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Biomedical subjects

F Picó-Aracil

Publications and source records attributed to F Picó-Aracil.

6 recordsLinked to original sources
PubMed2001

Effects of early use of atenolol or captopril on infarct size and ventricular volume: A double-blind comparison in patients with anterior acute myocardial infarction.

BACKGROUND: beta-Blockers and ACE inhibitors reduce early mortality when either one is started in the first hours after myocardial infarction (MI). Considering the close correlation between morphological changes and prognosis, we aimed to investigate whether the benefit of both beta-blockers and ACE inhibitors might reside in a similar protective effect on infarct size or ventricular volume. METHODS AND RESULTS: In a randomized, double-blind comparison between early treatment with captopril or atenolol in 121 patients with acute anterior MI, both drugs showed a similar reduction in mean blood pressure. However, only the atenolol-treated patients showed a significant early reduction in heart rate. Infarct size, obtained from the perfusion defect in resting single photon emission imaging, was higher in captopril-treated patients than in atenolol-treated patients: 29.8+/-12% versus 20.8+/-12% (P:<0.01) by polar map and 28.3+/-13% versus 20.0+/-13% (P:<0.01) by tomography. Changes from baseline to 1 week and to 3 months in ventricular end-diastolic volume, assessed by echocardiography, were as follows: 58+/-14 versus 64+/-19 (P<0.05) and 65+/-21 mL/m(2) (P<0.05), respectively, with captopril, and 58+/-18 versus 64+/-18 (P<0.05) and 69+/-30 mL/m(2) (P<0.05), respectively, with atenolol. Neither group showed significant changes in end-systolic volume. Among patients with perfusion defect >18% (n=51), those treated with atenolol showed a significant increase of end-systolic and end-diastolic ventricular volumes, whereas captopril-treated patients did not. CONCLUSIONS: Although early treatment with atenolol or captopril results in similar overall short- and medium-term preservation of ventricular function and volumes, in patients with larger infarctions, a beta-blocker alone does not adequately protect myocardium from ventricular dilatation.

Acute Disease↗
PubMed1999

Head-up tilt test in patients with high pretest likelihood of neurally mediated syncope: an approximation to the "real sensitivity" of this testing.

UNLABELLED: This study was designed to examine the "true sensitivity" of a specific head-up tilt (HUT) testing protocol using clinical findings. The HUT protocol used 45 minutes at 60 degrees for the baseline portion and intermittent boluses of 2, 4, and 6 micrograms of isoproterenol in the second phase. Eighty-eight patients (40 men and 48 women; mean age of 33.8 +/- 16 years) with recurrent syncope and high pretest likelihood of neurally mediated syncope were included. The following were considerated as high pretest likelihood criteria: (1) at least two syncopal episodes; (2) no structural heart disease and normal baseline ECG; (3) age < 65 years; (4) a typical history of neurally mediated syncope, triggering factors plus premonitory signs; and (5) short duration of symptoms and fast recovery without neurological sequelae. Fifty-four patients (61%) had a positive tilt test (34/88 baseline [39%] and 20/50 with isoproterenol [40%]). The shorter time interval between the last syncopal episode and baseline HUT test was the only predictor for a positive response (P < 0.003). Conversely, this time interval was not predictor of positive responses during isoproterenol-tilt testing. IN CONCLUSION: (1) we claim a "sensitivity" for this combined protocol of 61%; and (2) our results indicate that patients with syncope of unknown origin must be tilted nearest as possible to the last syncope to increase the positive responses of HUT test.

Adolescent↗
PubMed1998

Role of endogenous opioids in syncope induced by head-up tilt test and its relationship with isoproterenol-dependent and isoproterenol-independent neurally-mediated syncope.

This study was designed to evaluate the role of endogenous opioids in neurally-mediated syncope. Head-up tilt test was performed on 35 patients with syncope of unknown origin. Plasma beta-endorphin was measured (1) at baseline, (2) at the end of tilt test or at time of syncope, (3) 15 min before isoproterenol-test, (4) at the end of the isoproterenol-test or at time of syncope. Subjects with a positive tilt testing showed a larger rise in plasma beta-endorphin concentrations at time of syncope (baseline 13.7+/-8.0 vs. syncope 41.4+/-26.4 pmol l(-1); P<0.01). On the contrary, patients with a positive isoproterenol-test showed no rise in plasma beta-endorphin levels (baseline 7.9+/-3.6 vs. syncope 7.4+/-2.7 pmol l(-1); P=ns). Patients with a passive negative tilt test (baseline 6.7+/-2.8 vs. end of test 7.0+/-3.3 pmol l(-1); P=ns) and negative isoproterenol tilt test (baseline 7.4+/-3.8 vs. end of test 8.1+/-3.4 pmol l(-1); P=ns) showed no changes in beta-endorphin concentrations. To further examine the efficacy of i.v. naloxone to prevent syncope, 10 patients were randomized to naloxone (0.02 mg/kg) or placebo. Second head-up tilt testing was negative in 1/5 patients with naloxone and in 2/5 patients with placebo. We conclude that, (1) endogenous opioids seem to be involved in vasovagal syncope induced by baseline head-up tilt test, (2) changes in plasma beta-endorphin concentrations show significant differences between patients who have isoproterenol-dependent and isoproterenol-independent syncope, this finding might occur in the setting of different pathophysiologic mechanisms, and (3) intravenous naloxone at a dose of 0.02 mg/kg was not superior to placebo in order to prevent positive responses to baseline tilt test.

Adolescent↗