Bilirubin interference with a salicylate assay performed on an Olympus analyser.
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Adolescent↗
Biomedical subjects
A Broughton
Publications and source records attributed to A Broughton.
Efficacy and safety of direct stenting in coronary angioplasty.
BACKGROUND: Direct stenting is the deployment of an intracoronary stent without lesion predilation. Potential advantages include shorter procedural time, lower contrast dose and reduced spiral dissections. There is also the potential financial benefit of less balloon and/or stent usage. Concern still exists among some operators, however, regarding failure of stent deployment and local complications. METHODS: Of 467 consecutive angioplasty cases at the Alfred Hospital between August 1, 1997 and May 22, 1998, direct stenting was attempted in 93 patients (20%). Interventionalist preference determined whether direct stenting was attempted. Vessels with excessive calcification, severe proximal tortuosity or small caliber were typically considered unsuitable for direct stenting. RESULTS: A total of 102 lesions (38 type A, 60 type B, and 4 type C) were treated with direct stenting. Initial deployment was successful in 98 of 102 lesions, with a further 3 lesions successfully stented following predilation. A stent was unable to be deployed in only 1 case; however, the lesion was treated with balloon angioplasty alone. The majority of lesions required only 1 stent (an average of 1.1 stents were used per lesion). Distal complications occurred in 5 patients. In 3 patients, a small distal dissection was successfully stented, and in 1 case embolization of debris occurred down the distal vessel, resulting in a small procedural myocardial infarction. Only 1 patient out of 93 (1%) developed a large distal dissection requiring the deployment of multiple stents, compared with 22 of the remaining 374 patients (5.9%) who underwent conventional angioplasty. This was a significant difference in favor of direct stenting (Chi-square, p < 0.05). When compared with a cohort of patients matched by lesion grade treated with conventional stenting, direct stenting used significantly less contrast per case (154 +/- 7.6 ml compared with 202 +/- 9.5 ml for conventional stenting; p = 0.0001). CONCLUSION: Direct stenting is a safe and effective method for treating coronary artery disease. In appropriately selected cases, it has a low rate of procedural failure and results in less contrast usage and fewer distal complications than conventional angioplasty and stenting.
Angioplasty, Balloon, Coronary↗
Salivary creatinine assays as a potential screen for renal disease.
Salivary creatinine concentrations are 10-15% of serum creatinine concentrations in healthy populations but have not previously been measured in patients with renal disease. The Cobas Mira automated Jaffé method was adapted to measure salivary creatinine concentration. The method was linear to 1200 mumol/L, had a mean recovery of 78% and a detection limit of 6 mumol/L. Intra-assay variability was 13.5, 5.5 and 1.4% at 10.6, 17.8 and 128.4 mumol/L, respectively. Inter-assay variability was 35.0 and 4.8% at 6.2 and 130.4 mumol/L, respectively. The median salivary creatinine concentrations was 8.5 mumol/L (range 6-18 mumol/L) in healthy subjects (n = 23), and 84 mumol/L (range 18-591 mumol/L) in patients with renal disease (n = 25). Salivary and serum creatinine concentrations were not related in healthy subjects, however, a significant relationship was found in the patients (r = 0.784, P < 0.001). Using salivary creatinine concentration of 16.8 mumol/L as a cut off value, all patients would have been detected with one false positive result (sensitivity 100%, specificity 95.7%, efficiency 97.7%). Thus, salivary creatinine estimations may be used to identify subjects with serum creatinine concentrations above 120 mumol/L.
Adult↗
Adverse consequences of high sympathetic nervous activity in the failing human heart.
