Patent foramen ovale

INTRODUCTION: Intentional or unintentional placement of a pacemaker lead into the left ventricle is an uncommon clinical entity that is associated with a high risk for systemic embolization and enormous difficulties in case of explantation. Unintentional implantation through a patent foramen ovale via the mitral valve is the usual pathway for this malposition. METHODS: We report a case where a pacemaker lead was placed intentionally into the left ventricle via a patent foramen ovale for biventricular pacing for resynchronization therapy. Later, the patient developed life-threatening pacemaker lead-associated endocarditis with sepsis. Emergency open heart surgery for lead removal was necessary in the form of a reoperation after bypass graft surgery a number of years earlier. CONCLUSION: Although it is technically feasible to implant the pacemaker lead into the left ventricle via a patent foramen ovale, we consider this option to be obsolete for use with a biventricular pacemaker, due to the multitude of risks, which can, in part, be life-threatening for the patient.     

End-stage periventricular leukomalacia: MR evaluation

A prospective study was performed to assess the capabilities of magnetic resonance (MR) imaging in evaluation of end-stage periventricular leukomalacia (PVL) in six children, aged 31-54 months, in whom PVL had been documented by neurologic ultrasonography during the neonatal period. Eight children of similar age (four premature infants and four full-term infants) with normal neurologic development served as controls. A characteristic triad of PVL abnormalities was seen on MR images: (a) abnormally increased periventricular white-matter signal intensity on the first and second echo images of a T2-weighted sequence (repetition time = 2,000-2,400 msec, echo times = 20 or 30 and 80 msec), most commonly observed in the trigone regions of the lateral ventricles bilaterally; (b) marked loss of periventricular white matter in these regions of abnormal signal intensity, predominantly in the periatrial regions; and (c) compensatory focal ventricular enlargement adjacent to regions of abnormal signal intensity. In patients with the classic periatrial distribution of PVL lesions, general correlation between the degree of neurologic impairment and the severity of MR abnormalities was demonstrated. MR imaging was useful in detecting subtle forms of PVL in cases in which neurologic damage was subclinical.     

Procoagulant activity of reversibly acylated human factor Xa

The plasma clotting factors used to treat hemophiliacs who have developed inhibitory antibodies have a shared history of limited clinical safety and utility. To improve on existing bypass factors, we have developed a reversibly acylated form of human plasma factor Xa capable of providing a time-dependent release of procoagulant activity. Factor Xa was treated with p-amidinophenyl p'-anisate to generate anisoyl Xa. The chemical modification of the protein involves acylation of the active site serine residue of factor Xa. Anisoyl Xa deacylated in a time, pH, and temperature-dependent manner. Active factor Xa generated on deacylation of anisoyl Xa exhibited amidolytic and prothrombinase complex activities in in vitro assays, the level being comparable to those of untreated factor Xa. When Anisoyl Xa was infused into rabbits, active factor Xa was generated on deacylation of the acylated enzyme, which shortened the activated partial thromboplastin time (APTT) in a dose-dependent manner. The duration of effect on rabbit APTT could be directly correlated to the level of human plasma factor Xa. Because anisoyl Xa bypasses the "tenase" complex that is compromised in hemophilia A and B and is unaffected by inhibitory antibodies, it has the potential to be used as an effective bypass therapy.     

Monoclonal antibodies to human platelet glycoprotein IIb beta that initiate distinct platelet responses

Hybridomas secreting monoclonal antibodies (MoAbs) to human platelet membrane glycoprotein IIb (GPIIb) were prepared by fusing cells of a mouse myeloma line to spleen cells from a BALB/c mouse immunized with purified GPIIb. Six of the hybridomas secreted MoAbs that recognized epitopes on the 23,000-dalton, disulfide-linked subunit of GPIIb, GPIIb beta. All six of these MoAbs agglutinated platelets in the absence of calcium. The agglutination titers of three of the MoAbs, however, were enhanced between 2 and 6 log2 dilutions when titrated in the presence of mmol/L of calcium. The enhancement in titer was the result of MoAb- induced platelet activation followed by platelet aggregation, a reaction that could also be initiated by the monovalent Fab fragments prepared from one of the MoAbs. The MoAbs did not significantly agglutinate platelets from patients with Glanzmann's thrombasthenia, confirming biochemical evidence that there is a paucity of GPIIb beta in the membranes of these cells. Our results show that MoAbs to epitopes on GPIIb beta initiate distinct platelet responses; therefore, they should be useful for studying the ways in which regions of surface glycoproteins are involved in platelet-platelet interactions. In addition, these reagents may prove of value in diagnosing and typing patients with Glanzmann's thrombasthenia.     

