Hemodynamic Deterioration Research Articles

Hypertension restricts leg blood flow and aggravates neuromuscular fatigue during human locomotion in males.

Patients with hypertension (HTN) are characterized by exaggerated vascular resistance and mean arterial pressure (MAP) and a compromised leg blood flow (QL) response to exercise recruiting a small muscle mass. However, the impact of hypertension on peripheral hemodynamics and the development of neuromuscular fatigue during locomotor activities, which critically depends on QL, remain unknown. Eight HTN (143 ± 11 mmHg/95 ± 6 mmHg; 45 ± 13 yr) and eight matched (age and activity) controls (120 ± 6 mmHg/77 ± 7 mmHg; CTRL) performed constant-load cycling exercise at 25, 50, and 75 W (for 4 min each) and at 165 ± 41 W (for 5 min). Exercise-induced locomotor muscle fatigue was quantified as the pre- to postexercise change in quadriceps twitch-torque (ΔQtw, peripheral fatigue) and voluntary activation (ΔVA%, central fatigue). QL (Doppler ultrasound) and leg vascular conductance (LVC) were determined during cycling at 25, 50, and 75 W. Heart rate and ventilatory responses were recorded during all intensities. MAP during exercise was, on average, ∼21 mmHg higher (P = 0.002) and LVC ∼39% lower (P = 0.001) in HTN compared with CTRL. QL was consistently between 20 and 30% lower (P = 0.004), and heart rate was significantly higher in HTN. Exercise-induced peripheral (ΔQtw: -53 ± 19% vs. -25 ± 23%) and central (ΔVA%: -7 ± 5% vs. -3 ± 2%) fatigue was significantly greater in HTN compared with CTRL. In addition to an exaggerated MAP, LVC and QL were lower during exercise in HTN compared with CTRL. Given the critical role of QL in determining the development of neuromuscular fatigue, these hemodynamic impairments likely accounted for the faster development of neuromuscular fatigue characterizing hypertensive individuals during locomotor exercise. NEW & NOTEWORTHY The impact of primary hypertension on the cardiovascular and neuromuscular fatigue response to locomotor exercise is unknown. We compared central and peripheral hemodynamics and the development of central and peripheral fatigue during cycling exercise in patients with stage I/II hypertension and age- and activity-matched healthy individuals. In addition to a significantly elevated blood pressure, hypertensive patients were, compared with their nonhypertensive counterparts, also characterized by considerable leg blood flow limitations and impaired neuromuscular fatigue resistance.

Composite Pulmonary Embolism Shock Score and Risk of Adverse Outcomes in Patients With Pulmonary Embolism.

In hemodynamically stable patients with acute pulmonary embolism (PE), the Composite Pulmonary Embolism Shock (CPES) score predicts normotensive shock. However, it is unknown if CPES predicts adverse clinical outcomes. The objective of this study was to determine whether the CPES score predicts in-hospital mortality, resuscitated cardiac arrest, or hemodynamic deterioration. Patients with acute intermediate-risk PE admitted from October 2016 to July 2019 were included. CPES was calculated for each patient. The primary outcome was a composite of in-hospital mortality, resuscitated cardiac arrest, or hemodynamic decompensation. Secondary outcomes included individual components of the primary outcome. The association of CPES with primary and secondary outcomes was evaluated. Among the 207 patients with intermediate-risk PE (64.7% with intermediate-high risk PE), 29 (14%) patients had a primary outcome event. In a multivariable model, a higher CPES score was associated with a worse primary composite outcome (adjusted hazard ratio [aHR], 1.81 [95% CI, 1.29-2.54]; P=0.001). Moreover, a higher CPES score predicted death (aHR, 1.76 [95% CI, 1.04-2.96]; P=0.033), resuscitated cardiac arrest (aHR, 1.99 [95% CI, 1.17-3.38]; P=0.011), and hemodynamic decompensation (aHR, 1.96 [95% CI, 1.34-2.89]; P=0.001). A high CPES score (≥3) was associated with the worse primary outcome when compared with patients with a low CPES score (22% versus 2.4%; P=0.003; aHR, 6.48 [95% CI, 1.49-28.04]; P=0.012). CPES score provided incremental prognostic value for the prediction of primary outcome over baseline demographics and European Society of Cardiology intermediate-risk subcategories (global Χ2 value increased from 0.63 to 1.39 to 13.69; P=0.005). In patients with acute intermediate-risk PE, the CPES score effectively risk stratifies and prognosticates patients for the prediction of clinical events and provides incremental value over baseline demographics and European Society of Cardiology intermediate-risk subcategories.

The evolution and future directions of bypass surgery.

