Impact of wall thickness on conduit artery function in humans: Is there a “Folkow” effect?

Thijssen, Dick H. J.; Willems, Laura; Munckhof, Inge van den; Scholten, Ralph R.; Hopman, Maria T. E.; Dawson, Ellen A.; Atkinson, Greg; Cable, N. Timothy; Green, Daniel

doi:10.1016/j.atherosclerosis.2011.03.003

Cited by 35 publications

(41 citation statements)

References 26 publications

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“…Notwithstanding this limitation, the observation that smaller and more responsive vessels (with fewer endothelial cells for NO production via e-NOS) have larger e-NOS protein content in relation to the amount of smooth muscle to be relaxed is a novel and important one. Previous studies have shown regional differences in the lumen-to-wall ratio so that smaller arteries, despite the significantly smaller absolute wall thickness, have a relatively larger wall thickness and wall in relation to the lumen area [51]. In that study, a significant correlation between the wall-to-lumen ratio and flow-mediated dilation was observed.…”

Section: Discussionmentioning

confidence: 52%

High-Intensity Endurance Training Results in Faster Vessel-Specific Rate of Vasorelaxation in Type 1 Diabetic Rats

et al. 2013

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This study examined the effects of 6 weeks of moderate- (MD) and high-intensity endurance training (HD) and resistance training (RD) on the vasorelaxation responsiveness of the aorta, iliac, and femoral vessels in type 1 diabetic (D) rats. Vasorelaxation to acetylcholine was modeled as a mono-exponential function. A potential mediator of vasorelaxation, endothelial nitric oxide synthase (e-NOS) was determined by Western blots. Vessel lumen-to-wall ratios were calculated from H&E stains. The vasorelaxation time-constant (τ) (s) was smaller in control (C) (7.2±3.7) compared to D (9.1±4.4) and it was smaller in HD (5.4±1.5) compared to C, D, RD (8.3±3.7) and MD (8.7±3.8) (p<0.05). The rate of vasorelaxation (%·s−1) was larger in HD (2.7±1.2) compared to C (2.0±1.2), D (2.0±1.5), RD (2.0±1.0), and MD (2.0±1.2) (p<0.05). τ vasorelaxation was smaller in the femoral (6.9±3.7) and iliac (6.9±4.7) than the aorta (9.0±5.0) (p<0.05). The rate of vasorelaxation was progressively larger from the femoral (3.1±1.4) to the iliac (2.0±0.9) and to the aorta (1.3±0.5) (p<0.05). e-NOS content (% of positive control) was greater in HD (104±90) compared to C (71±64), D (85±65), RD (69±43), and MD (76±44) (p<0.05). e-NOS normalized to lumen-to-wall ratio (%·mm−1) was larger in the femoral (11.7±11.1) compared to the aorta (3.2±1.9) (p<0.05). Although vasorelaxation responses were vessel-specific, high-intensity endurance training was the most effective exercise modality in restoring the diabetes-related loss of vascular responsiveness. Changes in the vasoresponsiveness seem to be endothelium-dependent as evidenced by the greater e-NOS content in HD and the greater normalized e-NOS content in the smaller vessels.

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Section: Discussionmentioning

confidence: 52%

High-Intensity Endurance Training Results in Faster Vessel-Specific Rate of Vasorelaxation in Type 1 Diabetic Rats

et al. 2013

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“…The physiological significance of these sex differences remains unknown but may relate to artery size, which has impacts on functional responsiveness. 31 Our findings have potential clinical relevance. FMD of the brachial and femoral arteries, introduced by Celermajer et al 13 has been technically enhanced 24 and formalized as a measure of in vivo endothelial function and preclinical atherosclerosis in the past 2 decades.…”

Section: Sex Differencesmentioning

confidence: 85%

“…It is known that artery size influences the shear stimuli and functional responsiveness of an artery, which was potentially evident in the current study. 31 In addition, a previous magnetic resonance imaging study has reported greater distensibility in the CCA compared with the ICA within subjects. 32 This raises the interesting notion of the CCA's potential role in dampening the pressure waveform before the ICA and cranial vessels.…”

Section: Discussionmentioning

confidence: 99%

Evidence for Shear Stress–Mediated Dilation of the Internal Carotid Artery in Humans

