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Thormann J. The influence of clinical intervention on pressure-volume relationships--the conductance (volume) technique. Eur Heart J. 1992;13:69-79doi: 10.1093/eurheartj/13.suppl_e.69.
Thormann, J. (1992). The influence of clinical intervention on pressure-volume relationships--the conductance (volume) technique. European heart journal, 1369-79. https://doi.org/10.1093/eurheartj/13.suppl_e.69
Thormann, J. "The influence of clinical intervention on pressure-volume relationships--the conductance (volume) technique." European heart journal vol. 13 (1992): 69-79. doi: https://doi.org/10.1093/eurheartj/13.suppl_e.69
Thormann J. The influence of clinical intervention on pressure-volume relationships--the conductance (volume) technique. Eur Heart J. 1992 Nov;13:69-79. doi: 10.1093/eurheartj/13.suppl_e.69. PMID: 1478213.
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Eur Heart J. 1992 Nov;13:69-79. doi: 10.1093/eurheartj/13.suppl_e.69.

The influence of clinical intervention on pressure-volume relationships--the conductance (volume) technique.

European heart journal

J Thormann

Affiliations

  1. Kerckhoff-Klinik, Max-Planck-Gesellschaft, Bad Nauheim, Germany.

PMID: 1478213 DOI: 10.1093/eurheartj/13.suppl_e.69

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.

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