OBJECTIVES: In view of previous experimental evidence relating sympathetic nervous overactivity in the heart to myocardial necrosis and ventricular arrhythmias, we prospectively examined the hypothesis that heightened cardiac sympathetic nervous activity is associated with an adverse outcome in patients with moderate to severe heart failure. BACKGROUND: Despite recent therapeutic advances, patients with heart failure continue to have high mortality from progressive hemodynamic decompensation and lethal ventricular arrhythmias. It is believed that initially compensatory increases in sympathetic nervous system activity may ultimately be maladaptive, potentially contributing to subsequent adverse events. METHODS: Sixty patients with moderate to severe heart failure (left ventricular ejection fraction 18.9 +/- 0.9% [mean +/- SE]) were studied prospectively. In addition to the compilation of a hemodynamic, biochemical and electrocardiographic profile for each patient, whole-body and cardiac sympathetic activity were determined by isotope dilution. The relation of these variables to outcome was determined by Cox proportional hazards analysis. RESULTS: The mean follow-up period of the study group was 7 +/- 1 months (range 1 to 24) with a 12-month actuarial survival of 75%. Deaths (14 in all) were accounted for either by sudden death or progressive heart failure in equal numbers. The rate of release of norepinephrine from the heart was significantly higher in patients with heart failure than in healthy subjects (402 +/- 37 vs. 105 +/- 19 pmol/min, p < 0.01), although the values for heart failure ranged widely from normal to 10 times normal. By univariate Cox proportional hazards analysis, pulmonary capillary wedge pressure (p < 0.01), mean pulmonary artery pressure (p < 0.001), serum sodium levels (p < 0.01) and cardiac norepinephrine spill-over rate (p < 0.001) were identified as significant prognostic markers. In a multivariate analysis, cardiac norepinephrine spillover rate was identified as the most powerful prognostic marker (p = 0.0006) of those evaluated in this study. CONCLUSIONS: These results suggest that activation of the sympathetic nervous system in patients with heart failure, specifically the cardiac sympathetic nerves, may contribute to the poor prognosis associated with severe heart failure. The data therefore provide a rationale for the use of drugs such as beta-adrenergic blocking agents in the management of patients with heart failure.
Adult↗
Thrombolysis for presumed myocardial infarction--pitfalls in diagnosis.
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Diagnostic Errors↗
Evidence of a selective increase in cardiac sympathetic activity in patients with sustained ventricular arrhythmias.
BACKGROUND: Although enhanced efferent cardiac sympathetic nervous activity has been proposed as an important factor in the genesis of ventricular arrhythmias and sudden cardiac death, direct clinical evidence has been lacking. METHODS: We measured the rates of total and cardiac norepinephrine spillover into the plasma, which reflect respectively overall and cardiac sympathetic nervous activity, in 12 patients who had recovered from a spontaneous, sustained episode of ventricular tachycardia or ventricular fibrillation outside the hospital 4 to 48 days earlier. The results were compared with those from three age-matched reference groups without a history of ventricular arrhythmias: 12 patients with coronary artery disease, 6 patients with chest pain but normal coronary arteries, and 12 healthy, normal subjects. RESULTS: The patients who had had ventricular arrhythmias had reduced left ventricular ejection fractions, as compared with the patients with coronary artery disease or chest pain (mean [+/- SE], 46 +/- 3 percent vs. 58 +/- 4 percent and 69 +/- 5 percent, respectively; P less than 0.003). The rates of total norepinephrine spillover into the plasma were similar in the three reference groups, but 80 percent higher in the patients with ventricular arrhythmias (P less than 0.005). The rate of cardiac norepinephrine spillover was 450 percent higher in these patients (176 +/- 39 pmol per minute, as compared with 32 +/- 8 pmol per minute in the normal subjects; P less than 0.001), a disproportionate increase relative to the increase in total spillover, which indicated selective activation of the cardiac sympathetic outflow. This increase in cardiac norepinephrine spillover was probably caused by a reduction in left ventricular function. CONCLUSIONS: These results suggest that in some patients major ventricular arrhythmias are associated with and perhaps caused by sustained and selective cardiac sympathetic activation. We speculate that depressed ventricular function was present before the ventricular arrhythmia occurred, and that this resulted in reflex cardiac sympathetic activation, which in turn contributed to the genesis of the arrhythmia.
