Accurate localization of mitral regurgitant defects using multiplane transesophageal echocardiography

BACKGROUND: Appropriate patient selection for surgical repair of the mitral valve depends on the specific location and mechanism of regurgitation, which, in turn, has necessitated a more detailed method to accurately describe mitral pathology. This study tests a strategy of using multiplane transesophageal echocardiography to systematically localize mitral regurgitant defects and compares these results with the surgical findings. METHODS: Fifty patients with mitral regurgitation underwent intraoperative transesophageal echocardiography for the evaluation of mitral pathology and potential repair. Mitral regurgitant defects were localized using a systematic strategy and a simple nomenclature that divides each mitral valve into six sections (three sections per leaflet) and each prosthetic sewing ring into six sections (60 radial degrees = one section). RESULTS: Thirty-nine patients with native mitral valves were studied, for a total of 234 sections evaluated. Eighty-seven of these sections contained regurgitant defects by transesophageal echocardiography (mean number of regurgitant defects per valve, 2.2; range, 1 through 6). There was agreement between the transesophageal echocardiographic and surgical localizations in 96% (224/234; p < 0.0001) of the sections. Eleven patients with prosthetic mitral valves were studied, for a total of 66 sections evaluated. Twenty-three of these sections contained paravalvular leaks by transesophageal echocardiography (mean number of leaks per prosthesis, 2.1; range, 1 through 6). There was agreement between the transesophageal echocardiographic and surgical localizations in 88% (58/66; p < 0.001) of the sections. CONCLUSIONS: This transesophageal echocardiographic strategy provides a systematic method to accurately localize mitral regurgitant lesions and has the potential to improve the preoperative assessment of patients with significant mitral regurgitation.     

Body habitus as a predictor of burn risk in children: do fat boys still get burned?

Previous research at this institute has demonstrated that heavy-for-age boys are more burn prone than their normal sized counterparts. As this study is now 26 years old, we reexamined the anthropomorphic indices of 372 children admitted to one burn center between January 1991 and July 1997 to determine if this trend was still evident. Male children were over-represented in the < or =5th and >95th percentiles for both height (p < 0.001, p < 0.05) and weight (p < 0.01, p < 0.001). Female children were over-represented in the < or =5th and > 95th percentiles for height (p < 0.01, p < 0.05). Twenty-eight percent of boys at or below the 5th percentile for weight were burned as a result of known or suspected intentional injury, compared to 5.9% of the entire pediatric burn population. (p < 0.0004). 'Fat boys' continue to be over-represented in the pediatric burn population. Additionally, in the more recent time period, boys at or below the 5th percentile for height or weight and girls= < 5th percentile or >95th percentile for height are also over-represented. The increased frequency of burn injury in small-for-age children may reflect an increased risk of burn injury secondary to neglect or nonaccidental trauma.     

Pharmacodynamic efficacy, clinical safety, and outcomes after prolonged platelet Glycoprotein IIb/IIIa receptor blockade with oral xemilofiban: results of a multicenter, placebo-controlled, randomized trial

