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Biomedical subjects

G L Hammond

Publications and source records attributed to G L Hammond.

At least 19 recordsLinked to original sources
PubMed1998

Pathogenesis of systemic air embolism during bronchoscopic Nd:YAG laser operations.

BACKGROUND: The occurrence of systemic air embolism during bronchoscopic neodymium:yttrium-aluminum garnet laser operations has been suspected. Here we describe its mechanism. METHODS: Two patients with embolic cardiac and neurologic complications after bronchoscopic neodymium: yttrium-aluminum garnet laser tumor ablation are described. A subsequent third patient was monitored for intracardiac and aortic air by transesophageal echocardiography. A review of the literature and safety recommendations are discussed. RESULTS: The appearance of systemic air emboli was related to the use of the laser fiber air coolant at high flow and resolved by decreasing the air flow. The presence of intracardiac and aortic air was associated with hypotension and inferior ischemic electrocardiographic changes. CONCLUSIONS: Systemic air embolism during bronchoscopic laser operations is a potentially catastrophic complication and is related to the use of gas-cooled laser fibers and contact probes. We recommend using the noncontact mode whenever possible and maintaining the coaxial coolant air flow at the minimum level or using a fluid coolant if contact is necessary.

Aged↗
PubMed1998

Penetrating ulcer of the thoracic aorta: what is it? How do we recognize it? How do we manage it?

BACKGROUND: Although classic type A and B aortic dissections have been well described, less is known about the natural history of penetrating atherosclerotic ulcers of the thoracic aorta. This study differentiates penetrating ulcer from aortic dissection, determines the clinical features and natural history of these ulcers, and establishes appropriate correlates regarding optimal treatment. METHODS: A retrospective review of patient records and imaging studies was conducted with 198 patients with initial diagnoses of aortic dissection (86 type A, 112 type B) at our institution from 1985 to 1997. RESULTS: Of the 198 patients, 15 (7.6%) were found to have a penetrating aortic ulcer on re-review of computed tomographic scans, magnetic resonance images, angiograms, echocardiograms, intraoperative findings, or pathology reports. Two ulcers (13.3%) were located in the ascending aorta; the other 13 (86.7%) were in the descending aorta. In comparison with those with type A or B aortic dissection, patients with penetrating ulcer were older (mean age 76.6 years, p = 0.018); had larger aortic diameters (mean diameter 6.5 cm); had ulcers primarily in the descending aorta (13 of 15 patients, 86.7%); and more often had ulcers associated with a prior diagnosed or managed AAA (6 of 15 patients, 40.0%; p = 0.0001). Risk for aortic rupture was higher among patients with penetrating ulcers (40.0%) than patients with type A (7.0%) or type B (3.6%) aortic dissection (p = 0.0001). CONCLUSIONS: Accurate recognition and differentiation of penetrating ulcers from classic aortic dissection at initial presentation is critical for optimal treatment of these patients. For penetrating ulcer, the prognosis may be more serious than with classic type A or B aortic dissection. Surgical management is advocated for penetrating ulcers in the ascending aorta and for penetrating ulcers in the descending aorta that exhibit early clinical or radiologic signs of deterioration.

Aged↗
PubMed1998

Divergent changes in plasma ACTH and pituitary POMC mRNA after cortisol administration to late-gestation ovine fetus.

