Images in cardiology. Unusual dominant course of left circumflex coronary artery with absent right coronary artery.
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Biomedical subjects
Publications and source records attributed to E K Shin.
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We have evaluated the clinical outcomes of simple excision, ulnar lengthening and the Sauvé-Kapandji procedure in the treatment of deformities of the forearm in patients with multiple hereditary osteochondromas. The medical records of 29 patients (33 forearms) were reviewed; 22 patients (22 forearms) underwent simple excision (four with ulnar lengthening) and seven the Sauvé-Kapandji procedure. Simple excision increased the mean supination of the forearm from 63.2 degrees to 75.0 degrees (p = 0.049). Ulnar lengthening did not significantly affect the clinical outcome. The Sauvé-Kapandji technique improved the mean pronation from 33.6 degrees to 55.0 degrees (p = 0.047) and supination from 70.0 degrees to 81.4 degrees (p = 0.045). Simple excision may improve the range of movement of the forearm but will not halt the progression of disease, particularly in younger patients. No discernable clinical or radiological improvement was noted with ulnar lengthening. The Sauvé-Kapandji procedure combined with simple excision of osteochondromas can improve stability of the wrist, movement of the forearm and the radiological appearance.
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STUDY DESIGN: An anatomic study of cervical vertebral bodies. OBJECTIVES: To provide quantitative information on the cortical shell architecture of the middle and lower cervical vertebral bodies. SUMMARY OF BACKGROUND DATA: Some external dimensions have been measured, but little quantitative data exists for the cortical shell architecture of the vertebral bodies of the cervical spine. METHODS: Twenty-one human cervical vertebral bodies (C3-C7) were sectioned along parasagittal planes into five 1.7-mm thin slices for each vertebra. Radiographs of each slice were digitized, and external and internal dimensions were measured. Averages and standard deviations were computed. Single factor analysis of variance was used to determine significant (P < 0.05) differences between the vertebral levels. RESULTS: The superior endplate was thickest in the posterior region (range 0.74-0.89 mm) and thinnest in the anterior region (range 0.44-0.56 mm). The inferior endplate was thickest in the anterior region (range 0.61-0.81 mm) and thinnest in the posterior region (range 0.49-0.62 mm). In the central region, the superior endplate (range 0.42-0.58 mm) was thinner than the inferior endplate (range 0.53-0.64 mm). Variation with vertebral level was dependent on the dimension studied. CONCLUSIONS: Comprehensive quantitative anatomic data of the middle and lower cervical vertebral bodies have been obtained. This may be useful in improving the understanding of the three-column and other vertebral-fracture theories, the fidelity of the finite element models of cervical spine, and the designs of surgical instrumentation.
OBJECTIVES: We assessed the effects of estrogen on vascular dilatory and other homeostatic functions potentially affected by nitric oxide (NO)-potentiating properties in type II diabetic postmenopausal women. BACKGROUND: There is a higher cardiovascular risk in diabetic women than in nondiabetic women. This would suggest that women with diabetes do not have the cardioprotection associated with estrogen. METHODS: We administered placebo or conjugated equine estrogen, 0.625 mg/day for 8 weeks, to 20 type II diabetic postmenopausal women in a randomized, double-blinded, placebo-controlled, cross-over design. RESULTS: Compared with placebo, estrogen tended to lower low-density lipoprotein (LDL) cholesterol levels by 15 +/- 23% (p = 0.007) and increase high-density lipoprotein (HDL) cholesterol levels by 8 +/- 16% (p = 0.034). Thus, the ratio of LDL to HDL cholesterol levels significantly decreased with estrogen, by 20 +/- 24%, as compared with placebo (p = 0.001). Compared with placebo, estrogen tended to increase triglyceride levels by 16 +/- 48% and lower glycosylated hemoglobin levels by 3 +/- 13% (p = 0.295 and p = 0.199, respectively). However, estrogen did not significantly improve the percent flow-mediated dilatory response to hyperemia (17 +/- 75% vs. placebo; p = 0.501). The statistical power to accept our observation was 81.5%. Compared with placebo, estrogen did not significantly change E-selectin, intercellular adhesion molecule-1, vascular cell adhesion molecule-1, monocyte chemoattractant protein-1 or matrix metalloproteinase-9 levels. Compared with placebo, estrogen tended to decrease tissue factor antigen and increase tissue factor activity levels by 7 +/- 46% and 5 +/- 34%, respectively (p = 0.321 and p = 0.117, respectively) and lower plasminogen activator inhibitor-1 levels by 16 +/- 31% (p = 0.043). CONCLUSIONS: The effects of estrogen on endothelial, vascular dilatory and other homeostatic functions were less apparent in type II diabetic postmenopausal women, despite the beneficial effects of estrogen on lipoprotein levels.
