Jacqueline A. Augustine

Effect of acute resistance exercise on carotid artery stiffness and cerebral blood flow pulsatility

Arterial stiffness is associated with cerebral flow pulsatility. Arterial stiffness increases following acute resistance exercise (RE). Whether this acute RE-induced vascular stiffening affects cerebral pulsatility remains unknown. Purpose: To investigate the effects of acute RE on common carotid artery (CCA) stiffness and cerebral blood flow velocity (CBFv) pulsatility. Methods: Eighteen healthy men (22 ± 1 yr; 23.7 ± 0.5 kg·m−2) underwent acute RE (5 sets, 5-RM bench press, 5 sets 10-RM bicep curls with 90 s rest intervals) or a time control condition (seated rest) in a randomized order. CCA stiffness (β-stiffness, Elastic Modulus (Ep)) and hemodynamics (pulsatility index, forward wave intensity, and reflected wave intensity) were assessed using a combination of Doppler ultrasound, wave intensity analysis and applanation tonometry at baseline and 3 times post-RE. CBFv pulsatility index was measured with transcranial Doppler at the middle cerebral artery (MCA). Results: CCA β-stiffness, Ep and CCA pulse pressure significantly increased post-RE and remained elevated throughout post-testing (p < 0.05). No changes in MCA or CCA pulsatility index were observed (p > 0.05). There were significant increases in forward wave intensity post-RE (p < 0.05) but not reflected wave intensity (p > 0.05). Conclusion: Although acute RE increases CCA stiffness and pressure pulsatility, it does not affect CCA or MCA flow pulsatility. Increases in pressure pulsatility may be due to increased forward wave intensity and not pressure from wave reflections.

Hemodynamic Correlates of Late Systolic Flow Velocity Augmentation in the Carotid Artery

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.

Carotid Artery Stiffness and Hemodynamic Pulsatility During Cognitive Engagement in Healthy Adults: A Pilot Investigation

BACKGROUND The matching of vascular supply to neuronal metabolic demand during cognitive engagement is known as neurovascular coupling (NVC). Arterial stiffness is a prominent determinant of pulsatility in the systemic circulation and may thus indirectly impact NVC. In this pilot investigation, we explored changes in carotid artery stiffness and cerebrovascular hemodynamic pulsatiltiy during cognitive engagement in healthy adults. METHODS Twenty-seven adults (age 39 ± 3 years, BMI 24 ± 1 kg/m(2)) underwent Doppler ultrasonography of the common carotid artery (CCA) combined with applanation tonometry to derive (i) CCA elastic modulus (Ep) and β-stiffness index; (ii) CCA flow pulsatility index (PI); (iii) CCA pulse pressure, (iv) CCA augmentation index (AIx). Cerebral PI was assessed using transcranial Doppler at the middle cerebral artery (MCA). All measures were made at rest and during an incongruent Stroop task. RESULTS CCA PI was reduced (1.75 ± 0.06 to 1.57 ± 0.06, P < 0.05) while MCA PI was unchanged (0.75 ± 0.02 to 0.75 ± 0.02, P > 0.05) during Stroop. Brachial pulse pressure increased during Stroop (43 ± 1 to 46 ± 1 mm Hg, P < 0.05) while CCA pulse pressure was unchanged (36 ± 1 to 35 ± 1 mm Hg, P > 0.05). Similarly, CCA Ep (54.5 ± 5.5 to 53.8 ± 4.9 kPa, P > 0.05) and β-stiffness index (4.4 ± 0.4 to 4.2 ± 0.3 aU, P > 0.05) were unchanged. CCA AIx increased (1 ± 4 to 13 ± 4%, P < 0.05). CONCLUSION Carotid pressure pulsatility is unaltered while carotid flow pulsatility is reduced during cognitive engagement. Carotid artery stiffness does not change suggesting that factors other than the dynamic elastic properties of the CCA buffer cerebrovascular hemodynamic pulsatility during cognitive engagement.

Racial Differences in Aortic Stiffness in Children

Objective To investigate racial differences in central blood pressure and vascular structure/function as subclinical markers of atherosclerotic cardiovascular disease in children. Study design This cross‐sectional study recruited 54 African American children (18 female, 36 male; age 10.5 ± 0.9 years) and 54 white children (27 female, 26 male; age 10.8 ± 0.9 years) from the Syracuse City community as part of the Environmental Exposures and Child Health Outcomes study. Participants underwent blood lipid and vascular testing on 2 separate days. Carotid artery intima‐media thickness and aortic stiffness were measured by ultrasonography and carotid‐femoral pulse wave velocity, respectively. Blood pressure was assessed at the brachial artery and estimated in the carotid artery using applanation tonometry. Results African American children had significantly higher pulse wave velocity (4.8 ± 0.8 m/s) compared with white children (4.2 ± 0.7 m/s; P < .05), which remained significant after adjustment for confounding variables including socioeconomic status. African American children had significantly higher intima‐media thickness (African American 0.41 ± 0.06, white 0.39 ± 0.05 mm), and carotid systolic blood pressure (African American 106 ± 11, white 102 ± 8 mm Hg; P < .05) compared with white children, although these racial differences were no longer present after covariate adjustments for height. Conclusions Racial differences in aortic stiffness are present in childhood. Our findings suggest that racial differences in subclinical cardiovascular disease occur earlier than previously recognized.

