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Background Hypercoagulability in Coronavirus Disease 2019 (COVID-19) causes deep vein thrombosis and pulmonary embolism necessitating systemic anticoagulation. Case reports of intracerebral hemorrhages in ventilated COVID-19 patients warrant precaution. It is unclear, however, if COVID-19 patients with acute respiratory distress syndrome (ARDS) with or without veno-venous extracorporeal membrane oxygenation therapy (VV-ECMO) have more intracerebral hemorrhages (ICH) compared to other ARDS patients. Methods We conducted a retrospective observational single-center study enrolling all patients with ARDS from 01/2018 to 05/2020. PCR-positive SARS-CoV-2 patients with ARDS were allocated to the COVID-19 group. Propensity score matching was performed for age, VV-ECMO, and bleeding risk. Results A total of 163 patients with moderate or severe ARDS were identified, 47 (28.8%) in the COVID-19 group, and 116 (71.2%) in the non-COVID-19 group. In 63/163 cases (38.7%), VV-ECMO therapy was required. The ICU survival was 52.8%. COVID-19 patients were older, more often male, and exhibited a lower SOFA score, but the groups showed similar rates of VV-ECMO therapy. Treatments with antiplatelet agents (p = 0.043) and therapeutic anticoagulation (p = 0.028) were significantly more frequent in the COVID-19 patients. ICH was detected in 22 patients (13.5%) with no statistical difference between the groups (11.2 vs. 19.1% without and with SARS-CoV-2, respectively, p = 0.21). Propensity score matching confirmed similar rates of ICH in both groups (12.8 vs. 19.1% without and with SARS-CoV-2, respectively, p = 0.57), thus leveling out possible confounders. Conclusions Intracerebral hemorrhage was detected in every tenth patient with ARDS. Despite statistically higher rates of antiplatelet therapy and therapeutic anticoagulation in COVID-19 patients, we found a similar rate of ICH in patients with ARDS due to COVID-19 compared to other causes of ARDS.

Introduction Initiation of venoarterial extracorporeal membrane oxygenation (ECMO) under ongoing cardiopulmonary resuscitation (eCPR) in patients with refractory cardiac arrest may improve otherwise deleterious outcome. In general, the duration of mechanical resuscitation from collapse to ECMO ranges from 40 to 70 minutes. CPR-related injuries are reported frequently in non-eCPR patients. We wanted to quantify CPR-related injuries in eCPR patients. Methods All eCPR patients cannulated at a tertiary referral medical center between October 2010 and October 2017 were included in a retrospective registry study. A full-body CT scan was performed within the first 24 hours after eCPR. Results A total of 103 patients (mean age 58.8 ± 16.7 years, CPR duration 61.7 ± 31.9 min, and hospital survival 13.6%) underwent eCPR and immediate full-body computed tomography (CT). Full-body CT detected the cause for collapse in 16.5% of patients. Average number of pathologies detected per CT scan was 6.5 ± 3.3 findings per patient, of which 2.6 ± 1.5 findings were retrospectively considered of clinical relevance for subsequent treatment. Most frequent findings were multiple rib or sternal fractures (65.5%), pneumo- or hemothorax (32.3%) and pulmonary infiltrates (91.3%). Intracranial bleedings and cerebral edema were frequent (10.7% and 26.2%). A total of 20 patients (19.4%) had findings in whole-body CT that were considered to be so severe that further treatment was considered futile and therapy was subsequently discontinued. Most findings were associated with poor outcome with the exception of rib fractures, bleedings and abdominal trauma, which might have been caused by vigorous resuscitation efforts and were associated with favorable outcome. Conclusion A full-body CT scan performed after eCPR revealed substantial clinically significant findings. Therefore, it might be reasonable to routinely perform a full-body CT in all eCPR patients.

Aufgrund akut einsetzender Atemnot stellt sich ein 67-jahriger Patient vor. Er ist in der Praxis mit einem Lungenemphysem und einer COPD bekannt. Seine Medikation nimmt er regelmasig ein. Er berichtet, dass er in den letzten Tagen mehr Hustenanfalle gehabt habe als sonst.

