Introduction: Left ventricular assist devices have been successfully used as a bridge to cardiac transplantation. Because many patients exhibit marked clinical improvement of their heart failure after LVAD implantation, we studied the physiological effect of pulsatile and non-pulsatile devices on the neurohormonal axis and exercise capacity. Methods: We prospectively included 20 patients (17 men, 3 women) undergoing LVAD implantation between November 2001 and January 2004. Ten patients (1 woman and 9 men) were treated with the non-pulsatile INCOR-LVAD (Berlin Heart©) and ten patients received the pulsatile EXCOR LVAD (Berlin Heart©). Blood samples for plasma renin activity (PRA) were taken once a week over a period of ten weeks. All blood samples were collected in the morning before mobilization. Blood pressure, body weight, fluid intake and urine production were measured once a day. All patients received standard hospital diet with no limitation in fluid intake. Results: Body weight remained constant in both groups throughout the ten weeks' examination, and fluid intake and urine production were balanced in all patients. Although there was no significant difference in mean blood pressure (INCOR: 70 ± 10 mmHg; EXCOR: 73 ± 10 mmHg), plasma renin activity was substantially elevated in patients with non-pulsatile left ventricular support (INCOR: 94.68 ± 33.97 µU/ml; EXCOR: 17.06 ± 15.94 µU/ml; p < 0.05). Furthermore plasma aldosterone levels were significantly higher in patients supported by non-pulsatile INCOR LVAD (INCOR: 73.4 ± 9.6 µg/ml; EXCOR: 20.6 ± 4.6 µg/ml; p < 0.05). Conclusions: Our data suggest that pulsatile as well as non-pulsatile left ventricular assist devices are equally able to treat chronic heart failure. However pulsatile devices seem to have a greater impact on reversing the changes in plasma renin activity and might thus offer a greater advantage when recovery of left ventricular function is expected.

Objective Transcatheter aortic valve implantation (TAVI) has become an alternative to surgical aortic valve replacement (sAVR) in selected high risk patients. While improvement in left ventricular function after TAVI has been demonstrated, little is known about the impact on right ventricular (RV) function. Since postoperative RV dysfunction is linked to adverse outcomes, the authors sought to investigate the effect of TAVI and aortic valve replacement (AVR) on RV function using speckle tracking echocardiography. Design Cross-sectional study in tertiary healthcare setting. Setting 101 patients with severe symptomatic aortic stenosis (age 81±11 yrs) who underwent TAVI and 22 patients who underwent sAVR were included. RV function was assessed using 2D longitudinal strain (RV-LS), fractional area change and tricuspid annular plain systolic excursion before and after sAVR and TAVI (median 89 days). Results Although the TAVI group had worse baseline characteristics, RV function remained unchanged in this group whereas significant deterioration of RV function was observed in patients undergoing conventional AVR: RV-LS (−25.2±6.1 vs −20.0±7.0%; p=0.009), RV-fractional area change (47.0±7.0 vs 39.8±10.7%, p=0.019) and tricuspid annular plain systolic excursion (24±5 vs 16±4 mm, p=0.0001). Conclusion While TAVI did not affect RV function it deteriorated significantly in patients undergoing sAVR. The authors speculate that this may be related to the detrimental effects of pericardiotomy and, to a lesser degree, cardiopulmonary bypass. While further studies are required to assess the clinical significance of this finding, these data suggest that patients with pre-existing RV dysfunction may benefit from TAVI and that RV function should be incorporated into future risk scores.

It is known that the use of a cardiopulmonary bypass (CPB) during cardiac surgery leads to leukocyte activation and may, among other causes, induce organ dysfunction due to increased leukocyte recruitment into different organs. Leukocyte extravasation occurs in a cascade-like fashion, including capturing, rolling, adhesion, and transmigration. However, the molecular mechanisms of increased leukocyte recruitment caused by CPB are not known. This clinical study was undertaken in order to investigate which steps of the leukocyte recruitment cascade are affected by the systemic inflammation during CPB. We investigated the effects of CPB on the different steps of the leukocyte recruitment cascade in whole blood from healthy volunteers (n = 9) and patients undergoing cardiac surgery with the use of cardiopulmonary bypass (n = 7) or in off-pump coronary artery bypass-technique (OPCAB, n = 9) by using flow chamber experiments, transmigration assays, and biochemical analysis. CPB abrogated selectin-induced slow leukocyte rolling on E-selectin/ICAM-1 and P-selectin/ICAM-1. In contrast, chemokine-induced arrest and transmigration was significantly increased by CPB. Mechanistically, the abolishment of slow leukocyte rolling was due to disturbances in intracellular signaling with reduced phosphorylation of phospholipase C (PLC) γ2, Akt, and p38 MAP kinase. Furthermore, CPB induced an elevated transmigration which was caused by upregulation of Mac-1 on neutrophils. These data suggest that CPB abrogates selectin-mediated slow leukocyte rolling by disturbing intracellular signaling, but that the clinically observed increased leukocyte recruitment caused by CPB is due to increased chemokine-induced arrest and transmigration. A better understanding of the underlying molecular mechanisms causing systemic inflammation after CPB may aid in the development of new therapeutic approaches.

