Increase In Cardiac Output Research Articles

Septum displacement implications in the limited cardiac reserve, RV to pc uncoupling and oxygen uptake during exercise in heart failure

Abstract Background Exertional dyspnea is crucial in heart failure (HF) and may be determined by an unfavorable dynamic of ventricular interaction. This concept has been poorly addressed over time and we hypothesized that a careful study of the interventricular septum adaptations during maximal exercise in HF might be implicated in the limited cardiac reserve, uncoupling of right ventricular (RV) to pulmonary circulation (Pc), both yielding to a limited O2 uptake. Aim To address the pathophysiology behind biventricular interaction during exercise in HF, studying the role of l septum displacement during exercise and how and whether it would affect peak exercise oxygen consumption (VO2 peak). Through a limited cardiac output (CO) increase and some degrees of RV to PC uncoupling assessed by TAPSE/PASP. Methods 22 HF underwent a combined cardiopulmonary exercise testing imaging (CPET imaging) with RV 3D-imaging analysis and were compared with a control population. 3D imaging of the RV chamber was examined off-line using the 4D RV TomTec software and obtained 3D mesh of the RV model using custom software to obtain the mean curvature value of IVS in 4 regions of: inflow tract (RVIT), outflow tract (RVOT), apical and body. We acquired measurements of curvature during end-diastole (ED) and at end systole (ES) phases and obtained a parametric curvature map. Results HF patients (mean age 72±12, 27% female) typically exhibited an abnormal septal curve, with a more leftward configuration either at rest and under exercise (rest =−0.01±0.007 at ED, and −0.01±0.009 at ES; peak exercise= −0.01±0.006 at ED, and −0.01±0.007 at ES) compared to controls (rest =−0.02±0.002 at ED, and −0.02±0.006 at ES; peak exercise −0.02±0.0.006 at ED, and −0.02±0.01 at ES, Figure). Notably, the degree of the IVS curvature was found to linearly correlate with an impaired gas exchange performance as showed by a lower peak VO2, a limited CO and impairment of TAPSE/PASP in HF (respectively, r=0.64, p<0.001, r=0.5, p<0.001, r=0.53, p<0.001 at ED during exercise; r=0.61, p<0.001 at ES during exercise; Figure). Conclusions In HF, the occurrence of right to left IVS displacement appears worth of investigation, tightly contributing to a reduced CO response, and RV-PA uncoupling during exercise. These findings clearly point to the utility of assessing how therapeutic strategies may modulate the negative septum displacement and overall cardiac mechanics. RV colorimetric curvature map Septal curvature correlations

Comprehensive nursing interventions enhance sleep quality in patients with arrhythmia following AMI.

This study aims to assess the impact of comprehensive nursing care on sleep quality and rehabilitation duration in patients experiencing arrhythmia after acute myocardial infarction (AMI). Eighty-four patients with post-AMI arrhythmia treated at our hospital from February 2018 to February 2019 were selected and divided based on the nursing care received. The observation group (n = 44) underwent comprehensive nursing interventions, while the control group (n = 40) received standard nursing care. Evaluations of cardiac function indices and sleep quality were conducted before and after the nursing interventions. In addition, comparisons were made between the 2 groups regarding arrhythmia occurrence, patient compliance during care, visual analog scale scores for pain, self-rating anxiety scale scores, self-rating depression scale scores, and overall nursing satisfaction. Following the nursing interventions, the observation group exhibited a significant increase in cardiac output, unlike the control group, which showed no notable change. Both groups demonstrated significant improvements in left ventricular end-diastolic dimension and left ventricular ejection fraction; however, these enhancements were more pronounced in the observation group. Post-intervention, the Pittsburgh Sleep Quality Index scores were significantly lower in the observation group compared with the control group, indicating better sleep quality. The observation group also experienced a significant reduction in the incidence, frequency, and duration of arrhythmia episodes. Furthermore, this group showed a lower incidence of complications during the intervention period and reported lower visual analog scale, self-rating anxiety scale, and self-rating depression scale scores after nursing care. Nursing satisfaction rates were notably higher in the observation group than in the control group. Comprehensive nursing care significantly enhances sleep quality, speeds up rehabilitation, and increases patient satisfaction in individuals with arrhythmia after AMI. These findings support the clinical adoption of comprehensive nursing interventions for this patient population.

Acute maternal hyperoxygenation to predict hypoxia and need for emergency intervention in fetuses with transposition of the great arteries: a pilot study.