Plasma concentrations of cortisol and adrenocorticotropic hormone (ACTH) rise in the late-gestation sheep fetus at approximately the same time as there is an increase in the plasma levels of corticosteroid-binding globulin (CBG). We hypothesized that intrafetal cortisol infusion during late pregnancy would stimulate an increase in fetal plasma CBG, which in turn would bind cortisol and diminish glucocorticoid negative-feedback regulation of the fetal pituitary, leading to an increase in plasma ACTH concentrations. Cortisol was infused into chronically catheterized fetal sheep beginning at 126.1 +/- 0.5 days of gestation and continued for 96 h. Control fetuses were infused with saline. In cortisol-infused fetuses, the plasma cortisol concentrations rose significantly from control levels (4.4 +/- 0.6 ng/ml) to 19.3 +/- 3.1 ng/ml within 24 h and remained significantly elevated throughout the infusion period. Plasma immunoreactive (i.r.) ACTH concentrations were significantly elevated in cortisol-infused fetuses within 24-48 h and remained significantly higher than in controls throughout the 96-h experimental period. Plasma free cortisol concentrations increased 10-fold and remained significantly elevated in cortisol-infused animals, despite a rise in plasma corticosteroid-binding capacity. Levels of pituitary proopiomelanocortin (POMC) mRNA in the fetal pars distalis and pars intermedia were 96 and 38% lower, respectively, after 96 h of cortisol infusion. Therefore physiological elevations of plasma cortisol, in the late-gestation ovine fetus, lead to increases in mean plasma irACTH concentrations, but this is not associated with increases in fetal pituitary POMC mRNA levels.

Adrenocorticotropic Hormone↗
PubMed1998

Human sex hormone-binding globulin gene expression in transgenic mice.

The sex hormone-binding globulin gene (shbg) is expressed in the liver and testis as well as in several other tissues that play important roles in reproduction. Expression of shbg in the human liver results in the production of plasma sex hormone-binding globulin (SHBG), which regulates the bioavailability of sex steroids in the blood. Although shbg is not expressed in rodent livers postnatally, it gives rise to the androgen-binding protein in their testes upon sexual maturation. Human shbg is also expressed in the testis, but its products and their function are less well characterized. To study the expression of human shbg in different tissues and the consequences of overexpressing this gene in vivo, we have produced several lines of mice containing approximately 11-kilobase (kb; shbg11) or 4.3-kb (shbg4) human shbg genomic fragments that comprise all eight exons encoding SHBG as well as approximately 6 kb or approximately 0.9 kb of 5'-flanking DNA, respectively. Northern blots indicated that human shbg transcripts were most abundant in liver, kidney, and testis of the shbg11 mice. The 4.3-kb shbg transgenes were expressed at similar levels in liver and kidney, but the abundance of human shbg transcripts in their testes was much lower than that in shbg11 mice. Primer extension analysis indicated that transcription starts 60 bp from the translation initiation codon for SHBG in liver and kidney of shbg11 mice, and that the shbg transcripts in their testis are derived from a separate promoter flanking an alternative exon that replaces the exon containing the translation initiation codon for SHBG or androgen-binding protein. At the cellular level, the human shbg transgenes are expressed in clusters of hepatocytes located mainly within the periportal region of hepatic lobules and in the epithelial cells lining the proximal convoluted tubules of the kidney. This results in high levels of human SHBG in serum (1.45-1.72 nmol/ml) and urine (6-16 pmol/ml) of mature male shbg mice. The abundance and distribution of human shbg transcripts in the Sertoli cells of shbg11 mice vary throughout the spermatogenic cycle, with levels increasing in the Sertoli cell cytoplasm until stage VII of spermatogenesis and declining after stage IX. At stages X-XII of spermatogenesis, these transcripts concentrate at the adluminal compartment of the Sertoli cells, and this suggests that they have a role in the elongation phase of spermiogenesis. The presence of human SHBG in the blood of shbg transgenic mice may result in serum levels of testosterone that are 10-100 times higher than those in wild-type littermates. Despite this, their reproductive performance is normal, and there is no obvious phenotypic abnormalities even in animals homozygous for the transgenes.

Animals↗
PubMed1997

Hepatic nuclear proteins that bind cis-regulatory elements in the proximal promoter of the rat corticosteroid-binding globulin gene.

