Pressure-dependence of arterial stiffness

Spronck, Bart; Heusinkveld, Maarten H. G.; Vanmolkot, Floris; Roodt, Jos Op ‘t; Hermeling, Evelien; Delhaas, Tammo; Kroon, Abraham A.; Reesink, Koen D.

doi:10.1097/hjh.0000000000000407

Cited by 132 publications

(152 citation statements)

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“…Because cfPWV is highly influenced by BP,12,14,15,24 much of the increase in cfPWV observed in this study can be attributed to the increase in pressure. To determine whether HR further influenced cfPWV changes, we used 3 different methods to correct for BP; similar correction procedures were not conducted in previous studies.…”

Section: Discussionmentioning

confidence: 64%

“…28 Despite the decrease in SV and TPR, CO increased because of the large increases in HR, which likely drove the increase in MAP in addition to the increase in both peripheral and central diastolic BP. Because cfPWV is highly influenced by BP, 12,14,15,24 much of the increase in cfPWV observed in this study can be attributed to the increase in pressure. To determine whether HR further influenced cfPWV changes, we used 3 different methods to correct for BP; similar correction procedures were not conducted in previous studies.…”

Section: Discussionmentioning

confidence: 64%

“…9,10 In cross-sectional studies, only half of those that included HR as a parameter for predicting cfPWV in their model found a significant association. 11 Because cfPWV is known to be pressure dependent, [12][13][14][15] any change in cfPWV accompanied by a change in BP needs to be corrected for BP to isolate the true effect of the factor being investigated. This study aims to quantify the acute, BP-independent effect of HR on cfPWV.…”

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confidence: 99%

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Heart Rate Dependency of Large Artery Stiffness

et al. 2016

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Tan et al Heart Rate Dependency of Large Artery Stiffness 237 Hemodynamic MeasurementsBrachial BP, central aortic BP, and cfPWV were determined by cuffbased pulse wave analysis (SphygmoCor XCEL, AtCor, Sydney, Australia). Brachial BP was obtained by oscillometric method with a brachial cuff positioned on the right arm, and central aortic waveform was derived from the brachial BP volume displacement waveform using a validated transfer function. 16 For measurement of cfPWV, the carotid and femoral pulse waveforms were obtained by tonometry on the skin above the right carotid artery and by a cuff placed on the right upper thigh, respectively. 17,18 Subtraction method for path length was used to calculate cfPWV, whereby the path length was calculated as the distance between the sternal notch and the carotid site subtracted from the distance between the sternal notch and top of the thigh cuff. 17 In a subset of the study's cohort (n=45), beat-to-beat stroke volume (SV), cardiac output (CO), and total peripheral resistance (TPR) were determined from the finger arterial pressure waveform using the Modelflow method (Finometer PRO, Finapres Medical Systems, Amsterdam, The Netherlands). 19 Study ProtocolSubjects were advised to refrain from caffeine and fatty meals 4 hours before their study appointment, but to continue with their prescribed medications. There were no current tobacco users in the cohort. After 10 minutes of seated rest, seated brachial BP was measured in duplicate (SphygmoCor XCEL). After a further 10 minutes of supine rest, finger arterial pressure waveform was measured from the left middle finger (Finometer PRO) to obtain SV, CO, and TPR. Brachial and central aortic BP and cfPWV were then obtained (SphygmoCor XCEL). Subjects were then paced in a randomized sequence at 60, 70, 80, 90, and 100 bpm using their prescribed pacemaker settings, with BP and cfPWV measurements repeated at each pacing step after 3 minutes of stabilization. ECG was also acquired continuously for the duration of the study for monitoring of HR (PowerLab acquisition system, LabChart software, ADInstruments, Dunedin, New Zealand), and SV, CO, and TPR from the Finometer PRO device were also recorded via PowerLab and LabChart. The average duration for study protocol completion was 60 minutes. Data AnalysisFor pulse wave analysis, brachial and central aortic BP waveforms were averaged >5 s, and cfPWV was averaged >10 s. Observations with measured HR differing from the paced rate by >5 bpm were excluded from the analysis, and the lowest pace rates of 60 and 70 bpm were not achievable in some subjects because of a higher unpaced resting HR. A linear mixed model with maximum likelihood was used to determine the effects of HR on each measured variable, with paced HR modeled as the fixed effect and the random effect modeled as the intercept for each individual (Equation 1).where Yij denotes the outcome measure at a particular paced HR for one individual, ε ij , the residual of variances, and u j , the random effect becase of individual subjec...

