POSTEXTRASYSTOLIC POTENTIATION IN PATIENTS WITH ISCHEMIC-HEART-DISEASE - INFLUENCE OF INOTROPIC AGENTS

Citation
Y. Zhang et al., POSTEXTRASYSTOLIC POTENTIATION IN PATIENTS WITH ISCHEMIC-HEART-DISEASE - INFLUENCE OF INOTROPIC AGENTS, British journal of clinical pharmacology, 40(1), 1995, pp. 25-30
Citations number
33
Categorie Soggetti
Pharmacology & Pharmacy
ISSN journal
03065251
Volume
40
Issue
1
Year of publication
1995
Pages
25 - 30
Database
ISI
SICI code
0306-5251(1995)40:1<25:PPIPWI>2.0.ZU;2-R
Abstract
The extent of postextrasystolic potentiation (PESP) has been considere d a useful parameter for evaluating myocardial contractile reserve in the presence of myocardial stunning or hibernation. Extent of PESP app ears to reflect an interaction between myofibrillar calcium concentrat ion and function of the contractile apparatus. However, potential for cardiovascular drugs including agents modifying adenosine 3' 5'-cyclic monophosphate concentration to influence the extent of PESP in man ha s not been extensively studied. 2 In 35 patients undergoing diagnostic coronary angiography, we investigated the relationship between the ex trasystolic test pulse interval (ETPI) and left ventricular (LV) +dP/d t(max) of a postextrasystolic contraction. The influence of three inot ropically active agents on this relationship was examined following in travenous bolus injection (metoprolol, 4 mg; sotalol, 20 mg; and milri none, 1 mg). 3 The patient group examined had predominantly preserved LV function (LVEF 67% with 95% confidence intervals 63%, 71%). In the doses utilized, all agents exerted significant effects on LV+dP/dt(max ) during atrial pacing: reduction of 12.3% (6.4, 18.2) for metoprolol (P < 0.0005), and 10.9% (4.2, 17.6) for sotalol (P < 0.005); and incre ase of 11.8% (1.3, 22.3) for milrinone (P < 0.05), 4 With the postextr asystolic interval identical to baseline pacing cycle length, postextr asystolic potentiation of LV+dP/dt(max) varied inversely with ETPI. No ne of the three agents investigated significantly affected this relati onship. 5 These results demonstrate that the extent of PESP is unaffec ted by 'pure' beta-adrenoceptor antagonism, (+/-)-sotalol or phosphodi esterase inhibition in man. Hence pharmacotherapy with these agents is unlikely to affect assessment of extent of PESP.