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BackgroundCardiac physiology changes after heart transplant (HT), resulting in a restrictive physiology with an increase in both arterial elastance (Ea) and ventricular elastance (Ees). This leads to a higher susceptibility to develop afterload mismatch, although the early identification of this phenomenon has not yet been explored. The aim of this study is to identify the presence of afterload mismatch after HT, its determinants, and its impact on cardiac mortality.MethodsWe conducted an observational, single-centre study based on the historical cohort of patients who underwent HT from 1985 to 2015 at our institution. We included patients who had survived the first year after HT with left ventricular ejection fraction (LVEF) ≥ 50%, International Society of Heart and Lung Transplantation (ISHLT) cardiac allograft vasculopathy of grade 0–1, and ISHLT acute cellular rejection of grade 0–1R at 1 year after HT. Ea and Ees were calculated using a non-invasive method based on blood pressure and end-systolic volume and end-diastolic volume measured at transthoracic echocardiography. Patients were grouped in 3 categories according to the presence of increased afterload and afterload mismatch as follows: low afterload (LA - Ea lower the median), matched high afterload (MHA - Ea higher of equal than the median, Ees higher or equal than the median), afterload mismatch (AM - Ea higher or equal than the median, Ees lower than the median). The impact of AM on long-term outcome, defined as cardiac mortality, was investigated, as well as predictors of AM.ResultsThe study cohort consisted of 345 HT patients. The median of Ea and Ees were 4.0 mmHg/mL and 6.75 mmHg/mL, respectively. 49 patients (13%) developed AM, while LA and MHA groups accounted for 49% and 36% of the cohort, respectively. Patients with AM were mostly male (91%), with ischemic heart disease (45%) and a higher percentage of left ventricular assisted device prior to HT (8%). LVEF was lower in AM (57% vs 63% and 64% for LA and MHA respectively, p < 0.0001), while stroke volume was lower than LA and similar to MHA (27 ml vs 35 mL and 26 mL for LA and MHA respectively, p = 0.0001 ). Predictors of AM were male recipient from male donor (Mr/Md) (β 015, p = 0.0067) and Mr from female donor (Mr/Fd) (β 0.6, p = 0.0078). After a median of 11.3-year follow-up, 59 HT recipients died. Cardiac mortality was higher in AM than in the other groups (AM median survival 17.2 y vs 27.8 y and 24.1 y for LA and MHA respectively, log-rank p = 0.005). After adjusting for confounding variables, AM was a predictor of cardiac mortality (HR: 2.26; 95%CI 1.18 – 4.35), such as Mr/Fd (HR 2.94; 95%CI 1.18 – 4.35, p = 0.0358).ConclusionAM, in the context of a normal LVEF, is associated with male donor and sex mismatch, and negatively affects long-term outcome after HT.Abstract 144 Figure 1Cardiac mortality across the 3 groups of afterload conditionsAbstract 144 Figure 2Univariable and multivariable Cox proportional hazard modelConflict of InterestHeart Failure Unit

The hemodynamic effects of ventilation can be grouped into three concepts: 1) Spontaneous ventilation is exercise; 2) changes in lung volume alter autonomic tone and pulmonary vascular resistance and can compress the heart in the cardiac fossa; and 3) spontaneous inspiratory efforts decrease intrathoracic pressure, increasing venous return and impeding left ventricular ejection, whereas positive-pressure ventilation decreases venous return and unloads left ventricular ejection. Spontaneous inspiratory efforts may induce acute left ventricular failure and cardiogenic pulmonary edema. Reversing the associated negative intrathoracic pressure swings by using noninvasive continuous positive airway pressure rapidly reverses acute cardiogenic pulmonary edema and improves survival. Additionally, in congestive heart failure, states increasing intrathoracic pressure may augment left ventricular ejection and improve cardiac output. Using the obligatory changes in venous return induced by positive pressure breathing, one can quantify the magnitude of associated decreases in venous flow and left ventricular ejection using various parameters, including vena caval diameter changes, left ventricular stroke volume variation, and arterial pulse pressure variation. These parameters vary in proportion to the level of cardiac preload reserve present, thus accurately predicting which critically ill patients will increase their cardiac output in response to fluid infusions and which will not. Common parameters include arterial pulse pressure variation and left ventricular stroke volume variation. This functional hemodynamic monitoring approach reflects a practical clinical application of heart–lung interactions.