BACKGROUND: Synthetic, not natural, progestagen may negate the favorable effects of estrogen. Nonetheless, observational studies report no differences in risk for clinical cardiovascular events between users of unopposed estrogen and users of estrogen combined with synthetic progestin. METHODS AND RESULTS: In a double-blind study, we randomly assigned 20 healthy postmenopausal women to micronized progesterone (MP) 200 mg or medroxyprogesterone acetate (MPA) 10 mg for 10 days with conjugated equine estrogen (CEE) 0.625 mg for 25 days and the remaining 5 days off cyclically during 2 months, followed by crossover to the alternate therapy. CEE+MP and CEE+MPA significantly improved the percent flow-mediated dilator response to hyperemia relative to baseline measurements (P=0.004 by ANOVA) by a similar degree (P=0.863). Both therapies significantly decreased E-selectin, intercellular adhesion molecule (ICAM)-1, and vascular cell adhesion molecule (VCAM)-1 levels from baseline values (P<0.001, P=0.048, and P=0.016 by ANOVA, respectively) by a similar degree (P=0.977 for ICAM-1 and P=0.541 for VCAM-1, respectively). CEE+MPA decreased E-selectin levels more than CEE+MP did (P=0.040). Both therapies significantly decreased monocyte chemoattractant protein-1 levels from baseline values (P<0.005 by ANOVA) by a similar degree (P=0.194). Both therapies significantly decreased tissue factor antigen and increased tissue factor activity levels from baseline values (P=0.003 and P<0.001 by ANOVA, respectively) by a similar degree (P=0.652 for antigen and P=0.173 for activity). Both therapies significantly lowered plasma plasminogen activator inhibitor-1 levels from baseline values (P<0.001 by ANOVA) by a similar degree (P=0.533). CONCLUSIONS: CEE+MP and CEE+MPA provide similar improvement in endothelium-dependent vasodilator responsiveness and effects on markers of inflammation, hemostasis, and fibrinolysis inhibition in healthy postmenopausal women.
Primary stenting has been reported to be superior to balloon percutaneous transluminal coronary angioplasty (PTCA) in acute myocardial infarction (AMI) for recurrent ischemia, target lesion revascularization, and restenosis. However, concerns about early reocclusion or thrombosis after stenting in the very thrombotic environment of acute myocardial infarction still remain. Therefore, postprocedural short-term heparin or GpII(b)/III(a) receptor blockades has been used. The aim of our study was to evaluate the safety, feasibility, and long-term efficacy of heparin-coated stent in the early setting of AMI without postprocedural heparin or GpII(b)/III(a) receptor blockade infusion. We studied 102 consecutive patients presenting to cardiac catheterization laboratory < or = 6 hr from the onset of chest pain. No patients who were implanted with heparin-coated stents received heparin or GpII(b)/III(a) receptor blockade infusion after the procedures, not even patients who showed an angiographically large thrombus burden before stenting. Patients were evaluated for clinical endpoints at 30 days and 6 months. Coronary angiography was required for all patients at 2 weeks and 6 months after the procedure. Angiographic and procedural successes were 100% and 98%, respectively. Two patients (2%) died of heart failure without evidence of reocclusion of stented vessel during the hospitalization and 4 (4%) additional patients died of refractory heart failure within the first 6 months. Major bleeding complication occurred in one patient (1%). Recurrent myocardial infarction developed in one patient at 4 months. Early angiographic follow up at 2 weeks was performed in 88% of all patients, none of whom showed thrombotic stent occlusion. Six-month angiographic follow-up was completed in 71%(64/91) of eligible patients and binary restenosis was present in 17.2% of stented vessels. Eight(8%) patients underwent repeat PTCA. Cardiac event-free survival rate at 6 months was 86.3%. This study demonstrates that heparin-coated stents are safe in the early setting of acute myocardial infarction and no additional heparin infusion after stenting is necessary, which may reduce bleeding complications. Angiographic restenosis rate compares favorably to the binary restenosis rate from other studies with uncoated stents.
