Correction of carotid intima-media thickness for adaptive dependence on tensile stress: implication for cardiovascular risk assessment.

PURPOSE: Early artery wall-thickening detected by ultrasound-assessed increased carotid intima-media thickness (IMT) may reflect atherosclerosis or represent an adaptive response to keep homeostasis tensile stress that is related inversely to wall thickness by Laplace's equation. We attempted to discriminate between both mechanisms by correcting IMT for its inverse association with tensile stress. METHODS: Common carotid IMT and lumen diameter (D) where determined in 40 healthy controls and 119 never-treated asymptomatic patients with >or=1 traditional cardiovascular risk factor. The cross-sectional area (CSA) was calculated as pi x IMT x (IMT + D). Tensile stress was approximated by [mean blood pressure x (D/2 x IMT)], and wall shear stress by [(blood viscosity) x 4 x (mean blood velocity/D)]. Inverse regression line relating IMT and tensile stress in controls (p < 0.001) was used as a reference to determine in an individual at-risk patient the IMT deviation, defining DeltaIMT from the regression line of controls at the measured patient's tensile stress. RESULTS: DeltaIMT correlated positively with age (p < 0.05), body mass index (p < 0.05), blood pressure (p < 0.001), and glucose (p < 0.001). In multivariate analysis, DeltaIMT was independently associated with age (p < 0.01), male gender (p < 0.001), and blood pressure (p < 0.001). IMT showed positive association with age (p < 0.001) but not with other risk factors. Also, DeltaIMT, like CSA, correlated positively with tensile stress (p < 0.001) and negatively with wall shear stress (p < 0.05, p < 0.01), whereas IMT correlated negatively with tensile stress (p < 0.001) but not with wall shear stress. CONCLUSION: Correcting IMT for adaptive association with tensile stress may give more strength to carotid evaluation for assessing cardiovascular risk.

New assessment of endothelium-dependent flow-mediated vasodilation to characterize endothelium dysfunction.

The vascular endothelium plays an important role in the regulation of vascular tone, cell growth, inflammation, and thrombogenicity. Endothelium dysfunction, then, is considered to promote several disorders that initiate the atherosclerosis process. Vascular tone dysfunction can be determined by high-resolution ultrasonographic imaging of the brachial artery, enabling one to assess endothelium-dependent flow-mediated dilation (FMD). It is based on the principle that an increase in blood flow, specifically in shear stress, provokes the release of nitric oxide and then a vasodilation that can be quantified. In this study, brachial artery diameter evolution was continuously followed during baseline and hyperemia after forearm occlusion using a custom designed software. Some techniques used to measure FMD are limited by operator dependence. We present a new, automated, and versatile method of FMD quantification based on B-mode echographic images and edge detection algorithms. Edges for each image in the acquired sequences are recognized as interfaces based on the grey-level profiles of the averaged pixel values. Within-reading and within-subject FMD% coefficients of variation were 7% and 10%, respectively. This technique largely improves manual measurements and was shown to be appropriate for wide clinical use.

Impact of shear stimulus, risk factor burden and early atherosclerosis on the time-course of brachial artery flow-mediated vasodilation.

OBJECTIVES: Our aim was to analyze flow-mediated dilation (FMD) time-course in response to forearm occlusion in the clinical setting. METHODS AND RESULTS: In 50 asymptomatic subjects, monitoring software measuring continuous beat-to-beat change in brachial artery diameter was used to determine FMD magnitude in percentage change in peak diameter from baseline (FMD-DeltaD), time to peak diameter after occlusion release (FMD-t(peak)), integrated FMD response calculated as area under dilation curve (FMD-AUC), maximum FMD rate calculated as maximal slope of dilation (FMD-MDR). FMD-DeltaD and FMD-MDR correlated positively with peak wall shear stress (P < 0.05, P < 0.01). FMD-MDR correlated negatively with age (P < 0.001), Framingham risk score (P < 0.01) and carotid intima-media thickness (P < 0.05), while FMD-DeltaD correlated negatively with Framingham risk score only (P < 0.01). After adjustment, all these correlations were independent of antihypertensive, lipid-lowering and antidiabetic therapies. All but that of FMD-MDR with intima-media thickness were also found in a subgroup of 29 untreated subjects and in a subgroup of 24 untreated and low-risk (FRS < 10%) subjects. FMD-t(peak) and FMD-AUC were not associated with shear stimulus, Framingham risk score, and intima-media thickness. CONCLUSION: The kinetics of dilation (maximum rate) seem more sensitive than their magnitude in assessing FMD performance and its determinants.

