Atrial fibrillation after coronary artery bypass grafting An increase in high-frequency atrial activity in patients with right coronary artery revascularization

The increase in atrial high-frequency activity has been reported as a marker of the risk of paroxysmal atrial fibrillation. The presence of proximal right coronary artery disease is a predictor of atrial fibrillation after bypass surgery, however, the potential mechanism remains controversial. In this study, high-frequency atrial activity to clarify the electrophysiologic background for the predisposition to have proximal right coronary artery disease leading to atrial fibrillation after coronary revascularization was investigated. Before and soon after coronary revascularization, frequency analyses were performed on the 100 ms segment at the end of signal-averaged P waves in 22 patients with right coronary artery disease as opposed to the 23 patients without disease. Under the spectrum curve, area ratio (AR₅₀) and magnitude ratios (MR) were calculated as follows; AR₅₀ = (area 20–50 Hz/0–20 Hz)×100, and MR = (magnitude at 20, 30, 40 and 50 Hz, respectively/maximal magnitude)×100. In patients with proximal right coronary artery disease, high-frequency atrial components increased significantly in the 20 to 50 Hz range after coronary revascularization, and the incidence of postoperative atrial fibrillation was higher than in those without disease. In patients without right coronary artery disease, the frequency distribution of P waves was unchanged. Postoperatively, the two groups showed the same atrial frequency distribution. This data suggests that the increase in high-frequency atrial activity after right coronary artery revascularization might be associated with the pathogenesis of postoperative atrial fibrillation.     

Computerized antibiogram for methicillin-resistantStaphylococcus aureus in chest surgery

Background: An increasing number of cases of postoperative morbidity involving methicillin-resistantStaphylococcus aureus have been reported in thoracic surgery. To prevent its outbreak, cluster analysis using a personal computer was employed.Methods: A total of 120 patients undergoing operations on the lung and mediastinum were included into this study. Materials were isolates of methicillin-resistantStaphylococcus aureus newly recovered from across the hospital. The cluster analysis used antimicrobial susceptibility in 12 drugs, which were categorically valued to produce Euclidean distance to form clusters of similarity.Results: Six of the 120 patients were found to be positive for the microbe before or after thoracotomy. A total of two patients (1.7%) became symptomatic postoperatively, i.e., one of four preoperatively-positive patients and one of two postoperatively-positive cases. The analysis suggested that preoperative patients shared the strains in the same non-surgical ward.Discussion: A computerized antibiogram does not always strictly typeStaphylococcal strains but has advantages in typing with ease and at decreased cost. The current analysis suggested that patient harboring the strains migrated across wards.Conclusion: Computerized antibiograms forStaphylococcal strains may assist to prevent an outbreak of their infection in chest surgery.     

Haemodynamic changes in non-alcoholic (viral) liver cirrhosis studied by computed tomography (CT) arterial portography and CT arteriography

AIMS: To evaluate haemodynamic and vascular changes in non-alcoholic (viral) cirrhosis on conventional computed tomography (CT), CT arteriography (CTA) and CT arterial portography (CTAP), and to determine the cause of the observed reticular stain on angiography. METHODS: Using surgically resected liver specimens from 31 patients with viral hepatitis associated hepatocellular carcinoma, images of conventional CT, CTA, CTAP and the sinusoidal phase of hepatic arteriography were retrospectively analysed and compared with pathology of the non-cancerous portion of the liver. RESULTS: Computed tomography arteriography showed inhomogeneous enhancement (diffuse, low-density nodules) in a total of 16 samples (52%); in eight of 10 (80%) cirrhotic livers, three of six (50%) precirrhotic livers, five of 12 (42%) livers with chronic active hepatitis and none of three with no active liver disease. The frequency of inhomogeneous enhancement became significantly higher with increasing severity of parenchymal damage (P < 0.05). In contrast, conventional CT and CTAP showed homogeneous enhancement in all 31 (100%) patients. There was no correlation between inhomogeneous enhancement on CTA and reticular staining on sinusoidal-phase hepatic angiograms. Inhomogeneous enhancement was frequently seen in patients with hepatitis B surface antigen and/or anti-hepatitis C virus antibody compared with those without them (P < 0.05). CONCLUSION: The CTA was much more sensitive in detecting haemodynamic changes in the cirrhotic liver than CTAP, conventional CT and sinusoidal-phased hepatic angiography. Further study is required to clarify the mechanism of inhomogeneous enhancement on CTA and homogeneous enhancement on CTAP seen in cirrhosis.     