et al. 2016

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S mall cerebral arteries and arterioles (eg, pial vessels) respond rapidly to changes in their metabolic milieu and are highly sensitive to the partial pressure of arterial carbon dioxide (PaCO 2 ).1 Vasomotor responsiveness to PaCO 2 , termed CO 2 reactivity, is integral to stabilizing blood pH levels, and previous studies have associated lower CO 2 reactivity to increased cardiovascular and all-cause mortality.2 Recent magnetic resonance imaging studies in humans have revealed that vasomotor changes also occur in the middle cerebral artery (MCA) 3-5 and basilar artery 6 across the hypo-and hypercapnic range. These studies demonstrate the involvement of larger cerebral arteries in the PaCO 2 reactivity response, 7 findings consistent with well-controlled, animal studies. 8 Other recent studies using Duplex ultrasound have investigated extracranial artery responses during hypo-and hypercapnia.9,10 These studies provide direct evidence that changes in end-tidal CO 2 (PETCO 2 ) are associated with directionally similar, and dosedependent, changes in internal carotid artery (ICA) diameter. The mechanism(s), however, mediating these changes in extracranial ICA diameter remain unclear.Significant and rapid changes in extracranial artery blood flow occur across the hypo-and hypercapnic range. [9][10][11] In peripheral conduits such as the radial and brachial arteries, such changes in flow and attendant arterial shear stress represent potent vasoactive stimuli.12,13 Although Pohl et al 14 and Rubanyi et al 15 were the first to identify that flow-mediated dilation (FMD) is endothelium dependent, it is now well established that this phenomenon occurs in humans and that NO plays a significant role. [16][17][18][19] The widely used FMD test 13 relies on dilation of small arteries and arterioles in the limbs, as a consequence of cuff-induced ischemia, to induce an increase in upstream conduit artery shear stress and dilation. In the context of these studies, it is conceivable that rapid and profound dilation of intracranial vessels in response to hypercapnia induces extracranial (ICA) dilation as a consequence of increased shear stress. The aim of this study was to identify whether hypercapnia induces shear-mediated dilation in the carotid arteries. Using high-resolution Duplex ultrasound combined with novel, edge-detection software, we assessed simultaneous common Abstract-Increases in arterial carbon dioxide tension (hypercapnia) elicit potent vasodilation of cerebral arterioles. Recent studies have also reported vasodilation of the internal carotid artery during hypercapnia, but the mechanism(s) mediating this extracranial vasoreactivity are unknown. Hypercapnia increases carotid shear stress, a known stimulus to vasodilation in other conduit arteries. To explore the hypothesis that shear stress contributes to hypercapnic internal carotid dilation in humans, temporal changes in internal and common carotid shear rate and diameter, along with changes in middle cerebral artery velocity, were simultaneously assessed in 18 su...

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“…However, this paradoxical decrease in FMD, often used as a measure of endothelial function and artery health, may relate to the larger artery lumen size in athletes, who also exhibit decreased WT 38 39. It is well established that both artery size44 45 and WT46 impact upon functional responses. This may, in subjects who differ in arterial structural characteristics a priori, complicate the interpretation of between subject differences in FMD 36.…”

Section: Discussionmentioning

confidence: 99%

Peripheral vascular structure and function in hypertrophic cardiomyopathy

et al. 2012

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Background Hypertrophic cardiomyopathy (HCM) is characterised by idiopathic cardiac enlargement and represents the most frequent cause of sudden cardiac death in athletes under the age of 35 years. Differentiation between physiological (ie, exercise-related) and pathological (ie, HCM-related) cardiac remodelling is challenging. In line with cardiac remodelling, vascular structure and function are altered following training, but little is known about peripheral vascular adaptations in HCM. We hypothesised that, while HCM patients and athletes would exhibit similar cardiac characteristics, differences would be apparent in their brachial and carotid arteries. Methods In age-matched groups of HCM patients (n=18, 39±15 years), highly competitive athletes (n=18, 38±12 years) and recreational controls (n=10, 37 ±14 years), we used high-resolution ultrasound to assess the diameter and wall thickness of the carotid and brachial arteries, with flow-mediated dilator function (FMD) of the brachial arteries also assessed. Results A significant difference between athletes and HCM was evident in arterial wall thickness (carotid 519±60 vs 586±102 mm, p<0.05; brachial 345±80 vs 456±76 mm, p<0.05) and the brachial artery peak blood flow response following forearm ischaemia, an index of resistance artery remodelling (998±515 vs 725±248 ml/ min, p<0.05). Similar differences were noted between athletes and controls, while controls and HCM did not differ. Brachial FMD% was not different between groups. Conclusions Athletes and HCM subjects, who can be difficult to differentiate on the basis of cardiac measures, exhibit differences in indices of arterial structure. While this may be a disease-related effect, we cannot discount a generic impact of physical activity on arterial structure, as the athlete's arteries were also different to untrained control subjects. Future studies should assess artery function and structure in athletic HCM subjects.

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Impact of wall thickness on conduit artery function in humans: Is there a “Folkow” effect?

Cited by 35 publications

References 26 publications

High-Intensity Endurance Training Results in Faster Vessel-Specific Rate of Vasorelaxation in Type 1 Diabetic Rats

High-Intensity Endurance Training Results in Faster Vessel-Specific Rate of Vasorelaxation in Type 1 Diabetic Rats

Evidence for Shear Stress–Mediated Dilation of the Internal Carotid Artery in Humans

Peripheral vascular structure and function in hypertrophic cardiomyopathy

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