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Biomedical subjects

J Kobayashi

Publications and source records attributed to J Kobayashi.

At least 235 records · Page 13Linked to original sources
PubMed1997

Plasma collagen-binding vitronectin activated by heparin and dextran sulfate in chronic liver disease.

Plasma collagen-binding vitronectin was assayed in 62 patients with chronic liver disease and 14 healthy control subjects. It was measured by an enzyme immunoassay using type I collagen and monoclonal antibody to vitronectin before and after treatment with heparin or dextran sulfate in vitro. The pretreatment level of plasma collagen-binding vitronectin (mean +/- S.E.M.) was 5.5 +/- 0.5 micrograms/ml in the controls, 8.2 +/- 0.3 micrograms/ml in chronic persistent hepatitis, 8.3 +/- 0.7 micrograms/ml in chronic active hepatitis, 7.9 +/- 0.7 micrograms/ml in liver cirrhosis, and 8.2 +/- 0.5 micrograms/ml in hepatocellular carcinoma with cirrhosis. After treatment with heparin, the percent collagen-binding vitronectin to total vitronectin was 20.6 +/- 2.0% in the controls, 24.7 +/- 4.1% in chronic persistent hepatitis, 28.6 +/- 2.5% in chronic active hepatitis, 42.6 +/- 4.5% in liver cirrhosis, and 31.8 +/- 2.3% in hepatocellular carcinoma. All percents were significantly increased compared to the pretreatment percent. The same pattern was also found after dextran sulfate treatment. Compared to that in the pretreatment state, the collagen-binding vitronectin after these treatments was more closely correlated with the serum levels of 7S collagen and hyaluronic acid. These results suggest that the collagen-binding activity of vitronectin may play an important role in the progression of liver disease and/or fibrosis through its activation with some glycosaminoglycans.

Adult↗
PubMed1997

Long-term results of artificial chordae implantation in patients with mitral valve prolapse.

BACKGROUND AND AIMS OF THE STUDY: In terms of valve-related complication and ventricular function, mitral valve repair (MVR) is superior to valve replacement. To date, chordae shortening and transposition have been used for diffuse prolapses. We have used artificial chordae implantation for MVR since 1986, and here review our long-term results. METHODS: Pericardial strips were used in nine patients, and e-PTFE (Gore-Tex) sutures in 58. A degenerative lesion was present in 69% of cases, endocarditis in 16% and rheumatic valvulitis in 7%. Implantation of artificial chordae was indicated for treatment of diffuse prolapse. Annuloplasty was performed in patients with or without prosthetic ring. RESULTS: Actuarial survival rate was 78% for the pericardial chordae group at nine years, and 94% for the Gore-Tex chordae group at eight years. Thromboembolic events occurred in two pericardial chordae patients, and three Gore-Tex chordae patients required reoperation. Freedom from reoperation was 100% for pericardial chordae after nine years and 96% for Gore-Tex chordae after eight years. Quality of life among survivors is good: 83% are in NYHA class I, 89% are free from anticoagulation, and 60% require no medication. Mitral valve orifice area, estimated echocardiographically, was similar in both groups at discharge and at follow up. CONCLUSIONS: MVR with artificial chordae provided satisfactory valve function for up to nine years. Gore-Tex chordae are less prone to deterioration than pericardial chordae. Follow up observations support the use e-PTFE chordae to correct diffuse leaflet prolapse.

Chordae Tendineae↗
PubMed1997

Collection of anopheline mosquitos in three villages endemic for malaria in Khammouane, Lao PDR.

Anopheline mosquito collections were made during the months of May and June (dry season) and August (rainy season), 1996 at villages, Nakham, Namdik and Hinboon Neua in Khammouane Province. Larval collections were also made in 3 slow running streams around Nakham villages in May 1996. Altogether, 3,549 adult females consisting 19 Anopheles species were collected by 3 nights of human and 6 animal bait traps and 3 resting collections. Among them, Anopheles vagus (19.75%), An. philippinensis (15.02%), An. nivipes (11.55%), An. pallidus (11.27%), An. peditaeniatus (8.34%), An. kochi (8.00%) and An. barbirostris (7.27%) were predominant species. The immatures of An. barbirostris, An. minimus, An. maculatus sensu lato, and An. culicifacies were found in the streams of Nakham. It is noteworthy that An. minimus, An. dirus and An. maculatus sensu lato, which are well known malaria vectors in Thailand, were recorded for the first time in this area.

