Angela Kornberger

Percutaneous SAPIEN S3 Transcatheter Valve Implantation for Post-Left Ventricular Assist Device Aortic Regurgitation.

Aortic regurgitation was found to develop in a considerable share of patients supported with continuous flow left ventricular assist devices (LVADs). The resulting circulatory loop renders LVAD operation inefficient so that symptoms of heart failure develop in spite of high LVAD flows. In patients with a high reoperative risk, transcatheter aortic valve implantation may be considered as an alternative to reoperative valve surgical procedures. We report a case of percutaneous transcatheter aortic valve implantation using the SAPIEN S3 (Edwards Lifesciences, Inc, Irvine, CA) valve for post-LVAD aortic regurgitation.

Application of Intravascular Dissection Devices for Closed Chest Coronary Sinus Lead Extraction: An Interdisciplinary Approach

BACKGROUND Increasing application of cardiac resynchronization therapy is accompanied by an increase in patients requiring removal of coronary sinus (CS) leads. The aim of this study was to determine outcomes of closed chest CS lead extraction using intravascular dissection devices. METHODS Between 2000 and 2011, 41 patients (80.5% men; aged 64.2±13.8 years) underwent transvenous CS lead extraction procedures. Reasons for lead extraction were infection in 9, CS lead dislodgement in 15, lead malfunction, including manufacturer-initiated product recall in 6, phrenic nerve stimulation in 5, combinations of causes in 5, and elective extraction concomitant with generator replacement for battery depletion in 1. RESULTS In addition to 24 isolated CS lead extractions, we performed 17 multiple lead extractions (2 to 4 leads) after a mean of 30.6±32.5 months. The time elapsed from implantation was 4.6±9.1 months for isolated CS and 42.6±32.4 months for multiple lead extractions. Extraction by direct manual traction was feasible in 13 patients by locking stylets in 6. Escalation to mechanical sheaths was required in 17 patients and to electrosurgical sheaths in 5. More aggressive methods were associated with longer implantation times and positive infection status. No deaths or major periprocedural complications occurred. Six minor postprocedural complications, of which three were surgically related, occurred in 5 patients. CONCLUSIONS Closed chest CS lead extraction can be safely performed with excellent results. We recommend an escalating approach from isolated manual traction over locking stylets to mechanical sheaths and, eventually, electrosurgical dissection devices. The application in mainly high-risk patients demands an interdisciplinary approach to enhance safety and limit morbidity and death.

Suspected involvement of EPTFE membrane in sterile intrathoracic abscess and pericardial empyema in a multi-allergic LVAD recipient: a case report

Device-related infections in recipients of left ventricular assist devices (LVAD) have been recognized as a major source of morbidity and mortality. They require a high level of diagnostic effort as part of the overall burden resulting from infectious complications in LVAD recipients. We present a multi-allergic patient who was treated for persistent sterile intrathoracic abscess formation and pericardial empyema following minimally invasive LVAD implantation including use of a sheet of e-polytetrafluoroethylene (ePTFE) membrane to restore pericardial integrity. Sterile abscess formation and pericardial empyema recurred after surgical removal until the ePTFE membrane was removed, suggesting that in disposed patients, ePTFE may be related to sterile abscess formation or sterile empyema.

Left ventricular non-compaction cardiomyopathy and left ventricular assist device: a word of caution

BackgroundIn patients with left ventricular non-compaction (LVNC), implantation of a left ventricular assist device (LVAD) may be performed as a bridge to transplantation. In this respect, the particular characteristics of the left ventricular myocardium may represent a challenge.Case presentationWe report a patient with LVNC who required urgent heart transplantation for inflow cannula obstruction nine months after receiving a LVAD. LVAD parameters, echocardiography and examination of the explanted heart suggested changes of left ventricular configuration brought about by LVAD support as the most likely cause of inflow cannula obstruction.ConclusionsWe conclude that changes experienced by non-compacted myocardium during LVAD support may give rise to inflow cannula obstruction and flow reduction. Presence of LVNC mandates tight surveillance for changes in LV configuration and LVAD flow characteristics and may justify urgent transplantation listing status.

