[Show abstract][Hide abstract] ABSTRACT: Minimal invasive extracorporeal circulation (MiECC) systems have initiated important efforts within science and technology
to further improve the biocompatibility of cardiopulmonary bypass components to minimize the adverse effects and improve end-organ
protection. The Minimal invasive Extra-Corporeal Technologies international Society was founded to create an international
forum for the exchange of ideas on clinical application and research of minimal invasive extracorporeal circulation technology.
The present work is a consensus document developed to standardize the terminology and the definition of minimal invasive extracorporeal
circulation technology as well as to provide recommendations for the clinical practice. The goal of this manuscript is to
promote the use of MiECC systems into clinical practice as a multidisciplinary strategy involving cardiac surgeons, anaesthesiologists
Full-text · Article · Jan 2016 · Interactive Cardiovascular and Thoracic Surgery
[Show abstract][Hide abstract] ABSTRACT: In heart failure, left ventricular assist device (LVAD) implantation is performed to ensure sufficient cardiac output. Whereas some patients are subsequently weaned from LVAD support, other patients still need heart transplantation. To elucidate underlying mechanisms, we assessed the arrhythmogenic SR-Ca(2+) leak at the time of LVAD implantation (HF-Im) and heart transplantation (HF-Tx) and evaluated the effects of CaMKII-inhibition. Human left-ventricular cardiomyocytes were isolated, paced at 1 Hz for 10 beats to ensure SR-Ca(2+) loading and scanned for diastolic Ca(2+) sparks (confocal microscopy). In HF-Im, the high diastolic spark frequency (CaSpF) of 0.76 ± 0.12 × 100 μm(-1) × s(-1) could be reduced to 0.48 ± 0.10 × 100 μm(-1) × s(-1) by CaMKII inhibition (AIP, 1 μM). The amplitude of Ca(2+) sparks, width, and length was not significantly altered. In sum, CaMKII inhibition yielded a clear tendency toward a reduction of the SR-Ca(2+) leak (n cells/patients = 76/6 vs. 108/6, P = 0.08). In HF-Tx, we detected an even higher CaSpF of 1.00 ± 0.10 100 μm(-1) × s(-1) and a higher SR-Ca(2+) leak compared with HF-Im (increase by 81 ± 33%, n cells/patients = 156/7 vs. 130/7, P < 0.05), which fits to the further decreased LV function. Here, CaMKII inhibition likewise reduced CaSpF (0.35 ± 0.09 100 μm(-1) × s(-1,) P = 0.06) and significantly reduced spark duration (n sparks/patients = 58/3 vs. 159/3, P < 0.05). Conclusively, the SR-Ca(2+) leak was reduced by 69 ± 12% in HF-Tx upon CaMKII inhibition (n cells/patients = 53/3 vs. 91/3, P < 0.05). These data show that the SR-Ca(2+) leak correlates with the development of LV function after LVAD implantation and may represent an important pathomechanism. The fact that CaMKII inhibition reduces the SR-Ca(2+) leak in HF-Tx suggests that CaMKII inhibition may be a promising option to beneficially influence clinical course after LVAD implantation.
No preview · Article · Jan 2016 · Artificial Organs
[Show abstract][Hide abstract] ABSTRACT: In patients with left ventricular assist device implants (LVAD), pump thrombosis is a potential life-threatening complication. In a retrospective data analysis, we compared clinical outcomes in 50 patients with HeartWare or HeartMate II implants undergoing device exchange (DEx; n=21) or systemic thrombolysis (STL; n=29) for pump thrombosis. Primary endpoint was survival up to 90 days post-intervention. Secondary endpoints were the need of blood products post-intervention, duration of intensive care unit stay, in-hospital stay, 90-day and 2-year therapy failure (the need of additional surgical or nonsurgical intervention due to pump thrombosis), and 2-year survival. Ninety-day survival was 89.3% in the STL group and 91.0% in the DEx group (P=0.901). Compared with the DEx group, the average use of different blood products was lower (P-values <0.001), and duration of intensive care unit stay and in-hospital stay tended to be shorter in the STL group (P-values 0.086 and 0.048, respectively). However, 90-day freedom from therapy failure was significantly lower in the STL group than in the DEx exchange group (P=0.027), and so was 2-year freedom from therapy failure (P=0.006). Two-year survival was comparable between groups (P=0.267). Our data indicate that STL can be considered as therapeutic option in LVAD patients with pump thrombosis.
