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Biomedical subjects

J H Burgess

Publications and source records attributed to J H Burgess.

At least 19 recordsLinked to original sources
PubMed1994

Arboviruses in water birds (Ciconiiformes, Pelecaniformes) from Florida.

Sera from 360 ciconiform and pelecaniform birds collected in Florida (USA) from 1974 to 1990 were tested for serum neutralizing (SN) antibodies to eastern equine encephalitis (EEE), St. Louis encephalitis (SLE), and Everglades (EVE) viruses. Serum neutralizing antibodies to EEE virus were detected in 2%, to SLE virus in 7%, and to EVE virus in none of the samples. Pelecaniform birds (16%) had a higher antibody prevalence (P < 0.02) for SLE virus than did ciconiform birds (5%). Virus could not be isolated from 67 samples. Nestling birds with SN antibodies to both EEE and SLE viruses were found in both fresh water and marine colonies. Antibodies were more prevalent in adult and fledged juvenile birds than in nestlings.

Age Factors↗
PubMed1990

Pathophysiology of dynamic cardiomyoplasty: a clinico-pathological case study.

A 58-year-old man with end-stage ischemic cardiomyopathy underwent dynamic cardiomyoplasty. "On" and "off" studies with the cardiac assist device failed to show any significant hemodynamic changes despite improvement in functional status. The patient's late postoperative course was complicated by two episodes of acute pulmonary edema followed by cardiac arrest. These events were precipitated by ventricular tachycardia. The last episode led to myocardial infarction requiring diastolic counterpulsation and inotropic support. He died 4 1/2 months following the cardiomyoplasty. Postmortem findings revealed an anterior left ventricular infarct with aneurysm. There was fusion of skeletal muscle to the epicardium with minimal fibrosis and atrophy. The latissimus dorsi (LD) flap was viable, but myofibrillar ATPase stain revealed incomplete transformation. Several clinical observations have emerged from the early experience with dynamic cardiomyoplasty: (1) Important arrhythmias and cardiac arrest compromise the vascular supply and thus power of the muscular flap; (2) Resting ejection fraction does not correlate with exercise tolerance, therefore, other parameters must be sought to explain improved functional status; (3) Uniform muscle transformation in humans may be unpredictable with current clinical stimulation protocols. The conformation of LD to the epicardium underscores a potential remodeling phenomenon which may ultimately spare the diseased myocardium by altering its oxygen supply/demand ratio and thus the natural history.

Cardiac Output↗
PubMed1988

Idiopathic ventricular tachycardia. A review.

Idiopathic or unexplained VT occurs in a small but important subset of patients without clinically evident heart disease. The majority of these patients appear to have a structurally normal heart. The cause of the arrhythmias in these individuals is unclear and may never be recognized. Other patients with this condition may have minor abnormalities not sufficient to impair overall cardiac function. The significance of these abnormalities to the genesis of the arrhythmia is uncertain. Whether patients with minor abnormalities are more likely to harbor covert heart disease such as myocarditis or a focal defect is not known, nor is it resolved whether such patients warrant a more aggressive search for a structural cause. The question that remains in any patient not subjected to surgical or pathological exploration is whether undetermined heart disease is responsible for the arrhythmia. Continued correlation between functional (electrophysiological) and structural (pathological) data will provide meaningful information concerning the pathophysiology (substrate) of these arrhythmias. Because of the preservation of normal cardiac function, these arrhythmias are generally well-tolerated. Although the condition is usually associated with a favorable prognosis, the occasional deaths reported in patients with apparently idiopathic ventricular arrhythmias may not permit calling this condition benign. It would be important to know the extent to which unrecognized abnormalities play a role in the genesis of these tachycardias, and whether such patients are more predisposed to fatal arrhythmias or have a different natural history. If cases involving undetermined or covert heart disease were excluded from consideration, then a relatively homogeneous disease-free group may be identified with a truly benign condition and a uniformly favorable prognosis. In these cases, a primary electrical abnormality may prove to be the basis for the arrhythmia. These issues remain to be elucidated in future studies.

