Local Pulse Pressure and Regression of Arterial Wall Hypertrophy During Long-Term Antihypertensive Treatment

Boutouyrie, Pierre; Bussy, Caroline; Hayoz, Daniel; Hengstler, Jan G.; Dartois, Nathalie; Laloux, Brigitte; Brunner, Hans R.; Laurent, Stéphane

doi:10.1161/01.cir.101.22.2601

Cited by 203 publications

(184 citation statements)

References 21 publications

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“…According to our findings, ␤-blockers with vasodilating properties should be preferred because they reduce wave reflections and thus pulse pressure to a larger extent than ␤-blockers devoid of vasodilating effect. 13 In conclusion, in patients with acrogeric vEDS, an abnormally low IMT generates a higher wall stress than in control subjects at the site of an elastic artery and thus may increase the risk of arterial dissection and rupture.…”

Section: Clinical Implications Of Findingsmentioning

confidence: 83%

“…12,13 BP was monitored with an oscillometric method (Dinamap model 845, Critikon). Measurements of the right common carotid artery and radial artery parameters were obtained with high-precision echotracking devices (Wall Track System, PIE Medical, 14 and NIUS 02, SMH, 15 respectively), coupled with applanation tonometry as previously described, validated, and used in clinical studies.…”

Section: Arterial Parametersmentioning

confidence: 99%

“…The absolute difference between 2 determinations of carotid and radial artery internal diameter and wall thickness did not exceed 6% of the mean value for each parameter. 12,13 Arterial wall cross-sectional area (WCSA) was calculated in diastole as WCSAϭ Re 2 ϪRi 2 , where Re and Ri are the values of diastolic internal and external radii, respectively. 12,13 Wall-to-lumen ratio was calculated in diastole as 2 hour d /Dd.…”

Section: Arterial Geometrymentioning

confidence: 99%

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Increased Carotid Wall Stress in Vascular Ehlers-Danlos Syndrome

et al. 2004

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Background-Vascular Ehlers-Danlos syndrome (vEDS), also known as EDS type IV, an inherited disorder of connective tissue, results from mutations in the gene encoding type III procollagen (COL3A1). Affected patients are at risk for arterial dissection or rupture, the main cause of death. To understand the pathogenesis of the vascular lesions, we used a biomechanical approach and determined steady and pulsatile wall stress. Methods and Results-Sixteen patients with vEDS and 16 age-, gender-, and blood pressure-matched control subjects were included in this cross-sectional noninvasive study. Circumferential wall stress was determined under steady and pulsatile conditions at the site of an elastic (common carotid) and a muscular (radial) artery from the measurements of intima-media thickness and internal diameter with high-resolution echo-tracking systems and either mean blood pressure or pulse pressure, respectively. At the site of the carotid artery, steady circumferential wall stress was 43% higher in vEDS patients than in control subjects (68.9Ϯ14.3 versus 48.2Ϯ12.1 kPa, PϽ0.001), and pulsatile circumferential wall stress was 22% higher (28.2Ϯ7.7 versus 23.1Ϯ5.7 kPa, PϽ0.001). Carotid intima-media thickness was 32% lower (408Ϯ56 versus 598Ϯ171 m, PϽ0.001) in vEDS patients, and internal diameter was not different between groups. Radial artery parameters were not significantly different between groups. Conclusions-In vEDS patients, an abnormally low intima-media thickness generates a higher wall stress than in control subjects at the site of an elastic artery, which may increase the risk of arterial dissection and rupture.