„Bridge to transplant“ und Überleben nach Herztransplantation

Ergebnisse. Die mittlere Bridging-Dauer betrug 261 Tage. Die Patienten mit kurzem Bridging waren jünger als jene mit mittlerer und langer Bridging-Dauer, hatten eine bessere Nierenfunktion und waren vor Transplantation häufiger inotropieund intensivstationspflichtig. Eine Stratifizierung anhand der Karnofsky Performance Status Scale (KPS) ergab, dass die Anteile der Patienten mit KPS >70, KPS 50–70 und KPS <50 in den 3 Bridging-Gruppen bei der Listung vergleichbar waren. Zum Zeitpunkt der Transplantation war der Anteil von Patienten der niedrigsten KPS-Kategorie bei kurzem Bridging von 40,8 % auf 43,1% gestiegen, während bei mittlerer und langer Bridging-Dauer Reduktionen von 35,5 % auf 24,1 % bzw. von 33,6 % auf 26,4 % verzeichnet wurden. Dreißigtage-, Sechsmonatsund Einjahresüberleben betrugen 96,0 %, 92,2 % bzw. 89,0 % und variierten nicht in Abhängigkeit von der Bridging-Dauer. Das Einjahresüberleben der Patienten mit niedrigem KPS lag signifikant niedriger (81,9 %) als jenes der Patienten mit mittlerem (91,9 %) bzw. hohem (91,7 %) KPS. Bei kurzem Bridging war das Einjahresüberleben zwischen Patienten mit niedrigem, mittlerem und hohem KPS mit 94,2 %vs. 87,3 %vs. 94,4 %vergleichbar. Bei mittlerer und langer BridgingDauer jedoch lag das Einjahresüberleben jener mit niedrigem KPS (79,7 % bzw. 80,5%)signifikantunterjenemderGruppen mit mittlerem (90,2 % bzw. 94,4 %) bzw. hohem (93,2 % bzw. 90,0 %) KPS.

Levosimendan protects human hepatocytes from ischemia-reperfusion injury

Background Ischemia-reperfusion injury (IRI) is a major challenge in liver transplantation. The mitochondrial pathway plays a pivotal role in hepatic IRI. Levosimendan, a calcium channel sensitizer, was shown to attenuate apoptosis after IRI in animal livers. The aim of this study was to investigate the effect of levosimendan on apoptosis in human hepatocytes. Methods Primary human hepatocytes were either exposed to hypoxia or cultured under normoxic conditions. After the hypoxic phase, reoxygenation was implemented and cells were treated with different concentrations of levosimendan (10ng/ml, 100ng/ml, 1000ng/ml). The overall metabolic activity of the cells was measured using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), and aspartate aminotransferase (AST) levels were determined in order to quantify hepatic injury. Fluorescence-activated cell sorting (FACS) analysis was applied to measure necrosis and apoptosis. Finally, Western blotting was performed to analyze apoptotic pathway proteins. Results Administration of levosimendan during reperfusion increases the metabolic activity of human hepatocytes and decreases AST levels. Moreover, apoptosis after IRI is reduced in treated vs. untreated hepatocytes, and levosimendan prevents down-regulation of the anti-apoptotic protein Bcl-2 as well as up-regulation of the pro-apoptotic protein BAX. Conclusion The present study suggests a protective effect of levosimendan on human hepatocytes. Our findings suggest that treatment with levosimendan during reperfusion attenuates apoptosis of human hepatocytes by influencing BAX and Bcl-2 levels.

Identification of Factors Influencing Cumulative Long-Term Radiation Exposure in Patients Undergoing EVAR

Patients who undergo endovascular repair of aortic aneurysms (EVAR) require life-long surveillance because complications including, in particular, endoleaks, aneurysm rupture, and graft dislocation are diagnosed in a certain share of the patient population and may occur at any time after the original procedure. Radiation exposure in patients undergoing EVAR and post-EVAR surveillance has been investigated by previous authors. Arriving at realistic exposure data is essential because radiation doses resulting from CT were shown to be not irrelevant. Efforts directed at identification of factors impacting the level of radiation exposure in both the course of the EVAR procedure and post-EVAR endovascular interventions and CTAs are warranted as potentially modifiable factors may offer opportunities to reduce the radiation. In the light of the risks found to be associated with radiation exposure and considering the findings above, those involved in EVAR and post-EVAR surveillance should aim at optimal dose management.

Septic cardiomyopathy: evidence for a reduced force-generating capacity of human atrial myocardium in acute infective endocarditis

