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Eur J Cardiothorac Surg 2007;31:677-684. doi:10.1016/j.ejcts.2007.01.013
Copyright © 2007, European Association for Cardio-Thoracic Surgery. Published by Elsevier B.V. All rights reserved

Mechanical restitution curves — a possible load independent assessment of contractile function

Knut E. Kjørstada,b,*, Dag Ole Nordhaugc,d, Christian Korvalde, Stig Müllera,b, Tor Steensruda,b, Truls Myrmela,b

a Department of Cardiothoracic and Vascular Surgery, University Hospital North Norway, N-9038 Tromsø, Norway
b Department of Surgery, Institute of Clinical Medicine, Faculty of Medicine, University of Tromsø, N-9037 Tromsø, Norway
c Department of Cardiothoracic Surgery, St. Olavs University Hospital, N-7030 Trondheim, Norway
d University for Science and Technology, N-7491 Trondheim, Norway
e Department of Plastic Surgery, National Hospital, N-0027 Oslo, Norway

Received 18 April 2006; received in revised form 27 December 2006; accepted 5 January 2007.

* Corresponding author. Address: Department of Cardiothoracic and Vascular Surgery, University Hospital North Norway, N-9038 Tromsø, Norway. Tel.: +47 776 26 000; fax: +47 776 28 298. (Email: knutek{at}fagmed.uit.no).

Objective: The time constant of mechanical restitution (T (MRC)), proposed to reflect changes in calcium release and uptake, has been shown to increase in left ventricular (LV) failure, and might have a potential as an index of contractile function. However, in vivo studies of the effect on T (MRC) of changing loading conditions in the normal and failing heart have not been reported. Consequently, in this study, we tested the hypothesis that the increase in T (MRC) in vivo is independent of preload and afterload. Methods: Left ventricular pressure–volume loops were assessed at baseline in eight open chest pigs using the combined pressure–volume conductance catheter technique during right atrial pacing at 120 b/min. Mechanical restitution curves (MRC) were constructed during four different loading conditions in all eight animals: uninfluenced load, reduced preload (balloon catheter in v. cava inferior), increased afterload (balloon catheter in descending aorta), and increased preload combined with reduced afterload (aortocaval shunting). Acute LV failure was then induced by microembolization through the left main coronary artery, and the experimental protocol was repeated. Contractile response was defined as the maximal first derivative of pressure (dP/dt max), and T (MRC) was calculated using a least square approximation algorithm. Results: Hemodynamic data 30 min after microembolization showed decreased mean arterial pressure (98 ± 14–67 ± 10 mmHg, (mean ± SD) P < 0.0001) and dP/dt max (1482 ± 193–1001 ± 125 mmHg/s, P = 0.001). Stroke volume decreased from 30 ± 5 to 20 ± 5 ml (P < 0.0001) compared to baseline, and preload recruitable stroke work decreased from 52 ± 7 to 31 ± 10 mmHg (P = 0.002). T (MRC) increased in all eight animals after induction of LV failure at all loading conditions. There was no difference between the different loading conditions at baseline, nor at LV heart failure, but T (MRC) increased significantly after the induction of heart failure (ANOVA, two ways). Conclusions: We have shown that the left ventricular T (MRC) increases after developed heart failure. The increase in T (MRC) was independent on loading conditions and thus have a potential for a contractility index.

Key Words: Contractility index • Conductance catheter • Heart failure






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Copyright © 2007 European Association for Cardio-Thoracic Surgery. Published by Elsevier. All rights reserved.