in the context of heart failure but have not been well-studied in ischemic heart disease. We employed a large animal model of chronic coronary artery disease and metabolic syndrome (MS) to investigate the hemodynamic and metabolic consequences of SGLT2i administration. MethodsThirty-eight Yorkshire swine were divided into two groups, with half (n = 21) receiving a high fat diet to induce MS, and the other half fed a standard diet (n = 17). All animals underwent thoracotomy for ameroid constrictor placement over the left circumflex coronary artery. Treatment with SGLT2i was then initiated, generating four groups: regular diet placebo (CON, n = 9), regular diet canagliflozin (n = 8), high-fat control (n = 11), and high-fat canagliflozin (n = 10). After 5 wks, all animals underwent terminal myocardial harvest with pressure-volume loop acquisition, perfusion studies, and tissue resection for molecular analysis. ResultsSGLT2i improved multiple measures of myocardial performance, including a nearly 1.5-fold increase in both cardiac output and ejection fraction; these changes were associated with augmented capillary density and a twofold increase perfusion to the ischemic myocardium. These augmentations were blunted; however, in the presence of MS, and associated with modulated myocardial expression of multiple major metabolic enzymes. ConclusionsSGLT2i significantly improved cardiac function in our large animal model of coronary artery disease, with metabolic modulation of the myocardial tissue serving as a candidate account of these changes. The blunting seen with MS underscores the dependence of clinical translatability on faithful representation of the biochemical environment of human disease.

Performance and Robustness of Physiological Controllers With Integrated Pressure Sensors on Inflow Cannula.

The control of left ventricular assist devices (LVADs) requires sensors and/or estimators to account for the physiological state of the patient and apply advanced controllers. Sensor characteristics are a challenge when using implantable pressure sensors because they influence the quality of physiological control and the robustness of the controlled system. The objective of this work is to investigate the performance and robustness of LVAD controllers that operate based on LVAD integrated pressure sensors. Four pressure-based LVAD controllers are tested with a HeartMate 3 that has an integrated pressure sensor. Controller sensitivity as well as robustness to sensor drift and noise are evaluated based on controller response to large changes in preload and afterload. A fail-safe strategy for sensor failure used also to investigate the reliable operation of the LVAD in realistic conditions. All tested controllers are sensitive to drifting pressure signals, which can lead to unstable behavior. The results show that two controllers are robust to noise. The other two controllers show high deviation and oscillation in cardiac output even for small noise. Additionally, a noticeable difference of the controller's response between simulated and measured pressure input was observed, indicating the need for a robust controller design. Reliable operation even in the event of a sensor failure was achieved on the basis of a fail-safe control system.

Unravelling the noise in pharmacokinetic studies of epinephrine: time to focus on cardiac output?

Unravelling the noise in pharmacokinetic studies of epinephrine: time to focus on cardiac output?

A Change of Pace: Modifying Pacemaker Settings in the Emergency Department as Emergency Medicine Physicians, A Case Report

Background: Pacemakers are implantable or external devices that send electrical impulses allowing the heart to contract. Some common indications for permanent pacemaker placement include symptomatic bradycardia due to high grade atrioventricular (AV) block, sick sinus syndrome, chronic bifascicular block, and post-cardiac transplantation. Like all devices pacemakers can malfunction or stop working entirely. We present a patient with an implantable pacemaker/cardioverter and defibrillator (ICD) displaying symptomatic failure to capture and settings were adjusted in the emergency department. Adjustment in the emergency department (ED) resolved the patient's symptoms and required no further interventions.Case Report: An 82-year-old female with atrial fibrillation, heart failure, and a Medtronic dual chamber pacer/ICD presented to the emergency department for complaints of weakness and lightheadedness. Emergency medical services (EMS) noted intermittent bradycardia, hypotension, and decreased responsiveness. Electrocardiogram (ECG) revealed failure to capture. The Medtronic application was used to interrogate and reprogram the device. The settings were DDD at a rate of 60 beats per minute (BPM) with ventricular output of 4.5 millivolts (mV) and atrial output of 4.5 mV which were changed ventricular lead outputs from 4.5 mV to 8.0 mV and rate from 60 to 80 for additional cardiac output. After this adjustment, the bradycardia resolved, and ECG showed a successful AV-paced rhythm. Transcutaneous pacing was never required.Why should an emergency physician be aware of this?Adjustment of pacer settings in the ED in order to stabilize the critically ill patient is within the scope of the emergency physician. We can reduce stress to the patient and prevent hospitalizations. Pacemakers can become a tool to optimize treatment plans for an aging population where pacemakers are becoming more common.