BACKGROUND: Parenteral administration of platelet glycoprotein IIb/IIIa (GP IIb/IIIa) receptor blockers can reduce ischemic complications of coronary angioplasty. Orally active GP IIb/IIIa blockers may allow more sustained receptor antagonism with the potential for long-term secondary prevention. The pharmacodynamic efficacy, clinical safety, and outcomes after prolonged receptor blockade with an orally active GP IIb/IIIa antagonist are not known. The Oral Glycoprotein IIb/IIIa Receptor Blockade to Inhibit Thrombosis (ORBIT) Trial is a multicenter, placebo-controlled, randomized trial of xemilofiban, an oral platelet GP IIb/IIIa blocking agent, administered to patients after percutaneous coronary intervention. METHODS AND RESULTS: After successful elective percutaneous coronary intervention, 549 patients were randomized to receive either placebo or xemilofiban in a dose of 15 or 20 mg. Stented patients randomized to placebo also received ticlopidine 250 mg orally BID for 4 weeks. Patients who received abciximab during the coronary intervention and who were randomized to receive xemilofiban were administered a reduced dosage (10 mg TID for 2 weeks) followed by the randomized maintenance dose of 15 or 20 mg BID for 2 more weeks. All patients received 325 mg aspirin PO QD. Ex vivo platelet aggregation in response to 20 micromol/L ADP and 4 microg/mL collagen was measured over time after the initial dose of study drug and at days 14 and 28 of long-term therapy in 230 patients. All patients were followed clinically for 90 days. Xemilofiban inhibited platelet aggregation to both ADP and collagen with peak levels of inhibition that were similar at 14 and 28 days of long-term oral therapy. Plasma levels of xemilofiban correlated with the degree of platelet inhibition. Peak platelet inhibition on day 1 correlated with the subsequent occurrence of insignificant or mild bleeding events. Although this study was not powered to evaluate differences in clinical outcomes, a trend (P=0.04) was observed for reduction of cardiovascular events at 3 months in patients not treated with abciximab who received the highest dose (20 mg) of xemilofiban studied. CONCLUSIONS: Xemilofiban inhibited platelet aggregation and was well tolerated during 28 days of long-term oral therapy. The observed trend in reduction of cardiovascular events in follow-up awaits confirmation in the larger-scale phase III study (EXCITE trial) currently in progress.     

Leigh syndrome: clinical features and biochemical and DNA abnormalities

The morphology and number of cells in the trophectoderm (TE) and inner cell mass (ICM) of buffalo blastocysts derived from in vitro fertilization and cultured in the presence or absence of insulin-like growth factor-I (IGF-I) were analyzed by differential fluorochrome staining technique. The total cell number (TCN), TE number, and ICM cell number were significantly higher in blastocysts developed in vitro in the presence of IGF-I as compared to blastocysts developed without IGF-I (P < 0.01). It was observed that the buffalo blastocyst took 5-9 days postfertilization to develop in vitro. In order to correlate the time required for blastocyst development and the allocation of cells to TE and ICM, blastocysts were designated as fast (developing on or before day 7) or slow (developing after day 7). The TCN, TE, and ICM cells of fast-developing blastocysts cultured in the presence of IGF-I were significantly higher than slow-developing blastocysts (P < 0.01). The blastocysts developed on day 6 had a mean total cell number 118.6 +/- 21.4, which significantly decreased to 85.6 +/- 17.4, 62.0 +/- 14.5, and 17.0 +/- 4.0 on days 7, 8, and 9, respectively (P < 0.05). Normal development of buffalo embryo showed that, on average, embryos reached compact morula stage at the earliest between days 4.5-5.5. Blastocysts developed, at the earliest, between days 5.0-6.0, and it took them, on average, 6.5 days to hatch from the zona pellucida. TCN, TE, and ICM increased three times from morula to blastocyst; however, the proportion of ICM to TCN remained the same, in both embryonic stages. TE approximately doubled in hatched blastocysts, as compared to unhatched blastocysts (P < 0.05). However, ICM cells were decreased. The time required for development of parthenogenetic blastocysts was observed to be greater as compared to in vitro fertilized (IVF) blastocysts. The total cell number of parthenogenetic blastocysts was 100.8 +/- 11.3, including 59.2 +/- 8.4 cells of TE and 42.1 +/- 6.9 cells of ICM.     

Epidemiology of peripheral vascular disease: a predictor of systemic vascular disease

It is estimated that peripheral vascular disease (PVD) affects 30 percent of the adult population, and two-thirds of all cases are asymptomatic. Detecting PVD can be relatively easy and inexpensive, and based either on subjectively supplied historical information (claudication) or upon physical examination findings [ankle-brachial index (ABI)]. The ABI may serve as a marker for increased risk for systemic vascular disease as an abnormally low ABI has been shown to be associated with systemic vascular disease. Epidemiology of and risk factors for PVD are in similar to coronary heart disease. PVD is uncommon until middle age and then increases dramatically. Prevalence of PVD is slightly higher in men than women, yet this tends to diminish with age. Cigarette smoking is probably the most important risk factor for PVD. Hypertension, hypercholesterolemia, and diabetes are also risk factors for the development of symptomatic PVD. Conversely, the presence of a high degree of physical activity and higher levels of HDL-cholesterol as well as a lower body mass index (BMI) are protective. Patients who have vascular disease in one organ system often exhibit evidence of vascular disease elsewhere. Presence of coronary artery disease among patients with symptomatic PVD is between two and four times higher than those without PVD, and PVD is also associated with cerebrovascular disease.     

