Use of the operating microscope.
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Biomedical subjects
Publications and source records attributed to M D Feldman.
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Several studies have been performed in patients with a variety of myocardial diseases that have identified a prolongation of tau. However, it is not clear whether prolongation of tau represents abnormal myocardial physiology or the effect of excessive load associated with a particular disease process. Accordingly, we evaluate the effect on tau of an isolated decrease in preload induced by inferior vena cava occlusion before the appearance of reflex changes in six patients designated as normal by catheterization criteria. A computer-based digitization routine identified cardiac contractions in all patients early after inferior vena cava occlusion where left ventricular end-diastolic pressure decreased (18.3 +/- 6.3 to 9.3 +/- 5.8, p less than 0.05) while left ventricular systolic pressure (113.3 +/- 13.8 to 111.8 +/- 14.0, p = NS) and heart rate (66.0 +/- 10.0 to 65.9 +/- 10.3, p = NS) did not change. After this alteration in preload, no change in tau from baseline, as calculated by the logarithmic (TL), derivative (TD), or method of Mirsky (T1/2), was noted: TL, 47.4 +/- 6.5 to 44.6 +/- 7.6; TD, 39.3 +/- 8.1 to 39.8 +/- 8.4; T1/2, 33.0 +/- 4.0 to 31.8 +/- 4.6; all p = NS. The baseline pressure extrapolated from isovolumetric relaxation did not change in these preload beats compared with baseline (+4.26 +/- 6.20 to -0.80 +/- 4.87, p = NS). Subsequent beats were identified where left ventricular systolic pressure showed a numeric decrease compared with baseline (113.3 +/- 13.8 to 100.8 +/- 14.3, p = NS) despite no change in heart rate (66.0 +/- 10.0 to 66.8 +/- 10.5, p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)
Intramuscular hemangiomas make up less than 1% of all hemangiomas [1]. These invasive and aggressive lesions appear to have a predilection for large muscle masses. They can be strikingly aggressive in the head and neck, and persistence despite radical treatment is common. Spontaneous resolution in adults to our knowledge has not been reported in the literature. We present a case report of an invasive intramuscular hemangioma involving the parotid gland, the masseter and pterygoid muscles, and the infratemporal fossa after local resection of an apparently isolated lesion of the lip and the submandibular triangle. We describe a detailed course of treatment and review the literature.
A safe, effective method for securing autologous and alloplastic implants would benefit modern surgery substantially. We studied the effects of a new autologous fibrin tissue adhesive with various alloplastic implants and ear cartilage. Twelve rabbits had Proplast (a woven combination of Teflon and organic fibers), Silastic, Supramid polyfilament surgical sheeting, and ear cartilage implanted. One side of each animal had implants secured with tissue adhesive. The other, control side had identical implants placed in "subcutaneous tunnels." The tissue adhesive was biodegradable and produced no apparent toxic reaction, infection, or foreign-body reaction. It did not adhere to Silastic, but bound to the other implants. Glued implants had no more clinical or histologic evidence of inflammation than controls. Autologous fibrin tissue adhesive seems to be promising as a safe, biologic bonding material for securing certain alloplastic and autologous implants.
The giant cholesterol cyst is a clinical entity distinct from cholesterol granulomas and other destructive lesions of the petrous bone. Preoperative assessment by computed tomographic scan and magnetic resonance imaging is extremely helpful. Attempts at total resection of the lesion are not necessary. Adequate surgical drainage may be established through the mastoid or middle fossa.
With the advent of extremely rapid, powerful, compact, and inexpensive microcomputers, a revolution in data manipulation is ongoing. We have customized and used for over two years prepackaged software to track residents' operative experiences in the Department of Otolaryngology at Jefferson Medical College of Thomas Jefferson University, Philadelphia. An attempt is presently being made to develop a similar system that might be utilized by all otolaryngology teaching programs and thus enable the collection and review of residents' operative experiences nationally. A basic, relational database system is proposed for entering resident caseload data and generating reports for periodic review.
Although improvements in noninvasive external cardiac pacing have led to a technique with reliable electrical capture and reduced patient discomfort, hemodynamic responses to this pacing mode have not been described previously. Accordingly, this technique was applied to 16 patients with a clinical diagnosis of angina pectoris undergoing cardiac catheterization. Three patients had normal coronary arteries, whereas the remaining 13 had significant coronary artery disease. All patients had noninvasive pacing at increasing heart rates to 85 percent of age-predicted maximal heart rate. At maximal pacing, all patients demonstrated a rise in atrial, pulmonary artery, and mean aortic pressures. Cardiac index remained unchanged, reflecting parallel increases in arteriovenous oxygen difference and oxygen consumption. One minute after cessation of pacing, pulmonary artery pressure and oxygen consumption remained elevated, whereas arteriovenous oxygen difference returned to baseline with a subsequent rise in cardiac index. Angina occurred in eight patients with coronary artery disease at peak pacing and was accompanied by a rise in left ventricular end-diastolic pressure after pacing. In eight patients without pacing-induced angina, including the three patients with normal coronary arteries, there was no significant change in left ventricular end-diastolic pressure after pacing. It is concluded that noninvasive external cardiac pacing produces a rise in both right and left heart filling pressures and in oxygen consumption that persist after pacing, and may provoke angina and hemodynamic abnormalities consistent with myocardial ischemia. This mode of pacing appears hemodynamically safe with maintenance of cardiac index and aortic pressure at 85 percent of maximal age-predicted heart rate.
