Arterial Wave Reflection Research Articles

Effect of Vardenafil on Arterial Stiffness and Wave Reflection

Effect of Vardenafil on Arterial Stiffness and Wave Reflection

Arterial wave reflection during antihypertensive therapy with barnidipine: A 6-month, open-label study using an integrated cardiovascular ultrasound approach in patients with newly diagnosed hypertension

Background: Increased central aortic pressure resulting from large artery stiffening and increased wave reflection is associated with higher hypertension-related morbidity. Objective: The goal of this study was to evaluate the effects of a vasodilator-based therapy with the calcium channel blocker barnidipine on arterial stiffness, wave reflection, and left ventricular (LV) performance using an integrated cardiovascular ultrasound approach (including wave intensity analysis). Methods: Newly diagnosed, previously untreated patients with grade 1 or 2 essential hypertension (systolic blood pressure [BP] ≥140 and <180 mm Hg, and/or diastolic BP ≥90 and <110 mm Hg), and with no signs of clinical cardiovascular disease, were eligible for study. Carotid artery mechanics were investigated at baseline and after 3 and 6 months of barnidipine therapy (10–20 mg once daily, according to an open-label design) using a double-beam carotid ultrasound technique. This provided a simultaneous recording of diameter-derived pressure and flow velocity signals and allowed analysis of wave intensity. Indices of local arterial stiffness and wave reflection, as well as separated forward and backward pressure waves, were estimated. LV geometry, mass, and systolic and diastolic performance were also assessed using Doppler echocardiography. All ultrasound examinations and readings were performed by investigators blinded to patient demographics and treatment phase. Normotensive control subjects (office BP <140/90 mm Hg) were included as a reference group. Results: Twenty-one white, treatment-naive patients with hypertension (mean [SD] age, 58 [8] years; 14 males; mean body mass index, 27 [5] kg/m 2; mean BP, 159 [14]/96 [5] mm Hg) were enrolled. Twenty normotensive subjects comprised the control group. Compared with the control subjects, patients with hypertension had a higher mean augmentation index ([AIx] 22.0% [7.0%] vs 13.1% [5.2%]; P < 0.01), Peterson's pressure-strain elastic modulus (175 [49] vs 126 [41] kPa; P < 0.01), and forward and backward pressure waves (137 [17] vs 108 [7] mm Hg [ P < 0.001] and 21 [6] vs 17 [5] mm Hg [ P < 0.05], respectively) at baseline. After 6 months of barnidipine treatment, mean office BP in the patients with hypertension decreased from 159 (14)/96 (5) mm Hg at baseline to 138 (16)/81 (9) mm Hg ( P < 0.001) due to a significant reduction in forward and backward pressure waves, and AIx decreased to 17.0% (8.0%) ( P < 0.01); there were no significant changes in indices of intrinsic arterial stiffness. A significant direct relationship between AIx and pulse pressure ( r = 0.45 [ P < 0.05]) was observed at baseline in hypertensive patients but not after therapy ( r = 0.26 [ P = NS]). Mean stress-adjusted LV midwall shortening increased from 110% (17%) at baseline to 118% (13%) at 6 months ( P < 0.05), which was comparable to baseline values in the control subjects (119% [10%]). Conclusion: In these middle-aged patients with newly diagnosed mild to moderate hypertension, vasodilator therapy with barnidipine reduced central BP by a parallel reduction of forward and backward pressure waves, together with a later arrival of the reflected waves, with no significant changes in intrinsic arterial stiffness.

Arterial Stiffness and Hypertension

Arterial stiffness is increasingly recognized as an important prognostic index and potential therapeutic target in patients with hypertension. It is closely linked to, but by no means synonymous with, raised blood pressure, and its physiopathology is still not fully understood. Aortic stiffness and arterial pulse wave reflections are key determinants of elevated central systolic pressure and are associated with adverse cardiovascular outcomes, independent of blood pressure. Indeed, the 2003 European Society of Hypertension guidelines on the management of hypertension acknowledge the potential role of arterial stiffness measurement in clinical management1 and have prompted the publication of a consensus document on the measurement of central blood pressure and hemodynamics.2 A detailed expert consensus document has also been published on the methodologic and clinical issues around arterial stiffness.3 Broader implementation of these techniques into routine care seems inevitable. In this review, we have examined recent research in this field published in Hypertension , focusing on mechanistic work, methods for measuring stiffness, important clinical associations, and effects of treatment. ### Mechanisms and Causes of Arterial Stiffness Hypertension and arterial stiffness are closely associated with age.4 Degeneration of compliant elastin fibers, and deposition of stiffer collagen, is considered a key cause of age-related arterial stiffening. Moreover, blood pressure plays a significant role in determining vessel wall structure, with remodeling occurring to compensate for changes in wall stress. One potential mechanism is through matrix metalloproteinases, which modulate extracellular matrix proteins. When angiotensin II is given to mice, matrix metalloproteinase 9 activity is induced, resulting in enhanced collagen degradation. This improves the intrinsic distensibility of elastic arteries and, thus, blunts any blood pressure rise.5 Impairment of this compensatory mechanism may, therefore, contribute to increased stiffness. The organization of elastic fibers is also important. Inhibition of the vascular adhesion protein semicarbazide-sensitive amine oxidase in a rat model results in …