Cerebral bypass surgery is one of the most complex and elegant procedures in neurosurgery. It involves several meticulous steps that test the skills of even the most prepared neurosurgeons. This surgery has transcended its traditional role in arterial stenosis and atherosclerosis, expanding its applications to include flow preservation techniques for complex conditions such as aneurysms, tumors, and vascular malformations. The decreased number of procedures performed across many hospitals reflects the development of newer endovascular therapies but is also due to the results of the extracranial-intracranial bypass study, the Carotid Occlusion Surgery Study, and the Carotid and Middle Cerebral Artery Occlusion Surgery Study, which have raised questions about the efficacy of cerebral bypass surgery for individuals with carotid artery occlusion who are prone to ischemic stroke. Despite this, there is still a potential benefit of bypass surgery for patients with hemodynamic impairment refractory to medical management. Also, revascularization in moyamoya vasculopathy is an effective strategy for preventing ischemic and hemorrhagic events in both children and adults. Additionally, innovations in the technique, such as the flow-regulated bypass and intraoperative flow assessment, aim to minimize perioperative morbidity. Despite bypass surgery being less performed in this current era, the teaching and development of these skills are still encouraged for future neurosurgeons, as a role for bypass will exist for the foreseeable future.

BOLD Cerebrovascular Reactivity and NOVA Quantitative MR Angiography in Adult Patients with Moyamoya Vasculopathy Undergoing Cerebral Bypass Surgery.

Revascularization surgery for the symptomatic hemisphere with hemodynamic impairment is effective for Moyamoya vasculopathy patients. However, careful patient selection is crucial and ideally supported by advanced quantitative hemodynamic imaging. Recently, blood oxygenation level-dependent cerebrovascular reactivity (BOLD-CVR) and quantitative magnetic resonance angiography with non-invasive optimal vessel analysis (qMRA-NOVA) have gained prominence in assessing these patients. This study aims to present the results of BOLD-CVR and qMRA-NOVA imaging along with the changes in cerebral hemodynamics and flow status following flow augmentation with superficial temporal artery-middle cerebral artery (STA-MCA) bypass in our Moyamoya vasculopathy patient cohort. Symptomatic patients with Moyamoya vasculopathy treated at the Clinical Neuroscience Center of the University Hospital Zurich who underwent hemodynamic and flow imaging (BOLD-CVR and qMRA-NOVA) before and after bypass were included in the analysis. Reduced hemispheric volume flow rates, as well as impaired BOLD-CVR, were measured in all 12 patients with Moyamoya vasculopathy before STA-MCA bypass surgery. Following the surgical procedure, post-operative BOLD-CVR demonstrated a non-significant increase in BOLD-CVR values within the revascularized, symptomatic middle cerebral artery territory and cerebral hemisphere. The results of the statistical tests should be viewed as indicative due to the small sample size. Additionally, post-operative qMRA-NOVA revealed a significant improvement in the hemispheric volume flow rate of the affected hemisphere due to the additional bypass flow rate. Our findings affirm the presence of hemodynamic and flow impairments in the symptomatic hemisphere of the Moyamoya vasculopathy patients. Bypass surgery proves effective in improving both BOLD-CVR impairment and the hemispheric volume flow rate in our patient cohort.

Clinical Likelihood Prediction of Hemodynamically Obstructive Coronary Artery Disease in Patients With Stable Chest Pain

BackgroundSelection for invasive angiography is recommended to be based on pretest probabilities (PTPs), and physiological measures of hemodynamical impairment by, for example, fractional flow reserve (FFR) should guide revascularization. The risk factor–weighted clinical likelihood (RF-CL) and coronary artery calcium score–weighted clinical likelihood (CACS-CL) models show superior discrimination of patients with suspected obstructive coronary artery disease (CAD), but validation against hemodynamic impairment is warranted. ObjectivesThe aim of this study was to validate the RF-CL and CACS-CL models against hemodynamically obstructive CAD. MethodsStable de novo chest pain patients (N = 4,371) underwent coronary computed tomography angiography and subsequently invasive coronary angiography with FFR measurements. Hemodynamically obstructive CAD was defined as invasive FFR ≤0.80 or high-grade stenosis by visual assessment (>90% diameter stenosis). For comparison, a guideline-endorsed basic PTP model was calculated based on age, sex, and symptom typicality. The RF-CL model additionally included the number of risk factors, and the CACS-CL model incorporated the coronary artery calcium score into the RF-CL. ResultsIn total, 447 of 4,371 (10.9%) patients had hemodynamically obstructive CAD. Both the RF-CL and CACS-CL models classified more patients with a very low clinical likelihood (≤5%) of obstructive CAD compared to the basic PTP model (33.0% and 53.7% vs 12.0%; P < 0.001) with a preserved low prevalence of hemodynamically obstructive CAD (<5% for all models). Against hemodynamically obstructive CAD, calibration and discrimination of the RF-CL and CACS-CL models were superior to the basic PTP model. ConclusionsThe RF-CL and CACS-CL models are well calibrated and superior to a currently recommended basic PTP model to predict hemodynamically obstructive CAD. (Danish Study of Non-Invasive Diagnostic Testing in Coronary Artery Disease [Dan-NICAD]; NCT02264717; Danish Study of Non-Invasive Diagnostic Testing in Coronary Artery Disease 2 [Dan-NICAD 2]; NCT03481712, Danish Study of Non-Invasive Diagnostic Testing in Coronary Artery Disease 3 [Dan-NICAD 3]; NCT04707859)

Percutaneous mechanical support in catheter ablation of ventricular arrhythmias: hype or hope?

