Stiffening of the aorta often precedes coronary events, but little is known about the aetiological mechanism. We hypothesized that the predisposition to myocardial ischemia could be attributable to aortosclerosis-induced alterations in the central haemodynamics during diastole.
Using noninvasive tonometry and ultrasonography, we investigated the arterial pressure pulse waveforms, pulse wave velocities (PWVs) and compliance in 222 patients with hypertension. The diastolic pressure decay was quantified by fitting a mono-exponential curve as P(t) = P0e−λt [λ: decay index; P0: end-systolic pressure; t: time from end-systole]. The myocardial oxygen supply/demand balance was estimated from the subendocardial viability index (SVI).
The aortic pressure decay fit to an exponential curve significantly (R2 = 0.98 ± 0.02) and more closely than the radial pressure decay (P < 0.001). The aortic decay index (median, 0.59 s−1) was associated with the aortic PWV and compliance (but not with the peripheral PWV or resistance), even after controlling for age, sex, renal function, diabetes and hypercholesterolemia (P < 0.001). Also, both the aortic PWV and compliance (together with the augmentation index) were related to the SVI, although these relationships were no longer significant after accounting for the decay index. Mediation analysis revealed substantial mediating effects of the decay index on the relationship between aortic PWV or compliance and SVI (75–100%), despite the lack of similar effects of the augmentation index.
Aortic stiffening with reduced compliance potentially impairs myocardial viability by accelerating the diastolic exponential decay (rather than through enhancing late-systolic augmentation) of the central blood pressure, thus predisposing hypertensive patients to ischemic heart disease.