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Cerebrovascular mental stress reactivity is impaired in hypertension.

Naqvi TZ, Hyuhn HK - Cardiovasc Ultrasound (2009)

Bottom Line: Brachial artery reactivity in response to shear stress is altered in subjects with hypertension.Since endothelial dysfunction is generalized, we hypothesized that carotid artery (CA) reactivity would also be altered in hypertension.There was no difference in the CA response to nitroglycerin in healthy and hypertensive subjects.

View Article: PubMed Central - HTML - PubMed

Affiliation: Division of Cardiology at Cedars Sinai Heart Institute, Cedars-Sinai Medical Center, University of Southern California, Los Angeles, CA, USA. tnaqvi@usc.edu

ABSTRACT

Background: Brachial artery reactivity in response to shear stress is altered in subjects with hypertension. Since endothelial dysfunction is generalized, we hypothesized that carotid artery (CA) reactivity would also be altered in hypertension.

Purpose: To compare (CA endothelium-dependent vasodilation in response to mental stress in normal and hypertensive subjects.

Methods: We evaluated CA reactivity to mental stress in 10 young healthy human volunteers (aged 23 +/- 4 years), 20 older healthy volunteers (aged 49 +/- 11 years) and in 28 patients with essential hypertension (aged 51 +/- 13 years). In 10 healthy volunteers and 12 hypertensive subjects, middle cerebral artery (MCA) PW transcranial Doppler was performed before and 3 minutes after mental stress.

Results: Mental stress by Stroop color word conflict, math or anger recall tests caused CA vasodilation in young healthy subjects (0.61 +/- 0.06 to 0.65 +/- 0.07 cm, p < 0.05) and in older healthy subjects (0.63 +/- 0.06 to 0.66 +/- 0.07 cm, p < 0.05), whereas no CA vasodilation occurred in hypertensive subjects (0.69 +/- 0.06 to 0.68 +/- 0.07 cm; p, NS). CA blood flow in response to mental stress increased in young healthy subjects (419 +/- 134 to 541 +/- 209 ml, p < 0.01 vs. baseline) and in older healthy subjects (351 +/- 114 to 454 +/- 136 ml, p < 0.01 vs. baseline) whereas no change in blood flow (444 +/- 143 vs. 458 +/- 195 ml; p, 0.59) occurred in hypertensive subjects. There was no difference in the CA response to nitroglycerin in healthy and hypertensive subjects. Mental stress caused a significant increase in baseline to peak MCA systolic (84 +/- 22 to 95 +/- 22 cm/s, p < 0.05), diastolic (42 +/- 12 to 49 +/- 14 cm/s, p < 0.05) as well as mean (30 +/- 13 to 39 +/- 13 cm/s, p < 0.05) PW Doppler velocities in normal subjects, whereas no change in systolic (70 +/- 18 to 73 +/- 22 cm/s, p < 0.05), diastolic (34 +/- 14 to 37 +/- 14 cm/s, p = ns) or mean velocities (25 +/- 9 to 26 +/- 9 cm/s, p = ns) occurred in hypertensive subjects, despite a similar increase in heart rate and blood pressure in response to mental stress in both groups.

Conclusion: Mental stress produces CA vasodilation and is accompanied by an increase in CA and MCA blood flow in healthy subjects. This mental stress induced CA vasodilation and flow reserve is attenuated in subjects with hypertension and may reflect cerebral vascular endothelial dysfunction. Assessment of mental stress induced CA reactivity by ultrasound is a novel method for assessing the impact of hypertension on cerebrovascular endothelial function and blood flow reserve.

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Bar graphs showing the effect of mental stress on carotid artery diameter in hypertensive subjects with increasing mean blood pressure.
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Figure 2: Bar graphs showing the effect of mental stress on carotid artery diameter in hypertensive subjects with increasing mean blood pressure.

Mentions: We studied 28 hypertensive subjects. Baseline demographic characteristics along with differences with the normal subjects are summarized in Table 1. Hypertensives had a significantly increased size of CA (0.69 ± 0.05 vs. 0.61 ± 0.07 cm, p = 0.003), a significantly higher maximum CA IMT (0.070 ± 0.02 vs. 0.046 ± 0.02 cm, p = 0.005) and decreased CA distensibility (0.39 ± 0.19 vs. 0.62 ± 0.28, p < 0.01) than all normal subjects. The effects of mental stress on CA responses in hypertensive subjects are shown in Table 3. Compared to healthy volunteers, the hypertensive subjects demonstrated significantly reduced CA vasodilation (-2% ± 6% vs. 5 ± 4%, p < 0.0001), and CA flow reserve (3 ± 29 vs. 32 ± 35%, p < 0.01) in response to mental stress. A decrease in CA diameter occurred in 16 hypertensive subjects (52%), no change in 4 and an increase in CA diameter occurred in only 8 hypertensive subjects (29%). No difference in CA vasodilation was observed when hypertensives were divided into three groups based on baseline mean BP of <90, 91–105 and >105 mm Hg as shown in Figure 2. Figure 3 is a representative example of the effect of mental stress on CA diameter in a normal and hypertensive subject and Figure 4 shows effect of mental stress on CA PW Doppler velocities in a normal and a hypertensive subject. No difference in blood pressure response was seen in subjects with treated hypertension in whom medication was held for 24 hours prior to the study vs. untreated hypertensives (data not shown).