Angina Pectoris↗
The acetylcholine paradox: a constrictor of human small coronary arteries even in the presence of endothelium.
1. In animal experiments, acetylcholine is generally a vasodilator acting indirectly by releasing endothelium-derived relaxing factor (EDRF); for example, in dog and rabbit small coronaries mounted in a myograph, acetylcholine caused concentration-dependent relaxation. 2. In human small coronary arteries taken from the atrial appendage, however, acetylcholine caused concentration-dependent contraction with a functionally intact endothelium as shown by the relaxation in response to substance P, another stimulant of EDRF release. 3. We propose that coronary microvessels from various species have variable populations of acetylcholine receptors on the medial smooth muscle that cause contraction and on the endothelium that cause the release of EDRF. In humans, the medial smooth muscle receptors appear to predominate, and may thus play a role in coronary vasoconstriction.
Acetylcholine↗
Early and late results of surgery for Wolff-Parkinson-White syndrome.
Surgical treatment for accessory atrioventricular connections was performed in 60 patients with Wolff-Parkinson-White syndrome between 1981 and 1986. The initial procedure successfully divided 69 of 73 pathways identified preoperatively, including 39 of 40 left free wall pathways, 23 of 24 posteroseptal pathways, six of seven right free wall pathways, and one of two anteroseptal pathways. Three additional pathways were identified for the first time during follow-up. The primary procedure was successful in curing 53 (88%) of the 60 patients and in dividing 69 (91%) of the total of 76 pathways. Subsequent procedures increased the overall clinical cure rate to 97%. The surgery was performed with low morbidity and no perioperative or late mortality. Patients were followed-up for a mean of 6.4 years (range four to nine years). No patient showed clinical or electrocardiographic evidence of recurrence of a pathway which had been divided surgically. We conclude that regardless of pathway site, surgical treatment carries a low risk and has a high probability of avoiding lifelong antiarrhythmic therapy.
Adolescent↗
Left ventricular blood flow during aortic pressure reduction in hypertensive dogs.
We measured left ventricular blood flow with radioactive microspheres during aortic pressure reduction in 10 open-chest, anesthetized dogs with left ventricular hypertrophy due to chronic hypertension and in 10 matched normotensive dogs. Heart rate and left atrial pressure were held constant, and autonomic reflexes were abolished with ganglionic blockade. Aortic diastolic pressure was lowered from baseline to 90, 75, and 60 mm Hg with an arteriovenous fistula. During aortic pressure reduction, a stepwise decline in the endocardial-to-epicardial flow ratio in hypertrophied hearts from 1.23 +/- 0.04 at baseline to 0.96 +/- 0.09 at a diastolic pressure of 75 mm Hg parallelled that in normal hearts and was not associated with any deterioration in left ventricular performance. However, a further fall in the endocardial-to-epicardial flow ratio to 0.76 +/- 0.10 at a diastolic pressure of 60 mm Hg in hypertrophied hearts exceeded that in normal hearts (0.92 +/- 0.05, p less than 0.05) and was accompanied by evidence of left ventricular isovolumic and end-systolic dysfunction. We conclude that in hearts with pressure-overload left ventricular hypertrophy, aortic pressure reduction causes a transmural blood flow redistribution from subendocardial to subepicardial muscle layers. At moderately low aortic pressures, this redistribution is more pronounced than in normal hearts and is associated with functional evidence of myocardial ischemia.
Animals↗
Immunologic biomarkers associated with an acute exposure to exothermic byproducts of a ureaformaldehyde spill.
