Successful use of a percutaneous miniaturized extracorporeal life support system as a bridge and assistance to left ventricular assist device implantation in a patient with severe refractory cardiogenic shock

We present a 51-year-old man with cardiogenic shock in whom a percutaneous extracorporeal life support system (ECLS) was inserted to restore cardiopulmonary stability. After successful stabilization, a left ventricular assist device was implanted, using the ECLS without switching to a conventional cardiopulmonary bypass system to reduce its side effects

First experience with the new portable extracorporeal membrane oxygenation system Cardiohelp for severe respiratory failure in adults

Background: Over the last decade, technical improvements in extracorporeal membrane oxygenation (ECMO) equipment have reduced procedure-related complications and have made ECMO an effective option for patients with acute respiratory distress syndrome (ARDS) if conventional therapy fails. Methods: In this report, we present our early experience with the Cardiohelp, a new portable miniaturized ECMO system, in 22 consecutive patients with ARDS. All patients were placed on venovenous ECMO. Cannulas were inserted percutaneously, employing the Seldinger technique. Data were collected prospectively. Results: The median patient age was 47 years (36 to 61). Fifteen patients from regional hospitals were too unstable for conventional transport and were placed on Cardiohelp at the referring hospital and then transported to our institution. The patients were transported by ambulance (n=2) or helicopter (n=13) over a distance of 50-250 km. Cardiohelp support resulted in immediate improvement of gas exchange and highly protective ventilation. The median duration of support was 13 days (8 to 19). An exchange of the device was necessary in 9 patients. Sixteen patients (72.7%) were successfully weaned from ECMO and fifteen patients (68.2%) survived. Device-related complications were not observed. Conclusions: The compact portable ECMO device Cardiohelp is a highly effective method to secure vital gas exchange and to reduce further ventilator-induced lung injury in patients with acute respiratory failure. Crucial technical innovations and ease of device transport and implantation allow location-independent stabilization with consecutive inter-hospital transfer

Left ventricular support adjustment to aortic valve opening with analysis of exercise capacity

Background LVAD speed adjustment according to a functioning aortic valve has hypothetic advantages but could lead to submaximal support. The consequences of an open aortic valve policy on exercise capacity and hemodynamics have not yet been investigated systematically. Methods Ambulatory patients under LVAD support (INCOR®, Berlin Heart, mean support time 465 ± 257 days, average flow 4.0 ± 0.3 L/min) adjusted to maintain a near normal aortic valve function underwent maximal cardiopulmonary exercise testing (CPET) and right heart catheterization (RHC) at rest and during constant work rate exercise (20 Watt). Results Although patients (n = 8, mean age 45 ± 13 years) were in NYHA class 2, maximum work-load and peak oxygen uptake on CPET were markedly reduced with 69 ± 13 Watts (35% predicted) and 12 ± 2 mL/min/kg (38% predicted), respectively. All patients showed a typical cardiac limitation pattern and severe ventilatory inefficiency with a slope of ventilation to carbon dioxide output of 42 ± 12. On RHC, patients showed an exercise-induced increase of mean pulmonary artery pressure (from 16 ± 2.4 to 27 ± 2.8 mmHg, p < 0.001), pulmonary artery wedge pressure (from 9 ± 3.3 to 17 ± 5.3 mmHg, p = 0.01), and cardiac output (from 4.7 ± 0.5 to 6.2 ± 1.0 L/min, p = 0.008) with a corresponding slight increase of pulmonary vascular resistance (from 117 ± 35.4 to 125 ± 35.1 dyn*sec*cm−5, p = 0.58) and a decrease of mixed venous oxygen saturation (from 58 ± 6 to 32 ± 9%, p < 0.001). Conclusion An open aortic valve strategy leads to impaired exercise capacity and hemodynamics, which is not reflected by NYHA-class. Unknown compensatory mechanisms can be suspected. Further studies comparing higher vs. lower support are needed for optimization of LVAD adjustment strategies

Anaesthesia-related complications and side-effects in TAVI: a retrospective study in Germany

