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Biomedical subjects

G Cohen

Publications and source records attributed to G Cohen.

At least 91 records · Page 5Linked to original sources

Evaluation of differential growth and orthodontic treatment outcome by regional cephalometric superpositions.

Cephalometric superimposition on cranial base is the accepted method for evaluating mandibular displacement during orthodontic treatment and/or growth. However, assessing mandibular position relative to the maxillary base may yield different information. The aim of this study was to evaluate the effects of regional superpositions (cranial versus maxillary) on interpreting mandibular displacement. Both methods were applied to pre- and posttreatment cephalograms of 22 growing children (12 female, 10 male) treated for Class II Division 1 malocclusion. Differences in linear and angular measurements of three mandibular landmarks (pogonion, gnathion, menton) between cranial and maxillary superpositions were statistically significant (p = 0.0001). Vertical displacement of these landmarks contributed significantly to the differences (p = 0.0001). The contribution of horizontal displacement was not statistically significant. The results support the proposition that, in growing children, posttreatment displacement of mandibular skeletal and dental components should be assessed by both maxillary and cranial base superimpositions. The maxilla is subject to rotational and translational changes during growth that may affect the position of the mandible relative to the maxilla in a way inconsistent with the mandibular displacement perceived upon cranial superposition. Since occlusion is directly associated with the positions of the maxillary and mandibular basal bones, the positions of these bones relative to each other is critical in assessing occlusal changes in individual patients.

Adolescent↗

Monoamine oxidase and mitochondrial respiration.

Mitochondrial defects encompassing complexes I-IV of the electron transport chain characterize a relatively large number of neurodegenerative diseases. The relationships between mitochondrial lesions and recently described genetic alterations have not yet been defined. We describe a general mechanism whereby the enzymatic metabolism of neurotransmitters by monoamine oxidase (MAO) damages mitochondria, altering their protein thiol status and suppressing respiration. In these experiments, incubation of rat brain mitochondria with tyramine (a mixed MAO-A/MAO-B substrate) for 15 min at 27 degrees C suppressed state 3 respiration by 32.8% and state 5 respiration by 40.1%. These changes were accompanied by a 10-fold rise in protein-glutathione mixed disulfides. Direct comparison of effects on respiration and MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] dye reduction during electron flow gave similar results. It is suggested that certain mitochondrial lesions may derive from the natural turnover of monoamine neurotransmitters in susceptible individuals.

Animals↗

Systemic absorption of lidocaine after topical application for the treatment of oral mucositis in bone marrow transplantation patients.

This paper evaluates lidocaine absorption via oral mucosa following its topical application for symptomatic treatment of bone marrow transplantation (BMT)-induced oral mucositis. Five patients with high-grade oral mucositis after allogeneic BMT were entered consecutively into the study. Five healthy individuals served as controls. All 10 participants rinsed their mouth with 5 ml of a 2% lidocaine solution for 1 min, after which they expectorated the liquid. Blood samples were drawn at 1, 5, 10, 20, 30 and 60 min after rinsing and centrifuged. Plasma lidocaine levels were measured by fluorescence polarization immunoassay. In the BMT patients, plasma lidocaine levels were lower than the therapeutic range of this drug (0.2 microg/ml vs 1.5-5.5 microg/ml), while in the controls no detectable lidocaine levels were noted. The data from this preliminary study indicate that lidocaine prescribed as an anesthetic mouthwash in BMT patients with oral mucositis results in minor systemic absorption of the drug.

Administration, Topical↗

The involvement of the NMDA receptor complex in the protective effect of anticholinergic drugs against soman poisoning.