Cerebrovascular mental stress reactivity is impaired in hypertension.

Naqvi TZ, Hyuhn HK - Cardiovasc Ultrasound (2009)

Bar graphs showing the effect of mental stress on carotid artery diameter in hypertensive subjects with increasing mean blood pressure.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2710316&req=5

Figure 2: Bar graphs showing the effect of mental stress on carotid artery diameter in hypertensive subjects with increasing mean blood pressure.
Mentions: We studied 28 hypertensive subjects. Baseline demographic characteristics along with differences with the normal subjects are summarized in Table 1. Hypertensives had a significantly increased size of CA (0.69 ± 0.05 vs. 0.61 ± 0.07 cm, p = 0.003), a significantly higher maximum CA IMT (0.070 ± 0.02 vs. 0.046 ± 0.02 cm, p = 0.005) and decreased CA distensibility (0.39 ± 0.19 vs. 0.62 ± 0.28, p < 0.01) than all normal subjects. The effects of mental stress on CA responses in hypertensive subjects are shown in Table 3. Compared to healthy volunteers, the hypertensive subjects demonstrated significantly reduced CA vasodilation (-2% ± 6% vs. 5 ± 4%, p < 0.0001), and CA flow reserve (3 ± 29 vs. 32 ± 35%, p < 0.01) in response to mental stress. A decrease in CA diameter occurred in 16 hypertensive subjects (52%), no change in 4 and an increase in CA diameter occurred in only 8 hypertensive subjects (29%). No difference in CA vasodilation was observed when hypertensives were divided into three groups based on baseline mean BP of <90, 91–105 and >105 mm Hg as shown in Figure 2. Figure 3 is a representative example of the effect of mental stress on CA diameter in a normal and hypertensive subject and Figure 4 shows effect of mental stress on CA PW Doppler velocities in a normal and a hypertensive subject. No difference in blood pressure response was seen in subjects with treated hypertension in whom medication was held for 24 hours prior to the study vs. untreated hypertensives (data not shown).

Bottom Line: Brachial artery reactivity in response to shear stress is altered in subjects with hypertension.Since endothelial dysfunction is generalized, we hypothesized that carotid artery (CA) reactivity would also be altered in hypertension.There was no difference in the CA response to nitroglycerin in healthy and hypertensive subjects.

View Article: PubMed Central - HTML - PubMed

Affiliation: Division of Cardiology at Cedars Sinai Heart Institute, Cedars-Sinai Medical Center, University of Southern California, Los Angeles, CA, USA. tnaqvi@usc.edu

ABSTRACT

Background: Brachial artery reactivity in response to shear stress is altered in subjects with hypertension. Since endothelial dysfunction is generalized, we hypothesized that carotid artery (CA) reactivity would also be altered in hypertension.

Purpose: To compare (CA endothelium-dependent vasodilation in response to mental stress in normal and hypertensive subjects.

Methods: We evaluated CA reactivity to mental stress in 10 young healthy human volunteers (aged 23 +/- 4 years), 20 older healthy volunteers (aged 49 +/- 11 years) and in 28 patients with essential hypertension (aged 51 +/- 13 years). In 10 healthy volunteers and 12 hypertensive subjects, middle cerebral artery (MCA) PW transcranial Doppler was performed before and 3 minutes after mental stress.

Results: Mental stress by Stroop color word conflict, math or anger recall tests caused CA vasodilation in young healthy subjects (0.61 +/- 0.06 to 0.65 +/- 0.07 cm, p < 0.05) and in older healthy subjects (0.63 +/- 0.06 to 0.66 +/- 0.07 cm, p < 0.05), whereas no CA vasodilation occurred in hypertensive subjects (0.69 +/- 0.06 to 0.68 +/- 0.07 cm; p, NS). CA blood flow in response to mental stress increased in young healthy subjects (419 +/- 134 to 541 +/- 209 ml, p < 0.01 vs. baseline) and in older healthy subjects (351 +/- 114 to 454 +/- 136 ml, p < 0.01 vs. baseline) whereas no change in blood flow (444 +/- 143 vs. 458 +/- 195 ml; p, 0.59) occurred in hypertensive subjects. There was no difference in the CA response to nitroglycerin in healthy and hypertensive subjects. Mental stress caused a significant increase in baseline to peak MCA systolic (84 +/- 22 to 95 +/- 22 cm/s, p < 0.05), diastolic (42 +/- 12 to 49 +/- 14 cm/s, p < 0.05) as well as mean (30 +/- 13 to 39 +/- 13 cm/s, p < 0.05) PW Doppler velocities in normal subjects, whereas no change in systolic (70 +/- 18 to 73 +/- 22 cm/s, p < 0.05), diastolic (34 +/- 14 to 37 +/- 14 cm/s, p = ns) or mean velocities (25 +/- 9 to 26 +/- 9 cm/s, p = ns) occurred in hypertensive subjects, despite a similar increase in heart rate and blood pressure in response to mental stress in both groups.

Conclusion: Mental stress produces CA vasodilation and is accompanied by an increase in CA and MCA blood flow in healthy subjects. This mental stress induced CA vasodilation and flow reserve is attenuated in subjects with hypertension and may reflect cerebral vascular endothelial dysfunction. Assessment of mental stress induced CA reactivity by ultrasound is a novel method for assessing the impact of hypertension on cerebrovascular endothelial function and blood flow reserve.

Show MeSH
Related in: MedlinePlus