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Articles by T. Walther
Total Records ( 2 ) for T. Walther
  Y Wang , C Qian , A. J.M Roks , D Westermann , S. M Schumacher , F Escher , R. G Schoemaker , T. L Reudelhuber , W. H van Gilst , H. P Schultheiss , C Tschope and T. Walther

Background— Angiotensin (Ang)-(1-7) attenuates the development of heart failure. In addition to its local effects on cardiovascular tissue, Ang-(1-7) also stimulates bone marrow, which harbors cells that might complement the therapeutic effect of Ang-(1-7). We studied the effects of Ang-(1-7) either produced locally in the heart or subcutaneously injected during the development of heart failure induced by myocardial infarction (MI) and explored the role of cardiovascular progenitor cells in promoting the effects of this heptapeptide.

Methods and Results— Effects of Ang-(1-7) on bone marrow–derived mononuclear cells in rodents, particularly endothelial progenitor cells, were investigated in vitro and in vivo in rats, in mice deficient for the putative Ang-(1-7) receptor Mas, and in mice overexpressing Ang-(1-7) exclusively in the heart. Three weeks after MI induction through permanent coronary artery occlusion, effects of Ang-(1-7) either produced locally in the heart or injected into the subcutaneous space were investigated. Ang-(1-7) stimulated proliferation of endothelial progenitor cells isolated from sham or infarcted rodents. The stimulation was blunted by A779, a Mas receptor blocker, or by Mas deficiency. Infusion of Ang-(1-7) after MI increased the number of c-kit– and vascular endothelial growth factor–positive cells in infarcted hearts, inhibited cardiac hypertrophy, and improved cardiac function 3 weeks after MI, whereas cardiomyocyte-derived Ang-(1-7) had no effect.

Conclusions— Our data suggest circulating rather than cardiac Ang-(1-7) to be beneficial after MI. This beneficial effect correlates with a stimulation of cardiac progenitor cells in vitro and in vivo. This characterizes the heptapeptide as a promising new tool in stimulating cardiovascular regeneration under pathophysiological conditions.

  J Kempfert , J Blumenstein , M. W.A Chu , P Pritzwald Stegmann , T Kobilke , V Falk , F. W Mohr and T. Walther

Objective: Based upon recent developments in transcatheter technology, this study was designed to evaluate the feasibility and haemodynamic performance of transcatheter valve-in-a-ring (VinR) implantation for potentially failed mitral repair using a minimally invasive, transatrial, off-pump approach. Methods: Adult sheep (54.3 ± 3.0 kg) underwent mitral valve repair with a 26 mm complete annuloplasty ring (PhysioTM) using standard conventional techniques. To simulate the redo operation, a transcatheter 23 mm pericardial prosthesis (Edwards SapienTM) mounted on a balloon-inflatable steel stent was deployed within the annuloplasty ring. VinR implantation was performed off-pump under rapid pacing in four and on-pump in three animals using an antegrade transatrial approach under fluoroscopic guidance. Results: Transcatheter VinR implantation was successful in all seven sheep. Mean transvalvular gradient was 4.9 ± 0.3 mmHg. VinR function was excellent with no leak in one, good with mild leak in five (trans-stent: four, paravalvular: one) and sufficient with moderate central leak in one animal, respectively. Valve deployment required 10.0 ± 0.7 min and all transcatheter prostheses were confirmed in good position on postmortem analysis, without any signs of valve dislocation or embolisation. In an in-vitro model, the minimum force required to dislodge the valve was 32.9 ± 5.2 N, which was well above the normal estimated forces generated by the left ventricle. One animal was kept alive to assess mid-term outcome and is still well 12 months after the VinR implantation. Conclusions: Transatrial, transcatheter mitral VinR implantation is feasible using a minimally invasive off-pump approach. VinR implantation is a promising concept for re-operative surgery for selected patients after failed mitral valve repair.

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