[OP.5B.07] DIASTOLIC EXPONENTIAL DECAY OF CENTRAL BLOOD PRESSURE MEDIATES BETWEEN AORTIC STIFFNESS AND CORONARY PERFUSION: POTENTIAL IMPLICATION FOR AORTOSCLEROSIS-INDUCED MYOCARDIAL ISCHEMIA. (September 2016)

• Record Type: Journal Article
• Authors: Hashimoto, J.; Ito, S.
• Is Part Of: Journal of hypertension. Volume 34:(2016) Supplement 2
• Publication Date: 2016-09
• Subjects: Hypertension -- Periodicals; Hypertension -- Periodicals; 616.132005
• DOI: 10.1097/01.hjh.0000491488.28756.35
• Languages: English
• ISSNs: 1473-5598

Abstract

Abstract : Objective: Stiffening of the aorta often precedes coronary events in hypertension. However, little is known about the etiological mechanism by which aortic stiffening causes myocardial ischemia. Hemodynamic research suggests that most of coronary flow occurs during diastole, depending on lateral pressure in the central aorta. We hypothesized that predisposition to myocardial ischemia is attributable to aortosclerosis-induced alterations in central diastolic pressure. Design and method: The study group comprised 222 patients with uncomplicated hypertension. Tonometric signals were recorded to estimate the aortic waveform from the radial waveform and to measure the carotid-femoral (aortic) and femoral-pedis (peripheral) pulse wave velocities (PWVs). Aortic compliance was computed from aortic characteristic impedance and PWV. The least-squares method was used to fit a monoexponential curve to aortic pressure decay during diastole as P(t) = P0*exp(-λ*t) [λ: decay index; P0: end-systolic pressure; t: time from end-systole]. Myocardial perfusion was quantified using the subendocardial viability index (SVI), calculated as the central diastolic/systolic pressure-time integral ratio. Results: The central diastolic pressure decay fit closely to an exponential curve for all patients (R 2 = 0.98 ± 0.02). The median (interquartile range) of decay index was 0.59 (0.49–0.70) per second. The decay index was significantly (P < 0.001) correlated with aortic PWV (r = 0.53) and compliance (r = -0.65), but not with peripheral PWV or total peripheral resistance. The relationships of aortic PWV and compliance with decay index remained significant after controlling for age, gender, renal function, diabetes and end-systolic pressure (P < 0.001). Both aortic PWV and compliance were also associated with SVI (r = -0.39 and r = 0.37, P < 0.001); however, these associations were no longer significant after accounting for decay index. Mediation analysis revealed that 75% of the association between aortic PWV and SVI was mediated by decay index. A similar mediating effect of decay index was observed for the association between aortic compliance and SVI. In contrast, aortic augmentation index did not constitute a mediator of these associations. Conclusions: Our results suggest that associations between aortic stiffness and subendocardial viability are mediated through diastolic exponential decay (rather than late-systolic augmentation) of central pressure. Aortic stiffening potentially reduces myocardial perfusion by accelerating diastolic pressure decay, thus predisposing to ischemic heart disease.