A community was exposed for several days to formaldehyde (HCHO), hexamethylenetetramine, trimethylamine, and paraformaldehyde emitted from an overheated tanker car containing ureaformaldehyde resin. Residents experienced acute HCHO symptoms at the time of the accident. Many developed chronic, multiple organ health complaints. Three years following the accident, exposed subjects were compared to residents of a nearby unexposed community for the following immunological parameters: white blood cell count, total lymphocyte count, percent and total lymphocyte subsets (CD5, CD4, CD8, CD19, CD25, and CD26 cells), prevalence of autoantibodies, and antibodies to HCHO-human serum albumin (HCHO-HSA) conjugate. The data were adjusted for gender, age, history of smoking, mobile home residency, and use of wood stoves. There was a statistically significant difference for the following: elevated percent and absolute numbers of CD26 cells (p less than 0.0001); autoantibodies (p less than 0.004), and greater titers of isotypes IgG (p less than 0.0005) and IgM (p less than 0.005) to HCHO-HSA. It is concluded that the exposed subjects had an activated immune system in addition to the elevated autoantibodies. Also, isotypes to HCHO-HSA resulted from the exposure and no other sources, such as smoking, mobile home residency, and use of wood stoves.
Adolescent↗
Building-related illness and antibodies to albumin conjugates of formaldehyde, toluene diisocyanate, and trimellitic anhydride.
A case of building-related health complaints was investigated with respect to the relationship among frequency of symptoms, antibodies to albumin conjugates of formaldehyde (HCHO), toluene diisocyanate (TDI), and tirmellitic anhydride (TMA), and volatile organic chemicals (VOCs). The indoor air concentrations of VOCs, HCHO, TDI, and TMA did not exceed Fed-OSHA and ACGIH permissible standards. However, HCHO concentrations ranged between 0.05 and 0.08 ppm. The reported symptoms were multiple, involving the eyes, nose, sinuses, throat, lungs, skeletomuscular system, and central nervous system. Anti-HCHO, -TDI, and -TMA isotypes were found in 12 of 14 full-time employees and were nondetectable in one part-time employee. There was a positive, but not statistically significant, correlation (r values ranged between .24 and .55) between symptoms and the geometric mean titers to conjugates. The data suggest that a synergistic immunological response to airborne chemicals may be occurring in these subjects. In conclusion, immunological monitoring of affected individuals where chemicals are suspected may prove to be useful in future investigations of building-related illness.
Adult↗
Endothelin is blood vessel selective: studies on a variety of human and dog vessels in vitro and on regional blood flow in the conscious rabbit.
1. Endothelin (Et), a vasoconstrictor peptide, was 5-10-fold more potent (lower EC50) on isolated ring segments of large veins than on large arteries removed from dog coronary, mesenteric, femoral, renal and internal mammary vasculature and from the human internal mammary pedicle. 2. In the dog large coronary artery, Et (10-30 nmol/L) caused transient relaxations partway through the generation of a concentration-contraction curve. These relaxations were endothelium dependent. 3. In conscious rabbits treated with mecamylamine, Et (0.025-0.4 nmol/kg) caused a marked rise in renal vascular resistance but hindquarter vasodilation. Under the same conditions angiotensin II constricted both beds. 4. These studies suggest that Et is vascular bed and large vein selective in activity. It did not appear to be selective for large or small coronary arteries in vitro.
Animals↗
Immunological evaluation of four arc welders exposed to fumes from ignited polyurethane (isocyanate) foam: antibodies and immune profiles.
Four arc welders having a flu-like illness with multiple health complaints following an exposure to high concentrations of isocyanate fumes from ignited polyurethane foam underwent immunological tests as follows: ELISA antibody assays, activated lymphocyte profiles, and lymphocyte blastogenesis. ELISA procedures revealed the presence of antibodies to hexamethylene diisocyanate (HDI) and formaldehyde (F) conjugated to human serum albumin (HDI-SA and F-SA). The results from the activated lymphocyte profiles showed deviations from the norm as follows: three welders had elevated helper/suppressor (H/S) ratios; all four had elevated percentages of Tal positive cells; two had decreases in B cells; and one had low total white cell and lymphocyte counts. In contrast, the percentage and absolute numbers of ILS receptor cells were normal in the four subjects. T cell blastogenesis to PHA, Con A and PWM resulted in the following: T-cells from one subject responded normally; in another, a high response (212% of controls) to PHA occurred with normal mitogenesis to Con A and PWM. In the remaining two welders, the T cells responded abnormally low (50 to 75% of controls) to the three mitogens. In conclusion, the existence of IgG antibodies to HDI-SA and F-SA, the altered activated immune profiles, the elevated Tal cells, and the abnormal blastogenesis are interpreted as being linked with the episode of HDI and F exposure and the subsequent flu-like illness of the four welders.
