The Society of Thoracic Surgeons ad hoc Committee on AIDS. Report to the membership.
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Acquired Immunodeficiency Syndrome↗
Biomedical subjects
R E Clark
Publications and source records attributed to R E Clark.
Effect of left ventricular septal myectomy on concurrent mitral regurgitation.
To assess the impact of left ventricular septal myectomy (Morrow procedure) performed for obstructive hypertrophic subaortic stenosis on co-existing mitral regurgitation, we examined the preoperative and postoperative left ventriculograms of 35 patients (13 of them women) who underwent left ventricular septal myectomy alone or with concomitant operation. The mean age was 45 +/- 3 years (range, 19 to 74 years). Patients underwent left ventriculography at an average of 15 +/- 3 months postoperatively (range, 1 to 78 months). Severity of mitral regurgitation was evaluated by two teams of reviewers. Mitral regurgitation due to catheter entrapment or to premature ventricular contraction or other arrhythmia was excluded. Overall, 51% of patients showed improvement in the severity of mitral regurgitation, and all those with more severe mitral regurgitation (ie, 3+) demonstrated improvement. The population was subdivided for analysis into those with coronary artery disease requiring bypass grafting at the time of left ventricular septal myectomy (n = 7, 20%) and those without coronary artery bypass grafting. Among the 7 patients undergoing bypass grafting, 71% demonstrated improvement in the degree of mitral regurgitation as compared with only 46% of those without bypass grafting (p less than 0.005 by X2 analysis). Significant reductions in peak gradients at rest and in response to provocation, and in New York Heart Association functional class, also occurred in both groups.
Adult↗
Clinical and hemodynamic results after mitral valve replacement in patients with obstructive hypertrophic cardiomyopathy.
Mitral valve replacement has been performed in patients with obstructive hypertrophic cardiomyopathy if: (1) the interventricular septum is smaller than 18 mm in the region of usual resection; (2) atypical septal morphology is encountered; (3) a previous left ventricular myomectomy has been performed but residual major obstruction and symptoms persist; or (4) intrinsic mitral valve disease exists. Since 1983, mitral valve replacement has been performed in 58 patients with obstructive HCM only. Thirty-three female patients (mean age, 47.9 years) and 25 men (mean age, 45.7 years) met criteria 1 through 3 for mitral valve replacement. Patients with intrinsic mitral valve disease (criterion 4) were omitted from this study. All patients were in New York Heart Association functional class III or IV and had failed optimal medical therapy. Low-profile mechanical prostheses and bioprostheses were implanted, and the early mortality (less than 30 days or in the hospital) was 8.6% (5/58). Six patients (11.3%) died late, 3 suddenly of probably arrhythmia, 2 of respiratory failure, and 1 of an anticoagulant-related complication. After mitral valve replacement, 40 (83%) of 48 patients surviving operation and returning for evaluation were in functional class I or II, whereas 8 patients were in functional class III. Hemodynamic data obtained 6 months postoperatively showed that pulmonary artery wedge pressure was normal (13.7 +/- 4 mm Hg [+/- standard deviation]), left ventricular end-diastolic pressure had decreased (10.9 +/- 3.4 mm Hg), cardiac index was maintained (2.6 +/- 0.6 L/min/m2), and resting and provoked gradients were unremarkable. Mean follow-up was 24.2 months, actuarial survival was 86% at 3 years, and survival free from thromboembolism, anticoagulant-related complication, reoperation, and congestive heart failure for the same interval was 68%. Complications such as ventricular septal defect and complete heart block are avoided in patients undergoing mitral valve replacement, but device-related and cardiac-related complications can add to the morbidity and mortality in these patients in the long term.
Adult↗
It is time for a national cardiothoracic surgical data base.
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Cardiac Surgical Procedures↗
Differences in bone marrow cytogenetic characteristics between treated and untreated myeloma.