Abstract 5270: Vascular Function and Vascular Inflammation in Polycystic Kidney Disease

Background: Polycystins, which have been localized to vascular smooth muscle cells, may lead to vascular dysfunction and contribute to cardiovascular disease in autosomal dominant polycystic kidney disease (ADPKD). We examined vascular function and vascular inflammation in ADPKD. Methods: This is an ancillary study to the Halt Progression in PKD Study, which is examining the effect of renin-angiotensin-aldosterone blockade on progression of ADPKD. We used peripheral arterial tonometry to assess augmentation index (AIx), a measure of arterial stiffness and wave reflection, in 52 ADPKD patients with hypertension and glomerular filtration rate (GFR) 25– 60 ml/min/1.73 m 2 , 50 ADPKD patients with hypertension and GFR &gt;60 ml/min/1.73 m 2 , and 51 healthy controls. We measured serum levels of soluble intercellular adhesion molecule-1 (sICAM-1), vascular cell adhesion molecule-1 (VCAM-1), p-selectin, e-selectin, soluble Fas, and Fas ligand (FasL) as markers of vascular inflammation. Results: AIx, sICAM, p-selectin, and Fas were higher, and FasL was lower in subjects with ADPKD (p&lt;0.05, Table ). Adjusting for age, race, height, heart rate, and mean arterial pressure had no effect on group differences in AIx (healthy control = 8%, ADPKD GFR &gt;60 = 21%, ADPKD GFR 25– 60 = 20%). Group means were significantly different even after adjustment for vascular inflammatory markers (healthy control = 3%, ADPKD GFR &gt;60 = 24%, ADPKD GFR 25– 60 = 24%). There were no differences in AIx, sICAM, p-selectin, e-selectin, or FasL between the two ADPKD groups (Table 1 , p&gt;0.05). Conclusion: Vascular dysfunction and vascular inflammation are evident even in early stages of ADPKD with preserved GFR. Further research is needed to examine the relative contributions of genetic aberrations, hypertension, and reduced kidney function to the pathophysiology of vascular dysfunction in ADPKD. Table. Subject information.

Abstract 5151: Waveform Reflections and Arterial Stiffness in the Prediction of 15.1-Year All-Cause and Cardiovascular Mortalities: A Community-Based Study

Background- The role of arterial wave reflection, usually assessed by the transit-time dependent augmentation index (AI) and augmented pressure (Pa), in the prediction of cardiovascular events may have been underestimated. We investigated whether the transit-time independent measurements of reflected wave magnitude predict cardiovascular outcomes independently of arterial stiffness indexed by carotid-femoral pulse wave velocity (PWV). Method- A total of 1272 participants (47.0% women) from a community-based survey were studied. Carotid pressure waveforms derived by tonometry were decomposed to generate forward wave amplitude (Pf), backward wave amplitude (Pb), and reflection index (RI, = [Pb/(Pf+Pb)]), in addition to AI, Pa, and reflected wave transit time (RWTT). Results During a median follow-up of 15.1 years, 225 deaths occurred, including 64 cardiovascular origins. In univariate Cox proportional hazards regression analysis, PWV, Pa and Pb predicted all-cause and cardiovascular mortalities in both men and women whereas AI, RWTT and RI were predictive only in men. In multi-variate Cox analysis accounting for age, height, and heart rate, Pb predicted all-cause mortality in women and cardiovascular mortality in both men and women, whereas Pa only predicted cardiovascular mortality in men but not in women. When PWV and Pb were jointly entered into the multivariate model accounting for age, sex, height, heart rate, and brachial mean blood pressure, Pb (hazard ratio 1.066, 95% confidence interval 1.023–1.110) but not PWV (1.086, 0.993–1.189), independently predicted cardiovascular mortality. Conclusion- Pb, a transit-time independent measurement of reflected wave magnitude, predicted long term cardiovascular mortality in men and women independently of PWV.