Catheter ablation (CA) has become an established treatment strategy for managing recurrent ventricular tachycardias (VTs) in patients with structural heart disease. In recent years, percutaneous mechanical circulatory support (PMCS) devices have been increasingly used intra-operatively to improve the ablation outcome. One indication would be rescue therapy for patients who develop haemodynamic deterioration during the ablation. However, more efforts are focused on identifying subjects who are at high risk of such deterioration and could benefit from the pre-emptive use of the PMCS. The third reason to use PMCS could be the inability to identify diffuse substrate, especially in non-ischaemic cardiomyopathy. This paper reviews available experiences using various types of PMCS in different clinical scenarios. Although PMCS allows mapping during VT, it does not significantly influence acute outcomes and not convincingly long-term outcomes. On the contrary, the complication rate appears to be higher in PMCS cohorts. Our data suggest that even in patients with severe left ventricular dysfunction, the substrate modification can be performed without the need for general anaesthesia and risk of haemodynamic decompensation. In end-stage heart failure associated with the electrical storm, implantation of a left ventricular assist device (or PMCS with a transition to the left ventricular assist device) might be the preferred strategy before CA. In high-risk patients who are not potential candidates for these treatment options, radiotherapy could be considered as a bail-out treatment of recurrent VTs. These approaches should be studied in prospective trials.

Analysis of the perivascular fat attenuation index and quantitative plaque parameters in relation to haemodynamically impaired myocardial ischaemia.

To investigate the correlation between quantitative plaque parameters, the perivascular fat attenuation index, and myocardial ischaemia caused by haemodynamic impairment. Patients with stable angina who had invasive flow reserve fraction (FFR) assessment and coronary artery computed tomography (CT) angiography were retrospectively enrolled. A total of 138 patients were included in this study, which were categorized into the FFR < 0.75 group (n = 43), 0.75 ≤ FFR ≤ 0.8 group (n = 37), and FFR > 0.8 group (n = 58), depending on the range of FFR values. The perivascular FAI and CTA-derived parameters, including plaque length (PL), total plaque volume (TPV), minimum lumen area (MLA), and narrowest degree (ND), were recorded for the lesions. An FFR < 0.75 was defined as myocardial-specific ischaemia. The relationships between myocardial ischaemia and parameters such as the PL, TPV, MLA, ND, and FAI were analysed using a logistic regression model and receiver operating characteristic (ROC) curves to compare the diagnostic accuracy of various indicators for myocardial ischaemia. The PL, TPV, ND, and FAI were greater in the FFR < 0.75 group than in the grey area group and the FFR > 0.80 group (all p < 0.05). The MLA in the FFR < 0.75 group was lower than that in the grey area group and the FFR > 0.80 group (both P < 0.05). There were no significant differences in the PL, TPV, or ND between the grey area and the FFR > 0.80 group, but there was a significant difference in the FAI. The coronary artery lesions with FFRs ≤ 0.75 had the greatest FAI values. Multivariate analysis revealed that the perivascular FAI and PL density are significant predictors of myocardial ischaemia. The FAI has some predictive value for myocardial ischaemia (AUC = 0.781). After building a combination model using the FAI and plaque length, the predictive power increased (AUC, 0.781 vs. 0.918), and the change was statistically significant (P < 0.001). The combined model of PL + FAI demonstrated great diagnostic efficacy in identifying myocardial ischaemia caused by haemodynamic impairment; the lower the FFR was, the greater the FAI. Thus, the PL + FAI could be a combined measure to securely rule out myocardial ischaemia.