Newborns with transposition of the great arteries (TGA) are at risk of severe hypoxia from inadequate atrial mixing, closure of the arterial duct and/or pulmonary hypertension (PPHN). Acute maternal hyperoxygenation (AMH) might assist in identifying at-risk fetuses. We report pulmonary vasoreactivity to AMH in TGA fetuses and its relationship to early postnatal hypoxia and requirement for emergency balloon atrial septostomy (e-BAS). Standard fetal echocardiographic (FE) assessment of the foramen ovale (FO): total septal length and morphology of flap valve of FO were used to predict need for e-BAS. Following prospective recruitment, additional assessments were performed in fetuses with TGA at baseline and repeated after 10minutes of 10L/min of 100% oxygen delivered via non-rebreather mask to the pregnant mother. Analysis included measurement of atrial septal excursion, branch pulmonary artery pulsatility index (PA-PI), middle cerebral artery (MCA) PI and cardiac output. Delivery and newborn status were reviewed. Hypoxia was defined as preductal oxygen saturations <75% and e-BAS when undertaken within two hours of birth. Area under receiver operating characteristics curves (AUROC) were calculated. 30 cases underwent FE at 34.6weeks' gestation (IQR: 34.6-35.6). All 7 predicted to require e-BAS based on standard FE were correctly identified prenatally. 3/30 were hypoxic without FO restriction and treated with nitric oxide (PPHN). Change in PA-PI < 15% was associated with PPHN (p=0.001), but not with e-BAS. The MCA-PI response to AMH varied according to newborn condition, a mean reduction occurred in the non-hypoxic newborns (-7.8 ± 18.3, p=0.05). Increase in MCA-PI Z score AUROC 0.837 (95% CI: 0.663-1.00, p=0.01); reduction in right ventricular cardiac output 0.811 (95% CI: 0.623-0.998, p=0.04), reduction in combined cardiac output (0.851 (95% CI: 0.699-1.0, p=0.01)) were moderately associated with e-BAS. Changes in atrial septal excursion and FO flow direction with AMH did not correlate with newborn condition. PA-PI change < 15% to AMH was associated with postnatal hypoxia due to PPHN. Increase in right and combined cardiac output and reduced MCA resistance with AMH are seen in those who do not require e-BAS.

Maladaptive cardiomyocyte calcium handling in adult offspring of hypoxic pregnancy: protection by antenatal maternal melatonin.

Chronic fetal hypoxia is one of the most common complications of pregnancy and can programme cardiac abnormalities in adult offspring including ventricular remodelling, diastolic dysfunction and sympathetic dominance. However, the underlying mechanisms at the level of the cardiomyocyte are unknown, preventing the identification of targets for therapeutic intervention. Therefore, we aimed to link echocardiographic data with cardiomyocyte function to reveal cellular mechanism for cardiac dysfunction in rat offspring from hypoxic pregnancy. Further, we investigated the potential of maternal treatment with melatonin as antenatal antioxidant therapy. Wistar rats were randomly allocated into normoxic (21% O2) or hypoxic (13% O2) pregnancy with or without melatonin treatment (5µg/ml; normoxic melatonin in the maternal drinking water from gestational day 6 to 20 (term=22days). After delivery, male and female offspring were maintained to adulthood (16weeks). Cardiomyocytes were isolated from the left and right ventricles, and calcium (Ca2+) handling was investigated in field-stimulated myocytes. Systolic and diastolic function was negatively impacted in male and female offspring of hypoxic pregnancy demonstrating biventricular systolic and diastolic dysfunction and compensatory increases in cardiac output. Ca2+ transients from isolated cardiomyocytes in offspring of both sexes in hypoxic pregnancy displayed diastolic dysfunction with a reduced rate of [Ca2+]i recovery. Cardiac and cardiomyocyte dysfunction in male and female adult offspring was ameliorated by maternal antenatal treatment with melatonin in hypoxic pregnancy. Therefore, cardiomyocyte Ca2+ mishandling provides a cellular mechanism explaining functional deficits in hearts of male and female offspring in pregnancies complicated by chronic fetal hypoxia. KEY POINTS: This study identified significant changes in Ca2+ handling within cardiomyocytes isolated from offspring of hypoxic pregnancy including reduced systolic Ca2+ transients, impaired diastolic recovery of [Ca2+]i and a greater increase in systolic [Ca2+]i amplitude to β-adrenergic stimulation. These changes in cardiomyocyte Ca2+ handling help to explain dysregulation of biventricular systolic and diastolic dysfunction determined by echocardiography. The data show protection against maladaptive cardiomyocyte calcium handling and thereby improvement in cardiac function in adult offspring of hypoxic pregnancy treated with melatonin with doses lower than those recommended for overcoming jet lag in humans. Melatonin treatment alone in healthy pregnancy did cause some alterations in cardiac structure. Therefore, maternal treatment with melatonin should only be given to pregnancies affected by chronic fetal hypoxia.

Mitral Valve Transcatheter Edge-to-Edge Repair (MV-TEER) in Patients with Secondary Mitral Regurgitation Improves Hemodynamics, Enhances Renal Function, and Optimizes Quality of Life in Patients with Advanced Renal Insufficiency.