Background The optimal timing of left ventricular unloading in patients with cardiogenic shock receiving venoarterial extracorporeal membrane oxygenation therapy remains controversial. This systematic review evaluated the latest evidence on the impact of left ventricular unloading timing in patients with cardiogenic shock receiving venoarterial extracorporeal membrane oxygenation. Methods The PubMed, Embase and Cochrane Library databases were searched from inception to February 2025. The identified studies were screened based on predefined inclusion and exclusion criteria, and eligible studies were subjected to quality assessment and data extraction. Heterogeneity testing and meta-analysis were performed using Review Manager software version 5.4. Results Eight studies involving 2,117 patients (proactive unloading, 1,338; passive unloading, 779) were included in the meta-analysis, which revealed no statistically significant differences in extracorporeal membrane oxygenation weaning rates (relative risk = 1.06, 95% confidence interval: 0.87–1.28; P  = 0.59), in-hospital mortality (relative risk = 0.95, 95% confidence interval: 0.86–1.04; P  = 0.28), or 30-day all-cause mortality (relative risk = 0.75, 95% confidence interval: 0.52–1.10; P  = 0.14) between the proactive and passive unloading groups. However, the risks of sepsis (relative risk = 0.79, 95% confidence interval: 0.64–0.96; P  = 0.02) and abdominal complications (relative risk = 0.67, 95% confidence interval: 0.46–0.96; P  = 0.03) were lower following proactive unloading than following passive unloading. Conclusion Compared to passive left ventricular unloading, proactive left ventricular unloading did not confer significant benefits in terms of extracorporeal membrane oxygenation weaning success or short-term survival outcomes, but was associated with reduced risks of sepsis and abdominal complications. Registration The review protocol was registered in PROSPERO (ID: CRD42024499028).

Purpose The clinical significance of septic myocardial dysfunction is controversial, a fact that may be explained by the influence of loading conditions. Many indices may be useful to characterize cardiac function during septic shock, but their feasibility and physiological coherence in the clinical setting are unknown. Methods Hemodynamic and echocardiographic data with tissue Doppler and speckle tracking were prospectively recorded on the first 3 days of human septic shock. Hypokinesia, normokinesia, and hyperkinesia were defined as a left ventricular ejection fraction (LVEF) of <45, 45–60, and >60%, respectively. Twelve hemodynamic indices exploring contractility and loading conditions were assessed and analyzed. Results Two hundred and ninety-seven echocardiographies were performed in 132 patients. During the first 24 h (H 1–24 ), 48 (36.4%) patients were hyperkinetic, 55 (41.7%) were normokinetic, and 29 (22.0%) patients were hypokinetic. Thirteen patients had a secondary hypokinesia absent at H 1–24 but present at H 25–48 or H 49–72 , for an overall incidence of 42 (31.8%) during the first 3 days. Despite a limited feasibility (<50%), global LV longitudinal peak systolic strain was impaired in a majority (>70%) of the patients assessed, including all those with depressed LVEF, and declined early in patients whose LVEF secondarily deteriorated. Most contractility indices were inversely correlated with afterload indices. Hyperkinetic patients exhibited the worst reduction in afterload indices. Hospital mortality was significantly higher in patients with LV hyperkinesia than in their counterparts: 30 (62.5%) vs. 35 (41.7%), p  = 0.02. Conclusions Speckle tracking-derived strain was reduced in the majority of patients with septic shock, revealing covert septic myocardial dysfunction, but had poor feasibility. We found an inverse correlation between most of the contractility and afterload indices. Precise evaluation of afterload is crucial for adequate interpretation of LV systolic function in this setting.

