Ethanol ablation was used to create an interventricular septal infarction in 6 sheep, and 6 others served as the control sheep. The load-independent and in-series RV response to DCC was assessed using sonomicrometer heart dimension sensors. Triphenyltetrazolium perfusion delineated the septal damage.
LV DCC caused a greater increase of the RV preload recruitable stroke work in the control sheep than in the study sheep (190.6 ± 23.5 and 135.0 ± 40.8 erg*10^3, respectively, P < .001). In contrast, RV end-systolic elastance increased more in the septal-ablated sheep with RV DCC (17.29 ± 3.40 vs 9.88 ± 2.01 mm Hg/mL in the control sheep, P < .001). Abnormal RV diastolic function before device insertion in the septal-ablated sheep was normalized with both passive DCC placement and after activation (RV diastolic relaxation constant 23.5 ± 2.3 and 20.0 ± 2.1 ms, respectively, P < .001). Both biventricular and RV DCC actuation increased the RV systolic pressure more in the septal-ablated sheep than in the control sheep (37.9 ± 6.3 and 47.7 ± 4.6 mm Hg vs 29.7 % ± 4.8 % and 40.3 % ± 8.3 % , respectively, P < .001). In contrast, the RV end-systolic diameter decreased more during LV DCC (70.1 % ± 15.9 % vs 90.5 % ± 5.0 % , P < .001).
The HeartPatch DCC support of LV and RV function results from improvement of the systolic septal-lateral fractional change that is not influenced by septal infarction. The latter attenuated LV to RV device energy delivery during LV patch actuation but enhanced RV energy delivery during RV patch actuation. This DCC technique can provide effective support in high-risk RV failure situations arising from left ventricular assist device use.