Intracardiac teratoma in a newborn

Primary tumors of the heart are infrequent at all ages. We present a newborn with hypoxia and a heart murmur, in whom an echocardiogram revealed a large tumor filling the right ventricle and the pulmonary annulus. To maintain pulmonary blood flow, the patency of the ductus arteriosus was achieved by infusion of prostaglandin E1. Successful surgical resection was accomplished. The pathological examination was characteristic of a benign teratoma. The patient remains asymptomatic and has shown no evidence of recurrence of the tumor during a follow-up period of 34 months. This represents the eleventh case of intracardiac teratoma and only the fourth case to undergo successful surgical resection.     

PKCbeta regulates ischemia/reperfusion injury in the lung

Activation of PKCbetaII is associated with the response to ischemia/reperfusion (I/R), though its role, either pathogenic or protective, has not been determined. In a murine model of single-lung I/R, evidence linking PKCbeta to maladaptive responses is shown in the following studies. Homozygous PKCbeta-null mice and WT mice fed the PKCbeta inhibitor ruboxistaurin subjected to I/R displayed increased survival compared with controls. In PKCbeta-null mice, phosphorylation of extracellular signal-regulated protein kinase-1 and -2 (ERK1/2), JNK, and p38 MAPK was suppressed in I/R. Expression of the immediate early gene, early growth response-1 (Egr-1), and its downstream target genes was significantly increased in WT mice in I/R, particularly in mononuclear phagocytes (MPs), whereas this expression was attenuated in PKCbeta-null mice or WT mice fed ruboxistaurin. In vitro, hypoxia/reoxygenation-mediated induction of Egr-1 in MPs was suppressed by inhibition of PKCbeta, ERK1/2, and JNK, but not by inhibition of p38 MAPK. These findings elucidate key roles for PKCbetaII activation in I/R by coordinated activation of MAPKs (ERK1/2, JNK) and Egr-1.     

Comparison of patient reported outcomes after Triathlon? and Kinemax Plus prostheses

INTRODUCTION

The Triathlon^® (Stryker, Kalamazoo, MI, US) total knee replacement was designed to improve patient function and survivorship. The aim of this study was to determine whether the Triathlon^® prosthesis produces better patient reported outcomes than a previous design by the same manufacturer, the Kinemax Plus.

METHODS

The outcome of 233 knees of patients with a mean age of 68 years (range: 40–80 years) who received the Kinemax Plus prosthesis were compared with the outcomes of 220 knees of patients with a mean age of 70 years (range: 42–90 years) who received the Triathlon^® prosthesis. Data were collected via postal questionnaire prior to surgery as well as at 8–12 weeks and at 1 year following surgery. Validated questionnaires were used including the WOMAC^® (Western Ontario and McMaster Universities) pain and function scales, the Knee injury and Osteoarthritis Outcome Score quality of life scale and the self-administered patient satisfaction scale.

RESULTS

This study found that patients who had the Triathlon^® prosthesis had significantly better pain relief (p<0.0001), function (p=0.028), knee related quality of life (p<0.0001) and satisfaction (p=0.0003) at three months after surgery than those who received the Kinemax Plus prosthesis. In addition, knee related quality of life (p=0.002) and satisfaction (p=0.021) were significantly higher at one year after surgery in Triathlon^® patients.

CONCLUSIONS

The findings suggest that return to function and reduction in pain may occur more quickly in patients with a Triathlon^® prosthesis than in those with the Kinemax Plus.     

Monitoring the effect of CPAP on left ventricular function using continuous mixed-blood saturation

The hypothetic benefit of CPAP on cardiac performance and on a reduction in VO2 was tested in a patient before heart transplantation after acute myocardial infarction using continuous SvO2 monitoring. The CPAP added to inotropic support (enoximone plus dobutamine) and intraaortic balloon pumping dramatically increased SvO2 in relation to both an increase in cardiac output and a decrease in VO2 secondary to respiratory work reduction, validating the initial hypotheses.     

Dynamic right and left ventricular interactions in the rabbit: Simultaneous measurement of ventricular pressure-volume loops

: This study was performed to characterize the dynamic factors determining ventricular interdependence in an open-pericardium intact animal model. Materials and: Simultaneous measures of right ventricular (RV) and left ventricular (LV) pressures and volumes in 6 urethane-anesthetized openchested, open-pericardium rabbits. RV and LV V were calculated every 2 milliseconds. Measurements were made at initial baseline blood volume, and again after two infusions of 20 mL/kg isoconductive colloid solution. At each blood volume level, partial aortic (AO), pulmonary artery (PAO), and inferior vena caval (IVC) occlusions were performed. Biventricular diastolic compliance and end-systolic elastance were calculated from these data.: Baseline end-diastolic (ED) and end-systolic (ES) V were 3.29 ± 0.55 and 2.43 ± 0.33 mL (x ± SD) for the LV, and 3.38 ± 1.56 and 2.84 ± 1.36 mL for the RV, respectively. AO increased all LV pressure and volume (P < .05) but did not alter RV ED volume (2.85 ± 1.20 mL) or ED pressure (3.3 ± 2.0 to 3.6 ± 2.1 mm Hg). PAO increased RV ES pressure (P < .05) but did not alter RV ED volume, ED pressure, or ES volume, although it decreased LV ED volume (2.82 ± 0.59, P < .05). AO also immediately increased end-systolic RV elastance to a value greater than that defined by IVC (7.9 ± 4.4 to 10.9 ± 6.6 mm Hg/mL, P < .05). Intravascular volume expansion though increasing baseline pressure and volume, did not alter qualitatively biventricular responses to AO, PA, or IVC.: Ventricular interdependence has both systolic and diastolic components that have differing directional effects. In the pericardectomized rabbit, increases in RV ED volume decrease LV ED volume by decreasing LV diastolic compliance, but do not alter LV systolic function. Whereas, increases in LV ED volume decrease RV ES volume resulting in an increase in RV maximal elastance, but minimally alter RV diastolic function.