Abstract 4962: Influence of Adiposity on Carotid Wave Reflection and Arterial Stiffness: A Longitudinal Study in Healthy Children

Background: The relationship between childhood obesity and adverse cardiovascular outcomes during adulthood may be mediated through the promotion of impaired vascular function. Wave reflection is an index of arterial function that is determined by arterial stiffness and is predictive of adverse cardiovascular events in adults. We hypothesized that baseline and changes in adiposity during childhood have an adverse influence on future levels of wave reflection and arterial stiffness. Methods: In 514 healthy children (mean age 8.3±0.4, 50% boys); percentage body fat (%BF) was quantitated by dual-energy x-ray absorptiometry during a baseline assessment in 2005 and during a follow-up assessment in 2007. Baseline insulin resistance was evaluated using a homeostasis model assessment (HOMA-IR). Cardiorespiratory fitness (CRF) was assessed using a 20 meter shuttle run. Carotid artery wave reflection and carotid-femoral pulse wave velocity (PWV) was assessed in 2007 using applanation tonometry (SphygmoCor, Atcor Medical, Sydney, Australia). The second peak of carotid systolic blood pressure (SBP2) was obtained from the carotid arterial waveform. Results: In univariable analysis, baseline %BF was positively associated with carotid SBP2 and PWV measured in 2007. In multivariable analysis, baseline %BF and change in %BF was associated with carotid SBP2 after adjustment for age, sex, baseline blood pressure, heart rate, height, HOMA-IR, total cholesterol and CRF (Table ). Baseline %BF was also independently associated with PWV (Table ). Conclusion: Baseline adiposity was positively related to future carotid wave reflection and arterial stiffness. In addition, subsequent increase in adiposity over a 2-year period was associated a greater degree of wave reflection. Relationship between baseline and change in percent body fat and future wave reflection (carotid SBP2) and arterial stiffness (PWV) in multivariate models

Impact of human immunodeficiency virus infection on arterial stiffness and wave reflections in the early disease stages

Background Human immunodeficiency virus (HIV) infection is associated with subclinical inflammation and increased cardiovascular risk. Arterial stiffness and enhanced wave reflections are markers of cardiovascular disease and independent predictors of cardiovascular risk. The effect of HIV infection, per se, on aortic stiffness and wave reflections has not been clearly defined. Methods We studied 51 adults with a recent HIV infection, free of antiretroviral treatment and AIDS diagnosis, as well as 35 controls matched for age, sex and smoking status. Carotid-femoral pulse wave velocity (PWV) and timing of the reflected wave (Tr) were measured as indices of aortic stiffness, while aortic augmentation index (AIx) and augmented pressure (AP) were measured as indices of wave reflections. Results While PWV was similar in the two populations, Tr was significantly lower in HIV-infected subjects compared to controls (by 16.5 ms, p = 0.002). In addition, AIx and AP were decreased (by 6.4%, p = 0.048 and by 3.3 mmHg, p = 0.010, respectively) in subjects with HIV infection. Moreover, HIV-infected patients compared with controls had increased values of hs-CRP [1.37 (0.85–2.53) vs. 0.75 (0.41–1.90) mg/l, p = 0.007] and interleukin-6 [1.90 (0.91–3.9) vs. 1.28 (0.80–2.65) pg/ml, p = 0.048]. Tr was negatively correlated with hs-CRP ( r = −0.283, p = 0.010) and interleukin-6 ( r = −0.278, p = 0.018). Conclusions Our study provides evidence of decreased wave reflections and similar aortic stiffness, as assessed by PWV, in the early stages of HIV infection in treatment-naive patients compared to controls. Subclinical inflammation and resultant peripheral vasodilatation constitute potential mediators of the whole pathophysiological process.

The effects of passive leg raising on arterial wave reflection in healthy adults

Passive leg raising (PLR) produces hemodynamic and physiological changes related to centralizing blood volume and baroreceptor activation. To evaluate the effects of PLR on central hemodynamics, we prospectively studied 50 healthy participants (80% male, age 37 +/- 12 years). Central aortic blood pressures (CA-BPs) and reflected wave properties were evaluated using applanation tonometry at baseline and upon 1 min of PLR. Heart rate (HR) was unchanged. Brachial artery (BA)-systolic BP, BA-diastolic BP, and BA-pulse pressure (PP) all decreased from baseline to PLR. Changes in BA-PP were significantly greater than changes in CA-PP. Reflected wave augmentation pressure (P(s)-P(i)), HR corrected augmentation index (AIx@75), and augmentation index decreased significantly [(P(s)-P(i)): 5 +/- 6 vs. 4 +/-5, P < 0.001; AIx@75%: 10 +/- 13 vs. 7 +/- 12, P = 0.004; AI%: 14 +/- 12 vs. 12 +/- 12, P = 0.014, respectively]. HR corrected ejection duration (ED(c)), round trip travel time (deltat(p)), and reflected wave systolic duration (deltat(r)) all increased upon PLR [ED(c): 433 +/- 15 vs. 444 +/- 17, P < 0.001; deltat(p): 149 +/- 18 vs. 156 +/- 20, P = 0.003; deltat(r): 174 +/- 33 vs. 179 +/- 32, P = 0.046, respectively]. Indices of left ventricular (LV) workload including wasted LV energy and tension-time index decreased upon PLR. PLR decreases the amplitude and delays the onset of the reflected aortic pressure wave. This decreases wasted LV pressure energy and workload.