The plasma transport protein for glucocorticoids, corticosteroid-binding globulin (CBG), is produced by hepatocytes, and expression of the CBG gene (Cbg) in the liver is controlled by a variety of hormones, environmental stimuli, and developmental cues. The rat Cbg proximal promoter, including 145 base pairs (bp) from the transcription start site, contains two cis-regulatory elements (designated P1 and P2), and is as transcriptionally active as a much more extended region (approximately 1.2 kbp) of the promoter. We have now characterized the rat liver nuclear proteins that interact with P1 and P2. Several proteins interacted specifically with P1 during an electrophoretic mobility shift assay (EMSA), and based on ultraviolet (UV) cross-linking and Southwestern blot analyses, as well as an antibody-supershifting EMSA, one of these has been identified as hepatic nuclear factor (HNF)1 beta. The major band shift formed with P2 in an EMSA appears to comprise a protein that migrates as a doublet of 58 and 62 KDa on sodium dodecylsulfate-polyacrylamide gel ectrophoresis (SDS-PAGE) after UV cross-linking with an oligonucleotide containing P2, as well as during Southwestern blot analyses. Mutations of the CCAAT sequence within P2 also prevent binding to this protein, the physicochemical properties of which resemble the CCAAT-binding protein CP2. Functional analyses of this region of the rat Cbg proximal promoter fused to a luciferase reporter gene demonstrated that mutations within P1, which prevent its interaction with NHF1, do not influence adversely its transcriptional activity. Thus, although members of the HNF1 family of nuclear proteins play an essential role in the transcriptional activation of several other related genes (e.g., thyroxin-binding globulin and alphal-antitrypsin) in hepatocytes, HNF1 beta does not appear to be required for the basal activity of the rat Cbg promoter. In addition, deletion of P2 from the proximal promoter abolishes transcriptional activity and the CCAAT-binding protein that interacts with P2 probably represents an important determinant of Cbg expression under different physiological conditions.

Animals↗
PubMed1997

The effects of estradiol-17 beta infusion into fetal sheep in late gestation.

Activation of the hypothalamic-pituitary-adrenal (HPA) axis of fetal sheep during late gestation is associated with increases in plasma concentrations of adrenocorticotropic hormone (ACTH) and cortisol, and ultimately results in parturition. However, the mechanisms contributing to the concurrent increases in ACTH and cortisol are unclear. Plasma estradiol-17 beta (E2) concentrations increase progressively in the prepartum ovine fetus, and we hypothesized that E2 may influence HPA activity by affecting either basal and/or hypoxemia-stimulated ACTH release. We examined potential mechanisms, including altered expression of pro-opiomelanocortin (POMC) in fetal pituitary corticotrophs, and changes in corticosteroid binding globulin (CBG) and/or the enzymes 11 beta hydroxy steroid dehydrogenase (11 beta HSD)-1 or 11 beta HSD-2 in liver and placenta, that could alter negative feedback control. We infused fetal sheep at 127 d of gestation with either E2 (100 micrograms/24 h) or saline for 100 h. Fetal arterial blood samples were collected at 8 h intervals during the infusion of E2 or saline (n = 4), for measurement of basal plasma ACTH and cortisol concentrations, as well as plasma corticosteroid binding capacity (CBC). Placenta and fetal liver samples were collected at 100 h for measurement of placental 11 beta HSD-1 and 11 beta HSD-2 mRNA and hepatic CBG and 11 beta HSD-1 mRNA, by Northern blotting. Fetal pituitary samples were collected for measurement of POMC mRNA by in situ hybridization. In a separate experiment, fetuses were exposed to 2 h of hypoxemia at 75 h of E2 or saline infusion (n = 4), and fetal arterial blood samples were collected during the period of hypoxemia for measurement of plasma ACTH and cortisol concentrations. E2 infusion had no effect on basal plasma concentrations of ACTH or total cortisol, or on the stimulated levels of ACTH or total cortisol achieved in response to hypoxemia. Basal fetal pituitary POMC mRNA also did not change significantly with E2 infusion. No significant increases were observed in plasma CBC during E2 administration. However, hepatic CBG and 11 beta HSD-1 mRNA were significantly elevated in the livers of E2-treated fetuses. Placental 11 beta HSD-1 mRNA; but not 11 beta HSD-2 mRNA was increased by E2 treatment. These data do not support a direct effect of exogenous E2 at the level of basal or hypoxemia-stimulated ACTH output, but suggest that elevated E2 concentrations may alter the expression of genes encoding proteins implicated in tonic regulation of fetal HPA function.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed1997

What is the appropriate size criterion for resection of thoracic aortic aneurysms?