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Patients with aortic stenosis are susceptible to myocardial ischemia during hemodynamic stress, which may be caused by two mechanisms. First, vascular abnormalities inherent in myocardial hypertrophy may impair coronary vasodilation, limiting the ability to increase coronary blood flow to meet increased metabolic demands. Second, aortic stenosis itself may cause an imbalance between oxygen supply and demand during hemodynamic stress by decreasing aortic pressure (decreasing coronary perfusion or oxygen supply) and increasing left ventricular pressure (increasing oxygen demand). By decreasing aortic valve gradient without immediately altering ventricular hypertrophy, aortic balloon valvuloplasty offers the opportunity to distinguish these mechanisms. We hypothesized that aortic valvuloplasty would improve the balance between myocardial oxygen supply and demand, especially during isoproterenol infusion. Nine patients undergoing aortic balloon valvuloplasty were assessed at baseline and during isoproterenol infusion (5 +/- 2 micrograms/min, mean +/- SD) before and after valvuloplasty. Valvuloplasty increased myocardial oxygen supply. After valvuloplasty, isoproterenol decreased diastolic pressure time index (DPTI) less and increased coronary sinus blood flow more than before valvuloplasty (-630 +/- 367 vs. -292 +/- 224 mm Hg.sec/min, p = 0.02 and 53 +/- 137 vs. 179 +/- 145 ml/min, p = 0.001, respectively). Valvuloplasty also decreased oxygen demand, decreasing systolic pressure time index (SPTI) from 4,135 +/- 511 to 3,021 +/- 492 mm Hg.sec/min (p = 0.0002). Valvuloplasty improved the balance between myocardial oxygen supply and demand, increasing baseline DPTI:SPTI, decreasing aortocoronary sinus oxygen content difference (0.51 +/- 0.15 to 0.68 +/- 0.14, p = 0.005 and 96 +/- 14 to 78 +/- 15 ml O2/l, p = 0.002, respectively), and decreasing myocardial lactate production during isoproterenol infusion (mean lactate extraction fraction, -0.26 +/- 0.40 to 0.14 +/- 0.17; p = 0.01). We conclude that aortic valvuloplasty improves the balance between myocardial oxygen supply and demand during hemodynamic stress induced by isoproterenol infusion. We speculate that the clinical improvement, which often occurs in these patients after valvuloplasty despite persistence of hemodynamically "critical" aortic stenosis, is in part attributable to immediate improvement in the myocardial oxygen supply:demand ratio.
Previous reports have shown that increases in heart rate may result in enhanced left ventricular (LV) systolic and diastolic performance. To assess whether this phenomenon occurs in the presence of depressed LV function, the effects of pacing on LV pressure and volume were compared in seven patients with dilated cardiomyopathy (LV ejection fraction 0.19 +/- 0.11) and six patients with no or minimal coronary artery disease (LV ejection fraction 0.69 +/- 0.11). Patients with normal LV function demonstrated significant increases in LV peak-positive dP/dt, LV end-systolic pressure-volume ratio, LV peak filling rate, and a progressive leftward and downward shift of their pressure-volume diagrams, compatible with increased contractility and distensibility in response to pacing tachycardia. There was no change in LV peak-negative dP/dt or tau. Patients with dilated cardiomyopathy, in contrast, demonstrated no increase in either LV peak-positive dP/dt or the end-systolic pressure-volume ratio, and absence of a progressive leftward shift of their pressure-volume diagrams. Moreover, cardiomyopathy patients demonstrated no increase in LV peak-negative dP/dt or LV peak filling rate and a blunted downward shift of the diastolic limb of their pressure-volume diagrams. Tau, as determined from a derivative method, became abbreviated although never reaching control values. We conclude that patients with dilated cardiomyopathy may demonstrate little or no significant enhancement in systolic and diastolic function during atrial pacing tachycardia, suggesting a depression of both inotropic and lusitropic reserve.