Clonal karyotypic abnormalities in myelomatosis at initial diagnosis have been widely studied, but little data are available on the karyotypic status following treatment. We have studied bone marrow (BM) from 17 cases of untreated myelomatosis at initial diagnosis and from a further 29 cases who had received chemotherapy with regimens containing alkylating agents. At the time of study all previously treated cases had been off treatment for at least 152 days, had a paraprotein level in plateau phase, had a BM with less than 4% blasts, and in 28 of these 29 cases had less than 20% BM plasma cells. Two cases had more than 15% BM ringed sideroblasts; one other case was transfusion dependent. Clear differences in cytogenetic characteristics between the two groups were seen. At initial diagnosis clonal karyotypic abnormalities were observed in six of 11 accessible cases. All had hyperdiploid clones (of 49-54 chromosomes) and showed characteristic involvement of chromosomes 3, 5, 7, 9, 11, 15, 19 and 21. Additional structural rearrangements were present in only two of these cases. Following treatment, clonal abnormalities were seen in 10 of 25 assessible cases, of which only two showed hyperdiploidy (one with a hyperdiploid line, one with an additional derived chromosome). The remaining eight showed hypodiploid or pseudodiploid lines, and seven of these showed complex karyotypes with multiple rearrangements particularly affecting chromosomes 1, 2, 3, 6 and 7. After a minimum follow-up of 16 months, only four of these 10 cases (40%) remain alive compared with 12 of 15 (80%) with a normal karyotype after treatment (P = 0.03). No correlation was observed between the presence of an abnormal karyotype and the total dose or timing of previous therapy, though cases with an abnormal karyotype tended to have received treatment for longer (790 +/- 166 days) than cases with a normal karyotype (486 +/- 50 days). It is not clear whether the ploidy difference between the two groups represents a change in the disease state due to treatment or a direct effect of treatment itself.
Aged↗
Enhanced regional left ventricular function after distant coronary bypass by means of improved collateral blood flow.
To determine whether coronary artery bypass surgery can improve function in left ventricular regions not amenable to direct revascularization, 24 patients with multivessel coronary artery disease were studied by radionuclide angiography and coronary arteriography before and 6 months after coronary artery bypass surgery. All had proximal stenosis of the left circumflex artery or a major obtuse marginal branch. Left ventricular regional function was assessed by dividing the left ventricular region of interest into 20 sectors; the 8 sectors corresponding to the posterolateral free wall were used to assess function in the left circumflex artery distribution. Change in function in the left anterior descending territory was not analyzed because of the non-specific septal hypokinesia that develops postoperatively. For the total group, coronary artery bypass surgery significantly increased both global left ventricular ejection fraction during exercise (43 +/- 13% to 50 +/- 14%, p less than 0.001) and the change in ejection fraction from rest to exercise (-7 +/- 10% to 0 +/- 6%, p less than 0.001). Such improvement was observed in 9 of 10 patients with all stenoses bypassed, and to an equivalent degree in 9 of 10 patients in whom the left circumflex artery either could not be bypassed or the bypass graft was occluded (but bypass grafts to other coronary arteries were patent). Similarly, regional ejection fraction in posterolateral segments during exercise also increased comparably after operation in patients with a patent (from 57 +/- 18% to 70 +/- 19%, p less than 0.001) or nonpatent (from 51 +/- 14% to 68 +/- 14%, p less than 0.001) left circumflex graft.(ABSTRACT TRUNCATED AT 250 WORDS)
Aged↗
Results of operation for coexistent obstructive hypertrophic cardiomyopathy and coronary artery disease.
