The purpose of this study was to assess the effect of heart rate on left ventricular (LV)-arterial coupling and LV mechanical efficiency before and after @entity712 (CHF). The production of @entity64 work (SW) and mechanical efficiency depends on the coupling of the LV and arterial system. The response of @entity1002 to @entity591 may be altered in @entity712 . We compared the response of @entity1002 to increased heart rate (HR) in six conscious, instrumented @entity235 before and after pacing-induced CHF. Coupling was quantified as E(ES)/ E(A), where E(ES) is the slope of end-systolic pressure ( P)-volume ( V) relation, and E(A) is arterial elastance. Mechanical efficiency was determined as the ratio of SW to a total P-V area ( @entity939 ). Before CHF, E(ES) and E(A) increased similarly with increased heart rate to 180 min(-1). Thus, E(ES)/ E(A) remained unaltered (0.96 +/- 0.08 vs 0.94 +/- 0.35), and SW/ @entity939 was unchanged (0.62 +/- 0.03 vs 0.59 +/- 0.06). Compared with the results prior to CHF and after CHF the resting E(ES) was decreased, thus both E(ES)/ E(A) (0.58 +/- 0.09) and SW/ @entity939 (0.48 +/- 0.06) were less ( P < 0.05) than baseline. After CHF, an increase in HR to 180 min(-1) increased E(A) but not E(ES), thus E(ES)/ E(A) fell to 0.44 +/- 0.06 ( P < 0.05) and SW/ @entity939 fell to 0.41 +/- 0.05 ( P < 0.05). Under normal conditions, @entity1002 remains optimal during increases in HR. After CHF, @entity591 exacerbates the suboptimal baseline @entity1002 , reducing the efficiency of producing SW.

@entity591 exacerbates abnormal left ventricular-arterial coupling in XXXX .

@entity64 :: ('MESH:D020521', 'Disease') :: ['LV stroke'] @entity712 :: ('MESH:D006333', 'Disease') :: ['heart failure'] @entity939 :: ('CHEBI:17246', 'Chemical') :: ['PVA'] @entity235 :: ('9615', 'Species') :: ['dogs'] @entity591 :: ('MESH:D013610', 'Disease') :: ['tachycardia'] @entity1002 :: ('MESH:D018487', 'Disease') :: ['LV-arterial coupling']
@entity712 :: (MESH:D006333,Disease) :: ['heart failure']