The impact of blood viscosity modeling on computational fluid dynamic simulations of pediatric patients with Fontan circulation

For univentricular heart patients, the Fontan circulation presents a unique pathophysiology due to chronic non-pulsatile low-shear-rate pulmonary blood flow, where non-Newtonian effects are likely substantial. This study evaluates the influence of non-Newtonian behavior of blood on fluid dynamics and energetic efficiency in pediatric patient-specific models of the Fontan circulation. We used immersed boundary-lattice Boltzmann method simulations to compare Newtonian and non-Newtonian viscosity models. The study included models from twenty patients exhibiting a low cardiac output state (cardiac index of 2 L/min/m2). We quantified metrics of energy loss (indexed power loss and viscous dissipation), non-Newtonian importance factors, and hepatic flow distribution. We observed significant differences in flow structure between Newtonian and non-Newtonian models. Specifically, the non-Newtonian simulations demonstrated significantly higher local and average viscosity, corresponding to a higher non-Newtonian importance factor and larger energy loss. Hepatic flow distribution was also significantly different in a subset of patients. These findings suggest that non-Newtonian behavior contributes to flow structure and energetic inefficiency in the low cardiac output state of the Fontan circulation.

Comparison of cardiac output index in dogs before and after mitral valve repair as determined using pulse pressure recording analytical methods

Comparison of cardiac output index in dogs before and after mitral valve repair as determined using pulse pressure recording analytical methods

Electrical cardiometry significance in postoperative cardiac ICU; a single center study

BackgroundHemodynamic monitoring is a cornerstone of critical care; in fact, the techniques available for this purpose are either unreliable or operator-dependent or intermittent (echocardiography) and invasive (thermodilution). Objectives: To evaluate the effectiveness of electrical cardiometry (EC) in assessing hemodynamics in pediatric postoperative cardiac intensive care unit (ICU) and the agreement between EC and trans-thoracic echocardiography (TTE) as bedside tools for hemodynamic monitoring and early diagnosis of cardiovascular compromise. We included 70 pediatric patients from the postoperative cardiac ICU. All participants underwent history-taking and clinical examination. emphasising vital signs, manifestations or signs of hemodynamic instability, calculation of RACH score and vasoactive inotropic score. EC was applied for all patients, and TTE.ResultsThe study included 40 males and 30 females with a mean age of 2.6 ± 3.49 years, ranging between 2 weeks and 13 years, with a male to female ratio of 1.3:1. The median of EC parameters were comparable to TTE parameters stroke volume (SV) (9 vs. 8 p = 0.2), stroke index (SI) (23.5 vs. 22 p = 0.2), cardiac output (CO) (1.25 vs. 1.1 p = 0.3), and cardiac index (CI) (3.2 vs. 3.15 p = 0.2). Hemodynamic parameters correlated significantly between EC and echocardiography, with significantly observed agreement between them. Four equations were postulated successfully based on a linear regression model to predict echocardiographic hemodynamic parameters in comparable groups of children, i.e., SV, SI, CO, and CI.ConclusionEC is an excellent alternative to echocardiography in hemodynamic assessment of cardiac patients in the postoperative ICU.

Noninvasive Tools to Predict Necrotizing Enterocolitis in Infants with Congenital Heart Diseases: A Narrative Review

Background: Necrotizing enterocolitis (NEC) is the most frightening gastrointestinal emergency in newborns. Despite being primarily a disease of premature infants, neonates with congenital heart disease (CHD) are at increased risk of development. Acute and chronic hemodynamic changes in this population may lead to mesenteric circulatory insufficiency. Objectives: In this narrative review, we describe monitoring tools, alone or in multimodal use, that may help in the early recognition of patients with CHD at major risk of NEC development. Methods: We focused on vital parameters, echocardiography, Doppler flowmetry, abdominal near-infrared spectroscopy (aNIRS), and abdominal ultrasound (aUS). Results: The number of studies on this topic is small and includes a wide range of patients’ ages and types of CHD. Peripheral oxygen saturation (SpO2) and certain echocardiographic indices (antegrade and retrograde velocity time integral, cardiac output, etc.) do not seem to differentiate infants with further onset of NEC from those not developing it. Hypotensive events, persistent diastolic flow reversal in the descending aorta, and low mesenteric oxygen saturation (rsSO2) measured by aNIRS appear to occur more frequently in infants who later develop NEC. aUS may be helpful in the diagnosis of cardiac NEC, potentially showing air contrast tracked to the right atrium in the presence of pneumatosis. Conclusions: This narrative review describes the current knowledge on bedside tools for the early prediction of cardiac NEC. Future research needs to further explore the use of easy-to-learn, reproducible instruments to assist patient status and monitor patient trends.