This study describes the operative management and outcome of 28 patients with obstructive hypertrophic cardiomyopathy and hemodynamically significant coronary artery disease. Each patient underwent coronary artery bypass grafting and concomitant left ventricular myotomy-myectomy or mitral valve replacement. The mean age at operation was 59 years (range 42 to 74). Five patients (18%) died as a result of operation, four in the immediate postoperative period and one at 2 months postoperatively. Three patients died after the immediate postoperative period of causes unrelated to the operation. The mean follow-up period for the 20 currently surviving patients was 4.8 years (range 4 months to 10.8 years). Nineteen of these patients have experienced substantial functional improvement; all are currently asymptomatic or only mildly symptomatic. Twenty-one patients underwent cardiac catheterization before and after operation; each experienced relief of left ventricular outflow tract obstruction after operation. Twelve patients had a preoperative outflow gradient greater than or equal to 50 mm Hg (average 86 +/- 7) under basal conditions, which decreased to 3 +/- 1.8 mm Hg postoperatively (p less than 0.001). Nine patients had a severe preoperative gradient only with a provocative maneuver (average 93 +/- 6 mm Hg), which decreased to 24 +/- 8 mm Hg postoperatively (p less than 0.001). Five of the 24 patients undergoing left ventricular myotomy-myectomy incurred an iatrogenic ventricular septal defect. This operative complication occurred primarily in patients with a relatively thin ventricular septum (less than 20 mm) and contributed importantly to postoperative death in two of the patients.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Amiodarone-induced complications after cardiac operation for obstructive hypertrophic cardiomyopathy.
The occurrence of unanticipated and seemingly unexplicable major complications of hepatic, pulmonary, and cardiac dysfunction after palliative operation for obstructive hypertrophic cardiomyopathy prompted a review of 71 sequential patients. Fifty-five patients had been treated preoperatively with beta-blockers, calcium-channel inhibitors, or both, and 16 had received amiodarone for six to 566 days (mean time, 210 days) at total doses ranging from 8 to 175 g (mean dose, 82 g) and had drug-free intervals prior to operation of zero to 457 days (mean time, 91 days). Comparisons were made between the two treatment groups and between those with and without major complications within the amiodarone-treated group. Preoperative cardiac studies, sex, age, functional class, and type of operation were not related to outcome for the entire patient cohort. In amiodarone-treated patients, the major findings were as follows: a 50% incidence of hepatic dysfunction with a tenfold increase in concentrations of serum glutamic-oxaloacetic transaminase and serum glutamic-pyruvic transaminase; a 25% incidence of pulmonary dysfunction necessitating a fourfold increase in the number of days of ventilator support; and a 19% incidence of low cardiac output syndrome with two deaths. Only 44% of the amiodarone-treated group had no serious complications. The incidence of major complications of the liver, lungs, and heart was 2%, 0%, and 2%, respectively, in patients not treated with amiodarone. Abnormal preoperative pulmonary function studies were predictive of prolonged postoperative ventilatory support. Discontinuation of amiodarone for several months prior to operation appeared to reduce the incidence of major complications. The necessary drug-free interval required preoperatively could not be determined from this retrospective experience.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Cardiac allograft survival across major histocompatibility complex barriers in the rhesus monkey following T lymphocyte-depleted autologous marrow transplantation. II. Prolonged allograft survival with extensive marrow T cell depletion.
In the present study, we tested the possibility that a vascularized allograft might induce immunological tolerance in a myeloablated host, similar to the tolerance induced by allogeneic bone marrow grafts. To this end, we developed a rhesus monkey model consisting of myeloablative total-body irradiation and T cell-depleted autologous marrow transplantation followed by MHC-mismatched heterotopic cardiac allograft implantation. Limiting dilution analysis was used to quantify residual marrow T cells following depletion. We found that (1) allograft survival was substantially prolonged in the absence of immunosuppressive drugs (median survival = 160 days) over that seen in controls treated identically but receiving non-T cell-depleted marrow (median survival = 14 days); (2) there was a correlation between allograft survival prolongation and the extent of marrow T cell depletion, with a maximum survival of 329 days associated with a residual marrow T cell content of 0.00014%; (3) nonspecific immune deficiency--and, possibly, specific unresponsiveness of limited duration (determined by cryopreserved donor and third-party skin grafting)--contributed to the rejection-free period seen in recipients of extensively depleted marrow; (4) late allograft rejection occurred in 3 of 3 long-term survivors, thereby demonstrating that permanent tolerance was not induced by the allograft across MHC barriers; and (5) as few as 1.4 x 10(4) infused marrow T cells/kg were sufficient to mediate acute allograft rejection, a threshold approximately 10-fold lower than that reported for the induction of acute graft-versus-host disease following allogeneic bone marrow transplantation.
