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This letter critiques a prior study, arguing that carotid flow and pressure pulsations are closely related to lacunar infarction, challenging the previous finding of no relationship.
The authors challenge the findings of a previous study, arguing that carotid flow waveforms are closely related to intracerebral small vessel disease and questioning the reproducibility of the previous study's flow measurements.
To the Editor: The article by Ochi et al. titled “Association of Central Systolic Blood Pressure With Intracerebral Small Vessel Disease in Japanese”1 showed a significant correlation between small vessel disease (lacunar infarction (LI)) and brachial cuff systolic pressure, aortic systolic pressure (estimated from the second systolic shoulder of the radial pressure wave), and with brachial–ankle pulse wave velocity (a measure of aortic stiffness). They found no relationship between LI and flow velocity patterns in the carotid artery supplying the brain. These findings challenge our own2,3 and we seek an explanation. We found a close relationship between both pressure and flow pulsations in the carotid artery, with both highly correlated with LI. We explained findings as due to high aortic stiffening which permitted pressure and flow waves to extend into vasodilated organs (brain and kidney) and cause damage to endothelium and media of the microvessels. The close relationship between features of pressure and flow waveforms was predictable on the basis of previous studies of wave reflection and vascular impedance in central and peripheral vascular beds.4 Ochi et al. stressed a relationship between radial artery pressures—at considerable distance from the brain—and LI, but no relationship between flow (or pressure) in the brain's main artery of supply. Their carotid flow augmentation showed no clear relationship with aortic stiffness (B-A PWV) or with the reflected wave seen in the radial artery; both are expected but appear to be hidden by noise (authors' Figure 2). The only way we can explain disparities reported by Ochi is in their measurement of flow waveform features. They gave no data on reproducibility. Figure 1 appears not to be an actual recording using pulse Doppler. We must concede that there is no clear convention on measurement of flow augmentation at present, and that attention is rarely paid to features of carotid flow waveforms. We urge Ochi et al., and others interested in this field to ensure that their techniques are reproducible, and follow changes of pressure and flow waveforms with interventions in the carotid artery and elsewhere. We cannot concede that pressures in the wrist are more useful than flow values in the neck for determining presence and cause of cerebral vascular lesions. We do agree that the field is novel, the results are important, and that further data are needed. M.F.O. is a founding director of AtCor Medical, manufacturer of systems for analyzing the arterial pressure pulse. K.H. and M.S. declared no conflict of interest.
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Hirata et al. (2010) conducted a letter in Small vessel disease of the brain (lacunar infarction). This letter critiques a prior study, arguing that carotid flow and pressure pulsations are closely related to lacunar infarction, challenging the previous finding of no relationship.
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