Cardiomyopathies↗
PubMed1988

A reassessment of "chordoid sarcoma". Ultrastructural and immunohistochemical comparison with chordoma and skeletal myxoid chondrosarcoma.

The relationship of "chordoid sarcoma" (CS) to chordoma and myxoid chondrosarcoma has been debated for several years. In order to reassess this issue, we studied 5 CS, 5 chordomas, and 3 skeletal myxoid chondrosarcomas ultrastructurally and immunohistochemically. By electron microscopy, CS demonstrated smooth cellular outlines, macular intercellular junctions, and cytoplasmic inclusions of matrix-like material. Chordomas displayed a closely similar fine structural appearance, but in addition contained small, membrane-bound, glycogen-containing inclusions. Skeletal myxoid chondrosarcomas resembled CS, except that the former lesions had spiculated cell membranes and lacked intercellular junctions. Immunohistochemically, all CS cases expressed vimentin and lacked cytokeratin (CK). Leu 7 and S100 protein were seen in four cases each of CS, and three of these tumors demonstrated diffuse or focal reactivity for epithelial membrane antigen (EMA). Similar phenotypic features were seen in chordomas, except that all of them stained diffusely for CK, as well as EMA. Skeletal myxoid chondrosarcomas expressed vimentin, S100, and Leu 7 uniformly, but were devoid of epithelial markers. In aggregate, these data support the classification of "chordoid sarcoma" as a form of chondrosarcoma, but reveal that it may exhibit an "epithelial" antigen in some cases.

Adult↗
PubMed1988

Complete heart block in an Inuit family.

An Inuit family from Cape Dorset, Northwest Territories is described; six had documented complete heart block, one high grade atrioventricular block, one bi- or trifascicular block and all suffered syncope. One other member received a pacemaker for unknown reasons. Two of three middle-aged relatives had minor conduction abnormalities. All younger family members who were examined had no conduction problems. This suggests a heritable form of adult onset complete heart block, the largest series reported in the English literature.

Aged↗
PubMed1988

Association between immediate termination of supraventricular tachycardia by carotid sinus pressure and carotid sinus hypersensitivity.

An association between rapid reversion of supraventricular tachycardia by carotid sinus stimulation and carotid sinus reflex hypersensitivity during sinus rhythm is described in a 55-year-old patient. The findings indicate that a high level of vagal tone facilitates vagal maneuvers in terminating some supraventricular tachyarrhythmias. The briskness of the response during tachycardia may also be a marker for underlying carotid sinus hypersensitivity.

Carotid Sinus↗
PubMed1987

Metaiodobenzylguanidine [131I] scintigraphy detects impaired myocardial sympathetic neuronal transport function of canine mechanical-overload heart failure.

In heart failure secondary to chronic mechanical overload, cardiac sympathetic neurons demonstrate depressed catecholamine synthetic and transport function. To assess the potential of sympathetic neuronal imaging for detection of depressed transport function, serial scintigrams were acquired after the intravenous administration of metaiodobenzylguanidine [131I] to 13 normal dogs, 3 autotransplanted (denervated) dogs, 5 dogs with left ventricular failure, and 5 dogs with compensated left ventricular hypertrophy due to a surgical arteriovenous shunt. Nine dogs were killed at 14 hours postinjection for determination of metaiodobenzylguanidine [131I] and endogenous norepinephrine content in left atrium, left ventricle, liver, and spleen. By 4 hours postinjection, autotransplanted dogs had a 39% reduction in mean left ventricular tracer accumulation, reflecting an absent intraneuronal tracer pool. Failure dogs demonstrated an accelerated early mean left ventricular tracer efflux rate (26.0%/hour versus 13.7%/hour in normals), reflecting a disproportionately increased extraneuronal tracer pool. They also showed reduced late left ventricular and left atrial concentrations of tracer, consistent with a reduced intraneuronal tracer pool. By contrast, compensated hypertrophy dogs demonstrated a normal early mean left ventricular tracer efflux rate (16.4%/hour) and essentially normal late left ventricular and left atrial concentrations of tracer. Metaiodobenzylguanidine [131I] scintigraphic findings reflect the integrity of the cardiac sympathetic neuronal transport system in canine mechanical-overload heart failure. Metaiodobenzylguanidine [123I] scintigraphy should be explored as a means of early detection of mechanical-overload heart failure in patients.