O USO DOS INIBIDORES DO COTRANSPORTADOR DE SÓDIO-GLICOSE-2 (SGLT2) NA INSUFICIÊNCIA CARDÍACA: UMA REVISÃO BIBLIOGRÁFICA

Heart failure (HF) is not a single pathological diagnosis, but a clinical syndrome caused by a structural and/or functional abnormality of the heart, resulting in elevated intracardiac pressure or inadequate cardiac output at rest or during exercise. It is a common clinical condition found in various healthcare settings, with a vast socio-economic impact. In Brazil, HF is the leading cardiovascular cause of hospital morbidity. Thus, heart failure studies play a crucial role in the development of new drugs, enabling significant improvements in the efficacy, safety and tolerability of treatment, as well as the personalization of care for individual patients. Recent advances in pharmacotherapy have led to the evolution of new therapeutic agents with a decrease in hospitalization and mortality rates in HF. The 2023 update of the European Society of Cardiology (ESC) guidelines recommends (class IA) the administration of sodium-glucose transporter 2 inhibitors (SGLT2i) for patients with heart failure with preserved ejection fraction (HFpEF) and mildly reduced EF (HFpEF). This study aims to analyze the use of sodium-glucose cotransporter-2 inhibitors (SGLT2i) in heart failure. In order to arrive at these topics, articles were collected from the PUBMED and SCIELO databases, and an analysis was carried out based on the material found in order to be able to explain the information relevant to the topic.

Evaluating Impact of Surgical Myocardial Revascularization on Global Left Ventricular Systolic Function and Immediate Postoperative Outcome using Transesophageal Echocardiography

Abstract Background and Aims: Surgical myocardial revascularization is supposed to improve the global left ventricular (LV) function by improving the blood supply in significantly occluded coronary arteries. Transesophageal echocardiography (TEE) provides an excellent opportunity to evaluate cardiac function in operating room. Present study was aimed at evaluating impact of surgical myocardial revascularization on global LV systolic function. Comparison of LV fractional shortening (LV-FS), fractional area change (LV-FAC), ejection fraction (LV-EF), indexed LV volumes (indexed LV volumes at end diastole, LV volumes at end systole) and “Tei” (Myocardial performance) index obtained prior and after surgical myocardial revascularization was done for quantitative analysis. Also, the determinants of immediate postoperative outcome were evaluated based on need of pharmacological and/or mechanical cardiovascular support, mechanical ventilation, intensive care unit (ICU) stay, morbidity and mortality in immediate postoperative period. These outcome measures were correlated with baseline values of TEE derived echo indices. Methods: One hundred and ten subjects with significant coronary artery disease scheduled for elective myocardial revascularization surgery. Fourteen subjects were excluded due to presence of either hemodynamic instability requiring either pharmacological or mechanical cardiovascular support, before coronary revascularization (n = 6), presence of Grade III mitral regurgitation (MR) in baseline TEE (n = 2) and arrythmias (n = 6). Ninety six subjects were evaluated for global LV systolic function using TEE before and after surgical revascularization. Subjects were followed in ICU for the outcome. Immediate postoperative outcome was measured as “good” or “poor” based on vasoactive inotropic score, requirement of Intra-aortic balloon counter pulsation (IABP) and mechanical cardiovascular support (VA-ECMO) to maintain cardiac output, duration of mechanical ventilation, postoperative ICU stay, morbidity and mortality. Results: In 96 subjects analyzed, there was a significant improvement in TEE derived LV-FS (38.60 ± 16.38 vs. 31.31 ± 13.14) (P = 0.002), FAC (51.94 ± 16.06 vs. 43.99 ± 16.02) (P ≤ 0.001), EF (53.08 ± 9.97 vs. 46.71 ± 7.53) (P &lt; 0.00001), LV end diastolic volume index (34.84 ± 13.43 vs. 40.08 ± 17.22) (P = 0.0188) and “Tei” index (0.47 ± 0.13 vs. 0.53 ± 0.13) (P = 0.0007). Thirty three subjects required either prolonged stay in ICU (&gt;7 days), (n = 20) and/or mechanical ventilatory support (&gt;24 h), (n = 10) and/or mechanical cardiovascular support (IABP/VA ECMO placement), (n = 7) and/or suffered mortality (n = 2) in postoperative period were categorized as “poor” outcome. Presence of type II diabetes mellitus, Chronic obstructive pulmonary disease (COPD), higher grade of ischemic MR, larger LV end diastolic volume, use of cardiopulmonary bypass and allogenic blood transfusion during surgery were the determinants of “poor” outcome. Conclusion: Surgical myocardial revascularization improved global LV systolic function irrespective of baseline LV EF. Immediate postoperative outcome was strongly determined by presence of diabetes, COPD, higher grade of ischemic MR and larger LV end diastolic volumes. Preoperative (Baseline) LV EF and myocardial performance index did not determine “poor” postoperative outcome following surgical myocardial revascularization in subjects with LVEF &gt;35%.