No preview · Article · Jan 2016 · ASAIO journal (American Society for Artificial Internal Organs: 1992)
[Show abstract][Hide abstract] ABSTRACT: Aims:
New-onset conduction disturbances still represent a considerable problem after transcatheter aortic valve implantation (TAVI). The aim of this study was to identify calcification patterns with an elevated risk for permanent pacemaker implantation (PPI) after TAVI and investigate underlying mechanisms in an ex vivo setting.
Methods and results:
One hundred and sixty-two patients who underwent TAVI with the Edwards SAPIEN XT(®) or Medtronic CoreValve(®) at our institution were analysed. The calcium load of the device landing zone was quantified with 3mensio(®), and calcium patterns with an elevated risk for PPI were identified. Ex vivo simulations of balloon valvuloplasty were performed in 3D-printed silicone annuli of patients matching the identified risk profile. Patients with a calcium load of the left coronary cusp (LCC) above 209 mm(3) had a higher rate of PPI than patients below this threshold (16.7 vs. 2.6%, P = 0.003). Multivariate regression revealed pre-existing right bundle branch block (RBBB) and increased LCC calcification as independent predictors for PPI. Simulation of the TAVI procedure in a silicone annulus revealed an off-centreline shift of the valvuloplasty balloon and transcatheter heart valve away from the LCC towards the commissure between right- and non-coronary cusp.
Pre-existing RBBB and elevated LCC calcification were identified as independent predictors for PPI. These two risk factors enabled us to distinguish between patients according to their risk for PPI after TAVI. Ex vivo simulations suggested an off-centreline shift of the balloon as a possible explanation.
Full-text · Article · Jan 2016 · European Heart Journal Cardiovascular Imaging
[Show abstract][Hide abstract] ABSTRACT: Background
Dilated cardiomyopathy (DCM) could be caused by mutations in more than 40 different genes. However, the pathogenic impact of specific mutations is in most cases unknown complicating the genetic counseling of affected families. Therefore, functional studies could contribute to distinguish pathogenic mutations and benign variants. Here, we present a novel heterozygous DES missense variant (c.407C > T; p.L136P) identified by next generation sequencing in a DCM patient. DES encodes the cardiac intermediate filament protein desmin, which has important functions in mechanical stabilization and linkage of the cell structures in cardiomyocytes.
Methods and results
Cell transfection experiments and assembly assays of recombinant desmin in combination with atomic force microscopy were used to investigate the impact of this novel DES variant on filament formation. Desmin-p.L136P forms cytoplasmic aggregates indicating a severe intrinsic filament assembly defect of this mutant. Co-transfection experiments of wild-type and mutant desmin conjugated to different fluorescence proteins revealed a dominant affect of this mutant on filament assembly. These experiments were complemented by apertureless scanning near-field optical microscopy.
In vitro analysis demonstrated that desmin-p.L136P is unable to form regular filaments and accumulate instead within the cytoplasm. Therefore, we classified DES-p.L136P as a likely pathogenic mutation. In conclusion, the functional characterization of DES-p.L136P might have relevance for the genetic counseling of affected families with similar DES mutations and could contribute to distinguish pathogenic mutations from benign rare variants.
Full-text · Article · Dec 2015 · Journal of Molecular and Cellular Cardiology
[Show abstract][Hide abstract] ABSTRACT: We performed transapical transcatheter aortic valve implantation on an 87-year-old woman with severe aortic valve stenosis. Because of the narrow left ventricular outflow tract, annular positioning of the prosthetic valve proved challenging. During positioning, the prosthetic valve was accidentally dislodged from the balloon catheter and dropped into the left ventricle. Attempted catheter retrieval was unsuccessful. We therefore converted to open surgery without delay. After aortotomy, to our surprise, the prosthesis could not be found, neither in the left ventricle nor in the ascending aorta. Transesophageal echocardiography failed to reveal the location of the missing prosthesis. Fluoroscopy finally displayed the prosthesis in the descending aorta at the level of the left atrium. We proceeded with aortic and mitral valve replacement and closed the sternum. Under fluoroscopic guidance, the prosthetic valve was secured to the wall of the abdominal aorta in an infrarenal position by dilatation with a balloon catheter. This case shows that we should be alert to septum hypertrophy or a narrow left ventricular outflow tract during transapical aortic valve implantation. In such anatomical situations, we recommend advancing the sheath of the application system directly below the annular plane and positioning the prosthesis from this point.
Full-text · Article · Dec 2015 · Innovations Technology and Techniques in Cardiothoracic and Vascular Surgery