Effects of incoordination on left ventricular force-velocity relation in aortic stenosis.

OBJECTIVE

Tension development is often incoordinate in the hypertrophic left ventricle (LV). The present study aimed to elucidate the possible effects of incoordination on standard LV force-velocity relations in patients with aortic stenosis (AS).

DESIGN

Prospective study during aortic valve replacement with transoesophageal cross sectionally guided M mode echocardiogram, combined with high-fidelity LV pressure recorded by pressure transducer tip catheter, and thermodilution cardiac output.

SETTING

Tertiary cardiac referral centre.

PATIENTS

37 patients (mean (SD) age 63 (12)) years were studied before and 20 hours after aortic valve replacement.

MAIN OUTCOME MEASURES

LV function was assessed regionally by peak velocity of circumferential fibre shortening (peak Vcf), mean systolic wall stress, and peak myocardial power; and globally by LV stroke work index. LV coordination was quantified as cycle efficiency, derived from LV pressure-dimension loop (lower normal limit > or = 76%).

RESULTS

22 patients with a coordinate LV had significantly higher peak Vcf (1.85 (0.47) v 1.46 (0.64) s-1) peak myocardial power (20.8 (8.5) v 12.0 (6.1) mW.cm-3) and global stroke work index (440 (155) v 325 (150) mJ.m-2) than those of 15 patients with an incoordinate ventricle, all P < 0.05; though there was no significant difference in LV end diastolic dimension, mean systolic wall stress, LV mass index, or the incidence of coronary artery disease (P > 0.05, respectively). Furthermore, when contraction was coordinate, mean systolic circumferential wall stress correlated inversely with peak Vcf (r = - 0.71) and positively with peak myocardial power (r = 0.83), both P < 0.01. When contraction was incoordinate, these correlations did not apply; instead peak Vcf (r = 0.65) and peak myocardial power (r = 0.73) both correlated positively with cycle efficiency (P < 0.02 and 0.01, respectively). By 20 hours after surgery, values of cycle efficiency, peak Vcf, and myocardial power were indistinguishable in the previously coordinate and incoordinate groups.

CONCLUSIONS

In aortic stenosis, incoordination causes a fall in LV peak Vcf proportional to the increase in systolic wall stress, and thus modifies the standard LV force-velocity relation to mimic depressed contractility. However, incoordination and subsequent ventricular dysfunction were largely reversible once the aortic stenosis had been relieved.