Regional geometry and function during myocardial ischemia and recovery.
To define the effects of altered left ventricular (LV) geometry on regional myocardial function during ischemia and recovery, regional and global LV geometry and transmural pressure (P) were measured in seven conscious dogs with sonomicrometry and micromanometry. Data were obtained at steady state and during rapid vena caval occlusion (VCO) under control conditions, after 15 min of left anterior descending occlusion, and after 1, 4, and 24 hr of reperfusion. Regional midwall minor axis (MA) Lagrangian strain (epsilon) and stress (sigma) were calculated from measured MA segment length (L), MA midwall radius, and wall thickness. Unstressed regional geometry was quantified using L0, the value of L at P = 0 during maximal VCO. Conventional (SWL) and normalized (SW sigma epsilon) regional MA stroke work were calculated for each cardiac cycle as the area of P vs L and sigma vs epsilon relationships, respectively. Regional Frank-Starling mechanisms corrected for changes in unstressed LV geometry were quantified as the slope (M sigma epsilon) of the linear end diastolic epsilon vs SW sigma epsilon relationship for data obtained during VCO (mean r = 0.98). M sigma epsilon returned to baseline levels within 1 h of reperfusion (P = 0.314 vs control). In contrast, 15 min of ischemia increased L0 by 15.2 +/- 2.5% (P < 0.05), which remained increased 5.7 +/- 1.7% above control values after 1 hr of reperfusion (P < 0.05). Both steady-state SWL and SW sigma epsilon decreased with ischemia and slowly returned towards baseline, remaining 28.7 +/- 7.5% and 26.4 +/- 6.3% below control values after 1 hr of reperfusion (both P < 0.05). Therefore, late functional recovery from reversible ischemic injury is primarily correlated with reversal of changes in regional geometry, specifically the reversal of diastolic creep. As a result, adequate quantification of postischemic regional myocardial performance requires characterization of changes in regional geometry as well as indicators of Frank-Starling mechanisms.
Owen, CH; Lewis, CW; Zipprich, DA; Davis, JW; Sabiston, DC; Glower, DD
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