Organophosphate poisoning is associated with adverse effects on the central nervous system such as seizure/convulsive activity and long term changes in neuronal networks. This study reports on investigations designed to assess the consequences of soman exposure on excitatory amino acids receptors in the rat brain. In addition, the protective effects of caramiphen which acts at these receptors, and scopolamine, which does not, was determined on soman-induced alteration in rat brain functions. Administration of soman (1xLD50) to pyridostigmine pretreated rats produced seizure activity (measured by EEG monitoring) in all animals tested. Estimation of [3H]MK-801 binding to brain membranes from intoxicated rats revealed a marked decrease in Bmax value 24 but not 2 hrs following soman administration. The specific nature of these effects of soman was demonstrated by the findings that [3H]flunitrazepam binding to central benzodiazepine receptors remained unchanged in soman-poisoned rat brain membranes. Both scopolamine and caramiphen, when used prophylactically prevented the lethal effect of soman and completely blocked the development of electrographic seizure activity (EGSA). In contrast, only caramiphen abolished soman-induced modifications in NMDA/ion channel characteristics. Caramiphen displaced [3H]MK-801 bound to the NMDA/ion channel complex, possibly by interacting with the Zn2+ site whereas scopolamine did not. Moreover, caramiphen, but not scopolamine, partially protected mice from NMDA-induced lethality. Thus, it is suggested that an important component of the protective efficacy of caramiphen against organophosphate poisoning might be attributed to its ability to modulate NMDA receptors in addition to its anticholinergic properties.

Animals↗

Multiple arterial grafts. Radial versus right internal thoracic arteries.

BACKGROUND: Left internal thoracic artery (LITA) grafts to the left anterior descending coronary artery (LAD) during coronary bypass surgery (CABG) have greater patency rates than saphenous vein grafts and reduce long-term cardiac morbidity and mortality rates. The benefits of multiple versus single arterial grafts and the role of different arterial conduits with respect to short- and medium-term outcome remains controversial. The purpose of this study was to compare the perioperative and intermediate-term results of: (1) patients receiving 2 arterial grafts versus 1 arterial graft and (2) patients receiving a right internal thoracic artery (RITA) versus a radial artery (RA) as the second arterial graft. METHODS AND RESULTS: Retrospective analysis of prospectively gathered data on consecutive patients undergoing isolated CABG at our institution between 1989 and 1996 was conducted. The first section of the study compared outcomes for 1 arterial graft (LITA to LAD, n = 2333) versus 2 arterial grafts (LITA + RA or LITA + RITA, n = 378). The second section of the study compared outcomes for the RITA (n = 132) versus the RA (n = 171) as second arterial grafts since 1992, when the radial series was initiated. Part I: By multivariable stepwise logistic regression, the use of 1 arterial graft was associated with an increased incidence of perioperative cardiac morbidity and mortality (odds ratio 2.2, 95% confidence interval 1.4 to 3.3), with the use of our current patient selection criteria. Double-arterial graft patients had a nonsignificant trend toward increased intermediate-term actuarial survival (P = 0.12) and cardiac event-free survival (P = 0.09). Part II: Comparison of preoperative demographics revealed a higher incidence of diabetes (27% vs 11%, P < 0.001), peripheral vascular disease (16% vs 8%, P = 0.03), and elderly age (13% vs 2%, P = 0.001) in patients receiving an RA versus those receiving a RITA as the second arterial graft. Perioperative outcome analysis revealed a decreased intensive care unit stay in the RA versus RITA group (median 30.4 vs 36.2 hours, respectively, P = 0.005) but no significant difference in hospital length of stay. There was no significant difference in perioperative mortality or cardiac morbidity rates. RITA patients had a higher incidence of sternal wound infection (5.3% vs 0.6%, P = 0.01), however, and tended to have increased blood product transfusion rates (51% vs 40%, P = 0.06). CONCLUSIONS: The use of 2 arterial grafts is safe, with a reduction in perioperative cardiac morbidity or mortality rates compared with 1 arterial graft after adjustment for other risk variables. When comparing RITA to RA as second arterial grafts, patients receiving an RA have a lower incidence of sternal wound infection and decreased transfusion requirements, with no difference in perioperative or intermediate-term cardiac morbidity or mortality rates.

Aged↗

Decreasing incidence of stroke during valvular surgery.