Objectives This study was performed to analyse anaesthesia-related complications and side effects in patients undergoing transcatheter aortic valve implantation (TAVI) under general anaesthesia. Design Retrospective study. Setting The study was performed as a single-centre study in a hospital of tertiary care in Germany. Participants All 853 patients, who underwent TAVI at the Universitatsklinikum Regensburg between January 2009 and July 2015, were included. 52.5% were female patients. Primary and secondary outcome measures We gathered information, such as recent illness, vital parameters and medication administered during the intervention and postoperatively for 12 hours. We analysed all anaesthesia-related complications and anaesthesia-related side effects that occurred during the intervention and entire hospital stay. Results We analysed all 853 TAVI procedures. The mean patient age was 79 +/- 6 years. In 99.5% of cases, we used volatile-based anaesthesia. 2.8% (n=24; transfemoral (TF): n=19 [3.8%]; transapical (TA): n=5 [1.4%]) of all cases suffered from anaesthesia-related complications. 819 (TF: n=447; TA: n=372) anaesthesia-related side effects occurred in 586 (68.7%, TF: n=325 [64.2%], TA: n=261 [75.2%]) patients. Neither the complications nor the side effects had any serious consequences. Intraoperative hypothermia in 44% of cases (TF: n=202 [39.9%]; TA: n=173 [49.9%]) and postoperative nausea and vomiting in 27% (n=232; TF: n=131 [25.9%], TA: n=101 [29.1%]) of cases were the most common anaesthesia-related side effects. Conclusion In this study, serious anaesthesia-related complications were rarely seen, and non-critical anaesthesia-related side effects could have been avoided through consistent prophylaxis and management. Therefore, despite their high anaesthetic risk, general anaesthesia is justifiable in patients who underwent TAVI

Long-term follow-up and quality of life in patients receiving extracorporeal membrane oxygenation for pulmonary embolism and cardiogenic shock

Background Since 2019, European guidelines recommend considering extracorporeal life support as salvage strategy for the treatment of acute high-risk pulmonary embolism (PE) with circulatory collapse or cardiac arrest. However, data on long-term survival, quality of life (QoL) and cardiopulmonary function after extracorporeal membrane oxygenation (ECMO) are lacking. Methods One hundred and nineteen patients with acute PE and severe cardiogenic shock or in need of mechanical resuscitation (CPR) received venoarterial or venovenous ECMO from 2007 to 2020. Long-term data were obtained from survivors by phone contact and personal interviews. Follow-up included a QoL analysis using the EQ-5D-5L questionnaire, echocardiography, pulmonary function testing and cardiopulmonary exercise testing. Results The majority of patients (n = 80, 67%) were placed on ECMO during or after CPR with returned spontaneous circulation. Overall survival to hospital discharge was 45.4% (54/119). Nine patients died during follow-up. At a median follow-up of 54.5 months (25–73; 56 ± 38 months), 34 patients answered the QoL questionnaire. QoL differed largely and was slightly reduced compared to a German reference population (EQ5D5L index 0.7 ± 0.3 vs. 0.9 ± 0.04; p  < 0.01). 25 patients (73.5%) had no mobility limitations, 22 patients (65%) could handle their activities, while anxiety and depression were expressed by 10 patients (29.4%). Return-to-work status was 33.3% (average working hours: 36.2 ± 12.5 h/per week), 15 (45.4%) had retired from work early. 12 patients (35.3%) expressed limited exercise tolerance and dyspnea. 59% (20/34) received echocardiography and pulmonary function testing, 50% (17/34) cardiopulmonary exercise testing. No relevant impairment of right ventricular function and an only slightly reduced mean peak oxygen uptake (76.3% predicted) were noted. Conclusions Survivors from severe intractable PE in cardiogenic shock or even under CPR with ECMO seem to recover well with acceptable QoL and only minor cardiopulmonary limitations in the long term. To underline these results, further research with larger study cohorts must be obtained

Predictors of Nocturnal Hypoxemic Burden in Patients Undergoing Elective Coronary Artery Bypass Grafting Surgery

Nocturnal hypoxemia has been linked to increased cardiovascular morbidity and mortality. Several common diseases, such as sleep-disordered breathing (SDB), heart failure (HF), obesity, and pulmonary disease, coincide with an elevated nocturnal hypoxemic burden with and without repetitive desaturations. Research question: This study aimed to evaluate the association of relevant common diseases with distinctive metrics of nocturnal hypoxemic burden with and without repetitive desaturations in patients undergoing coronary artery bypass grafting surgery. Study design and methods: In this subanalysis of the prospective observational study, CONSIDER-AF (NCT02877745) portable SDB monitoring was performed on 429 patients with severe coronary artery disease the night before cardiac surgery. Pulse oximetry was used to determine nocturnal hypoxemic burden, as defined by total recording time spent with oxygen saturation levels < 90% (T90). T90 was further characterized as T90 due to intermittent hypoxemia (T90desaturation) and T90 due to nonspecific and noncyclic SpO2-drifts (T90non-specific). Results: Multivariable linear regression analysis identified SDB (apnea–hypopnea-index ≥ 15/h; B [95% CI]: 6.5 [0.4; 12.5], p = 0.036), obesity (8.2 [2.5; 13.9], p = 0.005), and mild-to-moderate chronic obstructive pulmonary disease (COPD, 16.7 [8.5; 25.0], p < 0.001) as significant predictors of an increased nocturnal hypoxemic burden. Diseases such as SDB, obesity and HF were significantly associated with elevated T90desaturation. In contrast, obesity and mild-to-moderate COPD were significant modulators of T90non-specific. Interpretation: SDB and leading causes for SDB, such as obesity and HF, are associated with an increased nocturnal hypoxemic burden with repetitive desaturations. Potential causes for hypoventilation syndromes, such as obesity and mild-to-moderate COPD, are linked to an increased hypoxemic burden without repetitive desaturations. Clinical Trial Registration: ClinicalTrials.gov identifier: NCT02877745

