Postextrasystolic potentiation in patients with ischaemic heart disease: influence of inotropic agents.
1. The extent of postextrasystolic potentiation (PESP) has been considered a useful parameter for evaluating myocardial contractile reserve in the presence of myocardial stunning or hibernation. Extent of PESP appears to reflect an interaction between myofibrillar calcium concentration 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 has not been extensively studied. 2. In 35 patients undergoing diagnostic coronary angiography, we investigated the relationship between the extrasystolic test pulse interval (ETPI) and left ventricular (LV) +dP/dtmax of a postextrasystolic contraction. The influence of three inotropically active agents on this relationship was examined following intravenous bolus injection (metoprolol, 4 mg; sotalol, 20 mg; and milrinone, 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/dtmax 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 increase of 11.8% (1.3, 22.3) for milrinone (P < 0.05). 4. With the postextrasystolic interval identical to baseline pacing cycle length, postextrasystolic potentiation of LV+dP/dtmax varied inversely with ETPI. None of the three agents investigated significantly affected this relationship. 5. These results demonstrate that the extent of PESP is unaffected by 'pure' beta-adrenoceptor antagonism, (+/-)-sotalol or phosphodiesterase inhibition in man. Hence pharmacotherapy with these agents is unlikely to affect assessment of extent of PESP.
Cardiology Unit, Queen Elizabeth Hospital, Adelaide, Australia.
Y I
YI
Zhang
R H
RH
Ritchie
J D
JD
Horowitz
D000319:Adrenergic beta-Antagonists / Q000494:pharmacology*; D000328:Adult; D000368:Aged; D005117:Cardiac Complexes, Premature / Q000188:drug therapy / Q000503:physiopathology*; D002316:Cardiotonic Agents / Q000494:pharmacology*; D005260:Female; D006801:Humans; D007275:Injections, Intravenous; D008297:Male; D008790:Metoprolol / Q000494:pharmacology; D008875:Middle Aged; D020105:Milrinone; D009200:Myocardial Contraction / Q000187:drug effects*; D017202:Myocardial Ischemia / Q000188:drug therapy / Q000503:physiopathology*; D017682:Myocardial Stunning / Q000503:physiopathology; D010726:Phosphodiesterase Inhibitors / Q000494:pharmacology; D011728:Pyridones / Q000494:pharmacology; D013015:Sotalol / Q000494:pharmacology; D016277:Ventricular Function, Left / Q000187:drug effects* / Q000502:physiology
D000319:Adrenergic beta-Antagonists; D002316:Cardiotonic Agents; D010726:Phosphodiesterase Inhibitors; D011728:Pyridones; D013015:Sotalol; D008790:Metoprolol; D020105:Milrinone