Arterial Wave Reflections During the Menstrual Cycle of Healthy Women

Increased wave reflection is an independent factor associated with cardiovascular diseases, risk, and mortality. The influence of the menstrual cycle on wave reflections and particularly on the reproducibility of their measurement has never been examined. The aim of the present study was to examine the reproducibility and variability of wave reflection indices in premenopausal healthy women during their menstrual cycle. Thirty-two women were examined at 3 phases of their menstrual cycle: days 1 to 2 (menstrual phase), days 6 to 14 (late follicular), and days 4 to 7 after ovulation (early luteal phase). Applanation tonometry of the radial artery and aortic pulse wave analysis were performed for the calculation of augmentation pressure, augmentation index, and timing of reflected waves. Reproducibility of these measures was evaluated by intraclass correlation coefficient and Bland-Altman analysis, whereas ANOVA was performed to assess their variability during the menstrual cycle. The SD of augmentation index differences between repeated measurements within the menstrual cycle ranged from 7.6% to 9.9%. Bland-Altman analysis indicated no evidence of systemic bias and no trend for the reproducibility of measurements to vary with their underlying mean value. Intraclass correlation coefficient indicated a moderate reproducibility of augmentation index and augmentation pressure (>0.80) and a rather low reproducibility for timing of reflected waves (0.43). Mean augmentation pressure, augmentation index, and timing of reflected waves did not vary significantly during the menstrual cycle (ANOVA). Measurement of wave reflections at the same phase of the menstrual cycle or statistical adjustment could be suggested for optimal study design and data interpretation.

Etanercept improves inflammation-associated arterial stiffness in rheumatoid arthritis

Increased arterial stiffness, an independent risk factor for premature coronary artery disease, has been reported in patients with RA. The objectives of this study were first to assess, in patients with RA, the relationship between disease activity, inflammation and augmentation index, which is a combined measure of arterial stiffness and pulse wave reflection. The second objective was to establish any effect anti-rheumatic treatment may have on augmentation index. One hundred and forty-eight RA patients with no previous history of cardiovascular disease (CVD) had their augmentation index corrected for a heart rate of 75 beats per minute (AIx@75), and parameters of RA disease activity and CV risk measured. Forty-seven patients were then treated with either MTX (n = 21) or etanercept (ETAN) (n = 26), and assessments were repeated at 2 and 4 months. Patients with high CRP (> 10 mg/l) showed significantly higher mean AIx@75 than those with low CRP (< or = 10 mg/l) (33 +/- 8 vs 30 +/- 8%; P = 0.033). On regression analysis, log(10) CRP (beta = 0.298; P = 0.002), gender (beta = 0.257; P = 0.007), BMI (beta = -0.292; P = 0.004), diastolic blood pressure (beta = 0.260; P = 0.009) and age (beta = 0.194; P = 0.046) were independently associated with AIx@75. Treatment with ETAN (35 +/- 9, 32.5 +/- 1 and 32.5 +/- 8%; P = 0.025) but not MTX (31 +/- 1, 31 +/- 1 and 31 +/- 1%; P = 0.971) attenuated the AIx@75 significantly from baseline to Visits 2 and 3. Systemic inflammation (CRP) is an independent predictor of arterial stiffness and pulse wave reflection in patients with RA. ETAN but not MTX therapy reduces arterial stiffness and pulse wave reflection and may thus improve CV morbidity in RA.