Aim Cardiac arrest is the most serious complication in acute coronary syndromes. Glycoprotein IIb/IIIa inhibitors (GPI) are used in selected acute coronary syndrome patients. If the use of GPI leads to an increase in bleeding events and influences survival in patients after cardiac arrest is unknown. Methods We report retrospective data of a single center registry of patients after successful intra- and out-of-hospital cardiac arrest between 2002 and 2013. Inclusion criteria were survival for at least 6 h and successful percutaneous coronary intervention (PCI) within the first 24 h. Patients treated with other fibrinolytic agents or being supported by an extracorporeal life support system were excluded from the analysis. Results 310 patients were included in our study. 204 received GPI (GPI+), 106 did not (GPI−). Patients in the GPI+ group were significantly younger (62.8 vs. 68.0 years, p

Veno-venous extracorporeal membrane oxygenation (V-V ECMO) is a last resort treatment option for patients with acute respiratory failure (acute respiratory distress syndrome [ARDS]). Cytokine adsorption has been incorporated in the management of some of these patients on an individual basis to control the imbalance of danger-associated molecular patterns and proinflammatory cytokines. However, little is known about the combination of V-V ECMO and cytokine adsorption as earlier reports contained mixed patient cohorts in terms of disease and mode of ECMO, veno-venous and veno-arterial. We here report single-center registry data of nine all-comers with severe ARDS treated with V-V ECMO and cytokine adsorption using the CytoSorb adsorber compared with a control group of nine propensity score matched patients undergoing V-V ECMO support without cytokine adsorption. Even though Respiratory ECMO Survival Prediction and PRedicting dEath for SEvere ARDS on V-V ECMO scores predicted a higher mortality in the cytokine adsorption group, mortality was numerically reduced in the patients undergoing V-V ECMO and cytokine removal compared with V-V ECMO alone. The need for fluid resuscitation and vasopressor support as well as lactate levels dropped significantly in the cytokine adsorption group within 72 hours, whereas vasopressor need and lactate levels did not decrease significantly in the control group. Therefore, our data suggest that cytokine adsorption might be beneficial in patients with severe ARDS requiring V-V ECMO support.

Veno‐venous extracorporeal membrane oxygenation (V‐V ECMO) is used to sustain blood oxygenation and decarboxylation in severe acute respiratory distress syndrome (ARDS). It is under debate if V‐V ECMO is as appropriate for coronavirus disease 2019 (Covid‐19) ARDS as it is for influenza. In this retrospective study, we analyzed all patients with confirmed SARS‐CoV‐2 or influenza A/B infection, ARDS and V‐V ECMO, treated at our medical intensive care unit (ICU) between October 2010 and June 2020. Baseline and procedural characteristics as well as survival 30 days after ECMO cannulation were analyzed. A total of 62 V‐V ECMO patients were included (15 with Covid‐19 and 47 with influenza). Both groups had similar baseline characteristics at cannulation. Thirty days after ECMO cannulation, 13.3% of all patients with Covid‐19 were discharged alive from our ICU compared to 44.7% with influenza (P = .03). Patients with Covid‐19 had fewer ECMO‐free days (0 (0‐9.7) days vs. 13.2 (0‐22.1) days; P = .05). Cumulative incidences of 30‐day‐survival showed no significant differences (48.6% in Covid‐19 patients, 63.7% in influenza patients; P = .23). ICU treatment duration was significantly longer in ARDS patients with V‐V ECMO for Covid‐19 compared to influenza. Thirty‐day mortality was higher in Covid‐19, but not significant., Patients with severe Covid‐19 supported with V‐V ECMO are less likely to be discharged from ICU within 30 days after initiation of V‐V ECMO than patients with influenza virus infection and V‐V ECMO. Hospital mortality was higher in patients with Covid‐19, but not significant.