Adult↗
Antibodies and immune profiles of individuals occupationally exposed to formaldehyde: six case reports.
Six patients with multiple subjective health complaints, which have been correlated with chronic exposure to formaldehyde during the course of their education and occupations, were tested for the existence of antibodies (IgE, IgM, and IgG) to formaldehyde (F) conjugated to human serum albumin (F-HSA). In addition, the percentage and absolute numbers of peripheral lymphocyte subpopulations as determined by surface markers were investigated. Antibody titers to F-HSA were present as follows: IgE (2 patients), IgM (3 of 4 tested patients), and IgG (5 patients). Analysis of lymphocyte subpopulations showed T-helper/suppressor (H/S) ratios ranging from 0.8 to 3.3. All 6 patients had elevated Tal cells (antigen memory cells), whereas interleuken 2 receptor positive cells were within expected values. Following formaldehyde exposure, 5 of the patients complained of an initial flulike illness from which they have not completely recovered. The sixth individual had a history of recurrent respiratory infections and surgical removal of hyperplastic ethmoid sinus tissue. The common occurrence of anti-F-HSA antibodies, flulike illness, and Tal cells are interpreted as suggestive of a chronic antigenic stimulation of the immune system in these 6 patients. Further immunological work-up of additional subjects and immune parameters with similar history of formaldehyde exposure and subjective health complaints is warranted.
Adult↗
Comparison of left and right ventricular blood flow responses during arterial pressure reduction in the autonomically blocked dog: evidence for right ventricular autoregulation.
The effect of reducing systemic arterial pressure with an arteriovenous fistula on left and right ventricular myocardial blood flow was studied in 17 anaesthetised, open chest, autonomically blocked dogs. Global and regional myocardial blood flows were measured with radioactive microspheres. As mean arterial pressure was reduced from 133 mmHg to 78 mmHg left ventricular myocardial blood flow and the left ventricular inner to outer flow ratio decreased progressively. By contrast, right ventricular myocardial blood flow remained constant (range 78-81 ml.min-1.100 g-1) whereas right ventricular vascular resistance fell linearly (from 235 to 130 kPa.litre-1.min.100 g-1). The inner to outer right ventricular free wall flow ratio (range 1.04-1.10) and blood flow to the right side of the interventricular septum also did not change significantly. It is concluded that the right ventricular myocardium shows effective autoregulation of total and regional tissue blood flow during changes in coronary perfusion pressure.
Animals↗
Role of alpha-adrenoceptors in constrictor responses of rat, guinea-pig and rabbit small arteries to neural activation.
1. We have investigated the adrenoceptors mediating the force and electrical responses of rat mesenteric small arteries (i.d. 100-300 microns). Some mechanical experiments were also performed using guinea-pig and rabbit mesenteric small arteries. 2. Vessels were mounted on an isometric myograph and stimulated either with short (3 s) trains of electric field stimuli (ca. 0.2 ms pulse width) at 25 Hz (nerve stimulation) or with 10 microM-exogenous noradrenaline. 3. Nerve stimulation caused a force response equal to ca. 40% of the response to exogenous noradrenaline and, in the rat vessels, excitatory junction potentials (EJPs), which normally summated to give a depolarization of ca. 10 mV (although action potentials were sometimes seen). 4. Almost complete and reversible inhibition of the force responses of all vessels to both exogenous noradrenaline and to nerve stimulation was obtained using prazosin (0.1 microM) or phentolamine (1 microM). 5. Irreversible blockade of alpha 2-receptors enhanced the force response of all vessels to nerve stimulation by ca. 50%, but did not affect the force response of rat and guinea-pig vessels to exogenous noradrenaline. In the rabbit vessels this force response was abolished by alpha 2-blockade. 6. Following alpha 2-blockade, in the rat vessels the alpha-antagonists prazosin (0.1 microM), phentolamine (0.1 microM), phenoxybenzamine (0.01 microM) and benextramine (10 microM) all totally abolished the force response to exogenous noradrenaline, and inhibited the response to nerve stimulation by at least 80%. Similar effects of phentolamine were seen in the guinea-pig and, for the response to nerve stimulation, in the rabbit vessels. 7. In the rat vessels, alpha-adrenoceptor antagonists did not affect the EJPs, but did inhibit the small depolarization which resulted from several seconds of nerve stimulation. The ATP analogue alpha, beta-methylene-ATP (3 microM) abolished the EJPs, but only slightly reduced the force responses. 8. The results suggest that the force response to nerve stimulation of the rat mesenteric small arteries is mediated primarily through alpha-adrenoceptors, but also to a small degree through non-alpha-adrenoceptors, possibly ATP receptors.
