title: Differences in haemodynamic response to beta-blocking drugs between stable coronary artery disease and acute myocardial infarction.
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)
authors.forename: B
authors.initials: B
authors.lastname: Silke
authors.forename: M A
authors.initials: MA
authors.lastname: Frais
authors.forename: S P
authors.initials: SP
authors.lastname: Verma
authors.forename: G
authors.initials: G
authors.lastname: Reynolds
authors.forename: S H
authors.initials: SH
authors.lastname: Taylor
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000494:pharmacology / Q000627:therapeutic use*; D000328:Adult; D002986:Clinical Trials as Topic; D003327:Coronary Disease / Q000188:drug therapy* / Q000503:physiopathology; D006339:Heart Rate / Q000187:drug effects; D006439:Hemodynamics / Q000187:drug effects*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000188:drug therapy*; D010869:Pindolol / Q000627:therapeutic use; D011433:Propranolol / Q000627:therapeutic use; D011897:Random Allocation; D013318:Stroke Volume / Q000187:drug effects; D014655:Vascular Resistance / Q000187:drug effects
chemical_list: D000319:Adrenergic beta-Antagonists; D011433:Propranolol; D010869:Pindolol