Angiotensin II, mechanotransduction, and pulsatile arterial hemodynamics in hypertension

The aortic blood pressure curve involves two components: a steady component, the mean arterial pressure (MAP), which is dependent on cardiac output and vascular resistance, and a pulsatile component pulse pressure (PP), which is dependent on arterial stiffness and pulse wave reflections. The transduction mechanisms of MAP and PP differ markedly, involving focal adhesion kinase for MAP and oxygen free radicals for PP. Angiotensin II (ANG II) and its blockade are associated with changed vascular resistance and MAP; however, their effects on PP (peripheral and mostly central PP) have been inadequately investigated. In hypertensive rats, when compared with their normotensive controls, ANG II blockade normalizes central PP (<50 mmHg) but not MAP when the same drug dosage is used for each. In hypertensive patients, ANG II blockade reduces arterial stiffness and pulse wave reflections, but with the same reduction in MAP, there is a greater reduction in central than peripheral PP, thereby increasing carotid-brachial PP amplification. With long-term ANG II blockade, the hypertensive arteriolar hypertrophy observed at baseline is corrected in association with reduced arteriolar reflection coefficients, reduced carotid arterial attachments linking alpha(5)-integrin to its ligand fibronectin, and decreased circulating C-reactive protein. When given a normal salt diet, each of these factors contributes separately in reducing arterial stiffness and wave reflections. These responses disappear with a high-salt diet, a condition that usually involves the activation of the local vascular renin-angiotensin-aldosterone system and can be prevented by its selective blockade. Thus ANG II inhibition seems to contribute independently in reducing central PP and aortic stiffness.

Low total antioxidative capacity levels are associated with augmentation index but not pulse-wave velocity

It is well known the relationship between oxidative stress and vascular function. However, association between total antioxidative capacity and arterial stiffness was not studied in patients with hypertension (HT). This study investigated whether total antioxidative capacity is associated with arterial stiffness and wave reflections. We studied 46 (age 48.5 +/- 10.6 years) never treated patients with HT and age-matched control group of 40 (age 47 +/- 8.6 years) normotensive individuals. Total antioxidative capacity level was determined in all subjects. We evaluated arterial stiffness and wave reflections of the study population, using applanation tonometry (SphygmoCor). Carotid-femoral pulse-wave velocity (PWV) was measured as index of aortic stiffness. The heart rate-corrected augmentation index (AIx@75) was estimated as a composite marker of wave reflections and arterial stiffness. Carotid-femoral PWV (10.5 +/- 2.2 vs 8.7 +/- 1.6, m/s, P = 0.0001) and AIx@75 (22.7 +/- 9.5 vs 15 +/- 11, %, P = 0.001) were significantly higher in patients with HT compared with age-matched control subjects. Total antioxidative capacity level (274 +/- 70 vs 321 +/- 56 micromol/l, P = 0.001) was significantly lower in hypertensive patients than controls. In the whole population, total antioxidative capacity level negatively correlated with AIx@75 (r = -0.24, P = 0.02) in univariable analysis, but not with carotid-femoral PWV (r = -0.08, P = 0.43). Also, we found that total antioxidative capacity level (beta = -0.21, P = 0.03) was an independent determinant of AIx@75 in multivariable analysis. Our results suggest that the decrease in the ability of antioxidant defenses contributes significantly to increased wave reflections.

Arterial Wave Reflection in HIV-Infected and HIV-Uninfected Rwandan Women

To assess differences in arterial wave reflection, a marker of atherosclerosis, in HIV-positive and HIV-negative Rwandan women, applanation tonometry was performed on 276 HIV(+) and 67 HIV(-) participants. Radial artery pressure waveforms were recorded and central aortic waveforms were derived by validated transfer function. Central augmentation index (C-AI), central pulse pressure (C-PP), and peripheral augmentation index (P-AI) were measured. HIV(+) participants were younger and had lower diastolic blood pressure (BP) and 41% of the HIV(+) women were taking antiretroviral therapy (ART). Mean C-AI and P-AI were significantly lower in HIV-infected than in uninfected participants (20.3 +/- 12.0 vs. 25.5 +/- 12.1, p = 0.002 and 74.6 +/- 18.8 vs. 83.7 +/- 20.0, p < 0.001). After age matching, C-AI, C-PP, and P-AI were similar among the groups. On multivariate analysis, age, heart rate, weight, and mean arterial pressure were independently associated with C-AI (R(2) = 0.33, p < 0.0001). Among HIV-infected women, current CD4 count did not correlate with C-AI (Rho = -0.01, p = 0.84), C-PP (Rho = 0.09, p = 0.16), or P-AI (Rho = -0.01, p = 0.83). In conclusion, HIV infection was not associated with increased arterial wave reflection in women with little exposure to antiretroviral therapy and without CV risk factors. Whether long-term ART increases measures of arterial stiffness remains unknown.

