Felix Hennig

Tricuspid Incompetence and Geometry of the Right Ventricle as Predictors of Right Ventricular Function After Implantation of a Left Ventricular Assist Device

BACKGROUND Implantation of a left ventricular assist device (LVAD) is an established treatment for end-stage heart failure. Right ventricular (RV) dysfunction develops in 20% to 50% of patients after LVAD implantation, leading to prolonged ICU stay and elevated mortality. However, the prediction of RV failure remains difficult. METHODS The pre-operative echocardiographic parameters, tricuspid incompetence (TI), RV end-diastolic diameter (cut-off >35 mm), RV ejection fraction (cut-off <30%), right atrial dimension (cut-off >50 mm) and short/long axis ratio (cut-off >0.6), were analyzed retrospectively in 54 patients. Patients were divided into two groups. One group consisted of patients with RV failure (n = 9), as defined by the presence of two of the following criteria in the first 48 hours after surgery: mean arterial pressure < or =55 mm Hg; central venous pressure > or =16 mm Hg; mixed venous saturation < or =55%; cardiac index 20 units; or need for an RVAD. The other patients comprised the non-RV-failure group (n = 45). RESULTS The RV failure group had a significantly higher short/long axis ratio of the RV (0.63 vs 0.52, p = 0.03; odds ratio 4.4, p = 0.011). For patients with a short/long axis ratio of the RV of <0.6, RV failure occurred in 7% of patients, as compared with 50% for patients with a ratio > or =0.6 (p = 0.013). Among patients with TI Grade III or IV, 75% developed RV failure as compared with 12% in patients with TI Grade I or II (p = 0.054). The odds ratio for RV failure after LVAD implantation for TI Grade III or IV was 4.7 (p = 0.012). CONCLUSIONS Pre-operative evaluation of tricuspid incompetence and RV geometry may help to select patients who would benefit from biventricular support.

Effect of surgical incision management on wound infections in a poststernotomy patient population.

Skin breakdown and infiltration of skin flora are key causative elements in poststernotomy wound infections. We hypothesised that surgical incision management (SIM) using negative pressure wound therapy over closed surgical incisions for 6–7 days would reduce wound infections in a comprehensive poststernotomy patient population. ‘All comers’ undergoing median sternotomy at our institution were analysed prospectively from 1 September to 15 October 2013 (study group, n = 237) and retrospectively from January 2008 to December 2009 (historical control group, n = 3508). The study group had SIM (Prevena™ Therapy) placed immediately after skin suturing and applied at −125 mmHg for 6–7 days, whereas control group received conventional sterile wound tape dressings. Primary endpoint was wound infection within 30 days. Study group had a significantly lower infection rate than control group: 1·3% (3 patients) versus 3·4% (119 patients), respectively (P < 0·05; odds ratio 2·74). In the study group, when the foam dressing was removed after 6–7 days, the incision was primarily closed in 234 of 237 patients (98·7%). SIM over clean, closed incisions for the first 6‐7 postoperative days significantly reduced the incidence of wound infection after median sternotomy. Based on these data SIM may be cost‐effective in patients undergoing cardiac surgery.

Neurohumoral and inflammatory markers for prediction of right ventricular failure after implantation of a left ventricular assist device

PurposeImplantation of a left ventricular assist device (LVAD) is an established treatment for end-stage heart failure. Right ventricular dysfunction develops in 20%–50% of patients after device implantation, leading to prolonged hospital stays and elevated mortality rates. However, prediction of right ventricular failure remains difficult.MethodsA total of 40 patients who received an LVAD for chronic end-stage heart failure between May 2001 and December 2002 were evaluated. The patients were divided retrospectively into two groups: group I (n = 26), with no apparent postoperative right ventricular failure; and group II (n = 14), with right ventricular failure after implantation defined by the presence of two of the following criteria during the first week after surgery: mean arterial pressure ≤55 mmHg, central venous pressure ≥16 mmHg, mixed venous saturation ≤55%, cardiac index <2 l/min/m2, inotropic support score >20 units or an apparent need for mechanical right ventricular support. Hemodynamic, echocardiographic, neurohumoral, and inflammatory parameters were evaluated 24 h before implantation of the LVAD.ResultsLevels of procalcitonin, neopterin, n-terminalpro-brain natriuretic peptide, and big endothelin-1 were significantly lower in group I: 0.106 vs. 0.322 ng/ml, P = 0.048; 10.5 vs. 20.7 ng/ml, P = 0.018; 6322 vs. 17174 pg/ml, P = 0.032; 1.6 vs. 19.5 pg/ml, P = 0.02, respectively. Levels of creatinine kinase and creatinine were significantly lower in group I than in group II: 24 vs. 40 U/l, P = 0.034; 1.3 vs. 2.3 mg/dl, P = 0.008, respectively.ConclusionPreoperative evaluation of markers of inflammation and neurohumoral activation may provide additional information for predicting right ventricular failure after implantation of an LVAD.