Secondary mitral regurgitation (MR) is a common valvular heart disease burdening the prognosis of patients with co-existing chronic heart failure. Transcatheter edge-to-edge mitral valve repair (MV-TEER) is a minimally invasive treatment option for high-risk patients. However, the effects of MV-TEER on expanded hemodynamics, tissue perfusion, and quality of life, particularly in patients with advanced renal failure, remain underexplored. This prospective, single-center study evaluated the impact of MV-TEER on hemodynamics, renal function, and quality of life in 45 patients with severe MR. Non-invasive bioimpedance monitoring with NICaS® was used to assess hemodynamics pre- and 3-5 days post-procedure. Quality of life was assessed using the EQ-5D-3L questionnaire before and 3 months post-procedure. For further analysis, patients were divided into subgroups based on the estimated baseline glomerular filtration rate (eGFR < 35 mL/min vs. eGFR ≥ 35 mL/min). A significant reduction in systemic vascular resistance (SVR; p = 0.003) and an increase in eGFR (p = 0.03) were observed in the entire cohort after MV-TEER, indicating improved tissue perfusion. Notably, particularly patients with eGFR < 35 mL/min showed a significant increase in cardiac output (CO; p = 0.035), cardiac index (CI; p = 0.031), and eGFR (p = 0.018), as well as a reduction in SVR (p = 0.007). Consistent with these findings, quality of life significantly improved, with the EQ-5D-3L index and EQ-VAS score increasing from 0.44 to 0.66 (p < 0.001) and from 51.7% to 62.9% (p < 0.001).

Anesthetic Management of Cesarean Delivery for a Parturient With Dextro-Transposition of the Great Arteries Post-Senning Procedure: A Case Report

The Senning procedure is a palliation technique for addressing dextro-transposition of the great arteries; deoxygenated blood is redirected to the left ventricle, making the right ventricle the systemic ventricle. The physiologic increase in cardiac output during pregnancy may place additional stress on the right ventricle and given the existence of atrial scar tissue, trigger arrythmias. Because the technique was gradually abandoned starting in the 1970s, few remaining patients of child-bearing age remain. We emphasize here the importance of interdisciplinary team planning for delivery. Preparation for possible arrhythmia and potential decompensation in right ventricular function are essential.

A new method to predict return of spontaneous circulation by peripheral intravenous analysis during cardiopulmonary resuscitation: a rat model pilot study

BackgroundEnhancing venous return during cardiopulmonary resuscitation (CPR) can lead to better hemodynamics and improved outcome after cardiac arrest (CA). Peripheral Intravenous Analysis (PIVA) provides feedback on venous flow changes and may indicate an increase in venous return and cardiac output during CPR. We hypothesize PIVA can serve as an early indicator of increased venous return, preceding end-tidal CO2 (etCO2) increase, before the return of spontaneous circulation (ROSC) in a rat model of CA and CPR.ResultsEight male Wistar rats were intubated and ventilated, and etCO2 was measured. Vessels were cannulated in the tail vein, femoral vein, femoral artery, and central venous and connected to pressure transducers. Ventilation was discontinued to achieve asphyxial CA. After 8 min, CPR began with ventilation, epinephrine, and automated chest compressions 200 times per minute until mean arterial pressure increased to 120 mmHg. Waveforms were recorded and analyzed. PIVA was calculated using a Fourier transformation of venous waveforms. Data are mean ± SE. Maximum PIVA values occurred in the tail vein 34.7 ± 2.9 s before ROSC, with subsequent PIVA peaks in femoral vein and centrally at 30.9 ± 5.4 and 25.1 ± 5.0 s, respectively. All PIVA peaks preceded etCO2 increase (21.5 ± 3.2 s before ROSC).ConclusionPIVA consistently detected venous pressure changes prior to changes in etCO2. This suggests that PIVA has the potential to serve as an important indicator of venous return and cardiac output during CPR, and also as a predictor of ROSC.

Abstract 4141469: Left Ventricular Septum Displacement Implications in the Limited Cardiac Reserve, RV to Pc Uncoupling and Oxygen Uptake During Exercise in Heart Failure

Background: Dyspnea on exertion is cardinal symptom in heart failure (HF) and may be caused by an unfavorable dynamic of ventricular interaction. This concept has been poorly addressed over time and we hypothesized that a careful study of the interventricular septum adaptations during maximal exercise in HF might be implicated in the limited cardiac reserve and uncoupling of right ventricular (RV) to pulmonary circulation (Pc), both yielding to a limited O2 uptake. Aim: To study the pathophysiology behind biventricular interaction during exercise in HF, evaluating the role of septum displacement during exercise and how and whether it would affect peak exercise oxygen consumption (VO 2 peak) through a limited cardiac output (CO) increase and some degrees of RV to PC uncoupling assessed by TAPSE/PASP. Methods: 22 HF performed a combined cardiopulmonary exercise testing imaging (CPET imaging) with RV 3D-imaging analysis and were compared with a control population. 3D imaging of the RV chamber was examined off-line using the 4D RV TomTec software and obtained 3D mesh of the RV model using custom software to obtain the mean curvature value of IVS in 4 regions of: inflow tract (RVIT), outflow tract (RVOT), apical and body. We acquired measurements of curvature during end-diastole (ED) and at end systole (ES) phases and obtained a parametric curvature map. Results: HF patients (mean age 72±12, 27% female) typically showed an abnormal septal curve, with a more leftward configuration either at rest and under exercise (rest =−0.01±0.007 at ED, and −0.01±0.009 at ES; peak exercise= −0.01±0.006 at ED, and −0.01±0.007 at ES) compared to controls (rest=−0.02±0.002 at ED, and −0.02±0.006 at ES; peak exercise −0.02±0.0.006 at ED, and −0.02±0.01 at ES, Figure). Notably, the degree of the IVS curvature showed a linear correlation with an impaired gas exchange performance as indicated by a lower peak VO 2 , a limited CO and impairment of TAPSE/PASP in HF (respectively, r=0.64, p&lt;0.001, r=0.5, p&lt;0.001, r=0.53, p&lt;0.001 at ED during exercise; r=0.61, p&lt;0.001 at ES during exercise; Figure). Conclusions: In HF, the evidence of right to left IVS displacement appears worth of investigation, by intervening strictly to a reduced CO response, and RV-PA uncoupling during exercise. These findings clearly point to the utility of assessing how new and current therapeutic strategies may modulate the negative septum displacement and overall cardiac mechanics.