Comparative performance of subclinical atherosclerosis tests in predicting coronary heart disease in asymptomatic individuals.

The prognostic performance of subclinical atherosclerosis in predicting coronary heart disease (CHD) needs to be clarified because of the existence of many non-invasive tests available for its detection in the clinical setting: ultrasound measurement of carotid intima-media thickness (IMT) and plaque, cardiac computed tomography assessment of coronary artery calcium, Doppler stethoscope measurement of ankle-arm index pressure (AAI), and mechanographic or Doppler determination of aortic pulse wave velocity (PWV). Data analysis of the main prospective studies in asymptomatic populations allows the establishment of a dose-response relationship between subclinical atherosclerosis burden and cumulative incidence of future CHD event (absolute risk). Negative subclinical atherosclerosis testing conveys a low 10-year CHD risk inferior to 10% whatever the test considered, i.e. IMT less than the 1st tertile or 1st quintile, AAI > or = 0.90, PWV less than the first tertile, no discernible carotid plaque, or zero coronary calcium score. Positive testing for IMT (>95th percentile or 5th quintile), AAI (<0.90), or PWV (>3rd tertile) conveys a moderately high 10-year CHD risk between 10 and 20%. Positive testing for carotid plaque (focal protrusion >1.5 mm or mineralization) or coronary calcium (total score >300 or 400 units) conveys a high 10-year CHD risk superior to 20%. Therefore, positive subclinical atherosclerosis measurement seems to have its place in the context of existing prediction models, namely for intermediate risk classification. It also remains to be established whether individuals with negative subclinical atherosclerosis may be considered at low CHD risk and receive conservative management.

Effects of enhanced external counterpulsation on carotid circulation in patients with coronary artery disease.

BACKGROUND: Enhanced external counterpulsation (EECP) is a noninvasive method previously shown to improve measures of myocardial ischemia in patients with coronary artery disease. However, the concomitant effects of EECP on large and small arterial properties have been poorly examined. In a randomized controlled study, we investigated whether arterial stiffness and resistance of the carotid circulation are altered by EECP. METHODS: Thirty patients with angiographically demonstrated coronary artery disease were randomized into two groups to receive either 'sham' or active EECP therapy for 35 1-hour sessions. The beta stiffness index was calculated by the ln(Ps/Pd)/DD equation where Ps and Pd = systolic and diastolic blood pressure, and DD = the ratio between carotid pulse and diastolic diameter, measured by ultrasound sequential frames during the cardiac cycle. Carotid vascular resistance was calculated as the ratio between mean arterial pressure and mean common carotid blood flow. RESULTS: No significant between-group differences were seen in clinical characteristics or carotid hemodynamics at baseline. The beta stiffness index and carotid vascular resistance were significantly reduced after 35 h of active EECP (p < 0.01), and the decrease was significantly different when compared with controls (p < 0.05 for beta stiffness index and p < 0.001 for carotid vascular resistance). These reductions persisted after multiple covariate adjustment. CONCLUSIONS: This study suggests that EECP exerts clear arterial effects on large and small vessels of the carotid circulation. The combined effects on arterial stiffness and vascular resistance are of particular interest in cardiovascular disease involving reduction in blood flow, in which techniques that increase regional blood flow may be beneficial.

New monitoring software for larger clinical application of brachial artery flow-mediated vasodilatation measurements.