Transcatheter aortic valve replacement with corevalve self-expanding bioprosthesis: Clinical and durability data up to 12 years

Background and aimsTranscatheter aortic valve replacement (TAVR) determined a paradigm shift in the treatment of patients with severe symptomatic aortic stenosis but data on very long-term durability are lacking. We sought to evaluate the clinical and hemodynamic outcomes of the CoreValve porcine pericardial self-expanding bioprosthesis at 12-year follow-up. Methods882 inoperable or high-risk patients were treated with the CoreValve bioprosthesis in 8 Italian high-volume centers between 2007 and 2011. The endpoints were 12-year all-cause and cardiovascular mortality, and Cumulative Incidence Functions (CIFs) for severe Structural Valve Deterioration (SVD), Bioprosthetic Valve Dysfunction (BVD), Bioprosthetic Valve Failure (BVF), and severe Hemodynamic Valve Deterioration (HVD). VARC-3 definitions were applied. ResultsBaseline characteristics included a mean age of 83 ± 6 years, and NYHA class III or IV in 76.3 % of patients. The actuarial risk of death at 12 years after TAVR was 95.5 % (CI 93.5 %- 97.1 %).The actual risk of cardiovascular death, weighted against the risk of non-cardiac death at 12 years was 23.9 % (21.0 %–26.8 %). The 12-year actual risk of BVD was 7.0 % (5.3 %–8.9 %), of SVD was 3.6 % (2.5 %–5.2 %), of BVF was 3.12 % (2.02 %–4.57 %), and of severe HVD was 1.7 % (0.9 %–2.9 %). Mean transaortic gradient significantly decreased after the procedure (52 ± 15 mmHg vs 9 ± 5 mmHg, p < 0.001), and remained stable up to 12 years (12 ± 4 mmHg, P = 0.08 vs. discharge). ConclusionsThe first-generation CoreValve bioprosthesis showed reassuring clinical and hemodynamic performance at 12-year follow-up.

Riociguat as bridging therapy to pulmonary endarterectomy in patients with chronic thromboembolic pulmonary hypertension: a retrospective cohort study.

In operable chronic thromboembolic pulmonary hypertension (CTEPH) patients, the utilization of bridging therapy with targeted medications prior to pulmonary endarterectomy (PEA) remains a topic of controversy, despite being common in cases of severe hemodynamic impairment. This study aims to assess the impact of riociguat as a bridging therapy on postoperative hemodynamics and outcomes. We conducted a retrospective study involving patients undergoing PEA from December 2016 to November 2023. Patients were categorized into two groups based on the use of riociguat before PEA. Pulmonary vascular resistance (PVR) following riociguat administration was assessed pre-PEA. Postoperative outcomes, including mortality, complications, and hemodynamics, were compared, employing propensity score matching analysis. Among the patients, 41.8% (n=56) received riociguat as bridging therapy. In patients with PVR ≥800 dynes·sec·cm-5, riociguat resulted in a reduction in PVR {1,207 [974-1,698] vs. 1,125 [928-1,486] dynes·sec·cm-5, P<0.01}, while no significant difference was observed in patients with PVR <800 dynes·sec·cm-5 {641 [474-740] vs. 600 [480-768] dynes·sec·cm-5, P=0.46}. After propensity score matching, each group included 26 patients. The overall perioperative mortality rate was 2.6%. Postoperative PVR {326 [254-398] vs. 361 [290-445] dynes·sec·cm-5, P=0.35} was similar in the riociguat group compared to the control group. The incidence of residual pulmonary hypertension (PH) and other postoperative outcomes were also comparable. The use of riociguat as bridging therapy demonstrated hemodynamic improvement before PEA in patients with high preoperative PVR. However, no additional benefits in postoperative mortality or hemodynamics were observed.

Inotropic Agents: Are We Still in the Middle of Nowhere?

Inotropes are prescribed to enhance myocardial contractility while vasopressors serve to improve vascular tone. Although these medications remain a life-saving therapy in cardiovascular clinical scenarios with hemodynamic impairment, the paucity of evidence on these drugs makes the choice of the most appropriate vasoactive agent challenging. As such, deep knowledge of their pharmacological and hemodynamic effects becomes crucial to optimizing hemodynamic profile while reducing the potential adverse effects. Given this perspective, it is imperative for cardiologists to possess a comprehensive understanding of the underlying mechanisms governing these agents and to discern optimal strategies for their application across diverse clinical contexts. Thus, we briefly review these agents' pharmacological and hemodynamic properties and their reasonable clinical applications in cardiovascular settings. Critical interpretation of available data and the opportunities for future investigations are also highlighted.

Hemodynamic Stroke: Emerging Concepts, Risk Estimation, and Treatment.

Ischemic stroke can arise from the sudden occlusion of a brain-feeding artery by a clot (embolic), or local thrombosis. Hemodynamic stroke occurs when blood flow does not sufficiently meet the metabolic demand of a brain region at a certain time. This discrepancy between demand and supply can occur with cerebropetal arterial occlusion or high-grade stenosis but also arises with systemic conditions reducing blood pressure. Treatment of hemodynamic stroke is targeted toward increasing blood flow to the affected area by either systemically or locally enhancing perfusion. Thus, blood pressure is often maintained above normal values, and extra-intracranial flow augmentation bypass surgery is increasingly considered. Still, current evidence supporting the superiority of pressure or flow increase over conservative measures is limited. However, methods assessing hemodynamic impairment and identifying patients at risk of hemodynamic stroke are rapidly evolving. Sophisticated models incorporating clinical and imaging factors have been suggested to aid patient selection. In this narrative review, we provide current state-of-the-art knowledge about hemodynamic stroke, tools for assessment, and treatment options.

