Non-invasive wave intensity analysis in the aorta and internal carotid using phase-contrast MR angiography: The effect of hypertension

Abstract

IntroductionHypertension is associated with stiffening of blood vessels, reduced arterial lumen and reduced cerebral blood flow; however, it is not known how lower cerebral blood flow relates to arterial structure or impacts on wave dynamics. We hypothesise increased backward wave energy and faster wave speed in the hypertensive internal carotid artery as an indication of increased resistance to flow.MethodsNormotensive, controlled and uncontrolled hypertensive participants were recruited (daytime ambulatory BP < 135/85 mmHg and >135/ 85 mmHg, respectively; n = 11 per group). Wave intensity analysis was performed on left internal carotid and ascending aorta phase-contrast magnetic resonance angiography.ResultsWhile ascending aortic wave speed increased significantly in the uncontrolled hypertensive compared to normotensive (p<0.001) and controlled hypertensive participants (p = 0.038), no significant difference was observed in the internal carotid. Carotid forward and backward wave intensity increased in uncontrolled hypertensives compared to normotensives (p = 0.036 and p = 0.033, respectively), and backward wave energy increased in the controlled hypertensives compared to normotensives (p = 0.041). There was no significant difference between uncontrolled and controlled hypertensives.Figure 1Analysis of the phase contrast MR angiography data. A) Magnitude imageB)Phaseimageoftheinternalcarotid arteriesC)Magnitude image and D) Phase image of the ascending aorta E) example of log(Area)-Velocity loop. Red line indicates the slope from which wave speed is calculated in early systole F) Exampleofthe wave Intensity components, where blueisthe forward wave energy, red is the backward wave energy and black is the net wave intensity.ConclusionWave intensity in the internal carotid artery is altered in uncontrolled hypertension. This is partly rescued when blood pressure is controlled by medication, although greater backward wave energy persists. This supports the hypothesis of increased resistance to flow in the cerebral circulation of the hypertensives. Whilst increased aortic wave speed confirmed an expected increase in stiffness, this was not observed in the internal carotid. This might suggest a protective mechanism in the cerebral circulation, in conjunction with the effect of vessel tortuosity.