Load dependence on left ventricular (LV) strain is under constant debate with its interference with prognostic implications remaining unclear. Consequently, we sought to investigate their interaction and prognostic value following acute myocardial infarction (AMI) using state-of-the-art cardiac magnetic resonance (CMR) imaging. In total, 1235 patients (n = 795 ST-elevation [STEMI] and 440 non-STEMI) underwent CMR in median 3 days following AMI. Infarct characteristics were described by CMR using tissue characterisation (infarct size, microvascular obstruction, area at risk) and deformation imaging including LV global longitudinal and circumferential strain (GLS/GCS). Non-invasive haemodynamic indices included effective arterial elastance Ea (end-systolic pressure (ESP)/stroke volume) and the non-geometric LV end-systolic afterload index NGI [(ESP × LV end-systolic volume (ESV))/LV mass] for estimation of LV afterload. LV contractility was assessed using end-systolic elastance Ees (ESP/LV ESV). Ventriculo-arterial coupling was described as Ea/Ees. Major adverse cardiac events (MACE) were recorded within the first year. All haemodynamic indices were impaired in patients with MACE during follow-up compared to patients without (p < 0.001-0.005). Ventriculo-arterial coupling showed the highest correlation to infarct properties (infarct size r = 0.51, p < 0.001) and deformation imaging (GLS r = 0.54, GCS r = 0.72, p < 0.001). GLS and GCS were associated with MACE independently of all haemodynamic indices (p < 0.001 for all except of GCS-Ea/Ees p = 0.024). Non-invasive haemodynamic indices are associated with outcome following AMI with ventriculo-arterial coupling showing the most prominent association to infarct properties and outcome. GCS showed higher correlation to haemodynamic indices compared to GLS whilst both are independent predictors for MACE.

While central blood pressure (BP) has been recognized as a major indicator of left ventricular (LV) afterload, the reduction of central pressure decreases LV afterload and may prevent heart failure (HF) decompensation. Non-invasive transcutaneous vagus nerve stimulation (tVNS) was shown to improve cardiac function in HF patients. In this study, the relationship between active tVNS and reduction of central BP was investigated in patients with acute HF (AHF). The 22 patients hospitalized for AHF after initial stabilization (median 80 yrs, males 60%) were randomly assigned to active or sham group. For 1 h daily over 5 days, low-level transcutaneous electrical stimulation (LLTS) (20 Hz, 1 mA) was performed after attaching an ear clip to the tragus (active group) or the earlobe (sham control group). Before and after stimulation, central aortic systolic pressure (CASP), brachial systolic BP (SBP), diastolic BP (DBP) as well as heart rate (HR) were noninvasively measured. No significant differences in baseline characteristics were observed between the active and sham groups. In the active group, CASP, SBP, DBP, and HR each decreased significantly after stimulation (all < 0.05), whereas in the sham group, CASP, SBP, DBP, and HR each increased significantly after stimulation (all < 0.05). All the changes in CASP, SBP, DBP and HR before and after stimulation were also significantly different between active and sham groups (all < 0.01). There were no device-related side effects. In this study, the left tragus tVNS resulted in an acute afterload reduction in the elderly AHF patients. Non-invasive LLTS may be useful and safe for reducing afterload in AHF. ClinicalTrials.gov, identifier UMIN000044121.

