Susanne Roedler

Blood rheology after cardiac valve replacement with mechanical prostheses or bioprostheses.

Arterial thromboembolism is a serious complication in patients after heart valve replacement. Abnormalities in blood rheology may contribute to this complication. Therefore, the aim of this study was to compare various determinants of blood rheology in patients with substitute heart valves with those in healthy controls; furthermore, differences between patients with mechanical valves and those with bioprostheses should be investigated. The hemorrheologic determinants--fibrinogen, plasma viscosity, red cell aggregation, hematocrit and platelet aggregation--were studied in 92 patients with mechanical bileaflet valves, in 28 patients with bioprostheses and in 29 control subjects; the time since valve replacement was greater than or equal to 9 months. Fibrinogen, plasma viscosity, red cell and spontaneous platelet aggregation were found to be increased in all patients after heart valve replacement compared with normal subjects (fibrinogen: 348 +/- 87 vs 267 +/- 66 mg/dl, p less than 0.01; plasma viscosity: 1.71 +/- 0.1 vs 1.66 +/- 0.1 mPas, p less than 0.05; red cell aggregation: 9.9 +/- 2 vs 7.8 +/- 2 U, p less than 0.01; platelet aggregation: 22 +/- 15 vs 13 +/- 13%, p less than 0.01); among patients, fibrinogen, plasma viscosity and spontaneous platelet aggregation were higher in mechanical valves than in bioprostheses (fibrinogen: 359 +/- 95 vs 314 +/- 41 mg/dl, p less than 0.01; plasma viscosity: 1.72 +/- 0.1 vs 1.68 +/- 0.1 mPas, p less than 0.1; platelet aggregation: 23 +/- 15 vs 16 +/- 11%; p less than 0.05), whereas no difference could be found for red cell aggregation (9.7 +/- 2 vs 10.5 +/- 2%, p greater than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Association of CD14+ monocyte-derived progenitor cells with cardiac allograft vasculopathy

Objective The pathogenesis of cardiac allograft vasculopathy after heart transplant remains controversial. Histologically, cardiac allograft vasculopathy is characterized by intimal hyperplasia of the coronary arteries induced by infiltrating cells. The origin of these infiltrating cells in cardiac allograft vasculopathy is unclear. Endothelial progenitor cells are reportedly involved in cardiac allograft vasculopathy; however, the role of CD14+ monocyte-derived progenitor cells in cardiac allograft vasculopathy pathogenesis remains unknown. Methods Monocyte-derived progenitor cells were isolated from blood mononuclear cell fractions obtained from 25 patients with cardiac allograft vasculopathy and 25 patients without cardiac allograft vasculopathy. Results Both patients with cardiac allograft vasculopathy and those without cardiac allograft vasculopathy had CD45+, CD34+, CD14+, CD141−, CD31− monocyte-derived progenitor cells that differentiated into mesenchymal lineages. Monocyte-derived progenitor cells formed significantly higher numbers of colonies in patients with cardiac allograft vasculopathy than in those without cardiac allograft vasculopathy; this correlated with posttransplant follow-up time. Importantly, monocyte-derived progenitor cells from patients with cardiac allograft vasculopathy expressed significantly more α smooth muscle actin and proliferated at a higher rate than did monocyte-derived progenitor cells of patients without cardiac allograft vasculopathy. In vitro experiments suggested a paracrine control mechanism in proliferation of monocyte-derived progenitor cells in cardiac allograft vasculopathy. Conclusions These results indicate that monocyte-derived progenitor cells are associated with cardiac allograft vasculopathy, have the ability to transdifferentiate into smooth muscle cells, and thus may contribute to intimal hyperplasia of coronary arteries in cardiac allograft vasculopathy. Targeting monocyte-derived progenitor cell recruitment could be beneficial in cardiac allograft vasculopathy treatment.