Background: SARS-CoV2 can cause pulmonary failure requiring prolonged invasive mechanical ventilation (MV). Lung protective ventilation strategies are recommended in order to minimize ventilator induced lung injury. Whether patients with COVID-19 have the same risk for complications including barotrauma is still unknown. Therefore, we investigated barotrauma in patients with COVID-19 pneumonia requiring prolonged MV. Methods: All patients meeting diagnosis criteria for ARDS according to the Berlin Definition, with PCR positive SARS-CoV2 infection and prolonged mechanical ventilation, defined as ≥2 days, treated at our ARDS referral center between March and April 2020 were included in a retrospective registry analysis. Complications were detected by manual review of all patient data including respiratory data, imaging studies, and patient files. Results: A total of 20 patients with severe COVID-19 pulmonary failure (Overall characteristics: median age: 61 years, female gender 6, median duration of MV 22 days) were analyzed. Eight patients (40%) developed severe barotrauma during MV (after median 18 days, range: 1-32) including pneumothorax (5/20), pneumomediastinum (5/20), pneumopericard (1/20), and extended subcutaneous emphysema (5/20). Median respirator settings 24 hours before barotrauma were: Peak inspiratory pressure (Ppeak) 29 cm H2O (range: 27-35), positive end-expiratory pressure (PEEP) 14 cm H2O (range: 5-24), tidal volume (VT) 5.4ml/kg predicted body weight (range 0.4-8.6), plateau pressure (Pplateau) 27 cm H2O (range: 19-30). Mechanical ventilation was significantly more invasive on several occasions in patients without barotrauma. Conclusion: Barotrauma in COVID-19 induced respiratory failure requiring mechanical ventilation was found in 40% of patients included in this registry. Our data suggest that barotrauma in COVID-19 may occur even when following recommendations for lung protective MV.

BACKGROUND Regional dispersion of prolonged repolarization is a hallmark of long QT syndrome (LQTS). We have also revealed regional heterogeneities in mechanical dysfunction in transgenic rabbit models of LQTS. OBJECTIVE In this clinical pilot study, we investigated whether patients with LQTS exhibit dispersion of mechanical/diastolic dysfunction. METHODS Nine pediatric patients with genotyped LQTS (12.2 ± 3.3 years) and 9 age- and sex-matched healthy controls (10.6 ± 1.5 years) were subjected to phase-contrast magnetic resonance imaging to analyze radial (Vr) and longitudinal (Vz) myocardial velocities during systole and diastole in the left ventricle (LV) base, mid, and apex. Twelve-lead electrocardiograms were recorded to assess the heart rate-corrected QT (QTc) interval. RESULTS The QTc interval was longer in patients with LQTS than in controls (469.1 ± 39.4 ms vs 417.8 ± 24.4 ms; P < .01). Patients with LQTS demonstrated prolonged radial and longitudinal time-to-diastolic peak velocities (TTP), a marker for prolonged contraction duration, in the LV base, mid, and apex. The longer QTc interval positively correlated with longer time-to-diastolic peak velocities (correlation coefficient 0.63; P < .01). Peak diastolic velocities were reduced in LQTS in the LV mid and apex, indicating impaired diastolic relaxation. In patients with LQTS, regional (TTPmax-min) and transmural (TTPVz-Vr) dispersion of contraction duration was increased in the LV apex (TTPVz_max-min: 38.9 ± 25.5 ms vs 20.2 ± 14.7 ms; P = .07; TTPVz-Vr: -21.7 ± 14.5 ms vs -8.7 ± 11.3 ms; P < .05). The base-to-apex longitudinal relaxation sequence was reversed in patients with LQTS compared with controls (TTPVz_base-apex: 14.4 ± 14.9 ms vs -10.1 ± 12.7 ms; P < .01). CONCLUSION Patients with LQTS exhibit diastolic dysfunction with reduced diastolic velocities and prolonged contraction duration. Mechanical dispersion is increased in LQTS with an increased regional and transmural dispersion of contraction duration and altered apicobasal longitudinal relaxation sequence. LQTS is an electromechanical disorder, and phase-contrast magnetic resonance imaging Heterogeneity in mechanical dysfunction enables a detailed assessment of mechanical consequences of LQTS.