Effect of sports activity on carnitine metabolism. Measurement of free carnitine, gamma-butyrobetaine and acylcarnitines by tandem mass spectrometry.

The effects of sports activity on carnitine metabolism were studied using mass spectrometry. Serum levels of free carnitine, acylcarnitines (acetylcarnitine, propionylcarnitine, C4-, C5- and C8-acylcarnitine) and gamma-butyrobetaine, a carnitine precursor, were determined by tandem mass spectrometry in liquid secondary ion mass ionization mode. The coefficients of variation at three different concentrations were 2.8-7.9% for gamma-butyrobetaine, and 1.2 to approximately 6.7% for free carnitine. The recoveries added to serum were 109.1% for gamma-butyrobetaine, 89.3% for free carnitine. Sports activity caused increased serum levels of gamma-butyrobetaine, acetylcarnitine, C4- and C8-acylcarnitines and decreased serum levels of free carnitine. This method requires a small amount of sample volume (20 microl of serum) and short total instrumental time for the analysis (1 h for preparation, 2 min per sample for mass spectrometric analysis). Therefore, this method can be applied to study carnitine metabolism under various conditions that affect fatty acid oxidation.     

Retrospective analysis of the clinical trends and current indications for perioperative intraaortic balloon pumping in high-risk coronary artery bypass surgery

We clinically evaluated the current indications for perioperative intraaortic balloon pumping (IABP) in high-risk patients undergoing coronary artery bypass grafting (CABG). Over the past 22 years, 196 CABG patients received perioperative IABP at our institution. We divided the 22 years into periods I–IV (earliest to latest) and investigated the annual changes in the indications for and mortality from IABP. In periods I and II, IABP was mainly employed for postoperative low-output syndrome (LOS) or perioperative myocardial infarction (PMI). The hospital mortality rate was 13.2%–18.5%. In period III, the mortality rate was markedly reduced by the use of preoperative scheduled IABP. In period IV, however, scheduled IABP was used less often for high-risk CABG, and IABP was mainly employed in patients having emergency CABG for acute coronary syndrome (ACS). The hospital mortality rate was reduced to 3.7%. In the last 2 years, 19 (65.5%) of 29 patients who received preoperative IABP had emergency CABG for ACS, while 27 high-risk CABG patients with poor left ventricular (LV) function or left main trunk (LMT) disease were treated successfully without scheduled IABP. There were no significant differences between the IABP and non-IABP patients in age, sex, number of bypasses, and aortic cross-clamp time. Because of improvements in anesthesia, operative techniques, perioperative management, and cardioplegic solutions, preoperative support with IABP is less often needed for high-risk CABG, except in patients undergoing emergency surgery for ACS.     

Complement-induced procoagulant alteration of red blood cell membranes with microvesicle formation in paroxysmal nocturnal haemoglobinuria (PNH): implication for thrombogenesis in PNH

Complement-induced procoagulant alteration of red blood cell (RBC) membranes in paroxysmal nocturnal haemoglobinuria (PNH) was examined. Microvesicles, deficient in acetylcholinesterase, were generated and released from PNH RBC upon complement activation. The microvesicles generated from complement-activated PNH RBC accelerated factor Xa-dependent plasma coagulation more than those generated from RBC by the treatment with ionophore A23187. When assessed by factor Xa-catalysed prothrombin activation, complement activation enhanced procoagulant properties of both normal and PNH RBC similarly, although PNH RBC were lysed but normal RBC were not. This enhancement of factor Xa-dependent prothrombinase activity of complement-activated RBC was inhibited by the treatment of the RBC with annexin V, a protein with binding affinity for anionic phospholipids especially for phosphatidylserine (PS). Neither the enhanced procoagulant properties of RBC nor apparent RBC population with annexin V-binding affinity were demonstrated before complement activation in any of the four PNH patients studied. PS-externalized PNH RBC and microvesicles may contribute to the removal of PNH RBC from the circulation. We conclude that although PNH RBC do not constantly exhibit enhanced procoagulant properties in vivo, complement activation induces a procoagulant alteration of RBC membranes with microvesicle formation, potentially contributing to the thrombogenesis in PNH.     

Effect of diesel exhaust on guinea pig nasal mucosa.