Arterial stiffness and cerebral hemodynamic pulsatility during cognitive engagement in younger and older adults

Abstract This study examined central artery stiffness and hemodynamic pulsatility during cognitive engagement in younger and older adults. Methods Vascular‐hemodynamic measures were completed in 19 younger (age 35 ± 1 yrs) and 20 older (age 69 ± 2 yrs) adults at rest and during a Stroop task. Aortic stiffness (carotid‐femoral pulse wave velocity, PWV) and carotid pulse pressure (PP) were assessed using applanation tonometry. Carotid stiffness was assessed as a single‐point PWV using Doppler Ultrasound. Middle cerebral artery (MCA) mean flow and flow pulsatility index (PI) were assessed using transcranial Doppler. Cognitive function was assessed as accuracy and reaction time from the Stroop task. Results Older adults had lower accuracy scores and longer reaction times on the Stroop task compared to younger adults (p < 0.05). Both age groups had similar increases in MCA mean flow during Stroop (p < 0.05). There were significant increases in aortic PWV, carotid PWV, carotid PP and MCA PI during Stroop in older but not younger adults (p < 0.05). Carotid PP and MCA PI assessed during Stroop were statistical mediators of the association between age group and Stroop performance metrics (accuracy and reaction time, p < 0.05), while aortic and carotid PWV were indirect statistical mediators of MCA PI through carotid PP (p < 0.05). Conclusions Older adults experience increases in large artery stiffness during cognitive engagement possibly preventing effective buffering of pulsatile hemodynamic energy entry into the cerebrovasculature. This is important as pulsatile flow during cognitive engagement, and not mean flow per se, was related to overall cognitive performance.

The Relationship Between Cardiorespiratory Fitness and Aortic Stiffness in Women with Central Obesity

PURPOSE To examine the association between cardiorespiratory fitness and aortic stiffness in women with central obesity. The secondary purpose was to examine whether traditional and nontraditional cardiovascular risk factors mediate the relationship between cardiorespiratory fitness and aortic stiffness. MATERIALS AND METHODS Eighty-seven centrally obese women (age, 42 ± 9 years, [body mass index (BMI)] 28 ± 3 kg/m(2)) participated in this cross-sectional study. Central obesity was defined as a waist circumference >85 cm. Pulse wave velocity (PWV) was obtained from the carotid and femoral pulse sites using applanation tonometry to measure aortic stiffness. Maximal aerobic capacity (VO2 Max) was estimated using a submaximal walk test and taken as a measure of cardiorespiratory fitness. Potential correlates of both cardiorespiratory fitness and aortic stiffness examined in this study included the following: triglycerides (TG), C-reactive protein (CRP), homeostasis model assessment of insulin resistance index (HOMA-IR), and pulsatile load (i.e., heart rate × aortic pulse pressure [aPP]). RESULTS Pearsons bivariate correlations indicated that estimated VO2 Max was inversely associated with PWV (r = -0.330, p < 0.05). Using hierarchical multiple regression, the association between estimated VO2 Max and PWV was no longer significant after controlling for traditional and nontraditional cardiovascular risk factors, age, BMI, TG, CRP, HOMA-IR, and pulsatile load (β = 0.121, p > 0.05). CONCLUSION In centrally obese women, cardiorespiratory fitness was inversely associated with aortic stiffness. Associations were not independent of traditional and nontraditional cardiovascular disease (CVD) risk factors. This suggests that higher levels of cardiorespiratory fitness may indirectly reduce aortic stiffness through its beneficial effects on traditional and nontraditional CVD risk factors in women with central obesity.

Subclinical atherosclerotic risk in endurance-trained premenopausal amenorrheic women.

