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Objectives The aim of this study was to determine the efficacy and safety of bivalirudin versus low-dose unfractionated heparin (UFH) in percutaneous peripheral intervention (PPI). Background Anticoagulation strategies used in PPI are based primarily on studies of percutaneous coronary intervention where higher doses of heparin are used usually in combination with a glycoprotein IIb/IIIa inhibitor. There are no studies comparing bivalirudin alone versus low-dose heparin in PPI. Methods Consecutive patients who underwent PPI at our institution were treated with either bivalirudin or low-dose UFH. Patients were assessed prospectively during index hospital stay for procedural success and bleeding complications. Of 236 patients, 111 were dosed with UFH at 50 U/kg (goal activated clotting time of 180 to 240 s), and 125 were dosed with bivalirudin at 0.75-mg/kg/h bolus followed by a 1.75-mg/kg infusion. Procedural success was defined as Results Procedural success and major bleeding rates were similar with bivalirudin versus heparin (98% vs. 99% and 2.4% vs. 0.9%, respectively). There were no differences in minor bleeding, time to ambulation, and length of hospital stay. The hospital cost for bivalirudin was $547 and Conclusions Low-dose UFH is as effective and safe as bivalirudin when used as an anticoagulation strategy in patients undergoing PPI, and low-dose UFH is less costly than bivalirudin. Larger randomized studies are required to further evaluate these findings.

Extracorporeal membrane oxygenation (ECMO) was developed as a supportive therapy for severe respiratory failure. It has been shown to be life-saving in neonates and children with isolated respiratory failure, however, its usefulness in adults remains controversial. We report the successful use of ECMO in an adult patient with severe hypoxemic respiratory failure secondary to diffuse alveolar hemorrhage from Wegener granulomatosis.

The incidence of anomalous coronary arteries is ∼1%, with heterogeneous clinical outcomes ([1][1]). Left circumflex coronary artery (LCX) entrapment is an infrequently reported complication of mitral valve surgery and correlates to the dominance and the distance of the artery from the mitral

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.