Although many articles have described techniques for resection of thoracic aortic aneurysms, limited information on the natural history of this disorder is available to aid in defining criteria for surgical intervention. Data on 230 patients with thoracic aortic aneurysms treated at Yale University School of Medicine from 1985 to 1996 were analyzed. This computerized database included 714 imaging studies (magnetic resonance imaging, computed tomography, echocardiography). Mean size of the thoracic aorta in these patients at initial presentation was 5.2 cm (range 3.5 to 10 cm). The mean growth rate was 0.12 cm/yr. Overall survivals at 1 and 5 years were 85% and 64%, respectively. Patients having aortic dissection had lower survival (83% 1 year; 46% 5 year) than the cohort without dissection (89% 1 year; 71% 5 year). One hundred thirty-six patients underwent surgery for their thoracic aortic aneurysms. For elective operations, the mortality was 9.0%; for emergency operations, 21.7%. Median size at time of rupture or dissection was 6.0 cm for ascending aneurysms and 7.2 cm for descending aneurysms. The incidence of dissection or rupture increased with aneurysm size. Multivariable regression analysis to isolate risk factors for acute dissection or rupture revealed that size larger than 6.0 cm increased the probability by 32.1 percentage points for ascending aneurysms (p = 0.005). For descending aneurysms, this probability increased by 43.0 percentage points at a size greater than 7.0 cm (p = 0.006). If the median size at the time of dissection or rupture were used as the intervention criterion, half of the patients would suffer a devastating complication before the operation. Accordingly, a criterion lower than the median is appropriate. We recommend 5.5 cm as an acceptable size for elective resection of ascending aortic aneurysms, because resection can be performed with relatively low mortality. For aneurysms of the descending aorta, in which perioperative complications are greater and the median size at the time of complications is larger, we recommend intervention at 6.5 cm.

Adolescent↗
PubMed1997

Glucocorticoids induce corticosteroid-binding globulin biosynthesis by immature mouse liver and kidney.

Marked changes in mouse corticosteroid-binding globulin (CBG) gene expression in the liver and kidney occur postnatally. To study the influence of glucocorticoids on the initiation of mouse CBG biosynthesis in these tissues during the first two weeks after birth, we administered dexamethasone (0.5 microgram/g body wt/day) to 4- and 11-day-old pups for three days. This resulted in higher serum CBG and hepatic CBG mRNA levels in animals, irrespective of their ages. Higher relative amounts of CBG mRNA in the kidneys of 14-day-old pups after three days of dexamethasone treatment co-incided with higher amounts of intact and proteolytically cleaved CGB in their urine, and both are indicative of increased CGB production by the developing renal tubules. When an additional group of 11-day-old pups (n = 4) was treated with 0.25 microgram dexamethasone/g body weight per day for five days, this also resulted in significantly higher levels of serum CBG (P < 0.01), hepatic CBG mRNA (P < 0.01) and renal CBG mRNA (P < 0.05), compared to littermates treated with the oil vehicle alone. In contrast, serum CBG levels progressively decreased in adult female mice during five days of treatment with 0.5 microgram dexamethasone/g body weight per day. Taken together, these data indicate that glucocorticoids induce murine CBG gene expression in the immature liver and kidney, and support the concept that the effects of glucocorticoids on CBG gene expression are developmentally stage-specific.

Age Factors↗
PubMed1997

Mitral, tricuspid, and aortic valve repair or reconstruction.

The term repair is most properly applied to disease affecting the mitral and tricuspid valves or their annuli. The rationale, description, and analyses of the most recent evolution in these repair techniques are reviewed. The aortic valve cannot easily be repaired in the true sense of the word. The more proper term is sparing of the aortic valve in diseases that primarily affect the aortic root and annulus or reconstruction of the valve using pericardium in disease that primarily affects the valve. The evolution and current rationale for these techniques are also reviewed, and opinions regarding their future potential are rendered.

Aortic Valve↗
PubMed1997

Rabbit sex hormone binding globulin: primary structure, tissue expression, and structure/function analyses by expression in Escherichia coli.