Myocardial Posttranscriptional Landscape in Peripartum Cardiomyopathy.

Pregnancy imposes significant cardiovascular adaptations, including progressive increases in plasma volume and cardiac output. For most women, this physiological adaptation resolves at the end of pregnancy, but some women develop pathological dilatation and ultimately heart failure late in pregnancy or in the postpartum period, manifesting as peripartum cardiomyopathy (PPCM). Despite the mortality risk of this form of heart failure, the molecular mechanisms underlying PPCM have not been extensively examined in human hearts. Protein and metabolite profiles from left ventricular tissue of end-stage PPCM patients (N=6-7) were compared with dilated cardiomyopathy (DCM; N=5-6) and nonfailing donors (N=7-18) using unbiased quantitative mass spectrometry. All samples were derived from the Sydney Heart Bank. Data are available via ProteomeXchange with identifier PXD055986. Differential protein expression and metabolite abundance and Kyoto Encyclopedia of Genes and Genomes pathway analyses were performed. Proteomic analysis identified 2 proteins, SBSPON (somatomedin B and thrombospondin type 1 domain-containing protein precursor) and TNS3 (tensin 3), that were uniquely downregulated in PPCM. SBSPON, an extracellular matrix protein, and TNS3, involved in actin remodeling and cell signaling, may contribute to impaired tissue remodeling and fibrosis in PPCM. Metabolomic analysis revealed elevated levels of homogentisate and deoxycholate and reduced levels of lactate and alanine in PPCM, indicating disrupted metabolic pathways and glucose utilization. Both PPCM and DCM shared pathways related to inflammation, immune responses, and signal transduction. However, thyroid hormone signaling was notably reduced in PPCM, affecting contractility and calcium handling through altered expression of PLN (phospholamban) and Sarcoendoplasmic Reticulum Calcium ATPase (SERCA). Enhanced endoplasmic reticulum stress and altered endocytosis pathways in PPCM suggested additional mechanisms of energy metabolism disruption. The present study reveals unique posttranslational molecular features of the PPCM myocardium, which mediates cellular and metabolic remodeling, and holds promise as potential targets for therapeutic intervention.

Elevated Perspectives: Unraveling Cardiovascular Dynamics in High-Altitude Realms.

High-altitude regions pose distinctive challenges for cardiovascular health because of decreased oxygen levels, reduced barometric pressure, and colder temperatures. Approximately 82 million people live above 2400 meters, while over 100 million people visit these heights annually. Individuals ascending rapidly or those with pre-existing cardiovascular conditions are particularly vulnerable to altitude-related illnesses, including Acute Mountain Sickness (AMS) and Chronic Mountain Sickness (CMS). The cardiovascular system struggles to adapt to hypoxic stress, which can lead to arrhythmias, systemic hypertension, and right ventricular failure. Pathophysiologically, high-altitude exposure triggers immediate increases in cardiac output and heart rate, often due to enhanced sympathetic activity. Over time, acclimatisation involves complex changes, such as reduced stroke volume and increased blood volume. The pulmonary vasculature also undergoes significant alterations, including hypoxic pulmonary vasoconstriction and vascular remodelling, contributing to conditions, like pulmonary hypertension and high-altitude pulmonary edema. Genetic adaptations in populations living at high altitudes, such as gene variations linked to hypoxia response, further influence these physiological processes. Regarding cardiovascular disease risk, stable coronary artery disease patients generally do not face significant adverse outcomes at altitudes up to 3500 meters. However, those with unstable angina or recent cardiac interventions should avoid high-altitude exposure to prevent exacerbation. Remarkably, high-altitude living correlates with reduced cardiovascular mortality rates, possibly due to improved air quality and hypoxia-induced adaptations. Additionally, there is a higher incidence of congenital heart disease among children born at high altitudes, highlighting the profound impact of hypoxia on heart development. Understanding these dynamics is crucial for managing risks and improving health outcomes in high-altitude environments.