For the past few years, children affected by an inherited channelopathy have been counseled to avoid (recreational) sports activities and all competitive sports so as to prevent exercise-induced arrhythmia and sudden cardiac death. An increased understanding of the pathophysiological mechanisms, better anti-arrhythmic strategies, and, in particular, more epidemiological data on exercise-induced arrhythmia in active athletes with channelopathies have changed the universal recommendation of "no sports," leading to revised, less strict, and more differentiated guidelines (published by the American Heart Association/American College of Cardiology in 2015). In this review, we outline the disease- and genotype-specific mechanisms of exercise-induced arrhythmia; give an overview of trigger-, symptom-, and genotype-dependent guidance in sports activities for children with long QT syndrome (LQTS), Brugada syndrome (BrS), catecholaminergic polymorphic ventricular tachycardia (CPVT), or short QT syndrome (SQTS); and highlight the novelties in the current guidelines compared with previous versions. While it is still recommended for patients with LQT1 and CPVT (even when asymptomatic) and all symptomatic LQTS patients (independent of genotype) to avoid any competitive and high-intensity sports, other LQTS patients successfully treated with anti-arrhythmic therapies and phenotype-negative genotype-positive patients may be allowed to perform sports at different activity levels - provided they undergo regular, sophisticated evaluations to detect any changes in arrhythmogenic risk.

AIMS Short-QT syndrome 1 (SQT1) is an inherited channelopathy with accelerated repolarization due to gain-of-function in HERG/IKr. Patients develop atrial fibrillation, ventricular tachycardia (VT), and sudden cardiac death with pronounced inter-individual variability in phenotype. We generated and characterized transgenic SQT1 rabbits and investigated electrical remodelling. METHODS AND RESULTS Transgenic rabbits were generated by oocyte-microinjection of β-myosin-heavy-chain-promoter-KCNH2/HERG-N588K constructs. Short-QT syndrome 1 and wild type (WT) littermates were subjected to in vivo ECG, electrophysiological studies, magnetic resonance imaging, and ex vivo action potential (AP) measurements. Electrical remodelling was assessed using patch clamp, real-time PCR, and western blot. We generated three SQT1 founders. QT interval was shorter and QT/RR slope was shallower in SQT1 than in WT (QT, 147.8 ± 2 ms vs. 166.4 ± 3, P

Key Clinical Message This case is a reminder not to overlook rare causes of electrolyte shifts, which may cause reversible changes in pacemaker pacing thresholds.

Purpose Patients hospitalized for infection with SARS-CoV-2 typically present with pneumonia. The respiratory failure is frequently complicated by pulmonary embolism in segmental pulmonary arteries. The distribution of pulmonary embolism in regard to lung parenchymal opacifications has not been investigated yet. Methods All patients with COVID-19 treated at a medical intensive care unit between March 8th and April 15th, 2020 undergoing computed tomography pulmonary angiography (CTPA) were included. All CTPA were assessed by two radiologists independently in respect to parenchymal changes and pulmonary embolism on a lung segment basis. Results Out of 22 patients with severe COVID-19 treated within the observed time period, 16 (age 60.4 ± 10.2 years, 6 female SAPS2 score 49.2 ± 13.9) underwent CT. A total of 288 lung segment were analyzed. Thrombi were detectable in 9/16 (56.3%) patients, with 4.4 ± 2.9 segments occluded per patient and 40/288 (13.9%) segments affected in the whole cohort. Patients with thrombi had significantly worse segmental opacifications in CT (p, Highlights (mandatory) • In COVID-19 respiratory failure, thrombi in segmental pulmonary arteries are common. • All Thrombi detected were localized in opacitated (presumably COVID-19 affected) lung segments. • This might suggest local clot formation.

