The impact of mitral valve morphology on the long-term outcome of mitral balloon valvuloplasty.

BACKGROUND: The effect of mitral valve morphology (MVM) on the long-term results of mitral balloon valvuloplasty (MBV) is not well established. The aim of the study was to evaluate the impact of MVM on long-term outcome of MBV. METHODS: Five hundred and eighteen consecutive patients (mean age, 31+/-11 years) who underwent successful MBV were followed up for 0.5-16.5 (mean, 6+/-4.5) years. Patients were divided into two groups according to their mitral echo score (MES) before MBV: group A (n=340; MES8). RESULTS: We report the immediate and long-term clinical and echocardiographic results of the above-mentioned 518 consecutive patients. The mitral valve area was significantly larger in group A than in group B, both immediately after MBV (2.0+/-0.3 vs. 1.82+/-0.3 cm2, respectively; P<0.0001) and also at the last follow-up (1.8+/-0.33 vs. 1.5+/-0.33 cm2, respectively; P<0.0001). Restenosis occurred in 38/340 (11%) in group A vs. 73/178 (41%) in group B (P<0.0001). Actuarial freedom from restenosis at 5, 10, 15 years were 92+/-2%, 85+/-3%, 65+/-6% for group A vs. 72+/-4%, 44+/-5%, 9+/-6% for group B (P<0.001). Event-free survival rates at 5, 10, 15 years for group A were 93+/-1%, 88+/-2%, 66+/-6% vs. 82+/-3%, 59+/-6%, 8+/-7% for group B (P<0.0001). Stepwise Cox multivariate regression analysis identified MES, preprocedure functional class, and postprocedure mitral valve area相似文献   

Hereditary deficiencies of antithrombin III, protein S, and the protein C pathway in Jordanian thrombosis patients.

Hereditary thrombophilia is caused by various inherited disorders. Most lead to a familial tendency to recurrent venous, not arterial, thrombosis, usually at a young age, and with spontaneous onset. Most of the genetic defects known today affect the function of natural anticoagulant pathways, in particular, the protein C system. In this study, 602 (265 female, 337 male) patients with suspected thrombosis, arterial or venous, were referred to King Hussein Medical Center in Amman, Jordan. The prevalence of hereditary deficiencies of antithrombin (AT), protein S (PS), and protein C (PC) were studied over a seven-year period (1993-2000). Activated protein C (APC-R) resistance subjects were studied over four years (1996-2000). The mean age was 30 years in females and 42 years in males. A diagnosis was established in 22.4% (n = 135) of the subjects (20.3% venous, 2.1% arterial). Protein C deficiency was found in 3.8%, protein S deficiency in 2.3% and antithrombin deficiency in 1.4% of our sample group. An APC-R problem was seen in 23.0% (n = 89) of the surveyed population. Out of the APC-R patients, 75.0% had the DNA analysis of a factor V Leiden mutation present. Of the subjects found to have the mutation 87.0% were heterozygous and 13.0% were homozygous. These results confirm that APC-R, as a result of factor V Leiden mutation, is the most prevalent cause of thrombosis, and thrombophilia is related to venous, not arterial, thrombosis.     

Dominant A1: angiographic and clinical correlations with anterior communicating artery aneurysms.

It has been observed but never proven that anomalies of the anterior communicating artery complex are associated with anterior communicating artery aneurysms (ACAA). Therefore, in an effort to understand the significance of haemodynamic factors in the genesis, as well as the clinical course of ACAA, we evaluated the correlation between certain angiographic patterns of flow in the anterior circulation and the clinical findings of 51 patients with ACAA compared with 50 matched controls. Four significant associations which have never been validated were identified: 1) a dominant A1 (filling both A2's) was found in 57% of ACAA patients versus 14% of controls (p less than 0.001). 2) Unilateral hypoplasia of the opposite A1 was present in 24% of ACAA patients versus 6% of controls (p = 0.01). 3) Exclusive filling of the ACAA from one A1 occurred in 78%. 4) No statistically significant relationship was found between the anatomic flow patterns studied and the patients clinical presentation including age, sex, or grade. We conclude that anterior communicating artery aneurysms are significantly related in a majority of patients with the presence of a dominant A1, probably as the result of enhanced haemodynamic stress caused by this anatomic abnormality in the circulation. However, this association is not constant, and a dominant pattern of flow did not correlate with the clinical course. This is probably a reflection of the differences between factors initiating aneurysm formation and those influencing its growth, as well as of the relative limitations of angiography when pathophysiological extrapolations are attempted.     

