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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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Carotid artery images in a normotensive (A) and a hypertensive subject (B). Intima media thickness is shown by white arrow heads. Carotid intima media thickness was measured in the far wall of the distal right common carotid artery over 1 cm below the carotid bulb. The image was frozen at end diastole (white arrows on EKG strip).
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Figure 1: Carotid artery images in a normotensive (A) and a hypertensive subject (B). Intima media thickness is shown by white arrow heads. Carotid intima media thickness was measured in the far wall of the distal right common carotid artery over 1 cm below the carotid bulb. The image was frozen at end diastole (white arrows on EKG strip).

Mentions: Maximum CA IMT was measured over 1 cm below carotid bulb at the common CA far wall at the onset of QRS complex from intimal-luminal interface to medial adventitial interface. This location was chosen because of its demonstrated reproducibility compared to CA IMT at other sites [28,29]. CA diameter was measured at the onset of QRS complex as the line identifying the media-adventitia interface in the near to the far wall. Figure 1 shows representative CA images from a normal and a hypertensive subject showing intima-media thickness (white arrows). All measurements were made in triplicate and averaged. CA diameter measurements were made over 3 cm of a straight segment below the CA bulb. PW Doppler measurements included: time averaged mean velocity (TAM), peak systolic (PSV), end diastolic velocity (EDV), pulsatility index (PI, (PSV-EDV)/TAM, resistive index (RI, PSV-EDV)/PSV) and blood flow (ml/min = 3.14× (r)2 × TAM × 60). All PW Doppler data was acquired using a 60° angle. CA distensibility was measured at baseline using the formula 2 × % change in CA diameter between systole and diastole/CA diameter systole × pulse pressure [30]. Five averaged Doppler measurements over at least 10 cardiac and 2 respiratory cycles were measured.


Cerebrovascular mental stress reactivity is impaired in hypertension.

Naqvi TZ, Hyuhn HK - Cardiovasc Ultrasound (2009)

Carotid artery images in a normotensive (A) and a hypertensive subject (B). Intima media thickness is shown by white arrow heads. Carotid intima media thickness was measured in the far wall of the distal right common carotid artery over 1 cm below the carotid bulb. The image was frozen at end diastole (white arrows on EKG strip).
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 1: Carotid artery images in a normotensive (A) and a hypertensive subject (B). Intima media thickness is shown by white arrow heads. Carotid intima media thickness was measured in the far wall of the distal right common carotid artery over 1 cm below the carotid bulb. The image was frozen at end diastole (white arrows on EKG strip).
Mentions: Maximum CA IMT was measured over 1 cm below carotid bulb at the common CA far wall at the onset of QRS complex from intimal-luminal interface to medial adventitial interface. This location was chosen because of its demonstrated reproducibility compared to CA IMT at other sites [28,29]. CA diameter was measured at the onset of QRS complex as the line identifying the media-adventitia interface in the near to the far wall. Figure 1 shows representative CA images from a normal and a hypertensive subject showing intima-media thickness (white arrows). All measurements were made in triplicate and averaged. CA diameter measurements were made over 3 cm of a straight segment below the CA bulb. PW Doppler measurements included: time averaged mean velocity (TAM), peak systolic (PSV), end diastolic velocity (EDV), pulsatility index (PI, (PSV-EDV)/TAM, resistive index (RI, PSV-EDV)/PSV) and blood flow (ml/min = 3.14× (r)2 × TAM × 60). All PW Doppler data was acquired using a 60° angle. CA distensibility was measured at baseline using the formula 2 × % change in CA diameter between systole and diastole/CA diameter systole × pulse pressure [30]. Five averaged Doppler measurements over at least 10 cardiac and 2 respiratory cycles were measured.

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