O2 consumption overshoot in patients with heart failure: crossing the line

Abstract Background Cardiopulmonary exercise testing (CPET) is among the most valuable clinical tools for evaluating disease severity and physical activity limitations in heart failure (HF) patients. Peak oxygen uptake (pVO2) reflects maximal cardiac output during exercise, and it is considered a major parameter in selecting candidates for cardiac transplantation. VO2 overshoot, a transient increase in VO2 during recovery from maximal exercise, has been frequently observed in HF patients and is attributed to the transient increase in cardiac output caused by the mismatch between cardiac contractility and afterload reduction. However, the prognostic significance of this phenomenon remains to be fully established. Purpose This study aimed to characterize the prognostic significance of VO2 overshoot following peak exercise in individuals with HF. Methods This retrospective single-center study included consecutive adult patients with chronic (&amp;gt;3 months) and stable HF, with left ventricular ejection fraction (LVEF) &amp;lt;50%, who underwent CPET between 2015 and 2020. Following maximal exercise, patients recovered over a 3-minute period (walking 2km/h for 1 minute and sitting passively for 2 minutes). VO2 overshoot kinetics during recovery were measured and described as the time until post-exercise VO2 fell below pVO2 for at least 15 seconds. Please refer to Figure 1A for an example of normal and prolonged VO2 overshoot. The study endpoint was time to cardiovascular (CV) death, urgent cardiac transplant, or left ventricular assist device (LVAD) over 1-year follow-up. Results A total of 254 patients were included (mean age 59 ± 12 years; 83% males; mean LVEF 34 ± 9%; 70% with ischemic HF; 77% in NYHA class II-III; mean pVO2 18 ± 6 mL/kg/min; mean predicted pVO2% 52 ± 16%; mean VE/VCO2 slope 41 ± 13). The VO2 overshoot had a normal distribution (Figure 1B) and lasted on average for 45 ± 33 seconds. There were no differences between patients that had an overshoot higher and below average. Overall, during follow-up, 25 patients met the composite endpoint (12 CV deaths, 9 urgent heart transplants, and 4 LVAD). Univariate analysis showed a significant relationship between VO2 overshoot and the outcome of interest (HR 1.01, 95% CI 1.00 – 1.02, p=0.027). In multivariate analysis, this association remained significant, even after adjusting for pVO2 and VE/VCO2 slope (HR 1.01, CI 95% 1.00– 1.02, p=0.026). Conclusion This study delves into the intriguing phenomenon of VO2 overshoot in patients with heart failure, shedding light on its potential prognostic significance. The independent association between VO2 overshoot and the composite endpoint suggests that this transient increase in oxygen consumption may carry prognostic value. Further studies should confirm these findings.

Evidence that mitral and/or tricuspid regurgitation diminishes stroke volume increase during exercise

Abstract Background and Purpose The severity of heart failure can be evaluated by peak oxygen consumption (VO2). Cardiac output is one of the major essential factors to determine the VO2. Therefore, cardiac output increases linearly as the exercise intensity increases. However, in mitral regurgitation, effective stroke volume decreases due to some blood flowing back into the left atrium from the left ventricle. This reduction may compromise oxygen delivery to working muscles and diminish oxygen uptake. Peak VO2/HR is known to indicate the stroke volume at the peak exercise, but since c(A-V)O2 difference shows almost a similar change pattern during a ramp protocol, VO2/HR during the load is also reported to be an indicator of stroke volume (SV) at that work rate. However, there are no investigations that have examined the extent to which the increase in cardiac output during stress is affected by the severity of mitral regurgitation. Therefore, we investigated the influence of the degree of regurgitant volume in mitral regurgitation (MR) and tricuspid regurgitation (TR) affects the SV increasing response to exercise load. Additionally, we examined whether blunted SV increase influences on the peak VO2. Methods Among 525 patients who underwent cardiopulmonary exercise test (CPX) at our institution from January 2023 to October 2023, 518 patients (143 females, 375 males, mean age 65.2±15.0 years old) where precise analyses of CPX was possible. CPX was performed using breath-by-breath gas analysis, and an incremental load test (10watts/min) was administered until exhaustion. The rate of increase in VO2/HR per watt during an incremental loading (Δ(VO2/HR)/ΔWR) was used as an indicator of the degree of increase in SV. Typically, SV increases up to 60% of maximum load, around AT, after which it stops increasing and plateaus. Therefore, the slope of Δ(VO2/HR)/ΔWR was examined from the initiation of ramp loading to AT. The degree of reflux was evaluated by echocardiography and classified as none/trivial, mild and moderate/severe. The number of people in each group of None/trivial, mild, moderate/severe was, 392, 83, 30 for MR, and 416, 64, 24 for TR. Δ(VO2/HR)/ΔWR was evaluated for each degree of reflux, using ANOVA to determine whether there was a difference between groups. Results As shown in the Figure1, Δ(VO2/HR)/ΔWR decreased as the reflux flow rate increased for both MR and TR. Concurrently, peak VO2 also decreased in the moderate/severe group compared to the non/trivial-reflux group for both MR and TR (MR: 17.5±5.4 mL/min/kg vs. 14.9±3.5 mL/min/kg, TR: 17.2±5.3 mL/min/kg vs. 13.6±3.8 mL/min/kg). Conclusion The Δ(VO2/HR)/ΔWR obtained through CPX has been shown to be an index that can evaluate the severity of reflux. Additionally, it was also demonstrated that as regurgitation flow increased, true stroke volume decreases, which is correlated with a reduction in peak VO2.