BACKGROUND: The predictors and causes of stroke after valvular surgery are incompletely defined. We examined the incidence, predictors, and mechanisms of stroke during valvular procedures over a 15-year time period. METHODS AND RESULTS: We retrospectively reviewed prospectively gathered data on 5954 consecutive patients undergoing valvular procedures at our institution from 1982 to 1996. Stroke was defined as persistent central nervous system deficit, usually with confirmatory CT imaging. Patients were divided into 3 groups according to date of operation: group 1, 1982 to 1986 (n = 1819); group 2, 1987 to 1991 (n = 2022); and group 3, 1992 to 1996 (n = 2113). Chart review was undertaken of all patients who developed stroke (n = 189). Stroke occurred in 3.8% of group 1 patients, 3.3% of group 2, and 2.6% of group 3 (P = 0.120). The decreasing incidence of stroke over time was confirmed by multivariable logistic regression analysis, in which earlier date of operation was an independent risk factor for stroke (P < 0.001). Predictors of stroke identified by multivariable logistic regression were (listed in decreasing order): (1) endocarditis (OR, 3.0; 95% CI, 1.8 to 5.0); (2) age > 74 years (OR, 2.3; 95% CI, 1.5 to 3.7); (3) earlier time period of operation (1982 to 1986: OR, 2.2; 95% CI, 1.5 to 3.2; 1987 to 1991: OR, 1.5; 95% CI, 1.0 to 2.2); (4) urgent timing (OR, 2.0; 95% CI, 1.4 to 2.8); (5) concomitant coronary bypass (OR, 2.0; 95% CI, 1.4 to 2.8); and (6) reoperation (OR, 1.7; 95% CI, 1.2 to 2.4). In more recent years of operation, we found an increasing prevalence of age > 74 years (7.4% in group 1, 9.5% in group 2, and 15.3% in group 3; P < 0.001), urgent timing (11%, 26%, and 34%, P < 0.001), and concomitant coronary bypass surgery (25%, 27%, and 33%; P < 0.001). CONCLUSIONS: The incidence of stroke during valvular surgery has decreased with time, despite an increased prevalence of risk factors. Predictors of stroke suggest 3 major causes (multivariable predictors in parentheses): atherosclerotic emboli (elderly age, concomitant coronary bypass), shock (urgent timing, reoperation), and septic emboli (endocarditis).

Aged↗

Optimal myocardial preconditioning in a human model of ischemia and reperfusion.

BACKGROUND: Adenosine (ADE) may mediate the protective effects of preconditioning (PC). However, human data are lacking, and the optimal method of ADE administration and the mechanism of protection remain unresolved. METHODS AND RESULTS: We have developed a model of simulated "ischemia" (I) and "reperfusion" (R) in quiescent human ventricular cardiomyocytes. Cellular injury and metabolic parameters were assessed after various interventions: Cells were preconditioned with anoxia (PC0), hypoxia (PC16), anoxic supernatant (SUP0), or hypoxic supernatant (SUP16) with or without the ADE receptor antagonist (SPT) or ADE deaminase (ADA). ADE was applied before, during, or after I or continuously with and without SPT. Cells were treated with the PKC agonist PMA. PC cells were incubated with the protein kinase-C (PKC) antagonist Calphostin-C (Cal-C). PKC translocation and PKC activity were assessed. PC0 was most protective. Protection was transferable via SUP0, which produced the highest concentrations of ADE. Protection was lost with SPT or ADA. Intracellular ATP fell after PC and prolonged I and R. Exogenous ADE was most protective when administered before I at 50 mumol. ADE during I was partially protective. No additional protection was provided with continuous ADE treatment. ADE prevented ATP degradation but increased lactate immediately after its administration. SPT abolished the protective effects of ADE. PMA conferred protection, which was abolished with Cal-C. ADE stimulated PKC translocation and PKC activity in the absence of SPT. CONCLUSIONS: Maximal I confers maximal PC. The degree of I is reflected in supernatant ADE concentrations. The initial ATP fall with PC may account for a lack of ATP preservation after I and R. ADE reproduces the protective effects of PC, preserves ATP, and increases lactate production, perhaps by stimulating glycolysis. Clinical trials of ADE administered during cardiac surgery are necessary to further define its beneficial effects in humans.