Reduced expression of tissue inhibitor of metalloproteinase in nodal metastasis of stomach cancer

The abuse of zipeprol, an antitussive agent, was found to be most prevalent among young people in Korea. Because abusers take large doses of this drug for its hallucinogenic effects, fatalities from zipeprol overdose abuse have been on the rise since 1991. Since 1991, a total of 69 zipeprol-related deaths have occurred throughout the nation. A demographic study shows that in ninety six percent of cases involving ziperol alone, the victims were in their teens and twenties. The male/female ratio in zipeprol related death was 3.5:1. Most of these zipeprol-associated deaths occurred in the larger cities of Seoul and Inchon. The blood concentration of zipeprol ranged from 0.8 to 38.3 micrograms/mL in single drug involved deaths, while zipeprol varied from 0.1 to 35.3 micrograms/mL in zipeprol and dextromethorphan victims.     

Circadian changes in PACAP type 1 (PAC1) receptor mRNA in the rat suprachiasmatic and supraoptic nuclei

A receptor for pituitary adenylate cyclase activating polypeptide (PACAP), denoted as PAC1, is expressed in the suprachiasmatic nuclei (SCN). Since the circadian clock demonstrates phase-dependent sensitivity to PACAP, we have used in situ hybridization histochemistry to examine whether PAC1 mRNA is differentially expressed in the rat SCN across the 24-h cycle. There was a significant variation in PAC1 mRNA within the SCN and supraoptic nuclei during the light-dark cycle and in constant darkness, with peaks at the middle of both the real and subjective day and night; no significant variation was observed in the cingulate cortex. The results suggest that the phase-dependent actions of PACAP on the clock may involve phase-specific changes in the availability of PAC1 receptors within the SCN.     

Disseminated intravascular coagulation and status epilepticus

Status epilepticus has been associated with disseminated intravascular coagulation (DIC), but little is known regarding the pathogenesis of this uncommon association. We describe a 41-year-old woman with status epilepticus resulting in death in whom laboratory data demonstrated profound activation of the coagulation and fibrinolytic systems; autopsy findings were consistent with DIC. The occurrence of DIC in status epilepticus may be related to widespread endothelial damage secondary to seizure-induced hyperpyrexia. Body temperature should be closely monitored in patients with prolonged seizures.     

Research on chronic, low-level exposure to formaldehyde: implications for neuropsychological assessment

Findings from empirical research serve as the foundation for neuropsychological assessment of individuals suspected of exposure to formaldehyde. Insofar as conclusions regarding causal relationships between exposure and neuropsychological deficits are based on research methodologies that are reliable, findings can be informative. Unfortunately, existing research is not rooted in sound methodology and findings may mislead rather than enlighten clinicians. Two prominent shortcomings in formaldehyde research are discussed: selection bias in recruitment of research participants and unreliability of participant recall for obtaining data on important background variables and exposure levels. Selected examples illustrate the influence of these shortcomings on research showing a causal relationship between long-term, low-level exposure to formaldehyde and chronic neurobehavioral deficiencies. The implications of these weaknesses for assessment of individual patients are discussed.     

Impact of Sandimmune, Neoral, and Prograf on rejection incidence and renal function in primary liver transplant recipients

Following primary liver transplantation, immunosuppressive efficacy of Neoral and Prograf was similar and superior to that of Sandimmune. Rejection incidence was statistically increased with Sandimmune therapy. Incidence of hypertension, posttransplant diabetes mellitus, and infectious complications was not statistically different. Although early compromise in renal function was associated with Sandimmune, Neoral, and Prograf immunosuppression, no progressive renal dysfunction was identified.