Postoperative cerebrospinal fluid (CSF) leakage continues to be one of the most common and potentially serious complications following translabyrinthine surgery despite numerous strategies aimed at its prevention. Fibrinogen-based tissue adhesives may be helpful in decreasing this complication rate. Although commercial glues have been used widely in Europe (especially for dural repairs), they are not approved for use in the United States. Recent investigation has provided a relatively simple technique for producing a comparable autologous glue that obviates the risks of the commercial product. Since this glue will bind fascia, fat, and dura in the watertight fashion, it is potentially ideal for preventing CSF leaks. Experimental studies in rabbits reveal that autologous tissue adhesive can be used safely around intact nerves, suggesting it can be used safely to supplement fat, fascia, or muscle plugs for closing translabyrinthine defects. Clinical trials to test the efficacy of tissue adhesives in this application are currently under way.
Improvements in noninvasive external cardiac pacing have led to a technique with reliable electrical capture and tolerable patient discomfort. To assess the use of this modality of pacing in combination with thallium scintigraphy as a noninvasive pacing stress test, we applied simultaneous noninvasive cardiac pacing, hemodynamic monitoring, and thallium-201 scintigraphy in 14 patients undergoing cardiac catheterization for chest pain syndromes. Two patients had normal coronary arteries, while the remaining 12 had significant coronary artery disease. Thallium scintigraphic responses to pacing were compared to routine exercise thallium stress testing in nine of these 14 patients. All patients were noninvasively paced to more than 85% of the age-predicted maximum heart rate. Twelve patients demonstrated reversible thallium defects, which corresponded in 11 cases to significant lesions seen on coronary angiography. Of nine patients who underwent both pacing and exercise thallium stress tests, comparable maximal rate-pressure products were achieved. Moreover, thallium imaging at peak pacing and during delayed views did not differ significantly from exercise thallium scintigraphy. A limiting factor associated with the technique was local patient discomfort, which occurred to some degree in all patients. We conclude that noninvasive external cardiac pacing together with thallium scintigraphy is capable of detecting significant coronary artery disease and may be comparable to routine exercise thallium stress testing. This new modality of stress testing could be useful in patients unable to undergo the exercise required for standard exercise tolerance testing, particularly if improvements in the technology can be found to reduce further the local discomfort.
The sciatic nerve in rabbits was exposed, transected, and repaired using either of two methods. The experimental group had an autologous fibrin-based adhesive repair. The control group had conventional perineural suturing. The autologous tissue glue is similar in composition, handling, and performance to the commercially available European product Tisseel. It can be prepared quickly without sophisticated equipment or expense. Autologous glue obviates the risk of transmissible disease that has precluded approval of the commercial product for use in the United States. The glued anastomosis can be performed with accurate apposition and minimal trauma to the nerve. By making a fibrin cocoon, the anastomosis can be insulated. This provides some of the benefits of sheathed anastomosis while minimizing foreign body reaction. Functional evaluation and histologic results comparing the amount of anastomotic fibrosis, axonal regeneration, and alignment of fascicles showed glue to be as good as, if not superior to, conventional suture technique.
We studied the effects of different classes of inotropic drugs on human working myocardium in vitro that was isolated from the hearts of patients with end-stage heart failure, and compared the responses to these drugs with those noted in muscles from nonfailing control hearts. Although peak isometric force generated in response to increased extracellular calcium reached control levels in the muscles from patients with heart failure, the time course of contraction and rate of relaxation were greatly prolonged. The inotropic effectiveness of the beta-adrenergic agonist isoproterenol and the phosphodiesterase inhibitors milrinone, caffeine, and isobutylmethylxanthine was markedly reduced in muscles from the patients with heart failure. In contrast, the effectiveness of inotropic stimulation with acetylstrophanthidin and the adenylate cyclase activator forskolin was preserved. After a minimally effective dose of forskolin was given to elevate intracellular cyclic AMP levels, the inotropic responses of muscles from the failing hearts to phosphodiesterase inhibitors were markedly potentiated. These data indicate that an abnormality in cyclic AMP production may be a fundamental defect present in patients with end-stage heart failure that can markedly diminish the effectiveness of agents that depend on generation of this nucleotide for production of a positive inotropic effect.
Intracellular Ca2+ release and reuptake are essential for contraction and relaxation of normal heart muscle. Intracellular Ca2+ transients were recorded with aequorin during isometric contraction of myocardium from patients with end-stage heart failure. In contrast to controls, contractions and Ca2+ transients of muscles from failing hearts were markedly prolonged, and the Ca2+ transients exhibited 2 distinct components. Muscles from failing hearts showed a diminished capacity to restore low resting Ca2+ levels during diastole. These experiments provide the first direct evidence from actively contracting human myocardium that intracellular Ca2+ handling is abnormal and may cause systolic and diastolic dysfunction in heart failure.
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