Animals↗
Anticalcification treatments of bioprosthetic heart valves: in vivo studies in sheep.
Studies performed by other investigators have shown that a number of preimplantation processes inhibit the calcification of pieces of porcine aortic valves and of bovine parietal pericardium subcutaneously implanted in rats. To evaluate biological reactivity with these biomaterials functioning in an intracardiac position, mitral and tricuspid valve replacements were performed in young sheep to assess the effects of the following preimplantation processes: (1) surfactants, including sodium dodecyl sulfate, polysorbate-80, Triton X-100 and N-lauryl sarcosine; (2) covalently bound aminohydroxypropane diphosphonic acid; (3) toluidine blue; and (4) incorporation of polyacrylamide into valvular tissues. Quantitative calcium analyses showed that only the surfactants substantially reduced calcification, and only in porcine aortic valvular bioprostheses. However, morphological studies showed that some of these agents also induced alterations that decreased the durability of the valves. Toluidine blue decreased calcification to a degree that was statistically significant, but not biologically important. Polyacrylamide incorporation and diphosphonate binding increased calcification. Thus, data regarding anticalcification treatments obtained from subcutaneous implantation studies in small animal models should be cautiously interpreted and validated by studies with intracardiac valvular implantation in large animals.
Acrylic Resins↗
Pharmacokinetics and distribution of heparin-binding growth factor I (endothelial cell growth factor) in the rat.
Heparin-binding growth factor I (HBGF I), previously designated as endothelial cell growth factor, is a potent mitogen for endothelial cells in vitro, which may prove useful for promoting endothelial regeneration in vivo. Analysis of the pharmacokinetics and organ distribution of HBGF I is necessary before use of HBGF I as a pharmacological agent. Consequently, pharmacological studies were carried out with [125I]HBGF I in the rat. Intravenous injections of HBGF I were given with or without heparin (2.5 units/ng HBGF I). Blood concentrations of HBGF I decreased by one half 17 seconds after HBGF I bolus. This time was prolonged to 60 seconds when HBGF I was injected with heparin. The elimination half-life of HBGF I was 14 minutes in the presence of heparin. The highest concentrations of HBGF I following intravenous bolus were found in kidney, liver, and spleen, and the lowest in fat and brain. Heparin increased HBGF I concentrations in blood and all organs measured except kidney, which was significantly decreased (p less than 0.01). Intact HBGF I was recoverable from blood 5 minutes following intravenous administration. HBGF I underwent near-complete proteolytic digestion after more prolonged ex vivo incubation with rat plasma, but HBGF I was protected from proteolysis when incubations were conducted in the presence of heparin. Thus, it is feasible that HBGF I can be administered as a pharmacological agent in the presence of heparin. Further studies assessing acceleration of in vivo endothelial growth using HBGF I with heparin appear warranted.
Animals↗
The effect of coronary artery bypass grafting on left ventricular systolic function at rest: evidence for preoperative subclinical myocardial ischemia.