Recovery of pulmonary vein (PV) conduction is a common mechanism of atrial fibrillation recurrence after PV isolation (PVI), underscoring the need for durable lesion formation. We aimed to evaluate the utility of an automated lesion annotation algorithm (ALAA) on acute isolation rates and resulting lesion characteristics. Fifty patients underwent PVI using a contact force (CF) sensing catheter and ALAA. Single antral circles around ipsilateral PVs were performed with ALAA-1 settings including catheter stability (range of motion ≤2 mm, duration >10 s). Target CF was 10–20 g but not part of ALAA-1 settings. If PV conduction persisted after circle completion, force over time was added to automated settings (ALAA-2). Emerging gaps were subsequently ablated, followed by re-assessment for PVI. ALAA-1 isolated 70 % of the left and 78 % of the right PVs using 756.3 ± 212.3 s (left) and 737.1 ± 145.9 s (right) of energy delivery. ALAA-2 settings identified 29 gaps in previously unisolated PVs, closure significantly increased isolation rates to 88 % of the left and 96 % of the right PVs with additional 325.4 ± 354.1 s (left) and 266.8 ± 279.5 s (right) of energy delivery (p = 0.001). Lesion characteristics significantly differed between ALAA-1 (n = 3521 lesions) and ALAA-2 (n = 3037 lesions) settings, and between isolated and non-isolated PV segments, particularly with respect to CF. Interlesion distances with ALAA-2 were significantly longer in the left superior, left superior-anterior, and right superior-posterior segments when compared to ALAA-1. Settings of an ALAA affect lesion characteristics reveal areas of insufficient lesion formation and influence acute effectiveness of PVI. Combination of CF and stability shows superior performance over stability alone.

Long QT syndrome (LQTS) is a rare inherited channelopathy caused mainly by different mutations in genes encoding for cardiac K(+) or Na(+) channels, but can also be caused by commonly used ion-channel-blocking and QT-prolonging drugs, thus affecting a much larger population. To develop novel diagnostic and therapeutic strategies to improve the clinical management of these patients, a thorough understanding of the pathophysiological mechanisms of arrhythmogenesis and potential pharmacological targets is needed. Drug-induced and genetic animal models of various species have been generated and have been instrumental for identifying pro-arrhythmic triggers and important characteristics of the arrhythmogenic substrate in LQTS. However, due to species differences in features of cardiac electrical function, these different models do not entirely recapitulate all aspects of the human disease. In this review, we summarize advantages and shortcomings of different drug-induced and genetically mediated LQTS animal models - focusing on mouse and rabbit models since these represent the most commonly used small animal models for LQTS that can be subjected to genetic manipulation. In particular, we highlight the different aspects of arrhythmogenic mechanisms, pro-arrhythmic triggering factors, anti-arrhythmic agents, and electro-mechanical dysfunction investigated in transgenic LQTS rabbit models and their translational application for the clinical management of LQTS patients in detail. Transgenic LQTS rabbits have been instrumental to increase our understanding of the role of spatial and temporal dispersion of repolarization to provide an arrhythmogenic substrate, genotype-differences in the mechanisms for early afterdepolarization formation and arrhythmia maintenance, mechanisms of hormonal modification of arrhythmogenesis and regional heterogeneities in electro-mechanical dysfunction in LQTS.

Long QT syndrome (LQTS) is a congenital arrhythmogenic channelopathy characterized by impaired cardiac repolarization. Increasing evidence supports the notion that LQTS is not purely an "electrical" disease but rather an "electro-mechanical" disease with regionally heterogeneously impaired electrical and mechanical cardiac function. In the first part, this article reviews current knowledge on electro-mechanical (dys)function in LQTS, clinical consequences of the observed electro-mechanical dysfunction, and potential underlying mechanisms. Since several novel imaging techniques - Strain Echocardiography (SE) and Magnetic Resonance Tissue Phase Mapping (TPM) - are applied in clinical and experimental settings to assess the (regional) mechanical function, advantages of these non-invasive techniques and their feasibility in the clinical routine are particularly highlighted. The second part provides novel insights into sex differences and sex hormone effects on electro-mechanical cardiac function in a transgenic LQT2 rabbit model. Here we demonstrate that female LQT2 rabbits exhibit a prolonged time to diastolic peak - as marker for contraction duration and early relaxation - compared to males. Chronic estradiol-treatment enhances these differences in time to diastolic peak even more and additionally increases the risk for ventricular arrhythmia. Importantly, time to diastolic peak is particularly prolonged in rabbits exhibiting ventricular arrhythmia - regardless of hormone treatment - contrasting with a lack of differences in QT duration between symptomatic and asymptomatic LQT2 rabbits. This indicates the potential added value of the assessment of mechanical dysfunction in future risk stratification of LQTS patients.