title: The influence of clinical intervention on pressure-volume relationships--the conductance (volume) technique.
abstract: We analysed end-systolic pressure-volume relations (ESPVR), using the conductance technique, to study the potential inotropic effects of (1) PDE inhibitor drugs, (2) class 1 anti-arrhythmic drugs and (3) PTCA-induced myocardial ischaemia (MIS). The question of contractility involvement is of clinical importance, since with inotropy-induced rise in MVO2 there is a risk of MIS, should any of the cardiotonic drugs (amrinone, enoximone, piroximone) be used in patients with CAD. Accordingly, we analysed their haemodynamic effects, identified improved contractility as one factor of these drugs' mode of action and proved their inability to induce MIS. Anti-arrhythmic drugs may cause cardiodepression, a risk theoretically well recognized but clinically poorly defined. We monitored the haemodynamics of six class 1 anti-arrhythmic drugs and found that drug-induced moderate impairments of contractility (at rest and during tachycardia) proved significant, but clinically asymptomatic, and did not differ significantly from drug to drug. PTCA provides routine models of MIS in man. We analysed ESPVR and haemodynamics during MIS with PTCA and coronary angiography (CORO) and the induced diminished LV function during CORO v PTCA appeared quantitatively less. Inotropy impairment was rather modest during ischaemia: dP/dtmax was reduced by 11%, slope k of the ESPVR by 14%, while the EDV was increased by 67%. All changes were reversible about 90 s after PTCA balloon occlusion and 20 s after CORO.
authors: Kerckhoff-Klinik, Max-Planck-Gesellschaft, Bad Nauheim, Germany.
authors: J
authors: J
authors: Thormann
mesh_terms: D015906:Angioplasty, Balloon, Coronary; D000889:Anti-Arrhythmia Agents / Q000009:adverse effects / Q000494:pharmacology* / Q000627:therapeutic use; D001794:Blood Pressure / Q000187:drug effects* / Q000502:physiology; D006328:Cardiac Catheterization / Q000295:instrumentation; D002304:Cardiac Pacing, Artificial; D002306:Cardiac Volume / Q000187:drug effects / Q000502:physiology; D003196:Computer Graphics; D017023:Coronary Angiography; D003327:Coronary Disease / Q000188:drug therapy* / Q000503:physiopathology / Q000628:therapy; D017335:Enoximone / Q000009:adverse effects / Q000627:therapeutic use; D006333:Heart Failure / Q000188:drug therapy / Q000503:physiopathology; D006801:Humans; D007093:Imidazoles / Q000009:adverse effects / Q000627:therapeutic use; D009200:Myocardial Contraction / Q000187:drug effects* / Q000502:physiology; D017202:Myocardial Ischemia / Q000188:drug therapy / Q000503:physiopathology / Q000628:therapy; D010726:Phosphodiesterase Inhibitors / Q000009:adverse effects / Q000494:pharmacology* / Q000627:therapeutic use; D013318:Stroke Volume / Q000187:drug effects* / Q000502:physiology; D016277:Ventricular Function, Left / Q000187:drug effects / Q000502:physiology
chemical_list: D000889:Anti-Arrhythmia Agents; D007093:Imidazoles; D010726:Phosphodiesterase Inhibitors; C039686:piroximone; D017335:Enoximone