3-Iodobenzylguanidine↗
PubMed1986

Effects of captopril and a combination of hydralazine and isosorbide dinitrate on myocardial sympathetic tone in patients with severe congestive heart failure.

Changes in circulating catecholamines and transmyocardial catecholamine balance associated with improved left ventricular function were studied in patients with chronic heart failure after treatment with captopril (10 patients) and hydralazine in combination with isosorbide dinitrate (eight patients). Cardiac performance improved in response to both captopril and hydralazine-nitrate treatment. The systemic haemodynamic effects were also qualitatively similar, but the hydralazine-nitrate combination caused a greater increase in cardiac index and heart rate. Captopril did not change arterial adrenaline concentrations (0.63 to 0.60 nmol/l), arterial noradrenaline (4.2 to 3.9 nmol/l), or net transmyocardial noradrenaline release (390 to 317 pmol/min), while hydralazine-nitrate increased arterial adrenaline (0.91 to 1.47 nmol/l) and transmyocardial noradrenaline release (225 to 554 pmol/min). Although both captopril and hydralazine-nitrate treatment improve left ventricular performance in patients with chronic heart failure, hydralazine-nitrate enhances cardiac sympathetic tone and captopril does not. The clinical relevance of these findings, however, is not known.

Aged↗
PubMed1985

Detrimental arrhythmogenic and sustained beneficial hemodynamic effects of oral salbutamol in patients with chronic congestive heart failure.

The long-term efficacy and potential side effects of oral sympathomimetic amines in the treatment of advanced congestive heart failure remain controversial. We studied the acute and chronic hemodynamic and arrhythmogenic effects of the beta-2 agonist, salbutamol, 6 mg by mouth four times/day, in 20 patients with NYHA classes III to IV congestive heart failure. Acutely, salbutamol increased the cardiac index (1.9 to 2.3 L/min/m2, p less than 0.01) and heart rate (92 to 97 bpm, p less than 0.01) while it decreased pulmonary capillary wedge pressure (35 to 31 mm Hg, p less than 0.01). Salbutamol increased the number of patients having episodes of ventricular tachycardia from two to six and increased the number of episodes of ventricular tachycardia from 2 to 27. Once salbutamol was discontinued, no further episodes of ventricular tachycardia occurred in these six patients. Six patients did not have long-term hemodynamic studies because of serious arrhythmias and two died. In the 12 patients who had long-term studies, the initial beneficial hemodynamic effects of salbutamol were maintained. Thus, although salbutamol may have beneficial long-term hemodynamic effects, it may cause serious arrhythmias in patients predisposed to develop arrhythmias.

Aged↗
PubMed1985

Percutaneous aspiration thromboembolectomy.

Percutaneous aspiration thromboembolectomy (PAT) was used as an angioplastic tool to remove from arteries of the lower limbs thromboembolitic material originating from any source. PAT was performed with a custom-designed catheter/sheath system, alone or in combination with balloon dilatation and/or local lytic infusion therapy with streptokinase or urokinase. PAT completed the restoration of blood flow, thus improving the results of the preceding angioplastic interventions. Clinical improvement was high, with 93% success (42 of 45 procedures). Only one below-the-knee amputation occurred, and could not be prevented. No patient became worse because of PAT intervention. The Fogarty catheter technique remains the method of choice for removing emboli within the aorto-iliac region, but in the smaller vessels below the inguinal ligament-especially in the distal superficial femoral, popliteal, and tibial regions--in our experience PAT is superior. This has been substantiated also in studies of laboratory animals, using barium-impregnated emboli.

Aged↗
PubMed1985

Lack of reflex increase in myocardial sympathetic tone after captopril: potential antianginal effect.