Animals↗
PubMed1996

Tetrodotoxin-resistant Na+ spikes of C fibers have at least two subtypes in the isolated bullfrog sciatic nerve.

The C fiber compound action potentials (C-CAPs) were studied for their properties with the vaseline gap method from the isolated bullfrog sciatic nerve. Two components (the fast and the slow C-CAPs) were found to be Na+ dependent and tetrodotoxin-resistant. The conduction velocities of the fast and the slow C-CAPs were 0.61 +/- 0.06 m/s (n = 13) and 0.42 +/- 0.05 m/s (n = 8), respectively; their time constants were 11.4 +/- 1.7 m/s and 16.3 +/- 1/7 ms, respectively, with both parameters being significantly different at P < 0.01. The slow C-CAP had about 1.3 times higher threshold than that of the fast C-CAP, with a significant difference (P < 0.01). They showed differential sensitivity to lidocaine and Cd2+. Capsaicin reduced the amplitudes of both fast and slow C-CAPs, but not abolished. These findings indicate that C fibers have at least two subtypes with different properties.

Action Potentials↗
PubMed1996

Analysis of protein structure-function in vivo. Adenovirus-mediated transfer of lipase lid mutants in hepatic lipase-deficient mice.

Hepatic lipase (HL) and lipoprotein lipase (LPL) are key enzymes involved in the hydrolysis of triglycerides and phospholipids present in circulating plasma lipoproteins. Despite their similarities, the role that each of these two lipases play in the metabolism of triglyceride-rich lipoproteins and high density lipoproteins is distinct. In order to identify structural domains that may confer the different substrate specificities between HL and LPL, we have utilized a novel approach for performing structure-function analysis of a protein, in vivo, by using recombinant adenovirus vectors to express native and mutant enzymes in an animal model for a human genetic deficiency. HL-deficient mice (n = 19) characterized by increased plasma cholesterol and phospholipid concentrations were injected with adenovirus expressing luciferase (rLucif-AdV), native hepatic (rHL-AdV), and lipoprotein lipase (rLPL-AdV) or lipase mutants in which the lid covering the catalytic site of either enzyme was exchanged (rHL+LPL lid-AdV and rLPL+HL lid-AdV). Mice injected with rLucif-AdV had no changes in post-heparin HL and LPL activities (217 +/- 29 and 7 +/- 2 nmol/min/ml, respectively) as well as plasma lipids. Despite expression of similar levels of post-heparin plasma lipase activity on day 5 post-adenovirus infusion (9806 +/- 915 and 9677 +/- 2033 nmol/min/ml, respectively) mice injected with rHL-AdV or rHL+LPL lid-AdV demonstrated marked differences in the reduction of plasma phospholipids (70% and 32%, respectively, p < 0.005). Similarly, despite post-heparin plasma lipolytic activities of 4495 +/- 534 and 4844 +/- 1336 nmol/min/ml, injection of rLPL-AdV or rLPL+HL lid-AdV resulted in phospholipid reductions of 31% and 81% (p < 0.005). Exchange of the lipase lid did not significantly alter plasma triglyceride concentrations. Thus, preferential in vivo hydrolysis of phospholipids was demonstrated in animals expressing lipases containing the HL lid but not the LPL lid. These studies identify the lipase lid as a major structural motif responsible for conferring the different in vivo phospholipase activities between HL and LPL, a function which may modulate the distinct physiological roles of these two similar lipolytic enzymes in lipoprotein metabolism. The use of recombinant adenovirus to express mutant proteins in animal models for human genetic deficiencies represents a powerful, new approach for performing structure-function analysis of proteins in vivo.

Adenoviridae↗
PubMed1996

Collagen-binding activity of plasma vitronectin in chronic liver disease.