Abstract Background: This study analyzes the myocardial force-generating capacity in infective endocarditis (IE) using an experimental model of isolated human atrial myocardium. In vivo, it is difficult to decide whether or not alterations in myocardial contractile behavior are due to secondary effects associated with infection such as an altered heart rate, alterations of preload and afterload resulting from valvular defects, and altered humoral processes. Our in vitro model using isolated human myocardium, in contrast, guarantees exactly defined experimental conditions with respect to preload, afterload, and contraction frequency, thus not only preventing confounding by in vivo determinants of contractility but also excluding effects of other factors associated with sepsis, hemodynamics, humoral influences, temperature, and medical treatment. Methods: We analyzed right atrial trabeculae (diameter 0.3–0.5 mm, initial length 5 mm) from 32 patients undergoing aortic and/or mitral valve replacement for acute valve incompetence caused by IE and 65 controls receiving aortic and/or mitral valve replacement for nonendocarditic valve incompetence. Isometric force amplitudes and passive resting force values measured at optimal length in the two groups were compared using Student’s t-test. Results: There were no significant differences between the groups in terms of the passive resting force. The isometric force amplitude in the endocarditis group, however, was significantly lower than in the nonendocarditis group (p=0.001). In the endocarditis group, the calculated active force, defined as the isometric force amplitude minus the resting force, was significantly lower (p<0.0001) and the resting force/active force ratio was significantly higher (p<0.0001). Using linear regression to describe the function between resting force and active force, we identified a significant difference in slope (p<0.0001), with lower values found in the endocarditis group. Conclusion: Our data suggest that the force-generating capacity of atrial myocardium is significantly reduced in patients with IE. In these patients, an elevated resting force is required to achieve a given force amplitude. It remains unclear, however, whether this is due to calcium desensitization of the contractile apparatus, presence of myocardial edema, fibrotic remodeling, disruption of contractile units, or other mechanisms.

Kinetics of circulating endothelial progenitor cells in patients undergoing carotid artery surgery

Aim Endothelial progenitor cells (EPCs) are primitive cells found in the bone marrow and peripheral blood (PB). In particular, the potential of EPCs to differentiate into mature endothelial cells remains of high interest for clinical applications such as bio-functionalized patches for autologous seeding after implantation. The objective of this study was to determine EPCs’ kinetics in patients undergoing carotid artery thromboendarterectomy (CTEA) and patch angioplasty. Methods Twenty CTEA patients were included (15 male, mean age 76 years). PB samples were taken at 1 day preoperatively, and at 1, 3, and 5 days postoperatively. Flow cytometric analysis was performed for CD34, CD133, KDR, and CD45. Expression of KDR, SDF-1α, and G-CSF was analyzed by means of enzyme-linked immunosorbent assay. Results Fluorescence-activated cell sorting analysis revealed 0.031%±0.016% (% of PB mononuclear cells) KDR+ cells and 0.052%±0.022% CD45−/CD34+/CD133+ cells, preoperatively. A 33% decrease of CD45−/CD34+/CD133+ cells was observed at day 1 after surgery. However, a relative number (compared to initial preoperative values) of CD45−/CD34+/CD133+ cells was found on day 3 (82%) and on day 5 (94%) postoperatively. More profound upregulated levels of CD45−CD34+/CD133+ cells were observed for diabetic (+47% compared to nondiabetic) and male (+38% compared to female) patients. No significant postoperative time-dependent differences were found in numbers of KDR+ cells and the concentrations of the cytokines KDR and G-CSF. However, the SDF-1α levels decreased significantly on day 1 postoperatively but returned to preoperative levels by day 3. Conclusion CTEA results in short-term downregulation of circulating EPCs and SDF-1α levels. Rapid return to baseline levels might indicate participation of EPCs in repair mechanisms following vascular injury.

Influence of hypothermia and subsequent rewarming upon leukocyte-endothelial interactions and expression of Junctional-Adhesion-Molecules A and B

Patients with risks of ischemic injury, e.g. during circulatory arrest in cardiac surgery, or after resuscitation are subjected to therapeutic hypothermia. For aortic surgery, the body is traditionally cooled down to 18 °C and then rewarmed to body temperature. The role of hypothermia and the subsequent rewarming process on leukocyte-endothelial interactions and expression of junctional-adhesion-molecules is not clarified yet. Thus, we investigated in an in-vitro model the influence of temperature modulation during activation and transendothelial migration of leukocytes through human endothelial cells. Additionally, we investigated the expression of JAMs in the rewarming phase. Exposure to low temperatures alone during transmigration scarcely affects leukocyte extravasation, whereas hypothermia during treatment and transendothelial migration improves leukocyte-endothelial interactions. Rewarming causes a significant up-regulation of transmigration with falling temperatures. JAM-A is significantly modulated during rewarming. Our data suggest that transendothelial migration of leukocytes is not only modulated by cell-activation itself. Activation temperatures and the rewarming process are essential. Continued hypothermia significantly inhibits transendothelial migration, whereas the rewarming process enhances transmigration strongly. The expression of JAMs, especially JAM-A, is strongly modulated during the rewarming process. Endothelial protection prior to warm reperfusion and mild hypothermic conditions reducing the difference between hypothermia and rewarming temperatures should be considered.