Effect of acute brain death on release of atrium and B-type natriuretic peptides in an animal model

Introduction. Atrium and B-type natriuretic peptides (ANP and BNP) and big endothelin (ET)-1 are markers for severity of heart failure and may be used in the quality assessment of donor hearts. Elevated cardiac troponins predict early graft failure after heart transplantation. This study evaluated the effects of acute brain death (BD) on the release of ANP, BNP, big ET-1, and cardiac troponins in an animal model. Materials and Methods. Pigs were randomized into a BD group (n=5) and a control group (n=5). In the first group, acute BD was induced, and anesthesia was stopped. In the control animals, a sham operation was performed, and anesthesia was continued. Parameters were measured at baseline and for 13 hours postoperatively. Results. After acute BD, there were significant hemodynamic changes. In the control group, the BNP level was higher than in the BD group and decreased over time (P =0.016). There was no significant change in BNP release in the BD group up to 13 hours (P =0.1). ANP release remained stable over time in the control group (P =0.35) but decreased in the BD group (P =0.043). The big ET-1 levels were not different between groups. Cardiac troponin I was elevated in the BD group 5 hours after BD (P< 0.05) but remained under 1.5 mg/L throughout the study. Conclusion. Acute BD did not lead to an increase of BNP and ANP levels. Moreover, intact brain function seems to augment the release of natriuretic peptides from the myocardium. Further clinical evaluation of prognostic values of natriuretic peptides for the assessment of donor hearts is necessary. Cardiac troponins are a useful additional tool in the evaluation of donor hearts.

Natriuretic peptides as predictors of clinical course in patients with end-stage heart failure

The optimal time-point for HTx or implantation of a VAD in patients with end-stage heart failure is a key issue. In 73 patients with heart failure requiring inotropic support blood was sampled daily and big endothelin-1 (big ET) and natriuretic peptides were measured at the end of the study. Clinical parameters were also evaluated daily. The patients were divided into groups with regard to the following endpoints: Group I immediate VAD placement due to profound cardiogenic shock on admission (n 9); Group II deterioration into cardiogenic shock after an initially stable clinical course (n 21); Group III stable clinical course allowed urgent HTx or VAD implantation (n 35); Group IV weaning from inotropic support (n 8). The parameters were evaluated as potential predictors for clinical course. On admission there were no significant predictors for the clinical course except lower ANP level in group IV compared to group II (p 0-005). Among the parameters evaluated, only BNP and big ET showed significant differences between groups II and III during follow up. BNP was elevated in group II compared to the group III three days, two days and one day before profound cardiogenic shock occurred (p 0.04; p 0.05; p 0.019 resp.). Big ET was elevated in group II only 1 day before profound cardiogenic shock occurred (p 0.02). ProBNP remained unchanged during treatment in groups II and III, but decreased significantly in group IV (p 0.9, p 0.6 and p 0.025 resp.). While clinical parameters on admission did not predict the clinical course, lower ANP was found in patients weaned from inotropic support. A decrease of proBNP was also found in these patients. Elevated BNP indicated cardiogenic shock up to 3 days before its occurrence. Daily measurement of natriuretic peptides may be used for determination of optimal time-point for VAD implantation in patients with severe end-stage heart failure.

Rapid Application Is Crucial.