In this study using guinea pigs, we investigated the effects of diesel exhaust (DE) containing diesel exhaust particulate (DEP) on 1) vascular permeability induced by histamine, 2) nasal mucosal permeability to horseradish peroxidase (HRP), and 3) eosinophilic epithelial infiltration. The vascular permeability induced by histamine was enhanced significantly and dose-dependently in DE-exposed guinea pigs. The HRP reaction products in epithelial cells and intercellular spaces were significantly and dose-dependently increased in those guinea pigs. Eosinophil infiltration into the epithelial layer was significantly increased in guinea pigs exposed to DE containing 3.2 mg/m3 DEP, and the reactivity of the nasal mucosa to histamine solution applied on the nasal mucosa was significantly enhanced in those guinea pigs. These findings suggest that DE may play an important role not only in promoting nasal hyperreactivity induced by the enhancement of absorption of antigen through the nasal epithelium, but also in inducing eosinophil infiltration in nasal mucosa and enhancing nasal mucosal reactivity.     

Recognition of L-amino acid ester compounds by rat peptide transporters PEPT1 and PEPT2.

Peptide transporters (PEPT1 and PEPT2) in epithelia play an important role in the absorption of small peptides and peptide-like drugs. Recently, it was demonstrated that various nonpeptidic compounds can be transported by these transporters. In the present study, we focused on the L-amino acid ester compounds and examined the mechanisms of their interaction with rat PEPTs (rPEPTs) using stable transfectants. Valacyclovir, the L-valyl ester prodrug of the antiherpetic agent acyclovir, competitively inhibited [(14)C]glycylsarcosine uptake in the rPEPT1- or rPEPT2-expressing cells. Dixon plot analyses showed that the inhibition constant (K(i)) values of valacyclovir were 2.7 and 0.22 mM for rPEPT1 and rPEPT2, respectively, suggesting that rPEPT2 had higher affinity for this agent. Various L-valine alkyl esters significantly inhibited [(14)C]glycylsarcosine uptake. L-Valine methyl ester (Val-OMe) competitively inhibited [(14)C]glycylsarcosine uptake with K(i) values of 3.6 and 0.83 mM for rPEPT1 and rPEPT2, respectively, indicating that Val-OMe is also a high-affinity substrate for rPEPT2. Val-OMe had a trans-stimulation effect on [(14)C]glycylsarcosine efflux from both transfectants, suggesting the translocation of L-valine methyl ester via rPEPTs. Val-OMe showed the most potent inhibitory effect among the several L-amino acid methyl esters examined. We conclude that Val-OMe, as well as valacyclovir, could be recognized and transported by rPEPT1 and rPEPT2 and that these L-valyl esters showed higher affinity for rPEPT2 as do most substrates of these transporters. Our results suggest that L-valine is a desirable L-amino acid for the esterification of poorly permeable drugs to enhance their oral bioavailability targeting intestinal PEPT1.     

An autopsy case of Goodpasture's syndrome with P-ANCA and systemic vasculitis]

A 72-year-old woman was admitted because of anorexia and dyspnea. She was given a diagnosis of pulmonary hemorrhage and renal failure. Despite treatment with high-dose steroid and hemodialysis, the patient died of disseminated intravascular coagulation on the 9th hospital day. Autopsy revealed intra-alveolar hemorrhage, crescentic glomerulonephritis, and systemic vasculitis with fibrinoid necrosis. A direct immunofluorescence study demonstrated linear deposition of IgG along the glomerular basement membrane (GBM). Both anti-GBM antibody and anti-neutrophil cytoplasmic antibody with perinuclear pattern (P-ANCA) were detected in the patient's serum by enzyme immunoassay. Goodpasture's syndrome with P-ANCA was diagnosed. There has been some controversy as to whether vasculitis occurs in patients with Goodpasture's syndrome. This was a rare example of well-documented Goodpasture's syndrome with P-ANCA and systemic vasculitis, the exact etiologic relationships among which remain to be clarified.     

The Long–Evans Cinnamon rat: An animal model for Wilson's disease

The Long-Evans Cinnamon (LEC) rat is known to develop hepatitis and liver cancer spontaneously, phenomena attributed to abnormal copper metabolism. This mutant strain of rat shows some clinical features that are similar to those of Wilson's disease, including excessive copper in the liver, reduced excretion of copper into bile, a reduced level of serum copper and a remarkable decrease in serum ceruloplasmin activity. Molecular studies have revealed that the copper transporting P-type ATPase, atp7b, which is the rat gene homologous to human ATP7B, was found to be defective in the LEC rat. These observations have confirmed that the LEC rat is a rodent model for Wilson's disease. In addition, recent studies have suggested that the ATP7B protein is involved in the intracellular transport of hepatic copper. The absence or diminution of ATP7B function results in abnormal copper metabolism in the LEC rat and in patients with Wilson's disease.