Current surgical management of @entity1284 -induced @entity712 ( @entity712 ) leads to variable recovery of left ventricular (LV) function despite a return of LV geometry. The mechanisms that prevent restoration of function are unknown but may be related to the timing of intervention and the degree of LV contractile impairment. This study determined whether @entity292 ( @entity292 )-induced LV @entity1284 during the compensatory stage of @entity712 results in @entity5707 and restoration of pump function. @entity35 were subjected to @entity292 for 4 wk; a subset then received a load-reversal procedure by closing the shunt using a custom-made stent graft approach. Echocardiography or in vivo pressure-volume analysis was used to assess LV morphology and function in sham @entity35 ; @entity35 subjected to 4-, 8-, or 15-wk @entity292 ; and @entity35 subjected to 4-wk @entity292 followed by 4- or 11-wk reversal. Structural and functional changes were correlated to LV collagen content, extracellular matrix (ECM) proteins, and @entity1184 markers. @entity292 -induced @entity1284 led to progressive @entity5988 and @entity409 . @entity35 subjected to short-term reversal (4-wk @entity292 + 4-wk reversal) exhibited improved chamber dimensions (LV diastolic dimension) and LV compliance that were associated with ECM remodeling and normalization of atrial and brain natriuretic peptides. Load-independent parameters indicated LV systolic (preload recruitable @entity64 work, Ees) and @entity67 (tau, arterial elastance). These changes were associated with an altered a/b-myosin heavy chain ratio. However, these changes were normalized to sham levels in long-term reversal @entity35 (4-wk @entity292 + 11-wk reversal). Acute hemodynamic changes following @entity292 reversal improve LV geometry, but @entity1002 persists. Gradual restoration of function was related to normalization of @entity1184 , LV wall stress, and ECM remodeling. These results suggest that mild to moderate @entity1002 may be an important indicator of the ability of the myocardium to remodel following the reversal of hemodynamic overload.

Temporal pattern of left ventricular structural and functional remodeling following reversal of @entity1284 XXXX .

@entity712 :: ('MESH:D006333', 'Disease') :: ['HF', 'heart failure'] @entity64 :: ('MESH:D020521', 'Disease') :: ['stroke'] @entity5988 :: ('MESH:C565277', 'Disease') :: ['LV chamber dilation'] @entity1184 :: ('MESH:D006984', 'Disease') :: ['eccentric hypertrophy', 'hypertrophic'] @entity409 :: ('MESH:D008107', 'Disease') :: ['contractile dysfunction'] @entity292 :: ('MESH:D005402', 'Disease') :: ['reduction of aortocaval fistula', 'ACF'] @entity5707 :: ('MESH:D020257', 'Disease') :: ['beneficial LV structural remodeling'] @entity35 :: ('10116', 'Species') :: ['Rats', 'rats'] @entity67 :: ('MESH:D018754', 'Disease') :: ['diastolic dysfunction'] @entity1002 :: ('MESH:D018487', 'Disease') :: ['LV dysfunction', 'LV systolic dysfunction'] @entity1284 :: ('MESH:D019190', 'Disease') :: ['volume overload']
@entity712 :: (MESH:D006333,Disease) :: ['heart failure']