Sex hormone binding globulin (SHBG) is a homodimeric plasma protein found in mammals that binds sex steroids with high affinity and regulates their bioavailability. The protein is identical in structure and properties to the androgen binding protein (ABP) found in the male reproductive tract. We have isolated a 1245-base pair rabbit SHBG cDNA encoding a reading frame for a signal peptide followed by a protein of 367 amino acids, which shares 79.0, 68.1 and 63.2% amino acid identity with the corresponding human, rat and mouse proteins respectively. Northern blot and hot-nested PCR analyses indicated that rabbit SHBG is produced from a 1.6 kilobase mRNA in the liver of both sexes and in the testis. The rabbit SHBG cDNA was inserted into pGEX-1 lambda T for expression of a glutathione S-transferase/SHBG fusion protein in Escherichia coli. The bacterial product bound 5 alpha-dihydrotestosterone (DHT) in the same manner as the corresponding protein in serum. The dissociation constants (Kd) for rabbit and human SHBGs produced in E. coli were 11.1 +/- 1.1 nM and 2.1 +/- 0.6 nM respectively, and rabbit SHBG formed a less stable protein-steroid complex (t1/2 = 5 min) than human SHBG (t1/2 > 60 min). Unlike human SHBG, rabbit SHBG does not bind estradiol with high affinity. To aid in the identification of differences in the sequences of rabbit and human SHBG, which determine species differences in steroid-binding affinity and specificity, chimeras containing the 5'-terminal half of SHBG from one species and 3'-terminal half of SHBG from the other species were constructed and expressed. It was found that the chimeric proteins assumed similar steroid-binding affinity and specificity as the wild-type proteins when the amino (N)-terminal half of SHBG was derived from the same species. Replacement of the carboxyl (C)-terminal half of rabbit SHBG by the corresponding region of the human molecule increased the integrity of its steroid-protein complex. This supports the concept that amino acids within the N-terminal half of SHBG constitute the steroid-binding domain while the C-terminal half of the molecule may provide structural stability to the protein and its steroid-binding site.

Amino Acid Sequence↗
PubMed1996

The mitochondria are recognition organelles of cell stress.

The cellular response to stress includes synthesis of specific stress proteins in the presence of a generalized suppression of protein synthesis. The response occurs in intact animals, individually stressed organs of intact animals, donor organs upon removal, regardless of preservation methods, and cells in culture. The molecular biology of stress protein induction is not understood. While stress proteins are beneficial, overall suppression of protein synthesis, if prolonged, is harmful. Since altered energy metabolism is integral to stress induction, we examined the mitochondria to determine if they could provide a possible molecular mechanism for initiating the response. Rat myoblasts were incubated at varying temperatures for up to 120 min in [35 S] methionine. Proteins were separated electrophoretically and newly synthesized proteins visualized autoradiographically. Isolated mitochondria from resting rat myoblasts were then stressed, label incorporation determined, and newly synthesized protein was visualized. Stress sharply suppressed protein synthesis in mitochondria but autoradiograms of stressed mitochondria showed that a single stress protein of 18 kDa was synthesized. Mitochondria independently respond to stress and synthesize a stress protein from their own DNA. This protein may provide an intermediary pathway that links stressful conditions in the environment to the overall response observed in the cell.

Animals↗
PubMed1996

Sex hormone-binding globulin: gene organization and structure/function analyses.

Human plasma sex hormone-binding globulin (SHBG) and testicular androgen-binding protein (ABP) are homodimeric glycoproteins with a single steroid-binding site. They share the same primary structure and differ only with respect to the types of oligosaccharides attached to them. Both are products of a single gene (Shbg), the expression of which has been detected in several tissues including liver, testis, placenta, brain and endometrium. The transcript encoding SHBG in hepatocytes and ABP in Sertoli cells is identical. Several other transcripts result from differential exon utilization in sex steroid-responsive tissues, but their biological significance remains obscure. Wild-type and mutant forms of human SHBG have been produced in mammalian cells and Escherichia coli, and have provided insight into the structural and functional properties of SHBG and its related gene products.