A 55-year-old man came to the hospital because of chest pain, mostly occurring in the early morning at rest. He had to get isosorbide dinitrate intravenously with continuous infusion. Following ergonovine provocation test, total occlusion of mid-left anterior descending artery was identified with marked elevation of ST segment as exercise test showed despite isosorbide dinitrate.
BACKGROUND: Vascular inflammation plays an important role in the pathogenesis of atherosclerosis. We investigated the effect of hormone replacement therapy (HRT) on vasomotor function and monocyte chemoattractant protein (MCP)-1 levels, an important serological marker of inflammation. METHODS: We administered micronized progesterone (MP) 200 mg for 10 days with conjugated equine estrogen (CEE) 0.625 mg for 25 days and remaining 5 days off cyclically during 2 months to 20 healthy postmenopausal women (PMW). We measured NO bioactivity and plasma levels of MCP-1 before and after HRT in 20 PMW. And we measured plasma levels of MCP-1 in each 20 subjects of premenopausal women, men <50, and men >50 years, respectively. RESULTS: MP combined with CEE significantly improved the percent flow-mediated dilator response to hyperemia relative to baseline measurements (P<0.001). PMW receiving HRT had lower levels of MCP-1 than those not receiving HRT (121+/-38 versus 146+/-44 pg/ml, P<0.001). In all comparisons, subjects with high estrogen status had significantly lower MCP-1 levels than subjects with low estrogen status (P<0.001 by ANOVA). Premenopausal women had lower levels of MCP-1 than men of a similar age (106+/-14 versus 164+/-40 pg/ml, P<0.001). PMW not receiving HRT had similar levels of MCP-1 compared with men of a similar age (146+/-44 versus 143+/-29 pg/ml, P=0.816). Premenopausal women had markedly lower levels of MCP-1 than PMW not receiving HRT (106+/-14 versus 146+/-44 pg/ml, P=0.001). PMW receiving HRT had similar levels of MCP-1 compared with premenopausal women (121+/-38 versus 106+/-14 pg/ml, P=0.323). CONCLUSION: These findings might provide at least a partial explanation for the protection against cardiovascular disease experienced by premenopausal women, and the loss of that protection following menopause.
BACKGROUND: Results of clinical trials of statin therapy demonstrate that an improvement in incidence of cardiovascular end points and coronary stenosis can be achieved. The beneficial effects of statins on clinical events may involve nonlipid mechanisms that affect endothelial function, such as inflammatory responses, formation of thrombi, and stabilization of plaque. OBJECTIVE: To investigate levels of serologic markers, which may be useful surrogates for activity of vascular disease after administration of statin. METHODS: We administered 20-40 mg simvastatin daily for 14 weeks to 13 patients established to have coronary artery disease who remained hypercholesterolemic during step-II diet therapy. RESULTS: Administration of simvastatin significantly lowered lipoprotein levels and the low: high-density lipoprotein cholesterol level ratio and apolipoprotein B:A-I level ratio compared with pretreatment values (P < 0.01). Administration of simvastatin significantly lowered plasma levels of matrix metalloproteinase-9 (MMP-9) and monocyte chemoattractant protein-I [33+/-46 and 13+/-19%, respectively (P = 0.027 and 0.020, respectively)]. Furthermore, administration of simvastatin tended to lower plasma levels of plasminogen activator inhibitor type-1 and tumor necrosis factor-alpha [by 20+/-44 and 13+/-29%, respectively (P= 0.066 and 0.110, respectively)]. There were significant inverse correlations between pretreatment levels of MMP-9 and the degree of change in those levels after administration of simvastatin (r = -0.714, P= 0.005). However, there was no significant correlation between levels of lipoprotein and levels of MMP-9, monocyte chemoattractant protein-I, and plasminogen activator inhibitor type-1 during administration of simvastatin. CONCLUSIONS: Our current data support the hypothesis that nonlipid mechanisms elicited by administration of simvastatin contribute to the decrease in incidence of cardiovascular events and explain the early clinical benefit observed in clinical trials, independent of changes in levels of lipoprotein.
