Extracardiac Right Atrium-to-Right Ventricle Homograft for Uncorrectable Tricuspid Valve Disease

Surgically uncorrectable tricuspid valve disease in children is rare. However, when it happens the surgical options are very limited. Tricuspid valve replacement using a mechanical valve or stented bioprosthesis is impractical. Use of homografts in the “anatomic position” has its limitations. We report here the use of an extracardiac homograft connection between the right atrium and right ventricle in a 16-month-old boy in whom severe tricuspid valve stenosis developed after surgical repair of a complex ventricular septal defect associated with dextrocardia and anomalous systemic venous drainage. The patient remains well receiving no cardiac medication 12 months after the procedure.     

Aneurysms complicating pulmonary autograft procedure for aortic valve replacement

Aneurysm formation in the left ventricular outflow tract related to the proximal end of the pulmonary autograft after the Ross procedure was present in 2 patients. Both occurred late after operation and were associated with prolapse of a leaflet of the autograft and significant regurgitation. Both were repaired with no immediate complications. There was no evidence of infection at time of operation. The probable mechanisms underlying this complication and the possibilities of avoiding it are discussed.     

Osmotic nephrosis with mannitol: review article

Mannitol is commonly used to lower intracranial and intraocular pressures. Large doses/massive infusions of mannitol have been found to be associated with acute renal failure (MI-ARF), that is, osmotic nephrosis. While many researchers have reported individual experiences with this pathology, we felt that there is need of an updated comprehensive review of all reported cases with elaboration of etiology, pathogenesis, diagnosis and management plan for MI-ARF. The purpose of the present communication is to share our own experience with MI-ARF, to review the effect of mannitol on kidney function and to highlight the dynamics of MI-ARF with considerations for the cautious use of mannitol in patients with risk factors for kidney diseases.     

Cerivastatin, an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme a reductase, inhibits endothelial cell proliferation induced by angiogenic factors in vitro and angiogenesis in in vivo models

Cerivastatin is an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase. It inhibits the biosynthesis of cholesterol and its precursors: farnesyl pyrophosphate and geranylgeranyl pyrophosphate (GGPP), which are involved in Ras and RhoA cell signaling, respectively. Statins induce greater protection against vascular risk than that expected by cholesterol reduction. Therefore, cerivastatin could protect plaque against rupture, an important cause of ischemic events. In this study, the effect of cerivastatin was tested on angiogenesis because it participates in plaque progression and plaque destabilization. Cerivastatin inhibits in vitro the microvascular endothelial cell proliferation induced by growth factors, whereas it has no effect on unstimulated cells. This growth arrest occurs at the G(1)/S phase and is related to the increase of the cyclin-dependent kinase inhibitor p21(Waf1/Cip1). These effects are reversed by GGPP, suggesting that the inhibitory effect of cerivastatin is related to RhoA inactivation. This mechanism was confirmed by RhoA delocalization from cell membrane to cytoplasm and actin fiber depolymerization, which are also prevented by GGPP. It was also shown that RhoA-dependent inhibition of cell proliferation is mediated by the inhibition of focal adhesion kinase and Akt activations. Moreover, cerivastatin inhibits in vivo angiogenesis in matrigel and chick chorioallantoic membrane models. These results demonstrate the antiangiogenic activity of statins and suggest that it may contribute to their therapeutic benefits in the progression and acute manifestations of atherosclerosis.     

Nonoperative management of stomal stenosis after gastroplasty for morbid obesity

Over a period of six years, 33 of 172 (19 per cent) patients who had gastric partitioning had stomal stenosis develop which was defined as an inability to drink fluids or swallow saliva, or both. All were managed conservatively in the hospital or on an outpatient basis. This consisted of total parenteral nutrition and endoscopy to evaluate the stoma with or without dilation; Eder-Puestow dilaters and long term jejunostomy feeding were used. Thirteen of these patients were dilated a total of 36 times. Three required three to six dilations each, up to the maximum size (45F). There were no complications. Twenty-nine required repletion by combined parenteral and enteral nutrition. Three required jejunostomy insertion as a separate procedure. Patients were observed for six to 60 months. Thirty-two did well. Gastrogastrostomy was required in one patient with a stenosis after the second gastroplasty. Three patients who were dilated regained over 20 per cent of their ideal weight.     

Characterization of lymphocyte beta 2-adrenoceptor signalling in patients with left ventricular volume overload disease

1. Studies using animal experimental models have suggested that the beta2-adrenoceptor is uncoupled in association with alterations in the expression of G-protein-coupled receptor kinases (GRK) 2/3 in heart failure. However, the functional expression of the components of this pathway in human disease has not been fully elucidated yet. In the present study, we evaluated the possibility that the regulation of beta2-adrenoceptor signalling components in patients with left ventricular volume overload (VOL) depends on the severity of the overload. 2. We characterized the lymphocyte GRK 2-6, beta-arrestins 1 and 2, beta2-adrenoceptor expression at the mRNA and protein levels, as well as the activity of adenylyl cyclase, protein kinases (PK) A and PKC in patients with VOL using healthy blood donors as controls. 3. In the patient group, GRK2 mRNA was increased by 61% (P < 0.001), GRK3 was increased by 54% (P < 0.005), GRK5 was increased fivefold (P < 0.001) and the beta-arrestin 2 mRNA was increased by 40% (P < 0.05). These increases were paralleled with a sixfold increase in GRK2, a twofold increase in GRK3 and a 1.3-fold increase in GRK5 protein levels. These changes were associated with a significant decrease in beta2-adrenoceptor mRNA, the basal, catalytic and receptor-mediated activity of adenylyl cyclase and sensitization of the forskolin-stimulated activity towards augmented inhibition by guanylimidodiphosphate. In general, the increase in GRK2 and 5 mRNA exhibited a positive correlation with the gravity of the haemodynamic load, as determined by changes in left ventricular fractional shortening. 4. The results suggest that VOL induces an increase in the expression of lymphocyte beta2-adrenoceptor-specific GRK and beta-arrestin 2 in association with an attenuation in beta2-adrenoceptor levels. It can be speculated that the cardiac circulatory system adapts itself to altered haemodynamic functional demands partly by altering beta2-adrenoceptor signalling.