Abstract Body: Impaired relaxation is a common feature in most cases of diastolic dysfunction, including heart failure with preserved ejection fraction. Isovolumetric relaxation is typically characterized by τ, an exponential time constant, but may be broken into relaxation and stiffness-like parameters (µ and Ek). Recent in vitro work suggests that strain during late systole (protodiastolic period) modifies relaxation. We hypothesize that late systolic pressure and time indexes correlate with myocardial relaxation.

Thirty-four (34) simultaneous aortic and left ventricular micromanometric (Millar) pressure traces were obtained from a comprehensive database of clinical cardiac catheterization patients. These patients underwent coronary artery disease screening and presented but did not have arterial blockages. Pressure and time parameters were calculated over a five-minute interval.

Relaxation rate (1/τ), and stiffness (Ek) correlated to end systolic parameters in an orthogonal pattern to relaxation (µ). 1/τ showed strong correlations with time from peak pressure to aortic valve divided by ejection time (t54/t52, r = .675, p < .01) and moderate correlation to the pressure decline after peak pressure to aortic valve pressure divided by the pulse pressure (P45/P42, r = .577, p < .01). In parallel Ek showed moderate correlation with t54/t52 (r = .592, p < .01), and a moderate correlation with P45/P42 (r = .470, p < .01), the pressure at aortic valve closure (r = -.420, p < .05), and aortic augmentation index (AIx, r = -.360, p < .05). Finally, µ presented a moderate correlation to P45/P42 (r = .501, p < .05), the pressure at aortic valve closure (r = .404, p < .05), and AIx (r = -.357, p < .05).

As predicted, ventricular relaxation in patients correlates with late systolic hemodynamics. Parameters or combinations of parameters may predict relaxation rates or correlate to in vivo late systolic strain. Prospective studies evaluating end systolic strain and relaxation merit consideration. Overall, these observations are consistent with in vitro studies that suggest that impaired cessation of contraction is a regulator of relaxation.