BACKGROUND: The reproducibility of brachial artery flow-mediated vasodilatation (FMD) is limited by the operator dependence of most measurement methods. METHODS: A new automated computerized analysis of brachial artery ultrasound scan providing a continuous evolution of the diameter during acute hyperemia, reactive to short hyperemia of the forearm and hand, was tested in 10 normal volunteers and 26 asymptomatic patients with cardiovascular risk factors such as hypertension, hypercholesterolemia, heavy smoking, history of premature coronary heart disease and the metabolic syndrome. FMD was the percentage of the maximum hyperemic diastolic diameter from baseline. Within-reading variations in FMD and diameters were assessed by reading one scan from the same subject twice by two observers. The within-subject variability of FMD was assessed by analysing two repeated measurements in the same subject by the same operator 1 h, 1 week or 1 month apart. RESULTS: Coefficients of variation (CV) of repeated FMD readings were 7.5% in normal volunteers and 6.9% in patients with risk factors. CV of repeated FMD measurements 1 h apart were 7.8% in normal volunteers and 16.5% in patients with risk factors. In normal volunteers, CV of repeated FMD measurements 1 week apart was 9.6%, and in patients with risk factors CV of repeated FMD measurement 1 month apart was 18.1%. CONCLUSION: This method overcomes the variability of FMD measurement seen with conventional manual analysis in normal volunteers, and to a lesser extent in patients with major cardiovascular risk factors, thus supporting its clinical applicability to patients with disease conditions.

Decreased number of circulating CD34+KDR+ cells in asymptomatic subjects with preclinical atherosclerosis.

OBJECTIVES: To assess whether circulating endothelial progenitor cells (CEPCs) can be considered as a cardiovascular risk marker before event has occurred, that is less firmly established than in clinically overt atherosclerosis. METHODS: Number of CD34+KDR+ cell number per ml blood was measured by flow cytometry in 84 untreated subjects without cardiovascular disease. Atherosclerotic plaque was detected by ultrasound in carotid, abdominal aortic and femoral sites and the number of sites affected by plaque among these three sites was counted as 0, 1, 2 or 3. Additionally, intima-media thickness (IMT) was measured by computerized ultrasound imaging of both common carotid segments. RESULTS: CD34+KDR+ cell number decreased by 48, 29 or 30% in the presence of carotid, aortic or femoral plaque (p<0.001, 0.05, 0.05, respectively) as compared to the absence of plaque and by 70% in the presence of three sites affected with plaque as compared with 0 site with plaque (p<0.01) but did not change with increasing IMT tertiles. Adjustment for Framingham risk score, that was also associated with decreased CD34+KDR+ cell number (p<0.001), made CD34+KDR+ cell number associations with plaque insignificant, except at the carotid site (p<0.01). CONCLUSIONS: Reduced CEPC number may participate to preclinical stage of atherosclerosis and provide additional information to traditional risk factors as regards global risk assessment.

Relationship of circulating biomarkers of inflammation and hemostasis with preclinical atherosclerotic burden in nonsmoking hypercholesterolemic men.

BACKGROUND: Relations of mediators of inflammation and hemostasis with preclinical atherosclerosis have been poorly analyzed. The aim of this study was to test potential associations of these blood markers with indicators of cardiovascular risk and atherosclerotic burden in asymptomatic, nonsmoking, hypercholesterolemic men. METHODS: A total of 87 men underwent cardiovascular risk assessment by means of 10-year Framingham risk calculation (median 9%) and atherosclerotic burden evaluation by means of ultrasonographic measurement of common carotid intima-media thickness and assessment of atherosclerotic plaques at three arterial sites (three-site plaques). RESULTS: Of the markers C-reactive protein, tumor necrosis factor-alpha, interleukin-10, factor VIIc, fibrinogen, plasminogen activator inhibitor-activator, soluble intercellular adhesion molecule-1, soluble P-selectin (sP-selectin), and von Willebrand factor, only sP-selectin was positively and independently associated with high Framingham risk score (>9%) (71.7 +/- 3.6 ng/mL, n = 33 v 59.6 +/- 2.8, n = 54; mean +/- SEM; P < .05) and with three-site plaques (75.4 +/- 5.7 ng/mL, n = 14 v 62.0 +/- 2.5, n = 73; P < .05). After adjustment for all of the above markers and for cardiovascular risk factors, odd ratios of having high Framingham risk and three-site plaques were 3.38 (1.43 to 10.21) and 5.23 (1.74 to 23.52) respectively, per 1-standard deviation increase in sP-selectin. CONCLUSIONS: These results confirm that among several hemostasis and inflammation mediators, only sP-selectin blood level was associated with preclinical atherosclerosis. It might confer to sP-selectin measurement a clinical usefulness for detecting and managing high cardiovascular risk in primary prevention.

