engleski

Differential regional adaptation to acute left ventricular afterload increase with retained pericardial constraint.

Purpose: Most studies on left ventricular (LV) morphology during afterload increase were performed on open chest/pericardium animals. Little is known about the acute afterload impact on LV wall thickness in a more physiological closed chest/closed pericardium model. Furthermore, regional LV postsystolic thickening (PST) was described in chronic pressure overload, but the onset of its occurrence is unknown. We aimed to study the impact of acute LV pressure overload on regional changes in LV wall thickening and its timing in the experimental setting. Methods: 7 anesthetised closed chest/closed pericardium pigs were instrumented with a descending aorta balloon, partially inflated during 5-10 heartbeats creating a 30% LV pressure increase. Echocardiographic LV LAX B-mode cine- loops were acquired (5 pre-, 5-10 inflation, 10 postinflation beats). End-diastolic and end- systolic thickness of the septum (IVS) and the posterior wall (LVPW) were measured from anatomic M-mode images of the LV base, mid and apex. The timing of thickening was defined as systolic or PST from simultaneous LV Millar pressure traces. Results: A reduction in IVS and LVPW thickness occurred in systole and diastole during balloon inflation. The basal segments demonstrated significantly supranormal values after balloon release (Table 1). During balloon inflation, PST was induced in the basal and apical segments of the IVS and LVPW in all pigs, in the mid LVPW in only 1 pig and in none in the mid IVS. Conclusions: This study demonstrates immediate reduction of LV wall thickening during acute pressure overload in a model with retained pericardial constraint. PST was revealed as an acute response to pressure overload in the basal and apical segments which were more sensitive to afterload. These findings provide better insight into acute LV remodelling in pressure afterload and, due to the selected model, should reflect changes in the clinical setting during e.g. systemic BP surges.

Afterloading; pressure increase; animal model; postsystolic thickening.

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