Interventricular abnormal septum displacement as contributory mechanism for impaired peak oxygen consumption and exercise cardiac output response in heart failure

Abstract Background In Heart failure (HF), the role of septum position and abnormal right ventricular (RV) geometry in determining exercise performance is unknown. Especially an abnormal interventricular septal (IVS) position is a well-known sign of RV pressure overload which affects left ventricular filling and output due to interdependence. Aim We postulated that an abnormal septum displacement during exercise and RV geometry alteration would affect peak exercise oxygen consumption (VO2) and cardiac output (CO) increase. Methods 17 HF patients with reduced ejection fraction (HFrEF) (mean age 71±12) underwent a cardiopulmonary exercise testing imaging (iCPET) with RV 3D-imaging analysis and were compared with a control population (mean age 67±14). 3D imaging of the RV chamber was examined off-line using the 4D RV TomTec software and obtained 3D mesh of the RV model using custom software to obtain the mean curvature value of IVS in 4 regions of: inflow tract (RVIT), outflow tract (RVOT), apical and body.We acquired measurements of curvature during end-diastole (ED) and at end systole (ES) phases and obtained a parametric curvature map. Results HF patients typically exhibited an abnormal of septal curve, with a more leftward configuration either at rest and under exercise (rest =−0.01±0.004 at ED, and −0.01±0.006 at ES; peak exercise= −0.01±0.004 at ED, and −0.01±0.004 at ES, Figure) compared to controls (rest=−0.02±0.003 at ED, and −0.02±0.005 at ES; peak exercise −0.02±0.008 at ED, and −0.03±0.006 at ES, Figure). Notably, the degree of the IVS curvature was found to linearly correlate with an impaired gas exchange performance as lower peak VO2 and a limited CO in HF (respectively r=0.62, p&amp;lt;0.001 and r=0.5, p&amp;lt;0.001 at ED during exercise; r=0.34, p&amp;lt;0.001 at ES during exercise, Figure). Conclusions In HF, the RV geometrical alterations reflected by an abnormal IVS displacement appear as novel contributory factors to a reduced exercise performance, impaired oxygen uptake and decreased CO.

Chronic cold exposure causes left ventricular hypertrophy that appears to be physiological.

Exposure to winter cold causes an increase in energy demands to meet the challenge of thermoregulation. In small rodents, this increase in cardiac output leads to a profound cardiac hypertrophy, 2-3 times that typically seen with exercise training. The nature of this hypertrophy and its relevance to winter mortality remains unclear. Our goal was to characterize cold-induced cardiac hypertrophy and to assess its similarity to either exercise-induced (physiological) hypertrophy or the pathological hypertrophy of hypertension. We hypothesized that cold-induced hypertrophy will most closely resemble exercise-induced hypertrophy, but be another unique pathway for physiological cardiac growth. We found that cold-induced hypertrophy was largely reversed after a return to warm temperatures. Further, metabolic rates were elevated while gene expression and mitochondrial enzyme activities indicative of pathology were absent. A gene expression panel comparing hearts of exercised and cold-exposed mice further suggests that these activities are similar, although not identical. In conclusion, we found that chronic cold led to a phenotype that most closely resembled physiological hypertrophy, with enhanced metabolic rate, without induction of fetal genes, but with decreased expression of genes associated with fatty acid oxidation, suggesting that heart failure is not a cause of winter mortality in small rodents and identifying a novel approach for the study of cardiac growth.

Inhaled argon dilates pulmonary vasculature in rat isolated lungs.

During cardiopulmonary resuscitation, pulmonary vasoconstriction due to hypoxia and hypercarbia restricts blood flow from the right to the left heart, resulting in reduced cardiac output that further inhibits adequate oxygenation and the ability to distribute oxygenated blood and medications. An inhaled pulmonary vasodilator could attenuate vasoconstriction and, therefore, increase cardiac output. We used rat isolated lungs to test if inhaled Argon leads to pulmonary vasodilation in phenylephrine-treated lungs. Lungs of 13 adult male Sprague-Dawley rats were isolated, ventilated, and perfused. Pulmonary artery and left atrium were cannulated and lungs perfused at constant flow with 4% albumin physiological saline solution. Controls (n=6) were ventilated with 65% N2, 5% CO2, 30% O2, and Argon lungs (n=7) with 65% Argon, 5% CO2, and 30% O2. Pulmonary mean arterial pressure (pMAP) and airway pressure (AWP) were recorded continuously, and pulmonary vascular resistance (PVR) was calculated. Following baseline readings, phenylephrine, a pulmonary vasoconstrictor, was perfused at increasing concentrations from 10-7 to 10-3mol/L every 5min. Statistics: Student's t test, α=0.05. Argon led to significantly lower pMAPs and PVRs, independent of AWP. Thus, it significantly dilated pre-constricted pulmonary vessels in an ex vivo lung model. When given during resuscitation, this might aid to increase cardiac output.

