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Evaluation of efficacy of nisoldipine in therapy of effort's stabile angina: comparison with propranolol
No full text
Two-dimensional echocardiographic evaluation of ventricular asynergy induced by dipyridamole: correlation with thallium scanning.
No full textMyocardial asynergies detected by two-dimensional echocardiography during
intravenous administration of Dipyridamole (0.75 mg/kg) were evaluated in 54
patients referred for angiographic evaluation of chest pain. Technically adequate
two-dimensional echocardiograms suitable for analysis were recorded in 42 of 54
(77.7%) patients studied. Thallium-201 myocardial perfusion scintigraphy, during
dipyridamole test was performed in the same patients. Thirty of the 42 patients
studied showed significant coronary narrowing at cardiac catheterization.
Dipyridamole-induced wall motion abnormalities and myocardial perfusion defects
were detected, respectively, in 19 (63.3%) and 21 (70%) of 30 patients with
significant coronary artery disease. Wall by wall comparison of the distribution
of dipyridamole-induced echocardiographic asynergy with reversible thallium-201
(201Tl) perfusion defects demonstrated complete correlation in 42 segments
examined. Three segments with perfusion defects at thallium scanning did not show
asynergy during the test while two segments showing wall motion abnormalities
during dipyridamole infusion did not manifest perfusion defects. Our study
demonstrates that two-dimensional echocardiography during dipyridamole testing is
useful in detecting patients with coronary artery disease. Furthermore,ventricular asynergies detected during the test show a high correspondence with
site of myocardial perfusion defects at thallium scanning
Effect of mexiletine on reperfusion-induced ventricular arrhythmias - comparison with lidocaine
No full textThirty mongrel dogs underwent proximal occlusion of the left anterior descending
coronary artery to evaluate the comparative action of mexiletine and lidocaine on
ventricular arrhythmias during myocardial reperfusion. Heart rate, arterial blood
pressure, left ventricular end-diastolic pressure and dp/dt max were evaluated
before and at the 20th and 25th min after coronary occlusion; at the 25th min
coronary occlusion was removed. Dogs were randomly assigned to one of the
following groups of 10: 1) control group; 2) dogs given i.v. mexiletine; 3) dogs
given i.v. lidocaine. As expected, during ischemia, myocardial contractility
decreased after mexiletine or lidocaine administration more than in the control
group. Ventricular arrhythmias during myocardial reperfusion occurred in 9 dogs
of the control group (ventricular tachycardia in 2 cases and ventricular
fibrillation in 7 cases). Among dogs given mexiletine only 1 had ventricular
fibrillation (p less than 0.001 vs control). Six of the 10 dogs given lidocaine
had ventricular arrhythmias (ventricular tachycardia in 5 cases and ventricular
fibrillation in 1 case) (p = ns vs control group; p less than 0.05 vs mexiletine
group). Thus mexiletine and lidocaine had similar effects on cardiac function
during myocardial ischemia and only mexiletine showed a protective effect against
reperfusion ventricular arrhythmias
Effect of beta-blockade on thallium-201 dipyridamole myocardial scintigraphy
No full textThe effect of beta-blockade on dipyridamole thallium-201 images was assessed in 8
patients with coronary artery disease and positive dipyridamole test. Three
dipyridamole thallium-201 tests were performed, the first in basal conditions,
the second 30' after propranolol and the third with propranolol and atrial
pacing. After dipyridamole heart rate and double product increased respectively
from 75 +/- 7 to 98 +/- 15 b/min (p less than 0.01 vs starting values) and from
10 551 +/- 1255 to 11 740 +/- 4542 mmHg X b/min (p less than 0.05 vs starting
values). Propranolol reduced heart rate to 64 +/- 6 b/min (p less than 0.05 vs
basal conditions), systolic blood pressure to 136 +/- 13 and double product to
8733 +/- 1248 (p less than 0.05 vs basal conditions). Dipyridamole when infused
after propranolol, induced an increase in heart rate to 70 +/- 5 b/min (p less
than 0.05 vs starting values) while double product was 9133 +/- 1189 mmHg X b/min
(p = NS vs starting values). Atrial pacing prevented the fall in heart rate and
double product induced by propranolol so during dipyridamole infusion double
product increased to 13 271 +/- 1868 (p less than 0.05 vs propranolol treatment;
p less than 0.05 vs starting values). Segmental score calculated after
dipyridamole was 5.2 +/- 2.0 in basal conditions, 5.1 +/- 1.3 after propranolol
