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  • Title: Differences in haemodynamic response to beta-blocking drugs between stable coronary artery disease and acute myocardial infarction.
    Author: Silke B, Frais MA, Verma SP, Reynolds G, Taylor SH.
    Journal: Eur J Clin Pharmacol; 1986; 29(6):659-65. PubMed ID: 2872054.
    Abstract:
    Theoretically the increased sympathoadrenal activity following acute myocardial infarction might augment the haemodynamic impact of beta-adrenoceptor blockade. To evaluate this question 32 haemodynamic studies were performed to compare the effects of equivalent beta-blocking doses of propranolol (8 mg i.v.) and pindolol (0.8 mg i.v.) in patients with a recent acute myocardial infarction (A.M.I.) or stable coronary artery disease (and a presumptive low sympathetic state). In stable coronary artery disease there were clear differences between the haemodynamic impact of propranolol and pindolol. Propranolol decreased both heart rate (delta HR -7 beat/min) and cardiac index (delta CI -0.4 l/min/m2), with an increased pulmonary artery occluded pressure (delta PAOP +4 mmHg) and systemic vascular resistance index (delta SVRI +358 dyn X s X cm-5 m2). However an equivalent beta-blocking dose of pindolol increased PAOP (delta PAOP +3 mmHg) leaving other variables unchanged. These differential actions of propranolol and pindolol have previously been ascribed to the intrinsic sympathomimetic activity (I.S.A.) of pindolol maintaining cardiac pumping function in a low sympathetic state. In contrast following myocardial infarction, both drugs reduced cardiac index to a significantly greater extent compared with stable coronary artery disease (delta CI propranolol -0.81/min/m2; pindolol -0.4 l/min/m2; p less than 0.05); propranolol also reduced the systemic arterial blood pressure (delta systolic -10 mmHg; delta mean -5 mmHg; p less than 0.05). The haemodynamic relevance of the I.S.A. of pindolol appeared attenuated following A.M.I. These data are compatible with experimental evidence of sympathetic nervous activation following coronary occlusion; the resulting hyperadrenergic state appears to condition an augmented haemodynamic response to beta-blocking drugs irrespective of their ancillary pharmacological properties.(ABSTRACT TRUNCATED AT 250 WORDS)
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