Age-Related Changes in Carotid Artery Flow and Pressure Pulses Possible Implications for Cerebral Microvascular Disease

Jichi Medical University, Totigi, Tochigi, Japan
Stroke (Impact Factor: 5.72). 10/2006; 37(10):2552-6. DOI: 10.1161/01.STR.0000242289.20381.f4
Source: PubMed


We sought to establish the relation between the pulsatile components of pressure and flow waveforms in the carotid artery and their change with age.
Distention (pressure) and axial flow velocity waveforms were recorded noninvasively and simultaneously from the common carotid artery of 56 healthy subjects aged 20 to 72 years.
There was a close relation between the time intervals of pressure and flow waves: from foot to first shoulder or peak, to second shoulder or peak, and to incisura (r=0.97, P<0.0001 for each), which approximated the line of identity. The peak and nadir of flow velocity decreased with age, but late systolic flow augmentation increased substantially (1.6 times in the older group); this can be attributed to earlier wave reflection from the lower body. Pressure augmentation index (PAI) and flow augmentation index (FAI) increased similarly with age (PAI (%) = 0.84 x age - 26.6; FAI (%) = 0.75 x age + 11.9; both P<0.0001).
Arterial stiffening with aging increases carotid flow augmentation and can explain the increasing flow fluctuations in cerebral blood vessels. Measurement of carotid FAI may provide a gauge for risk of cerebral microvascular damage, just as PAI provides a gauge for risk of left ventricular hypertrophy and failure.

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    • "Carotid late systolic flow velocity augmentation may be quantified using the carotid flow augmentation index (FAIx) [4]. It has been suggested that pressure from wave reflections is a primary determinant of late systolic flow augmentation as there is a strong association between carotid FAIx and carotid pressure AIx [4]. Additional vascular and hemodynamic correlates of FAIx remain unexplored. "
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    ABSTRACT: Background. The contour of the common carotid artery (CCA) blood flow velocity waveform changes with age; CCA flow velocity increases during late systole, and this may contribute to cerebrovascular disease. Late systolic flow velocity augmentation can be quantified using the flow augmentation index (FAIx). We examined hemodynamic correlates of FAIx to gain insight into determinants of CCA flow patterns. Methods. CCA Doppler ultrasound and wave intensity analysis (WIA) were used to assess regional hemodynamics in 18 young healthy men (age 22 ± 1 years). Forward waves (W 1) and backward waves (negative area, NA) were measured and used to calculate the reflection index (NA/W 1 = RIx). Additional parameters included W 2 which is a forward travelling expansion/decompression wave of myocardial origin that produces suction, CCA single-point pulse wave velocity (PWV) as a measure of arterial stiffness, and CCA pressure augmentation index (AIx). Results. Primary correlates of FAIx included W 2 (r = - 0.52, P < 0.05), logRIx (r = 0.56, P < 0.05), and AIx (r = 0.60, P < 0.05). FAIx was not associated with CCA stiffness (P > 0.05). Conclusions. FAIx is a complex ventricular-vascular coupling parameter that is associated with both increased expansion wave magnitude (increased suction from the left ventricle) and increased pressure from wave reflections.
    International Journal of Hypertension 11/2013; 2013:920605. DOI:10.1155/2013/920605
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    • "Correlation and regression analysis revealed strong interdependence between cc-TQ and PP during acute bilateral jugular vein compression in the initial position (Fig. 3). Exposure to highly pulsatile pressure and augmented flow is a known predictor of cerebral vascular damage, even in the absence of increases in mean BP [29]–[31]. We have already proved in an animal model that during hypercapnia pulsatile flow is directly transmitted into pial arteries [16]. "
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    ABSTRACT: Purpose The aim of this study was to assess the effect of acute bilateral jugular vein compression on: (1) pial artery pulsation (cc-TQ); (2) cerebral blood flow velocity (CBFV); (3) peripheral blood pressure; and (4) possible relations between mentioned parameters. Methods Experiments were performed on a group of 32 healthy 19–30 years old male subjects. cc-TQ and the subarachnoid width (sas-TQ) were measured using near-infrared transillumination/backscattering sounding (NIR-T/BSS), CBFV in the left anterior cerebral artery using transcranial Doppler, blood pressure was measured using Finapres, while end-tidal CO2 was measured using medical gas analyser. Bilateral jugular vein compression was achieved with the use of a sphygmomanometer held on the neck of the participant and pumped at the pressure of 40 mmHg, and was performed in the bend-over (BOPT) and swayed to the back (initial) position. Results In the first group (n = 10) during BOPT, sas-TQ and pulse pressure (PP) decreased (−17.6% and −17.9%, respectively) and CBFV increased (+35.0%), while cc-TQ did not change (+1.91%). In the second group, in the initial position (n = 22) cc-TQ and CBFV increased (106.6% and 20.1%, respectively), while sas-TQ and PP decreases were not statistically significant (−15.5% and −9.0%, respectively). End-tidal CO2 remained stable during BOPT and venous compression in both groups. Significant interdependence between changes in cc-TQ and PP after bilateral jugular vein compression in the initial position was found (r = −0.74). Conclusions Acute bilateral jugular venous insufficiency leads to hyperkinetic cerebral circulation characterised by augmented pial artery pulsation and CBFV and direct transmission of PP into the brain microcirculation. The Windkessel effect with impaired jugular outflow and more likely increased intracranial pressure is described. This study clarifies the potential mechanism linking jugular outflow insufficiency with arterial small vessel cerebral disease.
    PLoS ONE 10/2012; 7(10):e48245. DOI:10.1371/journal.pone.0048245 · 3.23 Impact Factor
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    • "Comparison of (a) cycle-averaged VFR, (b) pulsatility index, (c) resistance index, and (d) flow augmentation index for the three different age groups indicated by the legend of panel (a). Labels " Hir " and " Sch " identify data from Hirata et al (2006) and Scheel et al. (2000), respectively. " Hoi " refers to the present study, with " Hoi* " including young-adult ICA data from Ford et al (2005). "
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    ABSTRACT: While it is widely appreciated that volumetric blood flow rate (VFR) dynamics change with age, there has been no detailed characterization of the typical shape of carotid bifurcation VFR waveforms of older adults. Toward this end, retrospectively gated phase contrast magnetic resonance imaging was used to measure time-resolved VFR waveforms proximal and distal to the carotid bifurcations of 94 older adults (age 68 +/- 8 years) with little or no carotid artery disease, recruited from the BLSA cohort of the VALIDATE study of factors in vascular aging. Timings and amplitudes of well-defined feature points from these waveforms were extracted automatically and averaged to produce representative common, internal and external carotid artery (CCA, ICA and ECA) waveform shapes. Relative to young adults, waveforms from older adults were found to exhibit a significantly augmented secondary peak during late systole, resulting in significantly higher resistance index (RI) and flow augmentation index (FAI). Cycle-averaged VFR at the CCA, ICA and ECA were 389 +/- 74, 245 +/- 61 and 125 +/- 49 mL min(-1), respectively, reflecting a significant cycle-averaged outflow deficit of 5%, which peaked at around 10% during systole. A small but significant mean delay of 13 ms between arrivals of ICA versus CCA/ECA peak VFR suggested differential compliance of these vessels. Sex and age differences in waveform shape were also noted. The characteristic waveforms presented here may serve as a convenient baseline for studies of VFR waveform dynamics or as suitable boundary conditions for models of blood flow in the carotid arteries of older adults.
    Physiological Measurement 03/2010; 31(3):291-302. DOI:10.1088/0967-3334/31/3/002 · 1.81 Impact Factor
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