(p = NS) and 4.8 +/- 1.3 after propranolol plus atrial pacing (p = NS). Thus the
results of the study show that beta-blockade does not worsen dipyridamole
thallium-201 images. Furthermore the steal phenomenon seems to be the main
mechanism of the dipyridamole induced ischemia. In fact, also when the increase, oxygen consumption is blunted with beta-blockade the disparity in myocardial blood flow resulted unaffected
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Variations on the Author
Full text link“Variations on the Author” discusses two of Eduardo Coutinho’s recent films (Um Dia na Vida, from 2010, and Últimas Conversas, posthumously released in 2015) and their contribution to the general question of documentary authorship. The director’s filmography is characterized by a consistent yet self-effacing form of authorial self-inscription: Coutinho often features as an interviewer that rather than express opinions propels discourses; an interviewer that is good at listening. This mode of self-inscription characterizes him as an author who is not expressive but who is nonetheless markedly present on the screen. In Um Dia na Vida, however, Coutinho is completely absent form the image, while Últimas Conversas, on the contrary, includes a confessional prologue that moves the director from the margins to the center of his films. This article examines the ways in which these works stand out in the filmography of a director who offers new insights into the notion of cinematic authorship
Appropriate Similarity Measures for Author Cocitation Analysis
Full text linkWe provide a number of new insights into the methodological discussion about author cocitation analysis. We first argue that the use of the Pearson correlation for measuring the similarity between authors’ cocitation profiles is not very satisfactory. We then discuss what kind of similarity measures may be used as an alternative to the Pearson correlation. We consider three similarity measures in particular. One is the well-known cosine. The other two similarity measures have not been used before in the bibliometric literature. Finally, we show by means of an example that our findings have a high practical relevance.information science;Pearson correlation;cosine;similarity measure;author cocitation analysis
Effects of acetylstrophanthidin on baroreflex sensitivity in patients with acute myocardial infarction
No full textWe evaluated the effects of acetylstrophanthidin on baroreflex sensitivity in patients soon after an acute myocadial infarction. Baroreflex control of heart rate is frequently depressed after acute myocardial infarction and few data are available as to the effects of pharmacological intervention on this parameter. The reflex chronotropic response to arterial baroreceptor stimulation was assessed in 29 patients with uncomplicated acute myocardial infarction in control conditions (72-96 h after symptom onset) and 30 min after acetylstrophanthidin administration. To check for spontaneous baroreflex sensitivity variations, 24 patients with the same characteristics were evaluated at the same time intervals before and after a 10-cc bolus of saline placebo. Baroreflex sensitivity was assessed by calculating the regression line relating phenylephrine-induced increases in systolic blood pressure to the attendant changes in RR intervals. Mean baseline baroreflex sensitivity value for the whole study population was 7.4 ± 4.5 ms/mmHg and was unchanged, 7.0 ± 4.5 ms/mmHg, after acetylstrophanthidin (P=NS). Mean baroreflex sensitivity values were also comparable dividing patients according to the site of infarction both before and after acetylstrophanthidin. Despite the lack of difference in mean baroreflex sensitivity values between the two studies, at a post hoc analysis an inverse relation was found in the total study population between baseline baroreflex sensitivity values and their changes after acetylstrophanthidin (r = -0.62; P < 0.005). The inverse relation was also evident separately in anterior (r = -0.57; P < 0.05) and in inferior (r =-0.70; P < 0.005) myocardial infarction patients. In the control group no difference was observed between mean baroreflex sensitivity values obtained in the two studies, nor was there any relationship between baseline baroreflex sensitivity values and their changes after placebo administration. These data demonstrate that after myocardial infarction acetylstrophanthidin administration had no effect on mean baroreflex sensitivity value. However, this drug seems to improve baroreflex sensitivity when it is depressed and to worsen it when normal or nearly normal
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