Abstract

We aimed to assess whether myocardial postsystolic thickening (PST) can be induced by an acute increase in right ventricular (RV) afterload and, thus, demonstrate that PST may have a nonischemic cause. In 8 anesthetized open-chest pigs, radial strains of the interventricular septum (IVS) and left ventricular inferolateral wall were obtained by Doppler tissue echocardiography before and during constriction of the pulmonary artery. After each constriction, RV peak systolic pressure increased from 30 +/- 5 to 57 +/- 8 mm Hg (P < .001). Peak systolic radial strain of the IVS decreased from 20.8% +/- 5.3% to 9.5% +/- 4.1% (P = .003), and PST of the IVS increased from 0.3% +/- 0.5% to 6.1% +/- 4.8% (P = .01). The onset of PST started 41 +/- 20 milliseconds after peak negative dP/dt of RV pressure. The inferolateral wall did not show PST. An acute increase in RV pressure causes a significant reduction in peak systolic strain of the IVS associated with the nonischemic appearance of PST.

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