Animals↗
PubMed1996

Growth response of adult germ cells to rat androgen-binding protein and human sex hormone-binding globulin.

Androgen-binding protein (ABP) is produced by Sertoli cells depending on the development and the stage of the spermatogenic cycle. Germ cell proliferation is at its peak when ABP is at its peak and secreted towards the testicular basal compartment containing spermatogonia and premeiotic spermatocytes. Rat isolated adult germ cell DNA synthesis was studied in vitro in the presence of ABP with and without steroids and in the presence of pure or recombinant sex steroid hormone-binding globulin (SHBG) using thymidine incorporation. Results are: SHBG is able to promote DNA synthesis in the absence of cofactors. Testosterone reacted negatively to the stimulatory effect of SHBG. We conclude that ABP, the physiological steroid-binding protein, should be considered as a paracrine regulator of spermatogenic DNA synthesis in the adult rat.

Androgen-Binding Protein↗
PubMed1996

Developmental regulation of corticosteroid-binding globulin biosynthesis in the baboon fetus.

The present study determined the roles of estrogen and cortisol in maternal and fetal corticosteroid-binding globulin (CBG) levels and fetal hepatic messenger RNA (mRNA) expression in the baboon. Samples of fetal liver, kidney, and brain were obtained from untreated control animals at early (day 60; n = 4), mid (day 100; n = 8), and late (day 165; n = 5) gestation (term = day 184). Maternal and umbilical blood samples were collected on day 100 from baboons in which betamethasone was administered sc to the mother (n = 6) on days 60-99 of gestation and on day 165 from animals (n = 4) in which the fetus was administered betamethasone on days 150-164 of gestation. Maternal serum cortisol concentrations were similar at mid (43 +/- 2 micrograms/dl) and late (42 +/- 3 micrograms/dl) gestation and decreased (P < 0.05) at midgestation (1 +/- 1 micrograms/dl) and term (31 +/- 4 micrograms/dl) after betamethasone treatment. Umbilical serum cortisol levels were also reduced (P < 0.05) at both mid (1 +/- 1 micrograms/dl) and late (14 +/- 5 micrograms/dl) gestation by betamethasone treatment. Fetal serum CBG levels in untreated animals were lower (P < 0.05) on day 165 (444 +/- 29 pmol/ml) than on day 100 (844 +/- 35 pmol/ml) and increased (P < 0.05) at midgestation (1098 +/- 64 pmol/ml), but not at term (551 +/- 24 pmol/ml), after betamethasone treatment. In contrast, maternal serum CBG levels (range, 528-770 pmol/ml) were not altered by gestational age or betamethasone. The human CBG complementary DNA hybridized to a single mRNA species of 1.8 kilobases in baboon fetal liver; however, CBG was not expressed in fetal kidney and was detectable in fetal brain and pancreas only by reverse transcription-PCR. In untreated baboon fetuses, the mRNA levels of hepatic CBG, expressed as a ratio of 18S RNA, progressively decreased (P < 0.05) in early (1.83 +/- 0.17), mid (0.97 +/- 0.12), and late (0.51 +/- 0.04) gestation. These results demonstrate that fetal hepatic CBG mRNA expression and serum CBG concentrations were elevated early in baboon gestation and exhibited a progressive decline during the course of advancing pregnancy. We suggest that the increased levels of fetal CBG in the early stages of gestation reflect stimulation of hepatic CBG synthesis by maternal cortisol, which we previously demonstrated to occur in the fetus as a result of preferential 11 beta-hydroxysteroid dehydrogenase-catalyzed glucocorticoid reduction across the placenta. The decline in fetal CBG may reflect the developmental increase in catabolism of cortisol to bioinactive cortisone in target tissues of the fetus such as the liver.

Animals↗
PubMed1996

Reoperative mitral valve surgery via right thoracotomy: decreased blood loss and improved hemodynamics.