Performance of subclinical arterial disease detection as a screening test for coronary heart disease.

Traditional risk factors are poor screening tests for coronary heart disease, whereas clinical arterial disease represents its strongest predictor. This raises the question whether subclinical arterial disease may also predict coronary disease. Using published data of prospective studies of subclinical arterial disease, we calculated the incidence of coronary event associated with the absence or presence of atherosclerosis as defined by dichotomous characterization of the following markers: low or high intima-media thickness or the absence or presence of plaque, assessed by carotid ultrasound; zero or high total coronary artery calcium score assessed by computed tomography; normal or decreased ankle-arm index pressure assessed by Doppler stethoscope; and low or high aortic pulse wave velocity assessed by mecanography. A dose-response relationship was found between the absence and presence of atherosclerosis and coronary event incidence. Yearly incidence was <1% in the absence of atherosclerosis regardless of the marker used. Coronary event incidence was >1% in the presence of atherosclerosis and increased in a gradual way, depending on the marker tested, to reach 3% maximum with massive coronary calcifications. The relation between clinically overt arterial disease, such as angina, transient ischemic attack, stroke, or myocardial infarct, and yearly incidence of subsequent events reported in the literature prolonged the dose-response curve of subclinical disease. Therefore, detection of arterial disease, not only clinically overt but also subclinical asymptomatic, is a worthwhile screening test for future coronary event.

Cyclic GMP release by acute enhanced external counterpulsation.

BACKGROUND: Enhanced external counterpulsation (EECP) is a noninvasive, pneumatic technique that provides favorable effects in patients with coronary artery disease and heart failure. The mechanisms by which EECP exerts its beneficial effects remain poorly understood. Cyclic GMP (cGMP) regulates vascular smooth muscle tone that may improve arterial function. We investigated the effect of a single session of EECP on plasma and platelet cGMP in asymptomatic subjects with cardiovascular risk factors (HCVR) and in patients with coronary artery disease (CAD). METHODS: Fifty-five subjects were included (25 HCVR and 30 CAD) and randomized into two groups to receive either sham (control) or active EECP during 1 h. Plasma and platelet cGMP were measured immediately before and after EECP by radioimmunoassay. RESULTS: One hour of EECP increased cGMP plasma concentration by 52% +/- 66% (SD) (P < .001) and platelet content by 19% +/- 28% (P < .01). The increase in plasma cGMP was particularly marked in CAD patients receiving active EECP (P < .01), mainly in those with low LDL-cholesterol. Platelets, inhibition of nitric oxide synthesis by N(G)-monomethyl-l-arginine (L-NMMA) reduced cGMP by 23% +/- 31% (P < .001), whereas presence of superoxide dismutase and inhibition of phosphodiesterase-5 increased cGMP by 46% +/- 49% and 70% +/- 77%, respectively (P < .001). In all of the cases EECP increased additional platelet cGMP content, which suggests nitric oxide synthase activation. CONCLUSIONS: Acute external counterpulsation showed that very early treatment increases the cGMP production that may participate in the mechanism by which EECP exerts its clinical benefit. Analysis of the modulation of platelet cGMP content suggests that EECP activated the nitric oxide-dependent pathways.

Current possibilities for detecting high risk of cardiovascular disease.

Current possibilities for better detecting high risk of coronary heart disease (CHD) and stroke and peripheral arterial disease are described in this review. A first step is based on risk factors assessment that allows establishing high-risk diagnostic, either by detecting a condition termed as "CHD risk equivalent" and defined by one or more severe major risk factor, or by calculating multifactorial risk in asymptomatic subjects with a global risk score integrating several moderate risk factors. A second diagnostic step, concerning subjects not considered at high-risk by risk factors assessment, is based on non-invasive detection of sub clinical atherosclerosis via a wide variety of structural and functional arterial markers. A third step focuses on detection of myocardial ischemia that may add diagnostic and prognostic information in subjects with high CHD risk. The implementation of high-risk strategy is not yet standardized but it should allow improving cost-effectiveness of cardiovascular prevention, particularly in asymptomatic subjects.