The mismatch of elastic properties between the arterial tissue and the vascular grafts, commonly called compliance mismatch, is responsible for many deleterious post-operative complications. Currently, there is an absence of prostheses that conform with the compliance of healthy aortas. We aimed to evaluate the in vivo performance of novel compliance-matching grafts in a swine model and compare it to the native aorta and to gold-standard aortic grafts.We proposed a compliance-matching graft design, composed of a standard aortic graft surrounded by an optimized Nickel-Titanium compliance-augmenting layer. We replaced the thoracic aorta of six domestic pigs with compliance-matching grafts under cardiopulmonary bypass. We removed the compliance-regulating layer of the compliant grafts, so that gold-standard grafts remained implanted. The aortic pressure and flow rate were measured at the three stages of the experiment to assess hypertension and arterial stiffness. The compliance-matching grafts were implanted without inducing post-operative hypertension by maintaining systolic pressure (p = 0.26), aortic pulse wave velocity (p = 0.89) and aortic distensibility (p = 0.67) at healthy levels. The gold-standard grafts caused a significant rise in systolic pressure (p = 0.005), pulse wave velocity (p = 0.012) and they approximately doubled pulse pressure (p < 0.001). Our novel compliant grafts could diminish the complications caused by compliance-mismatch and they could surpass the clinical performance of existing prostheses. The proposed grafts comprise a step towards optimized treatment and improved life expectancy of patients subjected to aortic replacement.

Background Low-volume hypertonic solutions, such as half-molar lactate (LAC), may be a potential treatment used for fluid resuscitation. This study aimed to evaluate the underlying cardiovascular effects and mechanisms of LAC infusion compared to sodium-matched hypertonic sodium chloride (SAL). Methods Eight healthy male participants were randomized in a controlled, single-blinded, crossover study. Each participant received a four-hour infusion of LAC and SAL in a randomized order. Assessor-blinded echocardiography and blood samples were performed. The primary endpoint was cardiac output (CO) measured by echocardiography. Results During LAC infusion, circulating lactate levels increased by 1.9 mmol/L (95% CI 1.8–2.0 mmol/L, P  < 0.001) compared with SAL. CO increased by 1.0 L/min (95% CI 0.5–1.4 L/min, P  < 0.001), driven primarily by a significant increase in stroke volume of 11 mL (95% CI 4–17 mL, P  = 0.002), with no significant change in heart rate. Additionally, left ventricular ejection fraction improved by 5 percentage points ( P  < 0.001) and global longitudinal strain by 1.5 percentage points ( P  < 0.001). Preload indicators were elevated during SAL infusion compared with LAC infusion. Concomitantly, afterload parameters, including systemic vascular resistance and effective arterial elastance, were significantly decreased with LAC infusion compared with SAL, while mean arterial pressure remained similar. Indicators of contractility improved during LAC infusion. Conclusions In healthy participants, LAC infusion enhanced cardiac function, evidenced by increases in CO, stroke volume, and left ventricular ejection fraction compared with SAL. Indicators of contractility improved, afterload decreased, and preload remained stable. Therefore, LAC infusion may be an advantageous resuscitation fluid, particularly in patients with cardiac dysfunction. Clinical trial registrations https://clinicaltrials.gov/ct2/show/NCT04710875 . Registered 1 December 2020.

The impact of Aortic Stenosis (AS) on the left ventricle (LV) extends beyond the influence of the pressure drop across the stenotic valve, but also includes the additional serial afterload imposed by the vascular system. Aortic input impedance is the gold standard for comprehensively studying the contribution of the vascular system to total myocardial afterload, but in the past measurement has been challenging arising from the need for invasive catheterization or specialized equipment to precisely record time-resolved blood pressure and flow signals. The goal of this work was to develop and validate a novel simulation-based method for determining aortic input impedance using only clinically available echocardiographic data and a simple blood pressure measurement. A simulation-based method to determine vascular impedance was developed using echocardiographic data and a brachial blood pressure measurement. Simulation-based impedance was compared to impedance calculated from echocardiographic flow data and pressure data from a non-invasive central pressure measurement device. In validation analysis comparing patient-specific simulation-based vascular impedance to non-invasively measured impedance, correlation between methods across a range of vascular parameters varied between R  = 0.40 and 0.99. A tendency was seen toward underestimation of pressure waveforms in point-by-point comparison of measured and simulated waveforms with an overall mean difference of 4.01 mmHg. Requiring only non-invasive clinical data that are widely available, simulation-based vascular impedance has the potential to allow for easier, more widespread, and larger-scale investigation of the effect of vascular impedance on total LV afterload.