DNA-dependent protein kinase (DNA-PK) is utilized in both DNA double-strand break repair (DSBR) and V(D)J recombination, but the mechanism by which this multiprotein complex participates in these processes is unknown. To evaluate the importance of DNA-PK-mediated protein phosphorylation in DSBR and V(D)J recombination, we assessed the effects of the phosphatidyl inositol 3-kinase inhibitor wortmannin on the repair of ionizing radiation-induced DNA double-strand breaks and V(D)J recombination in the V(D)J recombinase inducible B cell line HDR37. Wortmannin radiosensitized HDR37, but had no affect on V(D)J recombination despite a marked reduction in DNA-PK activity. On the other hand, studies with mammalian expression vectors for wild-type human DNA-PK catalytic subunit (DNA-PKcs) and a kinase domain mutant demonstrated that only the kinase active form of DNA-PKcs can reconstitute DSBR and V(D)J recombination in a DNA-PKcs-deficient cell line (Sf19), implying that DNA-PKcs kinase activity is essential for both DSBR and V(D)J recombination. These apparently contradictory results were reconciled by analyses of cell lines varying in their expression of recombinant wild-type human DNA-PKcs. These studies establish that minimal DNA-PKcs protein levels are sufficient to support V(D)J recombination, but insufficient to confer resistance to ionizing radiation.
STUDY DESIGN: The internal architecture of cervical spine pedicles was investigated by thin sectioning and digitization of radiographic images. OBJECTIVES: To provide quantitative information on the internal dimensions and cortical shell thicknesses of the middle and lower cervical pedicles. SUMMARY OF BACKGROUND DATA: Although there have been a number of studies presenting data on the external dimensions of the cervical pedicle, little is known regarding its internal architecture and cortical shell thickness along the pedicle axis. METHODS: Twenty-five human cervical vertebrae (C3-C7) were secured to a thin-sectioning machine to produce three 0.7-mm-thick pedicle slices along its axis. Plain radiographs of the pedicle slices were scanned and digitized to facilitate measurement of the internal dimensions. Computer software was specifically developed to determine the external dimensions (i.e., pedicle height and width) and the internal dimensions (i.e., cortical shell thicknesses of the superior, inferior, lateral, and medial walls and the cancellous core height and width) of cervical pedicles. RESULTS: Superior and inferior wall cortical thicknesses of pedicle thin slices were similar, whereas the lateral wall cortical thickness was significantly smaller than the medial wall thickness. The medial cortical shell (average value range: 1.2-2.0 mm) was measured to be 1.4 to 3.6 times as thick as the lateral cortical shell (average value range: 0.4-1.1 mm). When medial and lateral cortical thicknesses were normalized for external dimensions, the combined cortical shell thickness was thinnest at C7 (average value range: 18. 6-25.6% of the external width), and this result was statistically significant when compared with other vertebral levels. CONCLUSIONS: The cervical pedicle is a complex, three-dimensional structure exhibiting extensive variability in internal morphology. Characteristics of the cervical pedicle at different spinal levels must be noted before transpedicular screw fixation.
We reported previously that the genetic SCID disease observed in Arabian foals is explained by a defect in V(D)J recombination that profoundly affects both coding and signal end joining. As in C.B-17 SCID mice, the molecular defect in SCID foals is in the catalytic subunit of the DNA-dependent protein kinase (DNA-PKCS); however, in SCID mice, signal end resolution remains relatively intact. Moreover, recent reports indicate that mice that completely lack DNA-PKCS also generate signal joints at levels that are indistinguishable from those observed in C.B-17 SCID mice, eliminating the possibility that a partially active version of DNA-PKCS facilitates signal end resolution in SCID mice. We have analyzed TCRB rearrangements and find that signal joints are reduced by approximately 4 logs in equine SCID thymocytes as compared with normal horse thymocytes. A potential explanation for the differences between SCID mice and foals is that the mutant DNA-PKCS allele in SCID foals inhibits signal end resolution. We tested this hypothesis using DNA-PKCS expression vectors; in sum, we find no evidence of a dominant-negative effect by the mutant protein. These and other recent data are consistent with an emerging consensus: that in normal cells, DNA-PKCS participates in both coding and signal end resolution, but in the absence of DNA-PKCS an undefined end joining pathway (which is variably expressed in different species and cell types) can facilitate imperfect signal and coding end joining.