Connecting the dots: A narrative review of the relationship between heart failure and cognitive impairment.

Large clinical data underscore that heart failure is independently associated to an increased risk of negative cognitive outcome and dementia. Emerging evidence suggests that cerebral hypoperfusion, stemming from reduced cardiac output and vascular pathology, may contribute to the largely overlapping vascular dementia and Alzheimer's disease. Despite these insights, cognitive outcomes remain largely overlooked in heart failure management. This narrative review outlines the prevalence and risk of cognitive impairment in heart failure patients, exploring potential shared pathophysiological mechanisms and examining the impact of heart failure therapy on cognitive deficits. Additionally, it discusses clinical implications and suggests future treatment approaches targeting therapeutic outcomes. Cognitive impairment is prevalent among individuals with heart failure, with reported rates varying widely depending on assessment methods. Shared pathological pathways and risk factors, including atrial fibrillation (AF), hypertension, obesity and type 2 diabetes mellitus, suggest a causal link. Mechanisms such as poor perfusion, microembolic events, ischaemic syndromes and cerebral inflammation contribute to this relationship. Moreover, heart failure itself may exacerbate cognitive dysfunction. This emerging understanding posits that vascular dementia and Alzheimer's disease may represent a pathophysiological continuum, driven by both the accumulation of misfolded proteins and cerebrovascular pathology due to cardiovascular dysfunction. Understanding these links is crucial for developing effective treatment strategies. The complex interplay between heart failure and cognitive impairment underscores the necessity for a holistic patient care approach. Both conditions share analogous disease processes, influencing self-management and independence in patients. Prioritizing brain health in heart failure management is essential to enhance patient prognosis and general well-being.

Retrospective evaluation of the impact of atropine administration on incidence of post-operative colic in healthy, isoflurane-anaesthetised horses.

In anaesthetised horses, bradycardia secondary to high vagal tone can reduce cardiac output and blood pressure. The use of anticholinergics in horses is limited due to concerns about ileus and abdominal discomfort. This retrospective study sought to determine the prevalence of post-operative abdominal discomfort in healthy horses that received atropine under isoflurane anaesthesia. A retrospective evaluation of 222 general anaesthesia events between January 2019 and December 2019 was undertaken. One hundred and eleven horses that received atropine were identified, and 111 case match controls that did not receive atropine were also selected. Information gathered from the medical records included signalment, anaesthetic drugs, surgical procedures, duration of anaesthesia and surgery, dobutamine and atropine administration, and the occurrence of abdominal discomfort for 24 h after anaesthesia. After initial data analysis, a second cohort of records was assessed separately. The horses in this group were castrated under general anaesthesia (with or without atropine; n = 68). Logistic regression models and Fisher's exact tests were used to look for factors contributing to abdominal discomfort post-anaesthesia. The significance level was set to 5% (p < 0.05). Atropine administration was not associated with the development of post-anaesthetic abdominal discomfort (OR = 2.121, 95% CI [0.767, 5.869]; p = 0.2). Overall, 18/222 (8.1%) incidences of abdominal discomfort were identified. All incidents occurred in colts undergoing castration. In a separate analysis of only horses anaesthetised for castration, atropine was associated with developing abdominal discomfort (OR = 3.143, 95% CI [1.082, 9.132]; p = 0.04). Atropine was not associated with post-operative abdominal discomfort except in colts undergoing castration. All episodes of discomfort were mild and resolved with minimal intervention. The potential impact of insufficient analgesia in horses undergoing castration is a confounding factor and requires prospective investigation. Overall, atropine at a dose of 0.006 mg/kg IV appears to be a safe method to treat bradycardia in otherwise healthy horses anaesthetised for orthopaedic and upper airway procedures. Further work is required to determine if atropine is safe for colts undergoing castration.