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Section: Discussionmentioning

confidence: 64%

Section: Discussionmentioning

confidence: 64%

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confidence: 99%

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Heart Rate Dependency of Large Artery Stiffness

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“…PWV was normalized to diastolic pressure to account for the known dependency of this variable on changes in arterial pressure (Spronck et al, 2015).…”

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confidence: 99%

Magnesium Modifies the Impact of Calcitriol Treatment on Vascular Calcification in Experimental Chronic Kidney Disease

Zelt

McCabe

Svajger

et al. 2015

J Pharmacol Exp Ther

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Chronic kidney disease (CKD) patients are commonly treated with vitamin D analogs, such as calcitriol. Recent epidemiologic evidence revealed a significant interaction between vitamin D and magnesium, since an inverse relationship between vitamin D levels and mortality mainly occurs in patients with a high magnesium intake. The aim of the study was to assess the mechanisms involved by determining whether magnesium alone or combined with calcitriol treatments differentially impacts vascular calcification (VC) in male Sprague-Dawley rats with adenine-induced CKD. Treatment with moderate doses of calcitriol (80 mg/kg) suppressed parathyroid hormone to near or slightly below control levels. Given alone, this dose of calcitriol increased the prevalence of VC; however, when magnesium was given in combination, the severity of calcification was attenuated in the abdominal aorta (51% reduction), iliac (44%), and carotid arteries (46%) compared with CKD controls. The decreases in vascular calcium content were associated with a 20-50% increase in vascular magnesium. Calcitriol treatment alone significantly decreased TRPM7 protein (↓ to ∼11%), whereas the combination treatment increased both mRNA (1.7Â) and protein (6.8Â) expression compared with calcitriol alone. In summary, calcitriol increased VC in certain conditions, but magnesium prevented the reduction in TRPM7 and reduced the severity of VC, thereby increasing the bioavailable magnesium in the vascular microenvironment. These findings suggest that modifying the adverse effect profile of calcitriol with magnesium may be a plausible approach to benefiting the increasing number of CKD patients being prescribed calcitriol.

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“…17 In the estimation of arterial stiffness and carotid-femoral pulse wave velocity, it is not possible to differentiate which part is directly attributable to BP level. 18 Spronck and colleagues 19 found that carotid tonometry builds pressure curves throughout the cardiac cycle to measure stiffness, as the average 10 mm Hg of systolic BP change resulted in a variation of 1 m/s of pulse wave velocity. Although Barochiner and colleagues compared HBPM vs office BP, and not the physiopathological role of BP in arterial stiffness, establishing the status of persistent office hypertension with only one BP office measurement may have caused misclassification of patients in this category.…”

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Is Persistent Office Hypertension in Treated Hypertensive Patients a Benign Condition?

Coll‐de‐Tuero

Vargas-Vila

Torguet

2016

J of Clinical Hypertension

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Arterial stiffness is a powerful and independent risk factor for cardiovascular (CV) disease.1,2 Its prognostic value is added to others including hypertension. 3 The estimation of both stiffness and blood pressure (BP) can provide advantages in individual CV risk determination. 4 "Out-of-office" BP has a better CV prognostic value than office BP in hypertensive patients. This is a common knowledge; however, it is unclear how clinicians use this information in their decision-making.In untreated hypertensive patients at baseline, some authors 5,6 have shown that those with white-coat hypertension (WCH) according to ambulatory BP monitoring (ABPM) have similar CV risk to normotensive patients. However, other cohort studies with longer follow-up periods have shown that the CV risk of patients with WCH according to ABPM or home BP monitoring (HBPM) is intermediate between normotension and sustained hypertension 7 or even higher. 8 There are some factors to consider when discussing these discordant results. First is the rate of detection of subclinical vascular disease in patients diagnosed with WCH. When a patient has subclinical vascular disease, the diagnosis of WCH is not possible. For this reason, it is important to perform the appropriate search of subclinical vascular disease. If not, CV morbidity and mortality can be influenced. Second, patients identified as having WCH have a different profile according to out-of-office BP measurements (ABPM or HBPM). Patients with normal BP by both measurements have a lower basal CV risk than those who have normal values according to only one measurement.9 According to the above, hypertensive patients in whom normal out-of-office BP required by both techniques, ABPM and HBPM, have an incidence of CV events similar to that of normotensive patients, while those with one of the two measures high and the other normal have an intermediate CV risk among normotensive and sustained hypertensive patients. 10,11When these out-of-office measurements apply to the monitoring of treated hypertensive patients, it seems that both are useful and reliable.12,13 When a patient has outof-office BP controlled according to any one of the measures, ABPM or HBPM, CV risk is independent of BP measurement in the office. The work by Barochiner and colleagues 14 published in this issue of the Journal shows that hypertensive patients with persistent office hypertension (high BP in the office and normal HBPM) have greater arterial stiffness, measured by pulse wave velocity, than those with sustained normotension. Previously, Cuspidi and colleagues 15 showed similar findings with both ABPM and HBPM in treated hypertensive patients in relation to left ventricular hypertrophy. The conclusion is that this condition (persistent office hypertension) is perhaps not so benign, as is the case of WCH in untreated hypertensive patients.The study discussed has limitations that require caution in interpreting its results, particularly referring to the BP measurement types: office BP was obtained with only one determ...

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Pressure-dependence of arterial stiffness

Cited by 132 publications

References 33 publications

Heart Rate Dependency of Large Artery Stiffness

Heart Rate Dependency of Large Artery Stiffness

Magnesium Modifies the Impact of Calcitriol Treatment on Vascular Calcification in Experimental Chronic Kidney Disease

Is Persistent Office Hypertension in Treated Hypertensive Patients a Benign Condition?

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