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Biomedical subjects

E Aimè

Publications and source records attributed to E Aimè.

4 recordsLinked to original sources
PubMed1990

Variable response to atrial pacing after intravenous propranolol in patients with stable exertional angina.

The effect of propranolol administration on regional coronary haemodynamics were investigated in 14 patients with stable exertional angina and isolated left anterior descending artery disease. Thermodilution was used to measure great cardiac vein flow (GCVF) and anterior regional coronary resistance (ARCR) under control conditions, at peak atrial pacing, after i.v. propranolol administration (0.1 mg kg-1) and at the peak of repeated atrial pacing. Propranolol did not change peak pacing heart rate, systolic blood pressure or double product. Peak pacing GCVF decreased slightly but non-significantly after drug administration from 84 +/- 20 to 79 +/- 24 ml min-1, while ARCR increased, but again non-significantly, from 1.36 +/- 0.44 to 1.45 +/- 0.45. Analysis of individual patient responses revealed that propranolol prolonged peak pacing time and hence peak pacing heart rate (from 126 +/- 24 to 140 +/- 23 beats min-1, P less than 0.05) in five patients. In such patients, peak pacing systolic blood pressure was lower than the pre-propranolol atrial pacing (145 +/- 35 vs 165 +/- 33, P less than 0.001) so that double product remained unchanged. Moreover, peak pacing ARCR did not change after propranolol (pre-propranolol 1.47 +/- 0.46, after propranolol 1.40 +/- 0.56 mmHg.ml-1.min, P = ns) while it increased significantly in the nine patients who did not improve after the drug (before propranolol 1.30 +/- 0.44, after propranolol 1.48 +/- 0.41 mmHg.ml-1.min, P less than 0.02). These data suggest that the response to atrial pacing after i.v. propranolol administration is variable as some patients tolerate higher heart rates while others do not.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1990

[Evaluation of the effects of vasodilator therapy in primary pulmonary hypertension. Experience in 7 cases].

Primary pulmonary hypertension is an uncommon but serious disease that often results in debilitating symptoms and early death. One approach to treatment has been to attempt a reduction of pulmonary artery pressure and vascular resistance by using vasodilator drugs with conflicting results in several studies. The aim of this study is to review the ten-years (1978-1988) experience of vasodilator therapy for primary pulmonary hypertension at our institute. In this period 7 patients, 5 women and 2 men, mean age 38.4 years (range 15-66) met clinical and hemodynamic criteria for primary pulmonary hypertension. At diagnosis 3/7 patients were in NYHA class III and 2/7 in class II. Diagnosis was confirmed by open lung biopsy in one case. Mean pulmonary artery pressure was 66 +/- 17 mmHg, mean value of pulmonary vascular resistances was 22.5 +/- 11 U.W. and of cardiac index 1.8 +/- 0.58 l/min/m2. Twelve different vasodilator drugs were tested during right heart catheterization in a non randomized manner. Various vasodilators were usually tested in the same patient (2 or more drugs in 6 patients). Only one patient did not tolerate acute therapy because of development of a persistent systemic hypotension. Hemodynamic responses to nitrates showed a general reduction in pulmonary artery pressure and pulmonary vascular resistances with marginal changes in cardiac index. Calcium channel-blocking agents elicited different responses in similar patients with favorable, little, no or adverse effects in pulmonary hemodynamics and sometimes a significant decrease in systemic vascular resistances. Also hydralazine showed favorable hemodynamic results in few cases but exacerbated pulmonary hypertension in others.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1986

Effects of diltiazem on regional coronary hemodynamics during atrial pacing in patients with stable exertional angina: implications for mechanism of action.

To investigate the mechanism of the antianginal action of diltiazem in stress-induced myocardial ischemia, we studied 12 patients with stable exertional angina and disease of the proximal left anterior descending artery by measuring great cardiac vein flow (GVCF) and calculating anterior regional coronary resistance (ARCR) during myocardial ischemia induced by atrial pacing before and after intravenous administration of diltiazem (0.25 mg/kg in a bolus dose followed by continuous infusion of 0.005 mg/kg/min). Diltiazem increased the pacing time to angina from 6.9 +/- 3.5 to 10.7 +/- 4 min (p less than .001). At peak pacing heart rate was increased after diltiazem (from 128 +/- 17 to 145 +/- 17 beats/min, p less than .005), while mean arterial pressure was decreased (from 131 +/- 19 to 113 +/- 17 mm Hg, p less than .025), leaving the double product unaltered. At peak pacing no changes were observed in GCVF (from 115 +/- 46 to 119 +/- 46 ml/min, p = NS), ARCR (from 1.3 +/- 0.4 to 1.1 +/- 0.4 mm Hg/ml/min), or myocardial oxygen consumption of the anterior region (from 14.5 +/- 4.2 to 13.4 +/- 4.7 ml/min). Reduction of myocardial oxygen demand plays a major role in the antianginal action of diltiazem in patients with stress-induced myocardial ischemia.

Adult↗