Adenosine↗

Phase 2 studies of adenosine cardioplegia.

BACKGROUND: Laboratory evidence supports the use of adenosine-supplemented cardioplegia. An initial phase 1 dose-ranging clinical evaluation demonstrated that an adenosine concentration of 15 mumol/L could be safely administered with warm blood cardioplegia and suggested that phase 2 studies were warranted. METHODS AND RESULTS: Two separate double-blind, randomized, placebo-controlled trials were performed in patients undergoing primary, isolated, nonemergent coronary artery bypass graft surgery. Patients were randomized to receive adenosine 15 mumol/L versus placebo in the first study (n = 200) and adenosine 50 or 100 mumol/L versus placebo in the second study (n = 128). Adenosine was infused with both initial and final doses of warm antegrade blood cardioplegia. The data from the 2 trials were combined using the methods of Mantel and Haenszel, and the results of the meta-analysis are presented as the relative risk with their associated 95% confidence intervals (CI). The different study groups were comparable with respect to all preoperative clinical characteristics, angiographic findings, and intraoperative variables. In both trials 1 and 2, no differences were found between groups in the incidence of the individual primary or secondary outcomes. Similarly, when both studies were combined, there was no significant evidence of any consistent treatment benefit (primary: death: relative risk [RR] = 1.02, 95% CI = 0.06, 16.6; myocardial infarction by CK-MB: RR = 0.84, CI = 0.54, 1.31; low output syndrome: RR = 1.38, CI = 0.29, 6.42; any of the above: RR = 0.98, CI = 0.78, 1.25; secondary: Q-wave myocardial infarction: RR = 1.30, CI = 0.41, 4.13; myocardial infarction by troponin T: RR = 0.7, CI = 0.40, 1.21; inotrope requirement: RR = 0.9, CI = 0.46, 1.79; intra-aortic balloon pump requirement: RR = 0.6, CI = 0.07, 4.81; P > 0.20). CONCLUSIONS: Despite promising experimental data, adenosine supplementation of warm blood cardioplegia did not demonstrate any statistically significant benefit in patients undergoing elective coronary artery bypass graft surgery. Although sample sizes were relatively small, based on our interim analyses, it is unlikely that increased patient enrollment would reveal any substantive clinical differences between groups.

Adenosine↗

Protein L-dopa as an index of hydroxyl radical attack on protein tyrosine.

It is widely believed that hydroxyl radicals generated in vivo contribute to damage to macromolecules, such as proteins and DNA. We evaluated methodology based on the transformation of protein tyrosine to L-Dopa, via aromatic ring hydroxylation, as an index of hydroxyl radical attack on proteins. The catechol structure of Dopa makes it amenable to isolation with alumina, followed by HPLC analysis, typically used for the measurement of catecholamines. Because a level of controversy exists about the formation of Dopa by hydroxyl radicals, we conducted a systematic study of the formation of Dopa from tyrosine, tyrosine dipeptides, pure proteins (chymotrypsin and myelin basic protein), and endogenous proteins in tissue homogenates (rat brain), exposed to hydroxylating conditions (Fe2+/EDTA/ascorbate at neutral pH). Dopa residues in peptides and proteins were liberated by acid hydrolysis with 6 M HCl at 145 degrees C for 1 h. A marked lability of Dopa in 6 M HCl under hydrolysis conditions was prevented with added phenol; chymotrypsin and precipitated pellets of brain protein were also protective. Overall recoveries (hydrolysis plus purification procedures) averaged 83.4 +/- 1.7%. This improved analytic procedure may be useful for studying protein damage by hydroxyl radicals.

Animals↗

Gene organization in the trxA/B-oriC region of the Streptomyces coelicolor chromosome and comparison with other eubacteria.