Arterial Stiffness and Other Vasculatures Impairments That Cause in Hypertensive Older Patients and Smoking Cognitive Impairments Are Not Linked to Gender

HomeStrokeVol. 40, No. 9Arterial Stiffness and Other Vasculatures Impairments That Cause in Hypertensive Older Patients and Smoking Cognitive Impairments Are Not Linked to Gender Free AccessLetterPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessLetterPDF/EPUBArterial Stiffness and Other Vasculatures Impairments That Cause in Hypertensive Older Patients and Smoking Cognitive Impairments Are Not Linked to Gender Karim Hnid Karim HnidKarim Hnid Mitochondrial Interest Group (MIG), Zemamra, Morocco Search for more papers by this author Originally published6 Aug 2009https://doi.org/10.1161/STROKEAHA.109.557181Stroke. 2009;40:e539Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: August 6, 2009: Previous Version 1 To the Editor:The article by Kearney-Schwartz et al1 explains the mechanism by which cognitive impairments in the elderly can happen in hypertensive patients.They suggest that memory impairment was only observed in men and explain this fact by possible differential effects of gender in hypertensive patients at an early stage of cognitive impairment.They omitted to tell us in their paragraph discussion, that only 15% of women were smokers or exsmokers versus 66% of men.Hill2 has done a study in which he concluded that the residual effects of current cigarette smoking negatively influenced speeded cognitive capabilities in older adults, and exsmokers did not differ from smokers in their performance on any of the cognitive tasks. Moreover, Reitz et al3 found that current smokers aged >75 years had cognitive and memory impairment than their peers who do not smoke. Finally, the Rotterdam Study4 demonstrates that current smoking increases the risk of dementia and Alzheimer disease.On the other hand, Mahmud et al5 in their study found that hemodynamic consequences of chronic smoking increase arterial stiffness and arterial wave reflection, which leads to increased aortic systolic blood pressure, and chronic smoking females are not protective from such vascular effects.This finding about smoking and genesis of arterial stiffness is comforted by Jatoi et al,6 Polonia et al,7 and Liang et al8 in their respective studies. They all demonstrate, after a long period of smoking cessation, a clear improvement of pulse wave velocity, central pressure, and vascular stiffness.Smoking has a central role in the genesis of vascular disturbances in this particular study, and gender is not the cause of the difference noted in the study.DisclosuresNone.1 Kearney-Schwartz A, Rossignol P, Bracard S, Felblinger J, Fay R, Boivin J-M, Lecompte T, Lacolley P, Benetos A, Zannad F. Vascular structure and function is correlated to cognitive performance and white matter hyperintensities in older hypertensive patients with subjective memory complaints. Stroke. 2009; 40: 1229–1236.LinkGoogle Scholar2 Hill RD. Residual effects of cigarette smoking on cognitive performance in normal aging. Psychol Aging. 1989; 4: 251–254.CrossrefMedlineGoogle Scholar3 Reitz C, Luchsinger J, Tang M-X, Mayeux R. Effect of smoking and time on cognitive function in the elderly without dementia. Neurology. 2005; 65: 870–875.CrossrefMedlineGoogle Scholar4 Reitz C, den Heijer T, van Duijn C, Hofman A, Breteler MMB. Relation between smoking and risk of dementia and Alzheimer disease: the Rotterdam Study. Neurology. 2007: 69: 998–1005.CrossrefMedlineGoogle Scholar5 Mahmud A, Feely J. Effect of smoking on arterial stiffness and pulse pressure amplification. Hypertension. 2003; 41: 183–918.LinkGoogle Scholar6 Jatoi NA, Jerrard-Dunne P, Feely J, Mahmud A. Impact of smoking and smoking cessation on arterial stiffness and aortic wave reflection in hypertension. Hypertension. 2007; 49: 981–985.LinkGoogle Scholar7 Polonia J, Barbosa L, Silva JA, Rosas M. Improvement of aortic reflection wave responses 6 months after stopping smoking: a prospective study. Blood Pressure Monitoring. 2009; 14: 69–75.CrossrefMedlineGoogle Scholar8 Liang Y-L, Shiel LM, Teede H, Kotsopoulos D, McNeil J, Cameron JD, McGrath BP. Effects of blood pressure, smoking, and their interaction on carotid artery structure and function. Hypertension. 2001; 37: 6–11.CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Li J, Bao J, Gao C, Wei Z, Tan L, Liu P, Wang Z and Tian S (2021) Increased Serum E-Selectin Levels Were Associated with Cognitive Decline in Patients with Stroke, International Journal of General Medicine, 10.2147/IJGM.S292171, Volume 14, (733-739) September 2009Vol 40, Issue 9 Advertisement Article InformationMetrics https://doi.org/10.1161/STROKEAHA.109.557181PMID: 19661473 Originally publishedAugust 6, 2009 PDF download Advertisement