BACKGROUND AND AIMS OF THE STUDY: Reoperative mitral surgery via sternotomy can be associated with significant complications, including excessive blood loss and injuries to the heart, great vessels and patent coronary artery grafts. The right antero-lateral thoracotomy offers excellent exposure with less risk from re-entry. MATERIALS AND METHODS: Between 1982 and 1992, 221 patients had repeat mitral valve procedures at our institution. Fifteen of these 221 underwent mitral valve replacement via right thoracotomy. Indications for surgery in each group included bioprosthetic valve failure, paravalvular leak and bacterial endocarditis. Fifteen patients having reoperative mitral valve surgery via right thoracotomy approach were compared with a control group of 33 patient who underwent surgery via repeat sternotomy. All thoracotomy patients underwent mitral replacement or repair with ventricular fibrillation without aortic cross-clamping. Operative time, cardiopulmonary bypass time, requirement for inotropic support, blood loss within the first six postoperative hours, number of blood units transfused, length of ICU stay, days to discharge, and 30-day survival were compared between the two groups. In addition, the preoperative PaO2/FiO2 (P/F) ratio was evaluated as a prognostic indicator. RESULTS: Bypass time (162 +/- 43 min thoracotomy group vs. 131 +/- 34 min sternotomy group), operative time (389 +/- 100 min thoracotomy group vs. 450 +/- 25 min sternotomy group), ICU stay (6 +/- 8 days thoracotomy group vs. 5 +/- 6 days sternotomy group), P/F ratio (352 +/- 142 thoracotomy group vs. 423 +/- 108 sternotomy group), and 30-day survival (93% thoracotomy group vs. 91% sternotomy group) were not found to be significantly different between groups. Of great significance was the reduction in blood loss (277 +/- 152 ml thoracotomy vs. 651 +/- 504 ml sternotomy, p < 0.05) and blood transfused (2.0 +/- 1.7 units thoracotomy vs. 6.5 +/- 3.3 units sternotomy, p < 0.01) with the thoracotomy approach. Also of significance was a reduction in frequency with which significant inotropic support was needed to separate from cardiopulmonary bypass (26% vs. 63%, p < 0.05). Despite decreased access to the heart for de-airing maneuvers, no cerebrovascular events whatsoever were noted with the thoracotomy approach. CONCLUSION: The right thoracotomy approach is recommended for redo mitral valve surgery. Despite these advantages, severe pulmonary dysfunction (as indicated by a P/F ratio less than 300) correlated with a prolonged hospital course in four thoracotomy patients; such patients should have repeat sternotomy.

Blood Loss, Surgical↗
PubMed1995

Optimal timing of coronary artery bypass graft surgery after acute myocardial infarction.

BACKGROUND: To assess optimal timing for coronary artery bypass graft surgery (CABG) after an acute myocardial infarction (AMI), all patients undergoing CABG without associated procedures at our institution from January 1, 1991, to July 30, 1992, were reviewed. Patients were divided into three groups based on time from infarct to revascularization. The control group consisted of patients operated on for angina refractory to medical management. Relative risks (incident infarction group divided by incident control group) were established for need of vasopressors, new balloon to separate from bypass, perioperative myocardial infarction, and hospital mortality. METHODS AND RESULTS: One hundred sixteen patients underwent CABG within 6 weeks of infarction. In the experimental group, 58 patients underwent CABG for non-Q-wave infarction, and 58 patients underwent CABG for Q-wave infarction. In the control group, 255 patients underwent surgery for angina without infarction. Patients were analyzed by group relative to the time between infarction and CABG. Patients were analyzed between infarction and CABG and assigned to one of three groups. Group 1 patients were revascularized within 48 hours; group 2, between 3 and 5 days; and group 3, after 5 days. Significance was determined by Fisher's exact or Mantel-Haenszel chi 2 test where appropriate. Multivariate analysis was performed on statistics that were significant. All patients within all groups after Q-wave or non-Q-wave myocardial infarction had a significantly higher risk of needing an intra-aortic balloon pump and vasopressors to be weaned from bypass and a greater incidence of perioperative MI compared with control patients. Surgical mortality is highest immediately after Q-wave infarctions. CONCLUSIONS: Patients with non-Q-wave infarction may undergo CABG relatively safely at any time. Acceptable timing for CABG after Q-wave infarction is after 48 hours.

Aged↗