Action Potentials↗
Aortic pressure reduction redistributes transmural blood flow in dog left ventricle.
We studied the effect of graded aortic blood pressure reduction on left ventricular (LV) blood flow in anesthetized, autonomically blocked, open-chest dogs at constant heart rate and mean left atrial pressure. Aortic diastolic pressure (ADP) was lowered from rest (average 116 mmHg) to 90, 75, and 60 mmHg with an arteriovenous fistula. Global and regional LV blood flow was measured with radioactive microspheres. Mean LV blood flow fell stepwise from 145 ml.min-1.100 g-1 at rest to 116 ml.min-1.100 g-1 at ADP of 60 mmHg, whereas the endocardial-to-epicardial flow ratio decreased from 1.20 to 0.84. The transmural redistribution of LV blood flow was not accompanied by increases in LV oxygen extraction, depression of LV contractility, LV dilatation or LV electrical dysfunction and also occurred in the presence of considerable coronary vasodilator flow reserve. Electrical evidence of subendocardial ischemia appeared at ADP of 32 mmHg and an endocardial-to-epicardial flow ratio of 0.41 in a subgroup of animals. We conclude that the redistribution of LV flow during moderate aortic pressure reduction was an appropriate physiological adjustment to uneven transmural alterations in regional LV wall stress and that it preceded a more pronounced redistribution evident with myocardial ischemia.
Animals↗
Induction of ventricular arrhythmias by programmed ventricular stimulation: a prospective study on the effects of stimulation current on arrhythmia induction.
A protocol for programmed ventricular stimulation is described in which the effect of increasing stimulation current on ventricular refractoriness and arrhythmia induction was specifically examined. The protocol was evaluated prospectively in 70 patients undergoing electrophysiological study for documented or suspected ventricular arrhythmias. Programmed electrical stimulation was performed at the right ventricular apex and outflow tract using single and double extrastimuli and burst pacing. Stimulation currents of 2, 5, 10, and 20 mA were used in ascending order. The initial (lowest) current was never less than twice diastolic threshold and was maintained during each stimulation run until refractoriness was reached. The current was then increased to the next level to facilitate premature capture until refractoriness was encountered at 20 mA or a sustained arrhythmia occurred. Ventricular arrhythmias were induced in 34 patients, 31 of whom had presented with a sustained ventricular arrhythmia. The incidence of induced arrhythmias was low in those patients who had presented with symptoms alone, a non-sustained arrhythmia, or a sustained arrhythmia in association with a predisposing clinical event. Only one patient with a negative result had further ventricular arrhythmias during the mean follow up period of 15 months. Although each increase in stimulation current caused a decrease in measured ventricular refractoriness, this resulted in only four arrhythmias. Only one arrhythmia was induced above 5 mA. These results suggest that this simple protocol using two extrastimuli and a single stimulation current of 5 mA will reliably identify most patients who have symptomatic ventricular arrhythmias.
Adolescent↗