engleski

A study of the proarrhythmogenic effect of acute left ventricular afterload increase: insights from a novel closed chest/pericardium model.

Purpose: To determine whether acute LV afterload increase is an additive risk factor in sudden cardiac death. Prior studies of mechano-electric coupling during acute afterloading were limited to open chest/pericardium preparations or ex vivo models. The aim of this study was to determine the interrelationships of an acute LV afterload challenge with the induction, presence and disappearance of delayed after depolarizations (DADs). Methods: Systolic blood pressure was raised by 30% during 5 to 10 beats by acute balloon inflation (2-3ml) in the mid-descending aorta. Echo guidance was used to position a contact electrode catheter to record monophasic action potentials (MAPs). Concomitant 12 lead ECG was recorded. Endocardial MAP registration was performed during 30 pressure challenges in 3 consecutive pigs. Results: In all cases MAP duration and MAP amplitude slightly decreased during the acute pressure challenge (242±6 to 237±6 ms, p<0.001 ; 21.8±0.9 to 21.3±0.8 mV, p<0.05) with a concomitant lengthening of the RR interval (521±9ms to 570±13ms, p<0.001). With balloon release these changes normalized over several beats. Moreover, acute afterloading caused beat-to-beat appearance of DADs during 16/30 pressure challenges (figure A, asterisks). In 10/30 these DADs caused premature ventricular complexes (PVCs) (figure B) and in 1/30 short non-sustained ventricular tachycardia. Conclusion: The feasibility of MAP registration in a near to physiological closed chest/pericardium model of acute LV pressure overload was demonstrated. Furthermore, a beat-to-beat development of DADs was demonstrated during acute pressure overload giving rise to PVCs, with immediate disappearance during pressure release.

Acute afterloading; pressure; animal model; sudden death; delayed after depolarizations

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