ACUTE EFFECTS OF NICOTINE ON ARTERIAL STIFFNESS AND WAVE REFLECTION IN HEALTHY YOUNG NON‐SMOKERS

1. Recently, we have demonstrated that cigarette smoke exposure proportionally increases plasma nicotine levels and arterial wave reflection to the aorta. However, the exact contribution of nicotine to the smoke-induced enhancement of wave reflection and the potential underlying mechanisms have not been fully investigated. 2. The present study was a prospective study in 15 healthy male non-smokers. All received a placebo and a 2 mg nicotine tablet, according to a randomized double-blind cross-over study design. Each subject underwent repeated measurements at baseline and for 1 h after nicotine or placebo intake, using carotid-femoral pulse wave velocity (PWV) to assess arterial compliance. Concurrently, aortic pressures and the augmentation index were evaluated using applanation tonometry. 3. Plasma nicotine concentrations achieved 1 h after intake of the nicotine tablet reached comparable levels to those achieved after 1 h exposure to passive smoke (3.6 +/- 0.4 vs 3.2 +/- 0.4 ng/mL, respectively; P = 0.4). 4. Nicotine enhanced arterial wave reflection to the aorta, as assessed by the augmentation index corrected for heart rate (4.2 +/- 1.3 vs-0.7 +/- 0.8% with placebo; P = 0.001). In addition, a progressive increase in carotid-femoral PWV was noted after nicotine administration (0.3 +/- 0.1 vs-0.02 +/- 0.1 m/s with placebo; P = 0.04). This remained significant even after adjustment for changes in mean blood pressure and heart rate (P = 0.01). 5. Plasma nicotine concentrations comparable to those achieved after exposure to passive smoke enhance arterial wave reflection to the aorta. This is accompanied by an increase in carotid-femoral PWV, denoting a deterioration of arterial compliance by nicotine.

Relationship between job strain and radial arterial wave reflection in middle-aged male workers

Objective This study examined the relationship between job stain and radial arterial wave reflection as expressed by the augmentation index (AI), a marker of cardiovascular risk, in middle-aged male workers. Methods Radial AI was measured using automated applanation tonometry in 808 working men (mean age; 47 ± 5 years) at a company in Kanagawa, Japan in 2007. An elevated AI represents the deterioration of arterial properties and increased cardiovascular risk. Job demand and job control (decision latitude) were evaluated by a self-administered, Brief Job Stress Questionnaire. High job strain was defined as the combination of high job demand and low job control. Results In the entire study population, the mean ± SD and the median of AI were 74 ± 13% and 75%, respectively. High job strain was seen in 267 subjects. In a multiple logistic regression analysis with adjustment for multiple potential confounders, high job strain showed a significantly increased odds ratio (1.47, 95% CI; 1.04–2.09, P = 0.029) for an elevated AI (≥ 75%). Conclusion High job strain was significantly associated with an elevated radial AI. The measurement of AI may be useful when incorporated in workplace interventions to reduce the risk of cardiovascular disease, especially at sites where workers tend to perceive high job strain.

Introduction to the Seventh International Workshop on Structure and Function of the Vascular System

The Seventh International Workshop on Structure and Function of the Vascular System was held in Paris from March 12 through March 14, 2009. As with the preceding workshop (2007) the focus of the meeting shifted from large arteries toward a more integrative view on the structure and function of the vascular system, including the microcirculation. Recent insights have underlined the two-way traffic between the macro- and the microcirculation. On the one hand, pulse pressure generated in the macrocirculation penetrates deeper into the microcirculation than was previously believed. Increased pulse pressure at the level of the microcirculation causes functional and structural changes in the small vessels that contribute importantly to target organ damage. This is particularly the case in the renal pre- and postglomerular arterioles. On the other hand, the microcirculation is an important site of wave reflections in the arterial tree. Thereby, abnormalities in the microcirculation influence the contour of the pressure wave and the height of pulse pressure in the macrocirculation. A third potential interaction between the macro- and the microcirculation is the vaso-vasorum. Small arterioles have been found in the walls of larger arteries and may play a role in the structure and function of these arteries. Hypertensive disease is characterized by a “bad loop” between the macro- and microcirculation that maintains elevated blood pressure and causes target organ damage. During the three-day symposium nine sessions were held. The first dealt with arterial stiffness and was opened with a lecture by Gary Mitchell. He reviewed how excessive pressure pulsatility leads to target organ damage on a microvascular level. Ian Wilkinson subsequently proposed that changes in endothelial nitric oxide production resulting from stiffness-induced alterations in local shear stress may underlie damage of the microcirculation.1 Patrick Lacolley focused on the role of integrins as mediators of stiffness-induced decrease of …