In Vivo Effects of TRH, T3 and cGH on Antibody Production and T- and B-Lymphocytes Proliferation in Immature Male Chickens

Newly hatched White Leghorn male chicks were used in this study. Different doses of T₃ (O.1 or 1 ppm) or TRH (1 or 5 ppm) were administered in the feed for an 8-week period. Chicken growth hormone (cGH) (10 μg/kg BW) was injected (i.v.) into a different group of chicks twice daily for 1 week starting at 7 weeks of age. A different group received both T₃ (0.1 and 1 ppm) and cGH. Serum concentrations of T₄, T₃ and GH, antibody production against sheep red blood cells (SRBC) and Brucella Abortus (BA), and in vitro proliferative response of both T- and B-lymphocytes to mitogenic stimulation were measured. Supplementation of T₃ (1 ppm) significantly lowered T₄ and increased T₃ concentrations. No effect of any hormone treatment on antibody production was observed. T₃ supplementation and cGH injection alone or with T₃ (0.1 ppm) significantly increased blastogenic response of lymphocytes to either Con-A or LPS mitogenic stimulation. It was concluded that T₃ and GH are involved in lymphocyte activity of chickens.     

Plasma beta-endorphin level in cases of luteal phase defect

OBJECTIVE: To evaluate beta-endorphin secretion in euprolactinemic cases of luteal phase defect (LPD). DESIGN: Serial blood samples from the 18th to the 26th day of the menstrual cycle were assayed for beta-endorphin, progesterone (P), estradiol (E2), and prolactin (PRL) in cases of LPD and controls. Diagnosis of LPD was based on determinations of serum P and premenstrual endometrial biopsy. SETTING: From Cairo University Hospitals. PATIENT, PARTICIPANTS: Twenty-six women with LPD and 8 normal fertile women (controls) were chosen. INTERVENTIONS: None. MAIN OUTCOME MEASURES: beta-Endorphin, P, E2, and PRL concentrations were determined by the corresponding 125I radioimmunoassay. RESULTS: Plasma beta-endorphin level in cases of LPD varied from 2.58 to 9.14 pmol/L, whereas the level of controls varied from 2.41 to 5.57 pmol/L. The mean value of plasma beta-endorphin in cases of LPD was significantly higher than that of controls by 146% (P less than 0.0005). In spite of the significant decrease of serum P in cases of LPD, serum E2 level did not differ significantly from that of controls. CONCLUSION: The possible sources of beta-endorphin rise and its implication in the etiology of LPD are explained.     

Brain tissue oxygenation in patients with cerebral occlusive disease and arteriovenous malformations

It is not clear if ventilation with oxygen increases brain tissue oxygen pressure (PO2) during ischaemia. We have measured brain tissue PO2, carbon dioxide pressure (PCO2) and pH during baseline anaesthesia and oxygen ventilation in non-ischaemic control patients (n = 9), patients with cerebral occlusive disease (n = 11) and patients with arteriovenous malformations (AVM, n = 12). The same anaesthetic treatment was given to all groups and anaesthesia was constant during the study. Arterial pressure, brain temperature and arterial blood-gas tensions were similar between groups. Under baseline conditions, brain tissue PO2 was mean 4.2 (SD 1.4) kPa in the controls and was 70% lower in patients with ischaemia and AVM. Patients with occlusive disease also had elevated tissue PCO2 and acidosis. During oxygen ventilation, PO2 increased to 7.5 (2.9) kPa in controls and this was 50% greater than the increase in the ischaemia and AVM patients. The results showed that baseline tissue oxygenation and increases in PO2 during hyperoxia were attenuated in patients with ischaemia or AVM.      

Heat-shock protein synthesis by human polymorphonuclear cells

Mature human neutrophils from peripheral blood are known to be capable of limited protein biosynthetic activity. We now show that these cells are inducible for heat-shock protein synthesis when placed in short-term culture. Synthesis of hsp70 and hsp85 as well as the response to various temperatures and the time course of induction were typical for mammalian cell systems. This heat-shock response was blocked by actinomycin D added before heat exposure. This demonstration that hsp genes can be activated by heat exposure of terminally differentiated neutrophils supports the hypothesis that gene activation can serve a physiological role in these cells and opens up the possibility that synthesis of other gene products is similarly inducible.     

Acute eosinophilic pneumonia with respiratory failure: a new syndrome?

Acute, noninfectious, eosinophilic pneumonia with respiratory failure has been described in adults. This new form of eosinophilic lung disease differs from the previously described types of eosinophilic pneumonia. Patients with this entity develop rapid progressive respiratory failure, which seems to respond to corticosteroid therapy. Eosinophilia in lung biopsy specimen, or in bronchoalveolar lavage fluid seems to be a common denominator. We present the first pediatric case of this new, distinct form of eosinophilic lung disease and review the pertinent literature.