Background: Mitral valve surgery for the correction of secondary mitral valve regurgitation (MR) in cardiomyopathy is associated with a poor outcome. Numerous studies have identified a severe left ventricular dysfunction as an indicator for a poor prognosis. The aim of the study was to asses the follow-up after mitral valve surgery and severe left ventricular dysfunction. Methods: Between 1994 and 2000, 31 patients with mitral regurgitation and a left ventricular ejection fraction of below thirty percent undergoing isolated repair (n = 16) or replacement (n = 15) were investigated. All patients received maximal drug therapy. Twenty-one patients were New York Heart Association (NYHA) class III and 10 were class IV. Follow-up with echocardiography, ECG, and chest x-ray was performed in 87 % of the survivors. The mean duration of follow-up was 39 ± 16 months. Results: The mean duration of ICU and hospital stay was 3.6 ± 2.1 days and 8.1 ± 5.4 days, respectively. The 1-, 2-, and 5-year survival rates were 91 %, 84 %, and 77 %, respectively. NYHA class improved from 3.3 ± 0.8 to 2.1 ± 0.7 at follow-up (p < 0.01). The ejection fraction improved from 23.1 ± 6.6 % to 36 ± 6.8 % at follow-up (p < 0.02). Freedom from readmission for heart failure was 85 %, 79 %, and 68 % at 1-, 2-, and 5 years, respectively. Conclusions: Mitral valve surgery improves left ventricular function and reduces heart failure severity in patients with MR and cardiomyopathy. High-risk mitral valve surgery may be an alternative to heart transplantation in selected patients.

The Trifecta valve (St. Jude Medical) was introduced into clinical practice as a tri-leaflet stented pericardial valve designed for supra-annular placement in the aortic position. The present study aims to evaluate the preliminary results with this new bioprosthesis. Seventy patients underwent aortic valve replacement (AVR) with the Trifecta valve between August 2010 and December 2011. Thirty-three patients were male and 37 were female (52.9%). Mean age was 74.65 ± 7.63 (range 47–90 years). Prevalent cause of AVR was aortic stenosis in 64 (91.43%) patients. The mean preoperative pressure gradient was 50 ± 17 (range 20–84 mmHg), and the mean aortic valve area was 0.77 ± 0.33. Five (7.14%) patients were operated on due to aortic valve endocarditis. One patient was operated on due to isolated, severe aortic insufficiency. All patients were in New York Heart Association functional class III or IV. Twenty-eight (40%) patients underwent concomitant procedures. Concomitant procedures were coronary artery bypass grafting (n = 25), mitral valve replacement (n = 1), ablation of atrial fibrillation (n = 1) and septal myomectomy (n = 1). There were no intraoperative deaths. The 30-day in-hospital mortality was 2.85% (2 of 70). One late death occurred during the in-hospital stay due to a multiorgan failure on postoperative day 60. There were 2 (2.85%) perioperative strokes. Mean pressure gradient decreased significantly from a preoperative value of 50 ± 17 mmHg to an intraoperative gradient of 9 ± 4 mmHg (Table 3). The mean gradients were 14, 11, 11, 8 and 6 mmHg for the 19, 21, 23, 25 and 27 mm valve size, respectively. No prosthesis dislocation, endocarditis, valve thrombosis or relevant aortic regurgitation was observed at discharge. The initial experience with the Trifecta valve bioprosthesis shows excellent outcomes with favourable early haemodynamics. Further studies with longer follow-up are needed to confirm those preliminary results.