Mixed Cardiogenic Shock: A Proposal for Standardized Classification, a Hemodynamic Definition, and Framework for Management.

The classification of cardiogenic shock (CS) has evolved from a singular cold-and wet-hemodynamic profile. Data from registries and clinical trials have contributed to a broader recognition that although all patients with CS have insufficient cardiac output leading to end organ hypoperfusion, there is considerable variability in CS acuity, underlying etiologies, volume status, and systemic vascular resistance. Mixed CS can be broadly categorized as CS with at least 1 additional shock state. Mixed CS states are now the second leading cause of shock in contemporary coronary intensive care units, but there is little high-quality evidence to guide routine care, and there are no standardized classification frameworks or well-established hemodynamic definitions. This primer summarizes the current epidemiology and proposes a classification framework and invasive hemodynamic parameters to guide categorization that could be applied to help better phenotype patients captured in registries and trials, as well as guide management of mixed CS states.

Age-dependent changes in cardiac output following balloon pulmonary angioplasty: Implications for combination therapy in chronic thromboembolic pulmonary hypertension

Abstract Background Balloon pulmonary angioplasty (BPA) is an accepted treatment for patients with chronic thromboembolic pulmonary hypertension (CTEPH). However, some patients still have exercise intolerance even after normalizing mean pulmonary arterial pressure with BPA. Although medical therapy may be a potential option for such patients, it cannot be necessary for all patients. Low cardiac output (CO) after BPA is associated with exercise intolerance. However, the change in CO with BPA could be affected by the patient’s age and pulmonary hypertension (PH) medication status. The specific patients’ characteristics that require medical therapy following BPA remain unknown. Methods This single-centre, retrospective observational study included 286 patients with CTEPH who underwent BPA and right heart catheterization one year BPA at our hospital. The patients were classified into three age groups (younger: age &amp;lt; 60 years, n=91; middle-aged: 60 ≤ age &amp;lt; 70 years, n=91; elderly: 70 years ≤ age, n=104), and also stratified by two groups based on PH medication status (Group 1: patients without PH medications before and after BPA, Group 2: patients who received PH medications before BPA and discontinued them after BPA). CO and its percent change were compared between Groups 1 and 2 in each age group. Results CO increased significantly in the younger group (4.3±0.2 to 4.5±0.1 L/min, p=0.040) and decreased in the elderly group (4.0±0.1 to 3.8±0.1 L/min, p=0.035), resulting in no significant change overall. CO in the younger and middle-aged groups significantly increased after BPA in Group 1, whereas in Group 2, those in the middle-aged and elderly groups significantly decreased after BPA. The percent CO changes declined in an age-dependent manner in both groups. Conclusions Increasing CO with BPA alone may be challenging in elderly patients. Adjuvant medical therapy might be necessary, even after successful BPA, especially in elderly patients.Percent change in CO stratified by age

Hemodynamic effects of right and biventricular pacing during exercise in hypertrophic obstructive cardiomyopathy