The gene organization was determined in the trxA/B-rnpA region of the Streptomyces coelocolor chromosome, near to the origin of replication, oriC. Previously, we showed that the trxA and trxB genes, coding for thioredoxin and thioredoxin reductase, respectively, occur in S. coelicolor as a gene cluster and are contained on a cosmid H24 that carries oriC and several genes involved in DNA replication. Here we show that the trxA/B locus is positioned approx. 9.4kb from oriC, present the nucleotide sequence of the trxA/B-rnpA region and use sequence analysis to identify the nature of the intervening genes. Seven open reading frames were found, all oriented in the same direction, five of which were identified as the S. coelicolor homologs of SpoIIIJ, Jag, GidB, Soj and SpoOJ in Bacillus subtilis and which have been ascribed different functions in this and other bacteria for either DNA replication, chromosomal partitioning or morphological development. The arrangement of the genes coding for the above five proteins in the trxA/B-rnpA region in S. coelicolor resembles that in Mycobacterium leprae, Mycobacterium tuberculosis, B. subtilis and Pseudomonas putida, and supports the view that many of the genes necessary for development and cell division in bacteria are organized in a similar fashion. In B. subtilis and P. putida, however, the trxA/B genes are not present in the above gene arrangement.

Bacillus subtilis↗

Disruption of the intracellular sulfhydryl homeostasis by cadmium-induced oxidative stress leads to protein thiolation and ubiquitination in neuronal cells.

Cadmium is a potent cell poison known to cause oxidative stress by increasing lipid peroxidation and/or by changing intracellular glutathione levels and to affect the ubiquitin/ATP-dependent proteolytic pathway. However, the cellular mechanisms involved in cadmium toxicity are still not well understood, especially in neuronal cells. To investigate the relationship between cadmium-induced oxidative stress and the ubiquitin/ATP-dependent pathway, we treated cultures of neuronal cells with different concentrations of the metal ion. In addition to decreases in glutathione levels, we observed marked increases in protein-mixed disulfides (Pr-SSGs) after exposure of HT4 cells (a mouse neuronal cell line) or rat primary mesencephalic cultures to Cd2+. The increases in intracellular levels of Pr-SSGs were concurrent with increases in the levels of ubiquitinated proteins (Ub proteins) when the HT4 cells were subjected to lower (25 microM or less) concentrations of cadmium. However, higher concentrations of cadmium (50 microM), which were toxic, led to increases in Pr-SSGs but inhibited ubiquitination, probably reflecting inhibition of ubiquitinating enzymes. The cadmium-induced changes in Pr-SSGs and Ub proteins were not affected when more than 85% of intracellular glutathione was removed from the cells by the glutathione synthetase inhibitor L-buthionine-(S,R)-sulfoximine. However, the reducing agent dithiothreitol, which prevented the build up of Pr-SSGs in the cell, also blocked the accumulation of Ub proteins induced by cadmium. In addition, dithiothreitol blocked the effects of the higher toxic (50 microM) concentrations of cadmium on cytotoxicity and on glutathione, Pr-SSGs, and Ub proteins. Together, these results strongly suggest that changes in the levels of intracellular Pr-SSGs and ubiquitin-protein conjugates in neuronal cells are responses closely associated with the disruption of intracellular sulfhydryl homeostasis caused by cadmium-mediated oxidative stress.

Animals↗

Evaluation of the gemini infusion pump for the safe delivery of peripheral blood progenitor cells (stem cells).

The purpose of this in vitro study was to determine whether the Gemini PC-2TX infusion pump could safely deliver peripheral stem cells (PSC) for an autologous PSC transplant. For purposes of hypothesis testing, it was assumed that there would be no significant difference in CD34+ cell counts and colony-forming units-granulocyte, macrophage (CFU-GM) when the PSCs were administered by an IMED PC-2TX infusion pump as opposed to an intravenous push method. The American Red Cross collected 50-ml samples of PSCs from four donors by apheresis. These cells were tested for CD34+ using flow cytometry and for functional progenitor cells using a CFU-GM assay. The cells were cryopreserved after testing. For our study, samples were tested simultaneously at a single facility. Each sample was individually thawed and a baseline thaw sample collected; 10 ml of the donor specimen was pushed through a syringe into a specimen container (intravenous push sample). The remainder of the specimen was infused through the IMED Gemini PC-2TX pump into a specimen container (intravenous pump sample). All samples were assayed for CD34+ cell counts and CFU-GM. Data analyses were conducted using the t-test for paired samples, with values of P < 0.05 considered significant. Results failed to demonstrate a statistically significant difference between the CD34+ or CFU-GM results of the intravenous push and intravenous pump specimens. Additionally, we failed to find a statistically significant difference when we compared the intravenous push and the intravenous pump specimens with the baseline thaw sample. The results of this study support the hypothesis that the Gemini PC-2TX infusion pump can safely deliver PSCs for the purposes of stem cell transplantation.