The collagen-binding activity of plasma vitronectin was measured in 15 control subjects and 64 subjects with chronic liver disease. The assay of collagen-binding vitronectin was performed by an enzyme immunoassay using a monoclonal antibody to human vitronectin and type I collagen from human placenta. The plasma collagen-binding vitronectin concentration (mean +/- S.D.) was 5.6 +/- 1.9 micrograms/ml in the controls, 8.3 +/- 1.1 micrograms/ml in chronic persistent hepatitis, 8.3 +/- 2.9 micrograms/ml in chronic active hepatitis, 7.8 +/- 2.9 micrograms/ml in liver cirrhosis and 8.2 +/- 2.1 micrograms/ml in hepatocellular carcinoma with cirrhosis. The percent collagen-binding vitronectin to total plasma vitronectin was 2.2 +/- 0.8% in the controls, 3.9 +/- 2.2% in chronic persistent hepatitis, 3.9 +/- 1.2% in chronic active hepatitis, 5.8 +/- 3.3% in liver cirrhosis and 4.1 +/- 1.2% in hepatocellular carcinoma with cirrhosis. The plasma collagen-binding vitronectin also correlated with the serum levels of 7S collagen and hyaluronic acid. These findings suggest that vitronectin may play an important role in the progression of liver disease and/or in hepatic fibrosis through its collagen-binding domain.

Aged↗
PubMed1996

DNA replication-related elements cooperate to enhance promoter activity of the drosophila DNA polymerase alpha 73-kDa subunit gene.

An analysis was carried out on the promoter region of the Drosophila DNA polymerase alpha 73-kDa subunit gene and the factor(s) activating the promoter. Transcription initiation sites were newly identified in the region downstream of the previously determined sites. Full promoter activity resided within the region from -285 to +129 base pairs with respect to the newly determined major site. Within this region, we found three sequences identical or similar to the DNA replication-related element (DRE), 5'-TATCGATA, which is known as a common promoter-activating element for the Drosophila DNA polymerase alpha 180-kDa subunit gene and the proliferating cell nuclear antigen gene. These sites were located at positions -77 to -70 (DREalpha-I), -44 to -37 (DREalpha-II), and +3 to +10 (DREalpha-III). Footprinting analysis using the recombinant DRE-binding factor (DREF) or Kc cell nuclear extract demonstrated that DREF can bind to all three DRE-related sites. Introduction of mutation in even one of the three DRE-related sequences caused extensive reductions of the promoter activity and also the DREF-binding activity of the promoter-containing fragment. The results indicate that the three DREF-binding sites cooperate to enhance promoter activity of the DNA polymerase alpha 73-kDa subunit gene.

Animals↗
PubMed1996

FISH detection of chromosome 15 deletions in Prader-Willi and Angelman syndromes.

We have evaluated fluorescence in situ hybridization (FISH) analysis for the clinical laboratory detection of the 15q11-q13 deletion seen in Prader-Willi syndrome (PWS) and Angelman syndrome (AS) using probes for loci D15S11, SNRPN, D15S10, and GABRB3. In a series of 118 samples from patients referred for PWS or AS, 29 had deletions by FISH analysis. These included two brothers with a paternally transmitted deletion detectable with the probe for SNRPN only. G-banding analysis was less sensitive for deletion detection but useful in demonstrating other cytogenetic alterations in four cases. Methylation and CA-repeat analyses of 15q11-q13 were used to validate the FISH results. Clinical findings of patients with deletions were variable, ranging from newborns with hypotonia as the only presenting feature to children who were classically affected. We conclude that FISH analysis is a rapid and reliable method for detection of deletions within 15q11-q13 and whenever a deletion is found, FISH analysis of parental chromosomes should also be considered.

Angelman Syndrome↗
PubMed1996

Hepatic lipase gene therapy in hepatic lipase-deficient mice. Adenovirus-mediated replacement of a lipolytic enzyme to the vascular endothelium.

Hepatic lipase (HL) is an endothelial-bound lipolytic enzyme which functions as a phospholipase as well as a triacylglycerol hydrolase and is necessary for the metabolism of IDL and HDL. To evaluate the feasibility of replacing an enzyme whose in vivo physiologic function depends on its localization on the vascular endothelium, we have infused recombinant replication-deficient adenovirus vectors expressing either human HL (HL-rAdV; n = 7) or luciferase cDNA (Lucif-rAdV; n = 4) into HL-deficient mice with pretreatment plasma cholesterol, phospholipid, and HDL cholesterol values of 176 +/- 9, 314 +/- 12, and 129 +/- 9, respectively. After infusion of HL-rAdV, HL could be detected in the postheparin plasma of HL-deficient mice by immunoblotting and postheparin plasma HL activities were 25,700 +/- 4,810 and 1,510 +/- 688 nmol/min/ml on days 5 and 15, respectively. Unlike the mouse HL, 97% of the newly synthesized human HL was heparin releasable, indicating that the human enzyme was virtually totally bound to the mouse vascular endothelium. Infusion of HL-rAdV in HL-deficient mice was associated with a 50-80% decrease in total cholesterol, triglyceride, phospholipids, cholesteryl ester, and HDL cholesterol (P < 0.001) as well as normalization of the plasma fast protein liquid chromatography lipoprotein profile by day 8. These studies demonstrate successful expression and delivery of a lipolytic enzyme to the vascular endothelium for ultimate correction of the HL gene defect in HL-deficient mice and indicate that recombinant adenovirus vectors may be useful in the replacement of endothelial-bound lipolytic enzymes in human lipolytic deficiency states.

