In aortic stenosis, incoordinate left ventricular contraction reduced peak Vcf (1.46 vs 1.85 s-1, P<0.05) and myocardial power, mimicking depressed contractility, but reversed 20 hours post-surgery.
Observational (n=37)
No
Does left ventricular incoordination affect the force-velocity relation in patients with aortic stenosis, and is it reversible after aortic valve replacement?
In aortic stenosis, left ventricular incoordination mimics depressed contractility by altering the force-velocity relation, but this dysfunction is largely reversible within 20 hours after aortic valve replacement.
Absolute Event Rate: 1.85% vs 1.46%
p-value: p=<0.05
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, 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.
Jin et al. (Sun,) conducted a observational in Aortic stenosis (n=37). Coordinate left ventricular contraction vs. Incoordinate left ventricular contraction was evaluated on Peak velocity of circumferential fibre shortening (peak Vcf) (s-1) (p=<0.05). In aortic stenosis, incoordinate left ventricular contraction reduced peak Vcf (1.46 vs 1.85 s-1, P<0.05) and myocardial power, mimicking depressed contractility, but reversed 20 hours post-surgery.