Cardiovascular Adaptation in Fetal Growth Restriction: A Longitudinal Study From Fetuses at Term to the First Year of Life.

To investigate longitudinal trends in fetal and offspring cardiovascular adaptation in fetal growth restriction (FGR). Prospective longitudinal study. Fetal Medicine Unit. Thirty-five FGR pregnancies and 37 healthy controls assessed as term fetuses (mean age 37 ± 1 weeks) and again in infancy (mean age 8 ± 2 months). Conventional echocardiographic techniques, tissue Doppler imaging and speckle tracking echocardiography. Left ventricular (LV) and right ventricular (RV) geometry and function. Echocardiographic parameters were normalised by ventricular size adjusting for differences in body weight between groups. Compared to healthy controls, late FGR fetuses showed significant alterations in cardiac geometry with more globular LV chamber (LV sphericity index, 0.56 vs. 0.52), increase in biventricular global longitudinal systolic contractility (MAPSE, 0.29 vs. 0.25 mm; TAPSE, 0.42 vs. 0.37 mm) and elevated cardiac output (combined CO: 592 vs. 497 mL/min/kg, p < 0.01 for all). Indices of LV diastolic function in FGR fetuses were significantly impaired with myocardial diastolic velocities (LV A', 0.30 vs. 0.26 cm/s; IVS E', 0.19 vs. 0.16 cm/s) and LV torsion (1.2 vs. 3.5 deg./cm, p < 0.01 for all). At postnatal assessment, FGR offspring revealed persistently increased SAPSE (0.27 vs. 0.24 mm), LV longitudinal strain (-19.0 vs. -16.0%), reduced LV torsion (1.6 vs. 2.1 deg./cm) and elevated CO (791 vs. 574 mL/min/kg, p < 0.01 for all). Perinatal cardiac remodelling and myocardial dysfunction in late FGR fetuses is most likely due to chronic placental hypoxaemia. Persistent changes in cardiac geometry and function in FGR offspring may reflect fetal cardiovascular maladaptation that could predispose to long-term cardiovascular complications in later life.

Central Hemodynamic and Thermoregulatory Responses to Food Intake as Potential Biomarkers for Eating Detection: Systematic Review.

Diet-related diseases, such as type 2 diabetes, require strict dietary management to slow down disease progression and call for innovative management strategies. Conventional diet monitoring places a significant memory burden on patients, who may not accurately remember details of their meals and thus frequently falls short in preventing disease progression. Recent advances in sensor and computational technologies have sparked interest in developing eating detection platforms. This review investigates central hemodynamic and thermoregulatory responses as potential biomarkers for eating detection. We searched peer-reviewed literature indexed in PubMed, Web of Science, and Scopus on June 20, 2022, with no date limits. We also conducted manual searches in the same databases until April 21, 2024. We included English-language papers demonstrating the impact of eating on central hemodynamics and thermoregulation in healthy individuals. To evaluate the overall study quality and assess the risk of bias, we designed a customized tool inspired by the Cochrane assessment framework. This tool has 4 categories: high, medium, low, and very low. A total of 2 independent reviewers conducted title and abstract screening, full-text review, and study quality and risk of bias analysis. In instances of disagreement between the 2 reviewers, a third reviewer served as an adjudicator. Our search retrieved 11,450 studies, and 25 met our inclusion criteria. Among the 25 included studies, 32% (8/25) were classified as high quality, 52% (13/25) as medium quality, and 16% (4/25) as low quality. Furthermore, we found no evidence of publication bias in any of the included studies. A consistent postprandial increase in heart rate, cardiac output, and stroke volume was observed in at least 95% (heart rate: 19/19, cardiac output: 18/19, stroke volume: 11/11) of the studies that investigated these variables' responses to eating. Specifically, cardiac output increased by 9%-100%, stroke volume by 18%-41%, and heart rate by 6%-21% across these studies. These changes were statistically significant (P<.05). In contrast, the 8 studies that investigated postprandial thermoregulatory effects displayed grossly inconsistent results, showing wide variations in response with no clear patterns of change, indicating a high degree of variability among these studies. Our findings demonstrate that central hemodynamic responses, particularly heart rate, hold promise for wearable-based eating detection, as cardiac output and stroke volume cannot be measured by any currently available noninvasive medical or consumer-grade wearables. PROSPERO CRD42022360600; https://www.crd.york.ac.uk/prospero/display_record.php?RecordID=360600.

Atrial Adaptations in Athletes Heart.