Transpedicular screw fixation has recently been shown to be successful in stabilizing the middle and lower cervical spine. Controversy exists, however, over its efficacy, due to the smaller size of cervical pedicles and the proximity of significant neurovascular structures to both lateral and medial cortical walls. To aid the spinal surgeon in the insertion of pedicle screws, a number of studies have been performed to quantify the gross dimensions and angulations of the cervical pedicle. Notwithstanding these quantitative studies, there has been a conspicuous absence of research reporting the qualitative characteristics of the cervical pedicle. The purpose of our study was to provide comparative graphical data that would systematically document the anatomic variability in cervical pedicle morphology. Such information should better elucidate the complexity of the pedicle as a three-dimensional structure and provide the spinal surgeon with a more complete understanding of cervical pedicle architecture. Twenty-six human cervical vertebrae (C3-C7) from six fresh-frozen spines were secured to a thin sectioning apparatus to produce three 0.7-mm-thick pedicle slices along its axis. Radiographs taken of these pedicle slices were scanned, digitized, and traced to facilitate visual comparison. The pedicle slices were found to exhibit substantial variability in composition and shape, not only between individual spines and vertebral levels, but also within the pedicle axis. However, the lateral cortex was consistently found to be thinner than the medial cortex in all samples. These physical findings must be noted by surgeons attempting transpedicular screw fixation in the cervical spine.
Direct surgical angioplasty or coronary artery bypass graft has been done in patients who have left main coronary ostial stenosis. Recent reports have demonstrated that stenting of unprotected left main coronary artery stenosis has been attempted as an alternative to bypass surgery in selected patients with normal LV function. We report two patients with isolated left main coronary ostial stenosis who are undergoing primary and elective stenting, respectively. Major cardiac events did not occur during a 3-month follow-up. This study suggests that stenting of isolated left main coronary ostial stenosis in acute coronary syndrome is feasible and results in excellent outcomes.
We report a patient with Takayasu's arteritis who had recurrent restenosis following intracoronary bifurcation stenting of proximal left anterior descending and first diagonal arteries, and rotational atherectomy for in-stent restenosis. After all, the patient underwent coronary artery bypass grafts (CABG) and has remained asymptomatic during 3 months without damaging myocardium. We suggest that endoluminal stenting or rotational atherectomy may be an alternative treatment for the patients with coronary artery stenosis due to active Takayasu's arteritis as a therapy to postpone CABG.
OBJECTIVE: To determine whether a recently developed test would correctly identify horses heterozygous for the severe combined immunodeficiency (SCID) trait. DESIGN: Case series. ANIMALS: 17 healthy Arabian horses that had previously produced foals with SCID, 1 healthy Arabian foal whose dam and sire had produced foals with SCID, 4 foals with SCID, and 1 healthy non-Arabian foal. PROCEDURE: DNA was extracted from leukocytes or fibroblasts, amplified by means of polymerase chain reaction, and hybridized with probes specific for the normal and mutant alleles of the catalytic subunit of DNA-dependent protein kinase, the factor whose absence is responsible for SCID in Arabian foals. RESULTS: Amplified DNA from the healthy non-Arabian foal hybridized only to the probe specific for the normal allele, whereas amplified DNA from the 4 foals with SCID hybridized only to the probe specific for the mutant allele. Amplified DNA from the 2 stallions and 15 mares hybridized with both probes, as did amplified DNA from the healthy foal whose dam and sire had previously produced foals with SCID, indicating that these horses were all heterozygous for the SCID trait. CLINICAL IMPLICATIONS: Results suggest that the genetic test will be useful in identifying Arabian horses heterozygous for the SCID trait and foals with SCID, provided that all Arabian horses with SCID have the same genetic mutation.
The equine SCID defect is more severe than its murine counterpart in that SCID foals are incapable of forming either coding or signal joints, whereas SCID mice manifest normal signal joint formation. To determine the basis of this difference and whether DNA-dependent kinase, catalytic subunit (DNA-PK(CS)), is involved in signal joint formation, equine DNA-PK(CS) transcripts were cloned and sequenced from normal and SCID cell lines. In the mutant allele, a frame-shift mutation truncates the protein N terminal of the domain with homology to the phosphatidylinositol 3-kinase family resulting in complete absence of full length DNA-PK(CS) and accounting for the kinase-negative phenotype of these cells; the mutation in SCID mice allows for some DNA-PK(CS) expression. The difference in DNA-PK(CS) expression in SCID mice and foals explains the more severe phenotype of equine SCID, and definition of DNA-PK(CS) as the defect in equine SCID demonstrates that DNA-PK(CS) is required for both coding and signal joint formation.