Hemodynamic Impairment of Blood Pressure and Stroke Mechanisms in Symptomatic Intracranial Atherosclerotic Stenosis.

Hemodynamic impairment of blood pressure may play a crucial role in determining the mechanisms of stroke in symptomatic intracranial atherosclerotic stenosis). We aimed to elucidate this issue and assess the impacts of modifications to blood pressure on hemodynamic impairment. From the Third China National Stroke Registry III, computed fluid dynamics modeling was performed using the Newton-Krylov-Schwarz method in 339 patients with symptomatic intracranial atherosclerotic stenosis during 2015 to 2018. The major exposures were translesional systolic blood pressure (SBP) drop and poststenotic mean arterial pressure (MAP), and the major study outcomes were cortex-involved infarcts and borderzone-involved infarcts, respectively. Multivariate logistic regression models and the bootstrap resampling method were utilized, adjusting for demographics and medical histories. In all, 184 (54.3%) cortex-involved infarcts and 70 (20.6%) borderzone-involved infarcts were identified. In multivariate logistic model, the upper quartile of SBP drop correlated with increased cortex-involved infarcts (odds ratio, 1.92 [95% CI, 1.03-3.57]; bootstrap analysis odds ratio, 2.07 [95% CI, 1.09-3.93]), and the lower quartile of poststenotic MAP may correlate with increased borderzone-involved infarcts (odds ratio, 2.07 [95% CI, 0.95-4.51]; bootstrap analysis odds ratio, 2.38 [95% CI, 1.04-5.45]). Restricted cubic spline analysis revealed a consistent upward trajectory of the relationship between translesional SBP drop and cortex-involved infarcts, while a downward trajectory between poststenotic MAP and borderzone-involved infarcts. SBP drop correlated with poststenotic MAP negatively (rs=-0.765; P<0.001). In generating hemodynamic impairment, simulating blood pressure modifications suggested that ensuring adequate blood pressure to maintain sufficient poststenotic MAP appears preferable to the reverse approach, due to the prolonged plateau period in the association between the translesional SBP drop and cortex-involved infarcts and the relatively short plateau period characterizing the correlation between poststenotic MAP and borderzone-involved infarcts. This research elucidates the role of hemodynamic impairment of blood pressure in symptomatic intracranial atherosclerotic stenosis-related stroke mechanisms, underscoring the necessity to conduct hemodynamic assessments when managing blood pressure in symptomatic intracranial atherosclerotic stenosis.

Epstein-Barr Virus Lytic Transcripts Correlate with the Degree of Myocardial Inflammation in Heart Failure Patients.

The Epstein-Barr virus (EBV) is frequently found in endomyocardial biopsies (EMBs) from patients with heart failure, but the detection of EBV-specific DNA has not been associated with progressive hemodynamic deterioration. In this paper, we investigate the use of targeted next-generation sequencing (NGS) to detect EBV transcripts and their correlation with myocardial inflammation in EBV-positive patients with heart failure with reduced ejection fraction (HFrEF). Forty-four HFrEF patients with positive EBV DNA detection and varying degrees of myocardial inflammation were selected. EBV-specific transcripts from EMBs were enriched using a custom hybridization capture-based workflow and, subsequently, sequenced by NGS. The short-read sequencing revealed the presence of EBV-specific transcripts in 17 patients, of which 11 had only latent EBV genes and 6 presented with lytic transcription. The immunohistochemical staining for CD3+ T lymphocytes showed a significant increase in the degree of myocardial inflammation in the presence of EBV lytic transcripts, suggesting a possible influence on the clinical course. These results imply the important role of EBV lytic transcripts in the pathogenesis of inflammatory heart disease and emphasize the applicability of targeted NGS in EMB diagnostics as a basis for specific treatment.

Central sleep apnea in chronic heart failure with hypoxemia - treatment efficacy and hemodynamic effects of three different treatment modalities: a case report