Antigens, CD34↗

Presumed macular choroidal watershed vascular filling, choroidal neovascularization, and systemic vascular disease in patients with age-related macular degeneration.

PURPOSE: To investigate the possible association of presumed macular choroidal watershed vascular filling (PMWF), choroidal neovascularization, and systemic vascular disease in patients with age-related macular degeneration. METHODS: In a retrospective study, we evaluated 74 randomly selected indocyanine green videoangiograms of 74 patients with age-related macular degeneration. We also reviewed the charts of 20 randomly selected, age-matched control patients without age-related macular degeneration, initially referred for uniocular conditions, and subsequently performed indocyanine green videoangiography on their normal fellow eyes. We evaluated these videoangiograms for the presence of PMWF, manifesting as characteristic early choroidal hypofluorescence and its relation to choroidal neovascularization when present. Additionally, the incidence of hypertension, coronary artery disease, peripheral vascular disease, and diabetes mellitus was determined. RESULTS: Forty-one (55.4%) of 74 patients with age-related macular degeneration vs three (15.0%) of 20 normal control patients exhibited PMWF on indocyanine green videoangiography (P = .0014). Of the 61 patients with age-related macular degeneration and choroidal neovascularization, 36 (59.0%) exhibited PMWF on videoangiography. Associated choroidal neovascularization arose from the PMWF zone in 33 (91.7%) of these cases. Hypertension was observed in 24 (58.5%) of 41 patients with age-related macular degeneration and PMWF vs nine (27.3%) of 33 patients with age-related macular degeneration who did not exhibit PMWF (P = .007). CONCLUSIONS: An increased incidence of PMWF occurs in patients with age-related macular degeneration with a possible predisposition for the development of associated choroidal neovascularization. Additionally, PMWF may be accentuated by associated hypertensive choroidal microvascular insult.

Aged↗

Aprotinin and dipyridamole for the safe reduction of postoperative blood loss.

BACKGROUND: Aprotinin (APR) reduces postoperative blood loss but may induce thrombosis. Dipyridamole (DIP) limits platelet aggregation and may reduce the thrombotic complications associated with APR. METHODS: To evaluate the safety and effectiveness of combined APR and DIP, we undertook a prospective randomized trial in patients undergoing cardiac operations. Patients were stratified according to risk for bleeding (low or high), and received either DIP with placebo (DIP group; n = 59) or DIP with APR (DIP + APR group; n = 56). Blood samples were obtained for the measurement of hematologic and biochemical parameters. Blood loss and transfusion requirements were documented postoperatively. RESULTS: Postoperative blood loss and transfusion requirements were significantly lower in the DIP + APR group at 6, 12, and 24 hours after bypass (p < 0.01). No significant differences were found between groups in the incidence of perioperative mortality (DIP, 0%; DIP + APR, 3%), myocardial infarction (DIP, 0%; DIP + APR, 3%), stroke (DIP, 1%; DIP + APR, 1%), or potential thrombotic events (death, myocardial infarction, and stroke: DIP, 2%; DIP + APR, 5%). In addition, these rates did not differ from those of nonparticipating matched control patients. CONCLUSIONS: Administration of both drugs simultaneously was more effective than DIP alone in reducing postoperative blood loss. A platelet inhibitor may be required to reduce the thrombotic complications associated with APR. Further studies evaluating graft patency and perioperative ischemia are necessary to confirm the potential benefits of the combination of a platelet inhibitor and APR.