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Section: Clinical Implications Of Findingsmentioning

confidence: 83%

Section: Arterial Parametersmentioning

confidence: 99%

Section: Arterial Geometrymentioning

confidence: 99%

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Increased Carotid Wall Stress in Vascular Ehlers-Danlos Syndrome

et al. 2004

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“…The decrease in mean blood pressure with losartan treatment was small in the present study compared to a previous study (101 mmHg versus 92 mmHg, respectively). 3) In the same study, a marked reduction in IMT of 0.025 to 0.040 mm was reported for 9-month treatment using either the β-blocker celiprol or the ACE inhibitor enalapril, both of which reduced mean blood pressure by 10-15 mmHg in hyper- tensive patients. We believe that the substantial reduction in IMT despite a modest reduction in blood pressure in the present study may have been caused by mechanisms independent from the direct antihypertensive effect as reported in other antihypertensive agents such as calcium antagonists, 20) β-blockers, or ACE inhibitors.…”

Section: Discussionmentioning

confidence: 79%

“…1) Longterm administration of angiotensin converting enzyme (ACE) inhibitors such as enalapril and fosinopril was found to reduce atherosclerosis in hypertensive patients with early carotid atherosclerosis or arterial hypertrophy. 2,3) Although the clinical efficacy of ACE inhibitors is well-documented, patients receiving these therapeutic agents suffer from distinctive adverse effects such as dry cough, making the development of better-tolerated agents clinically desirable. Angiotensin receptor blockers (ARB) have been shown to have an antiatherosclerotic effect in animal models.…”

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confidence: 99%

A One-Year Study of the Antiatherosclerotic Effect of the Angiotensin-II Receptor Blocker Losartan in Hypertensive Patients A Comparison With Angiotensin-Converting Enzyme Inhibitors

et al. 2008

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SUMMARYAngiotensin receptor blockers (ARB) have been emerging as drugs to treat atherosclerosis. The effectiveness of the ARB losartan at reducing atherosclerosis was compared with that of ACE inhibitors in hypertensive patients.A total of 50 patients with hypertension were divided into 3 groups: a control group receiving neither an ARB nor an ACE inhibitor (n = 14), a losartan group (n = 22) receiving 50 mg/day of losartan, and an ACE inhibitor group (n = 14) receiving either 5 mg/ day of enalapril or 5 mg/day of imidapril. Atherosclerosis was evaluated based on the intima-media thickness (IMT) of the common carotid artery measured by B-mode ultrasound at baseline and after approximately 12 months of treatment.After the treatment, IMT significantly decreased with losartan (from 0.87 ± 0.14 to 0.79 ± 0.16 mm, P < 0.05) and with ACE inhibitor (from 0.81 ± 0.14 to 0.74 ± 0.11 mm, P < 0.05). The reduction was comparable between the two groups, -0.078 ± 0.136 with losartan and -0.073 ± 0.109 mm with ACE inhibitor, and the rate of the reduction was similar between the two drugs; -0.098 ± 0.142 mm/year with losartan and (-0.076 ± 0.118 mm/year) with ACE inhibitor. On the contrary, IMT did not change in the control group (from 0.90 ± 0.20 to 0.95 ± 0.26 mm) during the treatment period. Concomitant medication and coronary risk factors such as hyperlipidemia, diabetes mellitus, and smoking did not differ significantly among the groups.The antiatherosclerotic effect of losartan on the carotid artery was comparable to that of ACE-inhibitors, and less adverse effects, such as coughing that occurs with ACE inhibitors, were observed. Losartan appears to be a better alternative to ACE inhibitors for treating atherosclerosis in Japanese hypertensive patients. (Int Heart J 2008; 49: 95-103)

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Drug Therapy and Follow-Up

Eandi

2010

Atherosclerosis Disease Management

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Local Pulse Pressure and Regression of Arterial Wall Hypertrophy During Long-Term Antihypertensive Treatment

Cited by 203 publications

References 21 publications

Increased Carotid Wall Stress in Vascular Ehlers-Danlos Syndrome

Increased Carotid Wall Stress in Vascular Ehlers-Danlos Syndrome

A One-Year Study of the Antiatherosclerotic Effect of the Angiotensin-II Receptor Blocker Losartan in Hypertensive Patients A Comparison With Angiotensin-Converting Enzyme Inhibitors

Drug Therapy and Follow-Up

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