BackgroundThe optimal treatment for central sleep apnea (CSA) depends on the underlying pathophysiology and should consider the potential for hemodynamic impairment when using positive airway pressure devices. While the long-term effects on overall cardiovascular outcome have been investigated for different device settings, the immediate hemodynamic consequences are not well understood. This is mainly due to a lack of hemodynamic monitoring during routine polysomnographic assessment. The application of most monitoring devices is either restricted by their invasiveness, e.g. in thermodilution, or cannot be used continuously like in echocardiography. Impedance cardiography (ICG), however, enables physicians to implement a continuous non-invasive monitoring of different hemodynamic parameters which can be useful in various clinical scenarios. In sleep medicine, the hemodynamic effect of initiating positive airway pressure treatment in patients with pre-existing heart failure should be of special concern.Case presentationIn this case report, we compare the efficacy of three different treatment modalities in a patient with CSA related to chronic heart failure considering the resolution of respiratory events on polysomnography (PSG). In addition, we outline the hemodynamic effects of each treatment device using ICG for non-invasive hemodynamic monitoring. Regarding the reduction of respiratory central events, long-term oxygen treatment (LTOT) and adaptive servoventilation (ASV) proved to be more efficient compared with automatic positive airway pressure (APAP). Hemodynamically, substantial differences of the cardiac performance were observed between the treatment devices. This especially applied to ASV which led to a pronounced drop in cardiac output.ConclusionOur case report indicates that treatment of CSA may induce significant changes of hemodynamic parameters which would remain undetected during routine polysomnographic assessment. We conclude that non-invasive hemodynamic monitoring may be considered when positive airway pressure treatment is initiated in patients at risk of hemodynamic impairment.

First experiences with protected VT ablation using surgical Impella 5.5

Abstract Introduction Ablation of ventricular arrhythmias (VA) is still challenging due to the complex substrate of the underlying heart disease. Depending on specific risk factors acute hemodynamic decompensation during or after VT ablation procedures may occur and hemodynamic support may be required. Protected VA ablation with different devices has been evaluated but associated complications like bleeding, vascular closure or weaning from the device have been restrictive. We present data on a dedicated approach to patients with anticipated hemodynamic deterioration using preventive surgical Impella support. Method 5 patients (2 female) underwent protected VT ablation under our standardized protocol. Indication for Impella support was severely impaired left ventricular function and multiple medical therapy refractory ventricular arrhythmias. 4 patients had conventional VT ablation before. Mean age was 66,8 years, mean CHADSVASC 4,4, 1 patient with non-ischemic cardiomyopathy (CMP), 1 with hypertrophic non-obstructive CMP, 3 patients with ischemic CMP. Mean EF was 20%, mean mixed venous saturation was 36 %, mean PAINESD score 27. In all patients a 5.5. Impella was implanted surgically 1 day before planned VT ablation via the right subclavian artery. VT ablation procedure started with substrate mapping, VT induction and activation mapping of the inducible VT to identify the critical VT isthmus. Ablation was directed to dissection of the critical isthmus of inducible VAs and elimination of all late potentials within low voltage areas. The Impella device was explanted after weaning off the hemodynamic support. Results Implantation of Impella 5.5 was successfully performed in all patients in general anesthesia without any complication via surgical approach. Specifically, no access site vascular complications were noted. In 4 patients the VT ablation procedure was performed in analgosedation, 1 patient in GA as this patient was intubated due to recurrent VA requiring defibrillation. Mean procedure time was 125 min, radiation time 1,3 min, inducible VTs 1,3 , median 2 morphologies. In all patients all inducible VTs could be eliminated, in 1 patient polymorphic VA was still inducible at the end of the procedure. Impella was explanted after mean 5,2 days (3-11 days). No complications occurred. All patients were discharged alive on heart failure medication and in 2 patients with amiodaron. At a mean follow up of 3.5 months, all patients are alive without VA recurrence and heart failure decompensation. Conclusion Surgical Impella implantation for protected VT ablation in severe heart failure patients is feasible and allows for effective VT mapping and ablation. Access site safety and protection for heart failure decompensation in addition to the possibility of individually mobilisation and weaning after the procedure make this protocol an attractive option. Prospective evaluation of standardized indication is needed.

Symposium review: high altitude travel with pulmonary vascular disease.

Pulmonary arterial hypertension and chronic thromboembolic pulmonary hypertension are the main precapillary forms of pulmonary hypertension (PH) summarized as pulmonary vascular diseases (PVD). PVDs are characterized by exertional dyspnoea and oxygen desaturation, and reduced quality of life and survival. Medical therapies improve life expectancy and physical performance of PVD patients, of whom many wish to participate in professional work and recreational activities including traveling to high altitude. The exposure to the hypobaric hypoxic environment of mountain regions incurs the risk of high altitude adverse events (AEHA) due to severe hypoxaemia exacerbating symptoms and further increase in pulmonary artery pressure, which may lead to right heart decompensation. Recent prospective and randomized trials show that altitude-induced hypoxaemia, pulmonary haemodynamic changes and impairment of exercise performance in PVD patients are in the range found in healthy people. The vast majority of optimally treated stable PVD patients who do not require long-term oxygen therapy at low altitude can tolerate short-term exposure to moderate altitudes up to 2500m. PVD patients that reveal persistent severe resting hypoxaemia ( <80% for >30min) at 2500m respond well to supplemental oxygen therapy. Although there are no accurate predictors for AEHA, PVD patients with unfavourable risk profiles at low altitude, such as higher WHO functional class, lower exercise capacity with more pronounced exercise-induced desaturation and more severely impaired haemodynamics, are at increased risk of AEHA. Therefore, doctors with experience in PVD and high-altitude medicine should counsel PVD patients before any high-altitude sojourn. This review aims to summarize recent literature and clinical recommendations about PVD patients travelling to high altitude.