PURPOSE In premenopausal women, amenorrhea contributes to endothelial dysfunction. It is unknown whether this vascular functional change is associated with vascular structural change. METHODS This study examined regional and systemic vascular structure and function to gain insight into subclinical atherosclerotic risk in 10 amenorrheic athletes, 18 eumenorrheic athletes, and 15 recreationally active controls. Brachial flow-mediated dilation (FMD) and low flow mediated constriction (L-FMC) were used to measure global endothelial function. Carotid-femoral pulse wave velocity (PWV) was used to measure aortic stiffness. Doppler-ultrasound of the superficial femoral artery (SFA) was used to assess intima-media thickness (IMT) and vessel diameter as indicators of vascular remodeling. RESULTS Amenorrheic athletes had significantly lower brachial FMD adjusted for shear stimulus (6.9 ± 1.3%) compared with eumenorrheic athletes (11.0 ± 1.0%) and controls (11.0 ± 1.1%, p = 0.05). Brachial L-FMC (-1.8 ± 4.3%) and aortic PWV (5.0 ± 1.0 m/s) of amenorrheic athletes were similar to those of eumenorrheic athletes (L-FMC, -1.6 ± 4.6%; PWV, 4.6 ± 0.5 m/s) and controls (L-FMC, -1.5 ± 2.8%, p = 0.98; PWV, 5.4 ± 0.7 m/s, p = 0.15). SFA diameters were similar in amenorrheic athletes (5.7 ± 0.7 mm) and eumenorrheic athletes (5.7 ± 0.7 mm), but amenorrheic athletes had larger SFA diameters compared with controls (5.1 ± 0.6 mm, p = 0.04). In amenorrheic athletes, SFA IMT (0.31 ± 0.03 mm) was similar to that of eumenorrheic athletes (0.35 ± 0.07 mm) but significantly thinner compared to that of controls (0.38 ± 0.06, p = 0.01). CONCLUSION Vascular dysfunction in female amenorrheic athletes is not systemic. Parenthetically, amenorrhea may not prevent favorable peripheral vascular structural adaptations to habitual exercise training.

Arterial stiffness as a noninvasive tissue biomarker of cardiac target organ damage

The primary prevention of cardiovascular (CV) disease is hindered by the inadequacy of traditional risk factors to stratify CV risk. The presence of cardiac target organ damage (cTOD), as detected by measures of left ventricular (LV) hypertrophy and dysfunction, is associated with future CV outcomes, but is not currently assessed in asymptomatic individuals. Arterial stiffness contributes to cTOD and may represent a biomarker that can detect vascular dysfunction before the clinical manifestations of cTOD. Measurement of arterial stiffness may provide insight into premature risk for cTOD and afford opportunity for early intervention to prevent further damage. The purpose of this review is to examine the utility of arterial stiffness as a noninvasive biomarker of subclinical cTOD. To this end, we will examine the evidence sup- porting the association between arterial stiffness and measures of cTOD. We will then explore the developmental origins of arterial stiffness and cTOD and outline the progression of CV damage that occurs with age. We discuss the mechanistic role of pressure from wave reflections as a crucial link between arterial stiffness and cTOD. Finally, we examine these associations in context by exploring sex and racial differences in arterial stiffness as related to cTOD. Our comprehensive examination of the literature suggests that early identification of arterial stiffness would be a useful biomarker of future cTOD risk.

Muscular Strength is Inversely Associated with Central Hemodynamic Load in Young Women.: 2249 Board #85 June 1 11

Muscular strength is important for overall fitness. Strength is also associated with cardiovascular health; individuals with higher strength have a lower risk of developing hypertension. Muscular strength has been shown to be inversely associated with aortic stiffness, a precursor of hypertension. PURPOSE: Determine the relationship between muscular strength, aortic stiffness, and central hemodynamic load in young women. METHODS: Forty-two healthy young women (age 24 ± 6 years, body fat 23.1 ± 8.3 %) underwent muscular strength and vascular testing. Muscular strength was evaluated using a five-repetition maximum bench press and expressed relative to body weight. An aortic blood pressure waveform was derived from the brachial artery via an oscillometric cuff and used to estimate aortic pulse wave velocity (PWV). From this waveform, we also derived measures of central hemodynamic load: augmentation index (AIx@75, at heart rate of 75 bpm), forward wave pressure (Pf) and reflected wave pressure (Pb). Body composition was evaluated using air displacement plethysmography. RESULTS: As seen in Table 1, there was a negative correlation between relative strength and Pf (p<0.05) and Pb (p<0.05). Correlations remained after adjusting for age and mean arterial pressure (Pf, r = -0.28, p<0.05; Pb, r = -0.31, p<0.05) but were lost after further adjusting for body fat (Pf, r = -0.22, p>0.05; Pb, r = -0.19, p<0.05). There were no associations between relative strength and aortic PWV or AIx@75 (p>0.05). CONCLUSIONS: Women who have higher relative strength have lower forward and reflected wave pressure suggesting lower central hemodynamic load. Favorable associations may be partially mediated by stronger women having lower body fat.