In the section on mechanical circulatory support , the authors mention the option of using ventricular assist devices (VADs) or extracorporeal membrane oxygenation (ECMO/ECLS) only if the cause of the cardiogenic shock is potentially reversible (1). The presence of a reversible cause is not crucial for the treatment with mechanical circulatory support (MCS) systems. On the contrary, we wish to suggest making the decision in favor of implantation on the basis of a patient’s prognosis once heart failure has been removed from the scenario. If cardiac function improves under MCS then the system can be explanted without any substitute. If the patient’s general condition stabilizes but his/her heart function remains unsatisfactory (in a scenario of an otherwise acceptable prognosis!) a change to a permanent VAD (or even heart transplantation) is possible. What is crucial is that mechanical support is administered as rapidly as possible, as the success rate of such systems decreases in tandem with the increasing extent of the shock (2). Acutely decompensated chronic heart failure is a primary focus of the article. In this context the role of MCS should be explicitly mentioned. According to the ESC guidelines, VAD implantation is indicated if a patient who receives adequate medication recurrently decompensates and, in addition to left ventricular heart failure, is found to have impaired right ventricular function and secondary organ function impairments (reduced liver or kidney function) (3). We see this constellation often in our clinical practice, with patients not being informed about the option of VAD implantation. If the device is implanted only in the context of hemodynamic decompression, the chance of success is clearly lower (4).

Inflammatory parameters as predictors of clinical course in patients with end-stage heart failure

Background: The optimal timing for heart transplantation (HTx) or implantation of a ventricular assist device (VAD) in patients with end-stage heart failure is a key issue. Methods: In 76 patients with severe heart failure requiring inotropic support and subsequent HTx or VAD implantation blood was sampled daily. TNF-alpha, E-selectin, IL-6 and 10, neopterin, high sensitive CrP and procalcitonin (PCT) were measured at the end of the study. Clinical and hemodinamic parameters were also evaluated daily. The patients were divided into groups with regard to the following endpoints: Group I – deterioration into cardiogenic shock after an initially stable clinical course (n 26); Group II – stable clinical course allowed urgent HTx or VAD implantation (n 41); Group III – weaning from inotropic support (n 9). The data are presented as median values. Results: On admission there were no differences in clinical and hemodynamical parameters between the groups. Higher E-selectin (107.6 vs. 55 ng/ml, p 0.0001) and IL-6 levels were found in group I compared to group II (34.1 vs. 18.1 pg/ml, p 0.015). E-selectin remained significantly higher three days, two days and one day before profound cardiogenic shock occurred (150 vs. 52.7, p 0.0001; 128.8 vs. 46.3, p 0.0001; 96.4 vs. 50.5 ng/ml, p 0.001), while IL-6, 10 and PCT showed significant elevation only 1 day before (31.5 vs. 16.9 pg/ml, p 0.015; 5.1 vs. 4.9 pg/ml, p 0.002; 0.38 vs. 0.19 pg/ml, p 0.026 resp.). There were no differences for TNF-alpha, neopterin and high sensitive CrP between groups. Conclusion: While routine parameters did not predict the clinical course, selected inflammatory markers, especialy E-selectin, showed significant differences between groups on admission and before clinical deterioration. Daily measurement of these markers may be used to determine optimal time-point for HTx or VAD implantation in patients with severe end-stage heart failure.

Der einfluss des hirntodes auf die freisetzung der atrialen und B-typ natriuretischen peptide und kardialen troponine in einem herzspendermodell