#1073 Changes in endothelial function in patients with impaired central and renal hemodynamics respiratory pathology

Abstract Background and Aims To determine the degree of influence of endothelial dysfunction on the hemodynamics of renal and central vessels in respiratory pathology, as well as to determine the effectiveness of complex therapy regimens with carvedilol. Method Studies were conducted in 26 patients with chronic obstructive pulmonary disease (COPD) of II- III severity (group 1, in whom the level of glomerular filtration rate of the kidneys eGFR CKD-EPI ≥6 ml/min/1.73 m2 was determined) and 32 patients with COPD of IV severity (group 2, they were determined e GFR CKD-EPI ≥60 ml/min/1.73 m2). Patients received one course of ten-day standard therapy (GOLD, 2020) in combination with a beta–blocker drug, T. carvedilol 5 mg (Vertex). Doppler echocardiographic examination of peripheral vessels, heart and renal vessels of patients was performed. Stable metabolites of nitric oxide (Cm NO) in blood plasma, ventilation and perfusion state of the lungs were determined. Results A significant decrease in the functional state of the respiratory system was parallel with a decrease in Cm NO synthesis, which was clearly reflected in the second group (by 11%) compared with the first group (by 7%). Pronounced structural changes with remodeling of the right parts of the heart, as well as a pronounced degree of pancreatic hypertrophy in the second group were accompanied by a sharp change in renal filtration function (eGFR ≤60 ml/min/1.73 m2). When measuring the state of diastolic dysfunction of the right parts of the heart, a decrease in E/As well as an increase in the circulatory vascular resistance index and mean blood pressure were significantly higher in the first group of patients (where еGFR ≥6 ml/min/1.73 m2). After a course of treatment with t. carvedilol, based on basic treatment, normalization of endothelial function was determined, reflected in an increase in the concentration of stable metabolites of nitric oxide by 1.05 and 1.5 times (p&amp;lt;0.05) in the biological fluid, respectively, in the first and second groups. In the dynamics of the course of therapy in groups of patients with 75% and 35% decrease in lung ventilation capacity, mean pulmonary arterial pressure decreased by 18.1 and 14.3%, respectively, and the hemodynamic resistance index decreased by 7.9% and 5.7% in parallel (p&amp;lt;0.05). Conclusion When monitoring the functional state of central and renal hemodynamics and ventilation-perfusion function of the bronchopulmonary system after complex treatment with carvedilol, a long-term hypotensive effect, a decrease in endothelial dysfunction, respectively, and an improvement in central and renal hemodynamics were determined.

Dynamic inflation prevents and standardized lung recruitment reverts volume loss associated with percutaneous tracheostomy during volume control ventilation: results from a Neuro-ICU population.

To determine how percutaneous tracheostomy (PT) impacts on respiratory system compliance (Crs) and end-expiratory lung volume (EELV)during volume control ventilation and to test whether a recruitment maneuver (RM) at the end of PT may reverse lung derecruitment. This is a single center, prospective, applied physiology study. 25 patients with acute brain injury who underwent PT were studied. Patients were ventilated in volume control ventilation. Electrical impedance tomography (EIT) monitoring and respiratory mechanics measurements were performed in three steps: (a) baseline, (b) after PT, and (c) after a standardized RM (10 sighs of 30 cmH2O lasting 3s each within 1min). End-expiratory lung impedance (EELI) was used as a surrogate of EELV. PT determined a significant EELI loss (mean reduction of 432 arbitrary units p = 0.049) leading to a reduction in Crs (55 ± 13 vs. 62 ± 13 mL/cmH2O; p < 0.001) as compared to baseline. RM was able to revert EELI loss and restore Crs (68 ± 15 vs. 55 ± 13 mL/cmH2O; p < 0.001). In a subgroup of patients (N = 8, 31%), we observed a gradual but progressive increase in EELI. In this subgroup, patients did not experience a decrease of Crs after PT as compared to patients without dynamic inflation. Dynamic inflation did not cause hemodynamic impairment nor raising of intracranial pressure. We propose a novel and explorative hyperinflation risk index (HRI) formula. Volume control ventilation did not prevent the PT-induced lung derecruitment. RM could restore the baseline lung volume and mechanics. Dynamic inflation is common during PT, it can be monitored real-time by EIT and anticipated by HRI. The presence of dynamic inflation during PT may prevent lung derecruitment.