Many vasodilators have been tried as antianginal agents, but the reflex increase in sympathetic tone produced by these drugs necessitate their use with caution in patients with angina. In the first part of this study, captopril was given to 14 patients with angina and systolic arterial pressures of greater than 120 mm Hg. Over the short term, captopril decreased arterial blood pressure (from 110 +/- 18 to 98 +/- 18 mm Hg, p less than .01) without increasing heart rate (75 +/- 15 vs 74 +/- 15 beats/min), arterial concentrations of epinephrine (0.38 +/- 0.28 vs 0.34 +/- 0.25 nM) or norepinephrine (2.7 +/- 2.1 vs 2.8 +/- 2.1 nM), or transmyocardial norepinephrine balance (216 +/- 254 vs 146 +/- 170 p mol/min). Captopril decreased average myocardial oxygen consumption (9.7 +/- 4.1 to 8.2 +/- 2.7 ml/min, p less than .01). Given over the long term (mean 5.5 months), captopril decreased the severity of angina from NYHA classification 3.0 +/- 0.8 to 1.6 +/- 0.8. In the second part of this study, captopril was given in a prospective, randomized, double-blind, placebo-controlled study to 21 patients with stable exercise-induced angina and systolic arterial pressures greater than 120 mm Hg. Captopril increased exercise time (309 +/- 137 vs 374 +/- 142 sec, p less than .05) without changing anginal threshold (rate-pressure product 17.0 +/- 6.0 vs 17.1 +/- 5.6 X 10(-3)). We conclude that captopril decreases mean arterial pressure without causing a reflex increase in myocardial sympathetic tone.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1985

Tracer norepinephrine kinetics in coronary circulation of patients with heart failure secondary to chronic pressure and volume overload.

Controversy exists over the nature of the abnormality in cardiac sympathetic nerves in heart failure. In the cardiomyopathy of the Syrian hamster, reduction in tissue stores and increased turnover of norepinephrine is clearly associated with excessive sympathetic stimulation but in animal models and humans with heart failure secondary to mechanical overload there is evidence for depression of neuronal uptake. Because norepinephrine is both released and taken up by sympathetic fibers it is impossible to assess norepinephrine kinetics in an intact heart without separating these two functions. A technique for doing so has recently been developed in normal dogs and we therefore acquired similar data in humans with heart failure secondary to chronic pressure and volume overload. The technique involves the combination of transient norepinephrine tracer coronary sinus outflow in relation to intravascular and interstitial references after simultaneous injection into the left coronary artery and the measurement of endogenous norepinephrine concentrations in artery and coronary sinus. We found a marked reduction in cardiac norepinephrine release and uptake in a group of patients with clinical left ventricular failure secondary to mechanical overload, relative to a group of patients with no failure. Norepinephrine balance and overflow across the heart were not significantly different. We conclude that there is hypofunction of the cardiac sympathetic nerves in heart failure secondary to mechanical overload and that traditional methods are inadequate in assessing cardiac norepinephrine kinetics when there are simultaneous changes in neuronal uptake and release.

Adult↗
PubMed1984

Acute effects of captopril on the coronary circulation of patients with hypertension and angina.

Patients with hypertension have a high incidence of coronary artery disease. Captopril, the angiotensin-converting enzyme inhibitor, was given to eight patients with hypertension and coronary artery disease; it decreased mean arterial pressure from 121 to 103 mm Hg (p less than 0.01) but had no effect on heart rate. The rate-pressure product decreased from 12.5 to 11.4 X 10(3) (p less than 0.01). The change in coronary blood flow (90 to 80 ml per minute) and myocardial oxygen consumption (965 to 852 ml per minute) tended to parallel the decrease in the rate-pressure product. Captopril did not change global myocardial lactate (20 to 34 percent) or oxygen (9.6 to 10.0 volume percent) extraction. Hence, captopril decreases the rate-pressure product and tends to decrease myocardial oxygen consumption without causing global myocardial metabolic deterioration.

Aged↗