Sodium Intake and Vascular Stiffness in Hypertension

The relationship between sodium and blood pressure (BP) continues to be the focus of intense research. In humans, the impact of sodium on systolic BP (SBP), diastolic BP (DBP), mean BP, and pulse pressure (PP) is currently thought to be quite similar for the 4 pressures and to occur practically with identical consequences (see reviews1–8). In this review, the effect of sodium on SBP is taken into consideration mainly for a very simple but important reason: in recent years, SBP and PP have become the parameters the most difficult to control in hypertensive subjects, which is the principal goal of most antihypertensive drugs.1 Central (aortic) SBP is a complex parameter that is influenced both by cardiac (stroke volume and ventricular ejection) and vascular (arterial and venous stiffness and wave reflections) factors.1 Stroke volume, the ratio between cardiac output and heart rate, depends not only on cardiac structure and function but also on venous return. Through the extracellular and intravascular spaces and their elastic properties, stroke volume and, hence, SBP are strongly associated with sodium balance, ie, with the relationship between sodium intake and its urinary elimination, and, finally, the traditional pressure-diuresis mechanism.4 This pathway, which mainly affects the venous circulation, requires a low and steady BP, together with a vast storage capacity for salt and water. Another important pathway affects the high-pressure pulsatile arterial system, in which the SBP level is achieved through increased arterial stiffness and disturbed wave reflections. These hemodynamic parameters are strongly influenced by sodium intake, and their anomalies are mostly seen in subjects >50 years old.1,2,5,7,9 Note that, in humans, the volume and elasticity of the arterial space are very low compared with the corresponding values for the venous system.1 We have 2 principal aims for this review. First, how …

Associations between plasma homocysteine levels, aortic stiffness and wave reflection in patients with arterial hypertension, isolated office hypertension and normotensive controls.

The aim of this study was to evaluate any possible association of homocysteine with arterial stiffness indices in patients with essential arterial hypertension (AH), isolated office hypertension (IOH) and normotensive controls. The final cohort comprised 231 normotensives (NTs, 119 males), 480 patients with IOH (196 males) and 1188 patients with essential AH (713 males). All patients were screened for plasma homocysteine levels and lipidaemic profile and underwent aortic compliance and wave reflection assessment by using carotid-femoral pulse wave velocity (PWVc-f) and aortic augmentation index corrected for heart rate (AIx) accordingly. In the total population, stepwise multiple linear regression analysis showed that homocysteine levels remained a significant determinant of PWV (beta (SE): 0.056 (0.007), P<0.001) and AIx (beta (SE): 0.236 (0.052), P<0.001) independently of the traditional factors affecting arterial stiffness and wave reflection. When the three groups were examined separately, homocysteine levels remained an independent determinant of PWFc-f in all groups (NT: beta (SE): 0.070 (0.022), P=0.002; IOH: beta (SE): 0.109 (0.015), P<0.001; AH: beta (SE): 0.040 (0.009), P<0.001). However, homocysteine levels remained an independent determinant of AIx only in the IOH and AH, but not in the NT group (IOH: beta (SE): 0.302 (0.124), P=0.015; AH: beta (SE): 0.183 (0.057), P=0.001; NT: beta (SE): 0.308 (0.240), P=0.200). This study points to an independent relationship between circulating homocysteine levels, aortic compliance and wave reflection.

Acute Effects of Acupuncture Treatment with Baihui (GV20) on Human Arterial Stiffness and Wave Reflection

Objectives Treatment by manual acupuncture needling affects the vascular wall tone, and hemodynamic parameters for arterial stiffness may be characterized by treatment at the traditional acupuncture point (acupoint) of Baihui (GV20). Methods The acute effects of acupuncture treatment on arterial stiffness and wave reflection were investigated and, simultaneously, an augmentation index (AI), as an index of wave reflection, was estimated. These parameters were measured in male volunteers using applanation tonometry during 20 minutes of acupuncture treatment and 40 minutes post-acupuncture. Results During treatment, diastolic blood pressure (BP), but not systolic BP, increased significantly. Heart rates (HR) initially tended to increase and then decrease. The AI from radial arteries increased significantly, while central aortic blood pressure (CBP) was unaffected. Post-acupuncture, the effects lasted for 30-40 minutes. The average BP and HR were +10.1±0.3% and −7.2±0.2%, respectively, and the CBPs were not altered, but the AI decreased markedly; this latter effect presumably resulted from the involvement of neurovascular modulators. Conclusions These results indicated that acute treatment at Baihui enhanced arteriosclerotic parameters. In post-acupuncture, the AI profoundly decreased, presumably resulting from the involvement with neurovascular modulators.