Acute and short-term effects of partial left ventriculectomy in dilated cardiomyopathy - Assessment by pressure-volume loops

OBJECTIVES The aim of this study was to evaluate the short-term effects of partial left ventriculectomy (PLV) on left ventricular (LV) pressure-volume (PV) loops, wall stress, and the synchrony of LV segmental volume motions in patients with dilated cardiomyopathy. BACKGROUND Surgical LV volume reduction is under investigation as an alternative for, or bridge to, heart transplantation for patients with end-stage dilated cardiomyopathy. METHODS We measured P-V loops in eight patients with dilated cardiomyopathy before, during and two to five days after PLV. The conductance catheter technique was used to measure LV volume instantaneously. RESULTS The PLV reduced end-diastolic volume (EDV) acutely from 141 +/- 27 to 68 +/- 16 ml/m(2) (p < 0.001) and to 65 +/- 6 ml/m(2) (p < 0.001) at two to five days postoperation (post-op). Cardiac index (CI) increased from 1.5 +/- 0.5 to 2.6 +/- 0.6 l/min/m(2) (p < 0.002) and was 1.8 +/- 0.3 l/min/m(2) (NS) at two to five days post-op. The LV ejection fraction (EF) increased from 15 +/- 8% to 35 +/- 6% (p < 0.001) and to 26 +/- 3% (p < 0.003) at two to five days post-op. Tau decreased from 54 +/- 8 to 38 +/- 6 ms (p < 0.05) and was 38 +/- 5 ms (NS) at two to five days post-op. Peak wall stress decreased from 254 +/- 85 to 157 +/- 49 mm Hg (p < 0.001) and to 184 +/- 40 mm Hg (p < 0.003) two to five days post-op. The synchrony of LV segmental volume changes increased from 68 +/- 6% before PLV to 80 +/- 7% after surgery (p < 0.01) and was 73 +/- 4% (NS) at two to five days post-op. The LV synchrony index and CI showed a significant (p < 0.0001) correlation. CONCLUSIONS The acute decrease in LV volume in heart-failure patients following PLV resulted at short-term in unchanged SV, increases in LVEF, and decreases in peak wall stress. The increase in LV synchrony with PLV suggests that the transition to a more uniform LV contraction and relaxation pattern might be a rationale of the working mechanism of PLV. (C) 2000 by the American College of Cardiology.