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Objectives to investigate the feasibility of placing stents across renal arteries.Design we have studied in pigs: (i) the feasibility of accurately placing a fenestrated stent in front of one renal ostium; (ii) the short-term effects on renal arteries and function after the placement of such a fenestrated stent. Materials and methods eight fenestrated Palmaz stents were placed over pigs» renal ostia under fluoroscopy. Five weeks later, angiograms were performed and the animals were sacrificed. Proliferation of the healing tissues over the ostia was measured and analysed by microscopy. Serum creatinine was measured prior to all angiograms and at 5 weeks. Results all eight stents were correctly placed. One stent later migrated and was excluded from the study. One pig died at day 1. Gross examination confirmed the correct placement of the fenestrations in four pigs out of seven (57%). In the six remaining pigs, at 5 weeks, there was no angiographic evidence of stent misplacement and all the kidneys were fully perfused. Nine renal ostia were covered by struts and neointima with a mean area of coverage of 38±5% altogether. No tissue proliferation was observed over the three renal ostia located in front of the fenestration. Serum creatinine did not significantly increase at 5 weeks. Conclusion creating a fenestration in a stent for renal arteries may be worth while in order to avoid neointimal covering of the renal ostia. However, accurate placement of such a fenestrated stent remains a difficult task.

Introduction: Both pressure overload hypertrophy (POH) and aging cause increased diastolic chamber stiffness. Whether and to what extent these changes are dependent on increased LV mass, increased myocardial viscoelastic stiffness, changes in the extracellular matrix (ECM) and/or changes in the constitutive properties of the cardiac muscle cells is not completely defined. Methods: Three groups of mice (C57Bl) were studied: young adults (controls; n 7, age 16 5 wks), POH (n 6, age 16 1 wks) and senescent (n 7, age 96 10 wks). POH was created by transverse aortic constriction (TAC) for 4 weeks. Left ventricular (LV) structure and function were determined by echocardiography. LV papillary muscles were isolated and viscoelastic properties studied. Cardiomyocytes were isolated (collagenase), embedded in a gel matrix and viscoelastic properties studied. In both papillary muscles and cardiomyocytes a stress vs strain hysteresis loop was derived, which was fit by a constitutive equation to derive the elastic stiffness constant β. Additionally, normalized area of the hysteresis loop was used to derive the viscosity constant η. Results: In the POH mice echocardiography showed a significant increase in LV/ Body Weight ratio (3.04 0.16 before vs 5.69 1.09* mg/gm after TAC) with no change in end diastolic volume or ejection fraction. Stiffness and viscosity were increased in papillary muscle and cardiomyocytes in both POH and senescent mice (Table). POH caused a 118% increase in myocardial stiffness and a 21% increase in cardiomyocyte stiffness. Aging caused a 29% increase in myocardial stiffness and a 31% increase in cardiomyocyte stiffness. Therefore, both the ECM and cardiomyocyte properties play a role in increased myocardial stiffness. Conclusion: Data suggest that the observed increase in myocardial stiffness may be more dependent on changes in the ECM in POH, but more dependent on changes in the cardiomyocyte in aging. Therefore, treatment developed to decrease myocardial stiffness may target either ECM or cardiomyocyte but must affect both to completely normalize the increased stiffness that occurs in POH and aging.