Adenoviridae↗
PubMed1996

Immunohistochemical demonstration of prostaglandins in various tissues of the rat.

To demonstrate the tissue localization of prostaglandin (PG) E2, PGF2 alpha and 6-keto-PGF1 alpha (a stable metabolite of PGI2) various tissues, including decalcified periodontal tissue of 7-week-old male Wistar strain rats, were immunohistochemically examined using a streptavidin-biotin complex method. Besides tissue macrophages and endothelial cells in various tissues, hepatocytes, renal tubular cells, and parietal and chief cells in the gastric mucosa showed a positive reaction for the various PGs examined. PGs were demonstrated in the cytoplasm or in association with the cell membrane. We generally observed no difference between the localization patterns of PGE2-, PGF2 alpha-, and 6-keto-PGF1 alpha-positive cells in these tissues. However, in the periodontal ligament and alveolar bone, 6-keto-PGF1 alpha was localized in the cytoplasm of osteocytes, osteoblasts, cementocytes, and cementoblasts, while no reaction for PGE2 or PGF2 alpha was revealed in these cells. We demonstrated the immunohistochemical localization of PGs in various rat tissues including decalcified periodontal tissue and discuss the important roles of PGs in the modulation of their normal functions in these tissues.

Animals↗
PubMed1996

Maze procedure and anomalous coronary artery repair.

A 60-year-old woman has anomalous origin of the left coronary artery from the pulmonary artery, mitral regurgitation with left ventricular dysfunction, and atrial fibrillation. We performed mitral valve annuloplasty, maze procedure, and intrapulmonary tunnel repair of anomalous origin of the left coronary artery. The patient regained normal sinus rhythm and showed improved left ventricular function and no mitral regurgitation.

Cardiac Surgical Procedures↗
PubMed1996

Pentoxifylline in flush solution improves early lung allograft function.

BACKGROUND: Postischemic ischemia reperfusion injury is a frequent and unpredictable problem in clinical lung transplantation. Pentoxifylline (PTX) has a number of effects that could decrease reperfusion injury: reduced neutrophil adhesion to endothelium, decreased production of tumor necrosis factor, decreased platelet aggregation, and increased production of vasodilatory prostaglandins by vascular endothelium. We have demonstrated previously that PTX administered before storage and again during reperfusion reduced lung reperfusion injury. The purpose of the present study was to determine whether these observations were storage or reperfusion effects. METHODS: Fourteen canine left lung allotransplantations were performed. Donor lungs were flushed with modified Euro-Collins solution and stored for 24 hours at 1 degree C. Immediately after transplantation, the contralateral right main pulmonary artery and bronchus were ligated to assess isolated allograft function. Hemodynamic indices and arterial blood gas analysis (inspired oxygen fraction 1.0) were assessed for 6 hours before sacrifice. Allograft myeloperoxidase activity was assessed. Bronchoalveolar lavage fluid was obtained from the allograft middle lobe for neutrophil counts. The animals were divided into three groups based on the timing of PTX administration. Group 1 (n = 5) animals received no PTX. Group 2 (n = 4) animals received PTX (20 mg/kg) just before reperfusion as well as continuous infusion (0.1 mg x kg-1 x min-1) during the assessment period. In group 3 (n = 5), donor lungs received PTX (200mg/L) in the flush solution only. RESULTS: Superior gas exchange was noted in the lungs receiving PTX only in the flush solution (group 3). Myeloperoxidase activity in group-3 allografts was significantly reduced. In addition, protein levels and neutrophil counts in the bronchoalveolar lavage fluid were significantly reduced in group-3 allografts. CONCLUSIONS: Pentoxifylline ameliorates lung allograft reperfusion injury when administered in the flush solution. Our data suggest that PTX will prevent graft endothelial dysfunction during 24-hour cold ischemic storage and consequently will prevent neutrophil activation and migration into lung tissue.

