Key result
Induction of acute LV failure in pigs decreased dP/dt(max) from 1482 to 1001 mmHg/s (P=0.001) and significantly increased the time constant of mechanical restitution independent of loading conditions.
Why the study?
Does acute left ventricular failure increase the time constant of mechanical restitution independently of loading conditions in an open chest pig model?
Does acute left ventricular failure increase the time constant of mechanical restitution independently of loading conditions in an open chest pig model?
The time constant of mechanical restitution (T(MRC)) increases in acute heart failure independently of loading conditions, suggesting it may serve as a load-independent index of contractile function.
Answers are grounded in this paper and cite their sources.
May support T(MRC) as load-independent contractile index in acute LV failure; leaves open translation to clinical settings.
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 120b/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 30min after microembolization showed decreased mean arterial pressure (98+/-14-67+/-10mmHg, (mean+/-SD) P<0.0001) and dP/dt(max) (1482+/-193-1001+/-125mmHg/s, P=0.001). Stroke volume decreased from 30+/-5 to 20+/-5ml (P<0.0001) compared to baseline, and preload recruitable stroke work decreased from 52+/-7 to 31+/-10mmHg (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.
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Kjørstad et al. (2007) studied Acute left ventricular failure (n=8). Induction of acute LV failure by microembolization vs. Baseline was evaluated on Time constant of mechanical restitution (T(MRC)). Induction of acute LV failure in pigs decreased dP/dt(max) from 1482 to 1001 mmHg/s (P=0.001) and significantly increased the time constant of mechanical restitution independent of loading conditions.
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