Aprotinin↗

Deep sternal wound infection: risk factors and outcomes.

BACKGROUND: Deep sternal wound infection (DSWI) is a serious complication of cardiac operations performed by median sternotomy. We attempted to define the predictors of DSWI and to describe the outcomes of two treatment strategies used at our institution. METHODS: Retrospective review was performed using prospectively gathered data on 12,267 consecutive cardiac surgical patients from 1990 to 1995. Chart review was performed on all patients in whom DSWI developed, and follow-up was obtained on 100% of these patients. RESULTS: Deep sternal wound infections developed in 92 patients (incidence 0.75%). Multivariable predictors for development of DSWI in all patients were (odds ratios and 95% confidence intervals in parentheses) (1) diabetes mellitus (2.6; 1.7 to 4.0) and (2) male sex (2.2; 1.3 to 3.9). In patients receiving coronary artery bypass grafting alone, independent predictors were (1) bilateral internal thoracic artery grafts (3.2; 1.1 to 8.9), (2) diabetes (2.7; 1.6 to 4.3), and (3) male sex (1.8; 0.9 to 3.7). For all other patients, predictors were (1) age more than 74 years (3.3; 1.1 to 10.1), (2) male sex (3.0; 1.1 to 8.1), and (3) diabetes (2.3; 0.9 to 5.8). Bilateral internal thoracic artery grafts increased the risk of DSWI in all subgroups of coronary artery bypass graft patients, particularly in diabetics who had a 14.3% incidence of DSWI after bilateral internal thoracic artery grafting. Patients with DSWIs received either sternal debridement with primary closure (n=45) or sternectomy with flap reconstruction (n=46). The 6-month freedom from adverse event rate (ie, readmission, reoperation, or death) was 76% for both groups of patients. CONCLUSIONS: Male sex and diabetes are predictors of DSWI in all cardiac surgical patients. Bilateral internal thoracic artery grafting may be contraindicated in diabetic patients.

Age Factors↗

Inaccurate and misleading valve sizing: a proposed standard for valve size nomenclature.

BACKGROUND: The sizes with which manufacturers label valves are nonuniform and haphazard. This has led to confusion and inappropriate comparisons of hemodynamics between valves with the same labeled size. Hemodynamic performance of valves is primarily determined by the internal diameter (ID) of their orifice. METHODS: The purpose of this study was to determine the ID and external diameter of aortic valves used at our institution and compare the measurements to manufacturers' labeled sizes. We also evaluated valve size (ID, manufacturers' labeled size) in 527 patients undergoing isolated aortic valve replacement between 1990 and 1996. RESULTS: We demonstrated that no two manufacturers' tissue or mechanical valves have the same ID or external diameter for a given labeled size. The labeled size of tissue valves was 1 to 4 mm larger than the measured ID. The labeled size of mechanical valves was 3 to 5 mm larger than the measured ID. The St. Jude HP mechanical valve has a greater ID than all other mechanical valves for each labeled size. Among 403 patients operated on for predominant aortic stenosis, those patients receiving the Toronto Stented Porcine Valve (n = 98) had a larger mean ID (22.3+/-1.9 mm) than 204 patients receiving stented tissue valves (ID = 20.9+/-1.9 mm) and the 101 patients receiving mechanical valves (ID = 19.3+/-1.9 mm, p < 0.0001). However, when the manufacturers' labeled size was used as a measure of the size, the results were greatly exaggerated in favor of the Toronto Stented Porcine Valve (ID = 26.3+/-1.9 mm) compared with stented tissue valves (ID = 23.1+/-2.1) or mechanical valves (ID = 23.6+/-1.9) (p < 0.0001). CONCLUSIONS: Manufacturers' labeling of valves is nonuniform and may lead to erroneous comparisons and conclusions of hemodynamic differences between valves. We therefore recommend a standardized nomenclature for the size of all valves based on the ID measurement.

Aortic Valve↗