Enhanced Cardiac CaMKII Oxidation and CaMKII-Dependent SR Ca Leak in Patients with Sleep-Disordered Breathing

Background: Sleep-disordered breathing (SDB) is associated with increased oxidant generation. Oxidized Ca/calmodulin kinase II (CaMKII) can contribute to atrial arrhythmias by the stimulation of sarcoplasmic reticulum Ca release events, i.e., Ca sparks. Methods: We prospectively enrolled 39 patients undergoing cardiac surgery to screen for SDB and collected right atrial appendage biopsies. Results: SDB was diagnosed in 14 patients (36%). SDB patients had significantly increased levels of oxidized and activated CaMKII (assessed by Western blotting/specific pulldown). Moreover, SDB patients showed a significant increase in Ca spark frequency (CaSpF measured by confocal microscopy) compared with control subjects. CaSpF was 3.58 ± 0.75 (SDB) vs. 2.49 ± 0.84 (no SDB) 1/100 µm−1s−1 (p < 0.05). In linear multivariable regression models, SDB severity was independently associated with increased CaSpF (B [95%CI]: 0.05 [0.03; 0.07], p < 0.001) after adjusting for important comorbidities. Interestingly, 30 min exposure to the CaMKII inhibitor autocamtide-2 related autoinhibitory peptide normalized the increased CaSpF and eliminated the association between SDB and CaSpF (B [95%CI]: 0.01 [−0.1; 0.03], p = 0.387). Conclusions: Patients with SDB have increased CaMKII oxidation/activation and increased CaMKII-dependent CaSpF in the atrial myocardium, independent of major clinical confounders, which may be a novel target for treatment of atrial arrhythmias in SDB

Effects of Atrial Fibrillation on the Human Ventricle

Rationale: Atrial fibrillation (AF) and heart failure often coexist, but their interaction is poorly understood. Clinical data indicate that the arrhythmic component of AF may contribute to left ventricular (LV) dysfunction. Objective: This study investigates the effects and molecular mechanisms of AF on the human LV. Methods and Results: Ventricular myocardium from patients with aortic stenosis and preserved LV function with sinus rhythm or rate-controlled AF was studied. LV myocardium from patients with sinus rhythm and patients with AF showed no differences in fibrosis. In functional studies, systolic Ca2+ transient amplitude of LV cardiomyocytes was reduced in patients with AF, while diastolic Ca2+ levels and Ca2+ transient kinetics were not statistically different. These results were confirmed in LV cardiomyocytes from nonfailing donors with sinus rhythm or AF. Moreover, normofrequent AF was simulated in vitro using arrhythmic or rhythmic pacing (both at 60 bpm). After 24 hours of AF-simulation, human LV cardiomyocytes from nonfailing donors showed an impaired Ca2+ transient amplitude. For a standardized investigation of AF-simulation, human iPSC-cardiomyocytes were tested. Seven days of AF-simulation caused reduced systolic Ca2+ transient amplitude and sarcoplasmic reticulum Ca2+ load likely because of an increased diastolic sarcoplasmic reticulum Ca2+ leak. Moreover, cytosolic Na+ concentration was elevated and action potential duration was prolonged after AF-simulation. We detected an increased late Na+ current as a potential trigger for the detrimentally altered Ca2+/Na+-interplay. Mechanistically, reactive oxygen species were higher in the LV of patients with AF. CaMKII (Ca2+/calmodulin-dependent protein kinase IIδc) was found to be more oxidized at Met281/282 in the LV of patients with AF leading to an increased CaMKII activity and consequent increased RyR2 phosphorylation. CaMKII inhibition and ROS scavenging ameliorated impaired systolic Ca2+ handling after AF-simulation. Conclusions: AF causes distinct functional and molecular remodeling of the human LV. This translational study provides the first mechanistic characterization and the potential negative impact of AF in the absence of tachycardia on the human ventricle