Zusammenfassung Das atriale natriuretische Peptid (ANP) und das B-Typ natriuretische Peptid (BNP) werden im Herzen vermehrt bei Volumenbelastung und Anstieg der Wandspannung sezerniert. Sie sind sensitive und spezifische Marker des Schweregrades einer Herzinsuffizienz, daher können diese Marker bei der Beurteilung der Qualität von Spenderherzen angewendet werden. Die Spiegel der kardialen Troponine des Herzspenders haben sich als Prediktoren des frühen Transplantatversagens nach Herztransplantation (HTx) erwiesen. Jedoch ist der Einfluss des Hirntodes und der nachfolgenden hämodynamischen Veränderungen, bekannt als Cushing Reflex, auf die Freisetzung von natriuretischen Peptiden und kardialen Troponinen beim Herzspender nicht geklärt. Diese Studie untersuchte den Einfluss des Hirntodes auf die Freisetzung von ANP, BNP, big Endothelin 1 (big ET-1) und kardialer Troponine in einem Tiermodell.Nach Einleitung der Anästhesie und Beginn der Überwachung wurden 10 Landschweine in eine Hirntodgruppe (n=5) und eine Kontrollgruppe (n=5) unterteilt. Der Hirntod wurde in der ersten Gruppe nach einer Trepanation durch Aufblasen eines subdural platzierten Ballons hervorgerufen und anschließend die Anästhesie beendet. Die zweite Gruppe diente nach einer Trepanation und fortgeführter Anästhesie als Kontrolle. Hämodynamische Parameter, big ET-1, ANP- und BNP-Werte im Plasma, sowie cTnT und cTnI im Serum wurden vor und zwei stündlich bis 13 Stunden nach der Operation gemessen. Statistische Analysen der Veränderungen im Zeitverlauf wurden mittels Friedman-Test durchgeführt.Die Hirntodgruppe zeigte signifikante Veränderungen der Hämodynamik, bedingt durch den Cushing Reflex. In der Kontrollgruppe war der BNP-Wert höher als in der Hirntodgruppe und nahm mit der Zeit ab (p=0,016). Es gab keine signifikante Veränderung der BNP-Freisetzung in der Hirntodgruppe bis 13 Stunden nach Hirntod (p=0,1). Die ANPFreisetzung blieb in der Kontrollgruppe konstant (p=0,35), aber verringerte sich in der Hirntodgruppe (p=0,043). Es gab keinen Unterschied in der ET-1-Freisetzung zwischen beiden Gruppen und auch keine Veränderung mit zunehmender Zeit. 5 Stunden nach Hirntod war cTnI in der Hirntodgruppe etwas erhöht (p<0,05), die Werte blieben aber unter 1,5 mg/l während des gesamten Experiments. cTnT blieb in beiden Gruppen nicht messbar.Hämodynamische Veränderungen nach Hirntod erzeugen keine vermehrte Freisetzung von BNP und ANP. Ferner scheint die Hirnfunktion die Freisetzung von BNP und ANP aus dem Myokard zu beeinflussen. Weitere klinische Studien sind nötig, um die Aussagekraft von BNP und ANP in der Begutachtung der Qualität von Spenderherzen zu beurteilen. Bei der Evaluation der Herzspender ist der zusätzliche Einsatz von kardialen Troponinen sinnvoll.Summary Atrium and brain natriuretic peptide (ANP and BNP) are secreted in the heart in response to pressure or volume overload and are sensitive and specific markers for severity of heart failure. Therefore, both markers may be used in the quality assessment of donor hearts. Cardiac troponins were shown to be predictors for early graft failure after HTx. However, the hemodynamic changes (Cushing reflex) due to brain death (BD) may affect levels of natriuretic peptides and cardiac troponins in heart donors. This study evaluated the effects of BD on the release of ANP, BNP, big endothelin 1 (big ET 1) and cardiac troponins in an animal model.After anesthesia and the initiation of monitoring, ten pigs were randomized into a BD group (n=5) and a control group (n=5). BD was induced by inflation of a subdurally positioned balloon catheter and anesthesia was stopped. In the control animals sham operation was performed and anesthesia was continued. Hemodynamics and BNP, ANP and big ET 1 plasma levels and cardiac troponin I and T (cTnI and cTnT) serum levels were measured before and up to 13 hours after operation. Statistical analysis of the changes over time was performed using the Friedman test.The BD group presented significant increase of preload, afterload and cardiac output due to the Cushing reflex. In the control group the BNP level was higher than in the BD group and decreased over time (p=0.016). There was no significant change in BNP release in the BD group up to 13 hours after BD (p=0.1). ANP release remained stable over time in the control group (p=0.35) but decreased in the BD group (p=0.043). The big ET 1 levels were not different between groups and there were no changes over the time. cTnI was slightly elevated in the BD group 5 hours after BD (p<0.05), but remained under 1.5 mg/l throughout the study. cTnT was undetectable in both groups.Hemodynamic stress after BD did not lead to an increase of BNP and ANP levels. Moreover, brain function seems to influence the release of BNP and ANP from the myocardium. Further clinical evaluation of prognostic values of BNP and ANP levels for assessment of the quality of donor hearts is necessary. Cardiac troponins are a useful additional tool in the evaluation of donor heart quality.