AUTOIMMUNE MYOCARDITIS IN MELANOMA IMMUNOTHERAPY–COMPLEX CLINICA PRESENTATION AND ADVERSE THERAPEUTIC RESPONSE

Abstract A 68–year–old Caucasian female presented to the ED with cardiac chest pain and dyspnea. The patient had a history of arterial hypertension and was equipped with a biventricular pacemaker due to atrial fibrillation with low ventricular response. She had recently been diagnosed with metastatic melanoma and initiated treatment with nivolumab and ipilimumab two weeks prior. Troponin levels were elevated (700 ng/ml), and no ST–segment elevation was observed on the electrocardiogram (ECG). In suspicion of NSTEMI–ACS, coronary angiography was performed, revealing an intact epicardial coronary circulation without stenotic lesions. The echocardiogram showed borderline left ventricular systolic function (EF 50%), and the right ventricle exhibited initial signs of reduced systolic function (TAPSE, 15 mm; S RV, 9.5 m/s). The following day, there was a deterioration in hemodynamics and respiratory exchange, with evidence of apical and mid–distal interventricular septum hypokinesia of the left ventricle (EF 40%) and dilated right ventricle (BD 4.8 cm; MD 4 cm) with severely reduced systolic function (TAPSE 10 mm, S RV 7 m/s, FAC, 20%), and severe tricuspid regurgitation. Urgent computed tomography pulmonary angiography (CTPA) excluded pulmonary embolism. Additionally, there was a new troponin increase (5000 ng/ml) and elevated hepatic biomarkers. The clinical picture raised suspicion of myocarditis related to immune checkpoint inhibitor therapy. Corticosteroid therapy was initiated with a daily administration of methylprednisolone 1000 mg. Diagnostic confirmation was sought through autoimmune panel and viral marker assessments, which yielded negative results. Endomyocardial biopsy (EMB) revealed CD4 and CD8–positive lymphocytic infiltration and myocardial necrosis. Despite initial clinical improvement, an arrhythmic storm developed. Despite treatment with a defibrillator, intravenous antiarrhythmic therapy (beta–blocker, amiodarone, and lidocaine), and sedation, the patient unfortunately succumbed. Immune checkpoint inhibitors (ICIs) have been revolutionary in the treatment of many solid tumors. However, the dysregulation of immune mechanisms can rarely (2%) lead to autoimmune events involving multiple organs. Myocarditis, despite optimal treatment, is characterized by a mortality rate exceeding 50%, representing a significant challenge in the Intensive Care Unit.

HCM AT THE CROSSROAD

Abstract Introduction Treatment of oHCM frequently requires difficult choices, especially when it is superimposed on other urgent clinical conditions,such as AMI or mechanical complications. Clinical Case A 52–year–old man with known oHCM, who spontaneously quickly discontinued recommended therapy, presents to theED with a sudden episode of dyspnea and presyncope. A firstECG was essentially normal for pathology. After 1h, the patient experiences a sudden episode of chest pain with rapid hemodynamic deterioration and cardiogenic shock(CS). The ECG shows changes compatible with inferolateral MI. The TTE shows severe LVOTO, SAM, severe MR and a suspicious oval image attached to the anterior mitral leaflet. The patient underwent orotracheal intubation, coronary angiography and TEE. Coronary angiography shows a thrombotic occlusion of the proximal circumflex artery, treated with pPCI. TEE confirms a partial rupture of the papillary muscle head. Treatment:The patient‘s CS can be caused by 2different conditions that require treatments with opposing pathophysiological principles. SevereMR due to papillary muscle rupture, as mechanical complication of MI, requires afterload reduction, hemodynamic stabilization with IABP and emergency transfer to a cardiac surgery center. In contrast, the treatment of the underlying pathology(severe LVOTO and severe rMR due to SAM)requires pharmacological stabilization with depression of cardiac contractility and increase in afterload. In the context of cardiogenic shock a rapid choice was required. To help us make the right choice, an Esmolol test was performed. After iv administration of 2mg Esmolol, heart rate was reduced without reduction in BP. The patient was then treated with esmolol in continuous infusion and norepinephrine. In oHCM the ventriculo–arterial coupling is reduced, less than 1. This treatment favored better V–A coupling, ensuring an increase in afterload and a reduction in myocardial contractility. The patient‘s clinical condition rapidly improved, allowing extubation at48h and early mobilization at96h. Myectomy and mitral repair surgery was scheduled 1 month afterPCI. Conclusions Through the use of a short–lived drug such as Esmolol, it was possible to trace the prevailing mechanism of the patient‘s CS. Differently from other cases of CS, to rebalance the V–Acoupling, it was crucial to reduce myocardial contractility and increase afterload. A pathophysiological pharmacological approach ensured a good outcome.