Analysis of Variance↗
PubMed1996

Induction of anti-malarial transmission blocking immunity with a recombinant ookinete surface antigen of Plasmodium berghei produced in silkworm larvae using the baculovirus expression vector system.

We have studied Pbs21, a major ookinete surface protein of Plasmodium berghei, for the development of a model transmission blocking immunogen. In the mouse, recombinant Pbs21 expressed in the Escherichia coli expression system (EcrPbs21) is not as effective in inducing transmission blocking antibodies as native Pbs21 (nPbs21), possibly because of differences in post-translational processing between EcrPbs21 and nPbs21. In an attempt to improve the efficacy of the recombinant molecule, we describe here the use of a baculovirus expression vector system in the silkworm Bombyx mori. Following an injection of recombinant baculovirus containing Pbs21 cDNA, B. mori larvae produced recombinant Pbs21 (BmrPbs21) with a molecular weight indistinguishable from nPbs21. Fifty micrograms of BmrPbs21 could be purified from the hemolymph of each infected larva using affinity chromatography. Immunization of Balb/c mice with BmrPbs21 induced high anti-BmrPbs21 and anti--ookinete antibodies but low anti-EcrPbs21 antibody. In contrast, EcrPbs21 induced high anti--EcrPbs21 antibody but low anti-BmrPbs21 and anti-ookinete antibodies. This suggests that most B-cell epitopes on nPbs21 are conformational and that many of the linear epitopes in EcrPbs21 are not normally exposed in nPbs21. Oocyst formation in Anopheles stephensi mosquitoes, which fed on mice immunized with purified BmrPbs21 and infected with P. berghei, was blocked by 85.5-97.1%. These results suggest that the baculovirus-silkworm system produces useful quantities of recombinant Pbs21 which in limited studies is structurally and immunogenically indistinguishable from the native molecule.

Animals↗
PubMed1996

Rationale of the Cox maze procedure for atrial fibrillation during redo mitral valve operations.

OBJECTIVE: The frequency of reoperation for mitral valve diseases with chronic atrial fibrillation has increased steadily. This study examined the rationale for using the Cox maze operation for atrial fibrillation during redo mitral valve operations. METHODS: Between June 1992 and July 1995, we performed the maze procedure in 42 patients as a concomitant operation with redo mitral valve surgery (maze group). Associated procedures were tricuspid valve surgery in 27 patients and aortic valve surgery in 15 patients. The mean age at operation was 57.3 +/- 9.7 years, and the mean interval from the previous operation was 14.3 +/- 10.5 years. The mean follow-up period after the maze procedure was 25.5 +/- 10.8 months. Atrial fibrillation was present at the time of the previous operation in 29 patients (69%). RESULTS: Neither hospital death nor late death occurred. Sinus rhythm was regained in 28 patients (67%), and an atrial A-wave was detected in 21 patients (50%) by pulsed Doppler study. Patients in whom sinus rhythm was restored had a shorter history of atrial fibrillation (9.0 +/- 6.0 years vs 15.9 +/- 4.6 years, p = 0.0009), a larger f-wave on lead V1 of the electrocardiogram (0.18 +/- 0.10 mV vs 0.10 +/- 0.08 mV, p = 0.017), and a smaller cardiothoracic ratio (63% +/- 8% vs 67% +/- 5%, p = 0.049) than patients with persistent atrial fibrillation. During the same period, 54 patients underwent mitral valve reoperation without the maze procedure (control group). The aortic crossclamp and cardiopulmonary bypass times were slightly longer (p = 0.048 and p = 0.012) in the maze group (133 +/- 28 minutes and 221 +/- 43 minutes) than in the control group (126 +/- 65 minutes and 197 +/- 78 minutes). There was no significant difference in the amount of chest tube drainage or transfusion between the two groups (890 +/- 510 ml and 2120 +/- 1600 ml, respectively, in the maze group and 840 +/- 480 ml and 2140 +/- 1760 ml, respectively, in the control group). It was not necessary to reopen the chest for bleeding significantly more often in one group than in the other (14% in the maze group and 7% in the control group), and it was possible to operate without transfusion with the same frequency in the two groups (17% in the maze group and 20% in the control group). CONCLUSION: These results suggest that the maze procedure should be considered in selected patients who have a high possibility of regaining sinus rhythm during redo mitral valve operations.

Adult↗
PubMed1996

Immunohistochemical demonstration of prostaglandins E2, F2 alpha, and 6-keto-prostaglandin F1 alpha in rat dental pulp with experimentally induced inflammation.