Intensive training efforts are associated with hemodynamic changes accompanied by increases in cardiac output and stroke volume related to higher peak oxygen consumption and better athletic performance during exercise. These hemodynamic changes induce an enlargement of cardiac chambers, but also of the atria and may result in an athletes' heart (AH). Data from large studies about atrial enlargement in AH are sparse. Competitive athletes aged ≥18years, who presented for pre-participation screening 04/2020-10/2021 were included in this study and stratified for AH (defined as physiologically increased heart volume >13.0 in males and >12.0mL/kg in females). Overall, 646 athletes aged ≥18years (median age 24.0 [20.0/31.0]years; 206 [31.9%] females) were included in our study 04/2020-10/2021; among these, 118 (18.3%) had an AH. The computed absolute heart volume was 969.4 (853.1/1083.0)mL in athletes with AH and 841.3 (707.4/966.3)mL in those without AH (p<0.001). AH was associated with larger left ventricular mass (206.6±39.0vs. 182.7±44.2g, p<0.001). LA area (15.4 [13.7/18.2] vs. 14.3 [12.0/16.3]cm2, p<0.001) and RA area (15.8 [13.8/18.6] vs. 14.5 [12.3/17.0]cm2, p<0.001) were enlarged in AH versus those athletes without AH. The logistic regressions confirmed an independent association of AH on LV mass (OR 1.05 [95% CI 1.04-1.06], p<0.001). LA area (OR 1.29 [95% CI 1.19-1.39], p<0.001) as well as RA area (OR 1.28 [95% CI 1.19-1.38], p<0.001) were afflicted by AH. An AH is accompanied by significant enlargement of the atria as well as increased cardiac muscle mass.

Hemodynamic Mechanisms Initiating Salt-Sensitive Hypertension in Rat Model of Primary Aldosteronism.

Few studies have investigated the hemodynamic mechanism whereby primary hyperaldosteronism causes hypertension. The traditional view holds that hyperaldosteronism initiates hypertension by amplifying salt-dependent increases in cardiac output (CO) by promoting increases in sodium retention and blood volume. Systemic vascular resistance (SVR) is said to increase only as a secondary consequence of the increased CO and blood pressure. Recently, we investigated the primary hemodynamic mechanism whereby hyperaldosteronism promotes salt sensitivity and initiation of salt-dependent hypertension. In unilaterally nephrectomized male Sprague-Dawley rats given infusions of aldosterone or vehicle, we found that aldosterone promoted salt sensitivity and initiation of salt-dependent hypertension by amplifying salt-induced increases in SVR while decreasing CO. In addition, we validated mathematical models of human integrative physiology, derived from Guyton's classic 1972 model - Quantitative Cardiovascular Physiology-2005 and HumMod-3.0.4. Neither model accurately predicted the usual changes in sodium balance, CO, and SVR that normally occur in response to clinically realistic increases in salt intake. These results demonstrate significant limitations with the hypotheses inherent in the Guyton models. Together these findings challenge the traditional view of the hemodynamic mechanisms that cause salt-sensitive hypertension in primary aldosteronism. Key words: Aldosterone, Blood pressure, Salt, Sodium, Rat.

Effects of integrative therapy with Du Meridian moxibustion, ear acupuncture, and alprazolam on cardiac function and neurotransmitter levels in patients with coronary heart disease and insomnia: An observational study.

To explore the effects of Du Meridian moxibustion combined with ear acupuncture on clinical symptoms and serum neurotransmitters in patients with coronary heart disease and insomnia. This study is a retrospective study. From June 2021 to May 2023, 116 patients with coronary heart disease and insomnia treated at our hospital were selected as subjects. They were divided into 2 groups according to the treatment. The control group received treatment with alprazolam, while the experimental group received Du Meridian moxibustion combined with ear acupuncture in addition to alprazolam treatment. The efficacy of the 2 groups was compared, and the levels of cardiac function indicators, serum melatonin, leptin, and neurotransmitters were measured. The total effectiveness rate in the experimental group was 93.10% (with a cure rate of 36.21%, a significant improvement rate of 41.38%, and an effective rate of 15.52%), which was significantly higher than the 79.31% in the control group (with a cure rate of 24.14%, a significant improvement rate of 32.76%, and an effective rate of 22.41%) (P < .05). Both groups exhibited an increase in left ventricular ejection fraction, stroke volume, and cardiac output after treatment compared to before treatment. Additionally, left ventricular end-systolic diameter decreased after treatment compared to before treatment, but the cardiac function was compared between the 2 groups after treatment (P > .05). In both groups, serum melatonin and serotonin (5-HT) levels increased after treatment compared to before treatment, while serum leptin, dopamine, and glutamate levels decreased after treatment compared to before treatment. Furthermore, the experimental group had higher serum melatonin, 5-HT, and gamma-aminobutyric acid levels compared to the control group, and lower serum leptin, dopamine, and glutamate levels compared to the control group (P < .05). The serum traditional Chinese medicine syndrome score and Pittsburgh sleep quality index score of the 2 groups decreased after treatment, and the experimental group was lower than the conventional group (P < .05). The combination of Du Meridian acupuncture with ear acupuncture in the treatment of insomnia in coronary heart disease can regulate the expression of serum melatonin, leptin, and neurotransmitters, alleviate symptoms, and improve therapeutic efficacy.