Successful coronary artery bypass grafting (CABG) improves exercise-induced left ventricular (LV) dysfunction in patients with coronary artery disease (CAD), but its potential for improving resting LV function remains controversial. To assess the influence of CABG on LV function at rest, 31 CAD patients without previous myocardial infarction were studied before and 6 months after CABG by radionuclide angiography after all cardiac medicines were withdrawn. No patient had angina or ischemic electrocardiographic changes at rest. In 27 patients with patent bypass grafts, CABG significantly increased LV ejection fraction during exercise (47 +/- 11% before to 63 +/- 9% after operation, p less than 0.001), indicating reduction in exercise-induced LV ischemia. Moreover, LV ejection fraction at rest also increased (55 +/- 9 to 60 +/- 8%, p less than 0.001), with 20 of 27 patients manifesting an increase compared with preoperative values. Eleven of these 20 patients had apparently normal LV function at rest (ejection fraction and regional wall motion) before CABG. LV regional ejection fraction was computed by dividing the LV region of interest into 20 sectors. Regional analysis indicated that improved ejection fraction at rest after CABG occurred in regions developing ischemia during exercise before CABG. In 4 patients with occluded grafts, the ejection fraction at rest was unchanged by CABG globally (59 +/- 8 to 58 +/- 9%, difference not significant) and regionally. Thus, LV global and regional function at rest improved after successful CABG, even in patients with normal global LV ejection fraction and no visually detectable wall motion abnormality before surgery.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Influence of minoxidil on myocardial hemodynamics, regional blood flow, and morphology in beagle dogs.
Studies were made of the effects of two doses of minoxidil (3 mg/kg), given 24 hours apart, on cardiovascular hemodynamics, regional myocardial blood flow, and cardiac morphology in beagle dogs. Minoxidil caused increases in mean right atrial and left ventricular end-diastolic pressure. Systemic and pulmonary vascular resistance were reduced; cardiac output was increased. Left ventricular stroke work and the systolic pressure time index were unchanged by monoxidil administration. The diastolic pressure time index and ratio of diastolic/systolic pressure time index were decreased by minoxidil. Regional myocardial blood flow, measured with radioactive microspheres, increased in all regions of the heart except to the left ventricular papillary muscles. Minoxidil increased blood flow to left ventricular subendocardial tissue; however, this increase was significantly less than that observed in corresponding areas of subepicardial tissue, thus reducing the subendocardial/subepicardial tissue blood flow ratio. These results suggest that minoxidil is an effective peripheral vasodilator but may result in inadequate subendocardial perfusion. Morphologic studies disclosed two types of minoxidil-induced cardiac lesions: left ventricular papillary muscle necroses, and hemorrhagic lesions which were most prominent in right atrium and were associated with inflammation, intramural hemorrhage, and fibrinoid necrosis of small arteries. The papillary muscle necrosis were attributed to hypoxia. The atrial lesions were not of ischemic or hypoxic origin, because minoxidil did not decrease blood flow to atrial tissue. It is suggested that the atrial lesions are related to excessive vasodilation.
Animals↗
Dental and occlusal characteristics of children with neuromuscular disease.
Seventy-nine pediatric patients with neuromuscular diseases were examined for dental and occlusal characteristics. Fifty-six patients suffered from primary muscle disease (myopathies) including 43 with Duchenne's muscular dystrophy. The neuromuscular disorders in 19 patients were of neuropathic origin, while four were caused by a fault in the neuromuscular junction. Posterior crossbites occurred more often in the myopathies (57%) as compared with the neurogenic dystrophies (14%) (P less than 0.003). Although not statistically significant, the prevalence of open bite was also higher in the combined myopathies (21%) as compared with neurogenic disorders (9%). The Duchenne patients exhibited a statistically significant delay in dental emergence (1.06 years), unlike the other myopathies (0.31 years) and the neurogenic disorders groups (-0.03 years). This study emphasizes the influence of muscular environment on dental development in general. The dentition may be more affected in muscular dystrophies stemming from degenerative or inflammatory muscle damage than in those originating from nerve malfunction or disorder of the neuromuscular junction.
Adolescent↗
Guidelines for reporting morbidity and mortality after cardiac valvular operations.
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Actuarial Analysis↗
Myelodysplastic syndrome in a kindred with ins(16) (p11.2).