Using formalin-fixed and EDTA-decalcified cryostat sections, the immunohistochemical localization of prostaglandin (PG) E2, PGF2 alpha, and 6-keto-PGF1 alpha (a stable metabolite of PGI2) was examined in normal rat and inflamed dental pulp. Inflammation was induced by opening the pulp chamber. There was no immunoreactivity for prostaglandins in normal dental pulp, whereas positivities for PGE2, PGF2 alpha, and 6-keto-PGF1 alpha were demonstrated in the cytoplasm of macrophages and endothelial cells in the inflamed dental pulp. In addition to these cells, numerous pulp cells and odontoblasts existing in the inflamed pulp and its apical noninflamed area also were intensely stained for PGF2 alpha. Such an area with positive cells gradually extended in an apical direction with the progression of inflammation. These findings suggested that PG production from these host cells is involved in development of inflammation of rat dental pulp.

6-Ketoprostaglandin F1 alpha↗
PubMed1996

Immunohistochemical detection of prostaglandins E2, F2 alpha, and 6-keto-prostaglandin F1 alpha in experimentally induced periapical inflammatory lesions in rats.

The immunohistochemical localization of prostaglandin (PG) E2, PGF2 alpha, and 6-keto-PGF1 alpha (a stable metabolite of PGI2) was demonstrated in rat periapical inflammatory lesions induced by opening the pulp chamber. Two wk postoperatively, suppurative periapical lesions were formed, and active bone resorption was seen surrounding these lesions. Immunohistochemical examination showed that macrophages infiltrating in inflammatory tissue were positively stained for the examined PGs. In some lesions, wherein acute inflammatory changes subsided and proliferation of fibroblasts started, the fibroblasts were positively stained for 6-keto-PGF1 alpha. Osteocytes and osteoblasts were also positive for 6-keto-PGF1 alpha not only in experimental animals, but also in untreated animals. However the staining intensity of the PG in these cells was higher in periapical lesions than in normal condition. These findings suggested that the cellular sources of the PGs in the periapical lesions are mainly macrophages and fibroblasts, and that the PGs produced by these cells, and possibly osteoblast and osteocytes, may contribute to the osteolytic resorption of periapical lesions.

6-Ketoprostaglandin F1 alpha↗
PubMed1996

Surgical stratification of patients with atrial fibrillation secondary to organic cardiac lesions.

BACKGROUND: While the maze procedure does not always eliminate atrial fibrillation (AF) secondary to organic cardiac lesions, concomitant performance of the procedure is associated with increased surgical complexity and potential risks. METHODS: To stratify the surgical approach for patients with AF secondary to underlying cardiac lesions, we analyzed 24 preoperative and perioperative variables in 115 consecutive patients with AF undergoing a modified maze procedure combined with valvular intervention (101), repair of congenital anomalies (13) and coronary revascularization (1). RESULTS: Patients who remained in AF (18) compared to patients with restored atrial rhythm (97), had a higher incidence of giant left atrium (56% vs 10%, P < 0.0001), larger cardiothoracic ratio (70 +/- 13 vs 62 +/- 8%, P = 0.001) and left atrial dimension (64 +/- 12 vs 55 +/- 12 mm, P = 0.004), a longer history of AF (13.7 +/- 6.8 vs 8.3 +/- 6.9 years, P = 0.003) and lower f-wave voltage (0.10 vs 0.15 mV, P = 0.004). Multivariate logistic regression analysis of 24 preoperative and perioperative variables identified the presence of giant left atrium, cardiothoracic ratio and age at operation as the significant risk factors predisposing patients to persistent postoperative AF. Retrospective estimation identified 73 (63.5%) patients with a high probability of atrial defibrillation (97.3%) and 42 (36.5%) patients with a high risk of failure (38.1%). Regardless of the preoperative risk analysis or the performance of left atrial plication, every patient with a postoperative left atrial dimension less than 40 mm or cardiothoracic ratio below 55% was successfully defibrillated. CONCLUSION: The results suggest performing the maze procedure before "risk factors" develop for patients with predicted maze-amenable AF. While omitting the maze procedure may be prudent for patients with suspected maze-refractory AF, the simultaneous reduction of left atrial size may offset the increased risk from preoperative size factors. A prospective study seems warranted to examine the effects of left atrial plication on postoperative rhythm.

Adult↗