Abstract Background One third of patients with hypertrophic cardiomyopathy present with dynamic left ventricular outflow tract obstruction (LVOTO), referred to as hypertrophic obstructive cardiomyopathy (HOCM). Symptomatic treatment aims at reducing LVOTO with either medications, invasive septal reduction, or pacing. The importance of pacing site is unclear, and effects of pacing during physical activity have not been investigated. Purpose To determine the effect of right ventricular (RV) and biventricular (BiV) pacing, respectively, on LVOTO and cardiac output (CO) during exercise in patients with HOCM. Methods Patients with symptomatic HOCM, sinus rhythm, and no bundle branch block, scheduled for alcohol septal ablation (ASA), were eligible for inclusion. The day before ASA, we placed temporary pacing leads in the right atrium, the RV apex, and on the left ventricle’s lateral wall via the coronary sinus. LVOTO was assessed by echocardiography, and CO was measured by thermodilution with a pulmonary artery catheter. Patients performed supine cycling for 2 minutes until heart rate (HR) increased ≥20 bpm. We measured LVOTO and CO in sinus rhythm, and during cycling with atrial sensed RV pacing, and atrial sensed BiV pacing. The order of pacing sites was randomized, and the personnel performing echocardiography and CO measurements were blinded to the order of pacing. Results We included six patients (54±15 years) with a mean maximal left ventricular wall thickness of 16.7±1.8 mm. Resting LVOTO was 55.7±30.9 mmHg. The figures show LVOTO and CO in sinus rhythm (HR 85±10 bpm), RV pacing (HR 90±10 bpm), and BiV pacing (HR 91±9 bpm) during supine cycling. The LVOTO declined from 56±34 mmHg in sinus rhythm to 27±12 mmHg and 25±5 mmHg respectively for atrial sensed RV and BiV pacing. CO remained unchanged during sinus rhythm (9.0±1.2 L/min), atrial sensed RV pacing (9.0±1.7 L/min), and BiV pacing (8.9±1.5 L/min). Conclusion In this ongoing study evaluating cardiac pacing in HOCM, preliminary data indicate that both RV and BiV pacing are effective in reducing LVOTO during exercise, without compromising CO.

Post-prandial acyl ghrelin infusion in heart failure patients increases gastric emptying rate

Abstract Background Acyl ghrelin (ghrelin) increases cardiac output (CO) and contractility in patients with heart failure with reduced ejection fraction (HFrEF). In healthy humans, ghrelin increases gastric emptying rate (GER) and hunger, a potential add-on benefit for HFrEF patients suffering from cachexia with symptoms of delayed gastric emptying and loss of appetite. Aim Determine if post-prandial ghrelin infusion increases GER and hunger in HFrEF patients; compare to CO. Methods This study was a component of a double-blind placebo-controlled trial of acyl ghrelin vs. placebo in HFrEF. Patients (n=29) arrived fasted and received a 500 kcal breakfast and 1.5 g paracetamol. They next received placebo (vehicle, n=15) or ghrelin infusion (0.1 µg/kg/min, n=14) for 120 min. Blood was tapped for plasma at 0, 30, 60, 120 and 150 min into the meal. Plasma concentration of paracetamol was measured to assess GER of a liquid bolus. Hunger scores and CO were recorded. Mann-Whitney rank sum test was used for statistics. Results Paracetamol peaked at 30 min in 8 of 14 (57%) in the ghrelin treatment group versus 1 of 15 (7%) in the placebo group (P=0.004, Fig 1). Remaining patients peaked at later time points. There were no anomalous peaks at 0 min baseline or 2880 min (2 days). The ghrelin treatment group data was segregated into rapid (peak at 30 min, n=8) and slow (peak &amp;gt;30 min, n=6) GER subgroups. The rapid subgroup had a ghrelin treatment effect on CO (one-way repeat measures) (P&amp;lt;0.001, Fig 2). Baseline (t=0) CO for the rapid GER subgroup was 4.06 ±1.41 L/min (median ±SD) and 3.95 ±0.62 L/min for the slow GER subgroup (P=0.31). Data points shown are median ± SEM, each patient normalized to own baseline (100%); * P&amp;lt;0.05, ** P&amp;lt;0.01, *** P&amp;lt;0.001, pairwise comparison to baseline. Hunger gradually increased. The greatest increase in hunger was at 150 min, at which time median fold increase in hunger relative baseline was 1.6 (placebo), 1.7 (ghrelin, slow GER) and 2.3 (ghrelin, rapid GER). These hunger differences between groups did not reach significance. However, this trend was consistent with ghrelin induction of hunger, especially in those with potent GER and CO responses. Conclusions Ghrelin increases GER, and potentially hunger, in HFrEF patients in addition to increasing CO. Some HFrEF patients may benefit from this add-on effect.Fig 1.Time of paracetamol peak.Fig 2.Cardiac output.