A constitutional karyotypic abnormality, ins(16)(p11.2), is described in a case of myelodysplastic syndrome (MDS). The source of material for this insertion could not be established, but did not arise from either a balanced deletion or translocation, and did not consist of constitutive heterochromatin as defined by C-banding. The same lesion was found in both sisters, both nephews and four of the five great-nephews. Of these, all were phenotypically and haematologically normal, with the exception of a great-nephew who at the age at the age of 6 exhibits features compatible with partial trisomy 16p. The relationship of the karyotypic abnormality to the MDS and partial trisomy 16p in this family is discussed.
Blood Cell Count↗
Long-term serial changes in left ventricular function and reversal of ventricular dilatation after valve replacement for chronic aortic regurgitation.
In most patients with aortic regurgitation, valve replacement results in reduction in left ventricular dilatation and an increase in ejection fraction. To determine the relation between serial changes in ventricular dilatation and changes in ejection fraction, we studied 61 patients with chronic severe aortic regurgitation by echocardiography and radionuclide angiography before, 6-8 months after, and 3-7 years after aortic valve replacement. Between preoperative and early postoperative studies, left ventricular end-diastolic dimension decreased (from 75 +/- 6 to 56 +/- 9 mm, p less than 0.001), peak systolic wall stress decreased (from 247 +/- 50 to 163 +/- 42 dynes x 10(3)/cm2), and ejection fraction increased (from 43 +/- 9% to 51 +/- 16%, p less than 0.001). Between early and late postoperative studies, diastolic dimension and peak systolic wall stress did not change, but ejection fraction increased further (to 56 +/- 19%, p less than 0.001). The increase in ejection fraction correlated with magnitude of reduction in diastolic dimension between preoperative and early postoperative studies (r = 0.63), between early and late postoperative studies (r = 0.54), and between preoperative and late postoperative studies (r = 0.69). Late increases in ejection fraction usually represented the continuation of an initial increase occurring early after operation. Thus, short-term and long-term improvement in left ventricular systolic function after operation is related significantly to the early reduction in left ventricular dilatation arising from correction of left ventricular volume overload. Moreover, late improvement in ejection fraction occurs commonly in patients with an early increase in ejection fraction after valve replacement but is unlikely to occur in patients with no change in ejection fraction during the first 6 months after operation.
Adult↗
Heparin-binding growth factor-I (endothelial cell growth factor) binds to endothelium in vivo.
Heparin-binding growth factor-I (HBGF-I) produces a significant increase in endothelial cell replication in vitro and may prove useful for endothelial regeneration and endothelial seeding in vivo. Heparin enhances the mitogenic effects of HBGF-I in vitro and may be an important adjunct to its pharmacologic use. Binding studies in the rat were undertaken to determine the feasibility of use of HBGF-I in vivo. For saturation studies, 125I-labeled HBGF-I was administered intravenously at various concentrations with heparin (approximately 5 U/ml blood volume). Further binding studies were conducted with the use of a constant concentration of 125I-labeled HBGF-I (40 ng) with or without heparin (2.5 U/ng HBGF-I). In each case, the rat was perfused with ice-cold saline solution 5 minutes after drug administration and the aorta or carotid arteries were harvested. 125I-labeled HBGF-I with heparin demonstrated saturation binding to rat aortic endothelium at an approximate blood concentration of 10 ng/ml. Scatchard plot analysis of in vivo data revealed a binding constant (KD) of 1.60 +/- 0.004 x 10(-9) mol/L compared with 2 to 8 x 10(-10) mol/L obtained for in vitro binding. Receptor number per cell was approximately 3000 for rat aortic endothelium, compared with a receptor number of 2000 to 20,000 for several endothelial cell lines, including bovine aortic endothelial cells, determined in vitro. 125I-labeled HBGF-I binding to uninjured rat carotid endothelium was significantly increased (p = 0.0001) by heparin (463 +/- 302 cpm to 1172 +/- 403 cpm).(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