Minactivin expression in human monocyte and macrophage populations

Adherent monolayer cultures of human blood monocytes, peritoneal macrophages, bone marrow macrophages, and colonic mucosa macrophages were examined for their ability to produce and secrete minactivin, a specific inactivator of urokinase-type plasminogen activator. All except colonic mucosa macrophages produced and secreted appreciable amounts of minactivin, but only blood monocytes were stimulated by muramyl dipeptide (adjuvant peptide) to increase production. The minactivin from each of these populations could be shown to preferentially inhibit urokinase-type plasminogen activator and not trypsin, plasmin, or "tissue"-type plasminogen activator (HPA66). A plasminogen-activating enzyme present in monocyte cultures appeared unaffected by the presence of minactivin and could be shown to be regulated independently by dexamethasone.     

p53基因cDNA突变及其蛋白高表达与大肠癌预后关系

１００份大肠癌组织，用ＲＴ－ＰＣＲ－ＳＳＣＰ检测Ｐ５３基因ＣＤＮＡ突变；ＰＡｂ１８０１单抗免疫组化检测Ｐ５３基因蛋白搞表达并对大肠癌术对后病人作５年生存随访，比较上述２结果与大肠癌预后的关系，１００例大肠癌中，ＲＴ－ＰＣＲ－ＳＳＣＰ显示５１例大肠癌Ｐ５３基因ＣＤＮＡ突变，ＰＡｂ１８０１阳性率６２％，Ｐ５３基因ＣＤＮＡ突变和Ｐ５３基因蛋白高表达与Ｄｕｋｅｓ分期无关，Ｐ５３基因ＣＤＮＡ突变与Ｐ５３基因     

Contralateral hip fractures and other osteoporosis-related fractures in hip fracture patients: incidence and risk factors. An observational cohort study of 1,229 patients

Purpose

To report risk factors, 1-year and overall risk for a contralateral hip and other osteoporosis-related fractures in a hip fracture population.

Methods

An observational study on 1,229 consecutive patients of 50?years and older, who sustained a hip fracture between January 2005 and June 2009. Fractures were scored retrospectively for 2005–2008 and prospectively for 2008–2009. Rates of a contralateral hip and other osteoporosis-related fractures were compared between patients with and without a history of a fracture. Previous fractures, gender, age and ASA classification were analysed as possible risk factors.

Results

The absolute risk for a contralateral hip fracture was 13.8?%, for one or more osteoporosis-related fracture(s) 28.6?%. First-, second- and third-year risk for a second hip fracture was 2, 1 and 0?%. Median (IQR) interval between both hip fractures was 18.5 (26.6) months. One-year incidence of other fractures was 6?%. Only age was a risk factor for a contralateral hip fracture, hazard ratio (HR) 1.02 (1.006–1.042, p?=?0.008). Patients with a history of a fracture (33.1?%) did not have a higher incidence of fractures during follow-up (16.7?%) than patients without fractures in their history (14?%). HR for a contralateral hip fracture for the fracture versus the non-fracture group was 1.29 (0.75–2.23, p?=?0.360).

Conclusion

The absolute risk of a contralateral hip fracture after a hip fracture is 13.8?%, the 1-year risk was 2?%, with a short interval between the 2 hip fractures. Age was a risk factor for sustaining a contralateral hip fracture; a fracture in history was not.     

Comparison of outcomes of minimally invasive mitral valve surgery for posterior, anterior and bileaflet prolapse

Objective: We sought to compare the outcomes of minimally invasive mitral valve (MV) surgery for anterior (anterior mitral leaflet, AML), posterior (posterior mitral leaflet, PML) or bileaflet (BL) MV prolapse. Methods: Between August 1999 and December 2007, 1230 patients who presented with isolated AML (n = 156, 12.7%), isolated PML (n = 672, 54.6%) or BL (n = 402, 32.7%) MV prolapse underwent minimally invasive MV surgery. The preoperative mitral regurgitation (MR) grade was 3.3 ± 0.8, left ventricular ejection fraction (LVEF) was 62 ± 12% and mean age was 58.9 ± 13.0 years; 836 patients (68.0%) were male. Mean follow-up time was 2.7 ± 2.1 years, and the follow-up was 100% complete. Results: Overall, the MV repair rate was 94.0% (1156 patients). Seventy-four patients (6.0%) received MV replacement. MV repair for PML prolapse was accomplished in 651 patients (96.9%), for AML in 142 patients (91%) and for BL in 363 patients (90.3%). Repair techniques consisted predominantly of leaflet resection and/or implantation of neochordae, combined with ring annuloplasty. Concomitant procedures were tricuspid valve surgery (n = 56), atrial fibrillation ablation (n = 286) and closure of an atrial septal defect or patent foramen ovale (PFO) (n = 89). The overall duration of cardiopulmonary bypass was 127 ± 40 min and aortic cross-clamp time was 78 ± 33 min. The mean postoperative hospital stay was 11.6 ± 9.7 days for the overall group. Early echocardiographic follow-up revealed excellent valve function in the vast majority of patients, regardless of the repair technique, with a mean MR grade of 0.3 ± 0.5. For the overall group, 5-year survival rate was 87.3% (95% CI: 83.9–90.1) and 5-year freedom from cardiac reoperation rate was 95.6% (95% CI: 94.1–96.7). The log-rank test revealed no significant difference between the three groups regarding long-term survival or freedom from reoperation. Conclusions: Minimally invasive MV repair can be achieved with excellent results. Long-term outcomes and reoperation rates for AML prolapse are not significantly different from PML or BL prolapse.