Differential associations of statin and fibrate treatment with carotid arterial remodeling.

BACKGROUND: The effects of statins on intima-media thickness (IMT) are well documented, whereas those of fibrates are unknown. Therefore we compared IMT under treatment with each class of drugs. METHODS: We studied a cohort of consecutive dyslipidemic subjects treated with statin (n = 291) or fibrate (n = 82) drugs. Fibrate-treated subjects were matched with the same number of statin-treated subjects to obtain two subgroups of similar demographic and risk factors including LDL cholesterol. Common carotid far wall IMT and lumen diameter were measured by ultrasonography. RESULTS: In the entire study population, IMT was greater in the fibrate group than in the statin group (P < .001), even after adjustment for LDL cholesterol and other covariates (P < .05). In the matched groups, IMT was greater in fibrate group than in the statin group (P < .01), even after adjustment for LDL cholesterol and other covariates including treatment duration (P < .01). The IMT correlated positively with treatment duration in the fibrate group (P < 0.05) but not in the statin group. In addition, IMT correlated positively with carotid lumen diameter in both the fibrate and statin groups (P < .05, P < .01) but with a lower slope in the former (P < .05). CONCLUSIONS: In this study fibrate treatment was associated with greater IMT, steeper IMT-time relationship, and lower compensatory carotid enlargement than was statin treatment. These differences were not explained by differences in LDL cholesterol.

May subclinical arterial disease help to better detect and treat high-risk asymptomatic individuals?

The diagnosis of high risk of cardiovascular disease (CVD) in subjects without clinically overt CVD has been somewhat improved by integrating multiple traditional risk factors via appropriate risk score programs. Nevertheless, novel measures of CVD risk are being proposed and debated to further improve high-risk detection by their addition to, or their use in place of, traditional risk factors. Among such measures, non-invasive detection of subclinical arterial disease is a subject of growing interest. It may improve CVD risk evaluation and enable more intensive risk-reduction therapy in subjects judged to be at intermediate risk after preliminary risk factor assessment. However, the clinical utility and cost-effectiveness of high-risk diagnostic and therapeutic strategy guided by subclinical arterial disease remain untested. This uncertainty precludes systematic detection of subclinical arterial disease in routine clinical management for primary prevention, but such detection may be used at the discretion of the physician as a part of CVD risk assessment.

Sialic acid as a protective barrier against neointima development.

Arterial sialic acid (SA) has been shown to attenuate the binding of fibrinogen and low-density lipoproteins (LDL) to the vessel wall, presumably protecting against atherosclerosis. This study was aimed to assess the effect of changes in SA content in intimal thickening, an early step in the development of atherosclerosis. New Zealand white rabbits were subjected to bilateral carotid periarterial collaring, followed by in situ-perfusion with neuroaminidase (random artery) and with vehicle (contralateral control artery). The efficiency of SA removal was evaluated in perfusates and arterial homogenates, and arterial tissue samples were obtained 7 and 14 days after the intervention to assess morphological changes. Neuraminidase significantly reduced SA by 16.7%. Arterial desialylation was associated with a significantly increased neointimal formation. Proliferation of smooth muscle cells (SMCs), assessed by incorporation of bromo-2'-deoxyuridine into replicating DNA was also significantly increased in desialylated arteries. In addition, immunohistochemical studies showed a slightly stronger oxidized-LDL (ox-LDL) immunostaining in neointima of desialylated arteries than in control vessels. A mild reduction of SA increases intimal thickening, at least partly due to an enhanced proliferation of SMCs, and may facilitate the accretion of atherogenic lipoproteins, providing evidence for the potential role of SA in the protection against neointimal development.

Differences between markers of atherogenic lipoproteins in predicting high cardiovascular risk and subclinical atherosclerosis in asymptomatic men.

OBJECTIVE: As main markers of atherogenic lipoproteins, apolipoprotein B (apoB), non-HDL cholesterol (non-HDLC), and LDL cholesterol (LDLC) do not seem equipotent to predict cardiovascular complications, we have compared simultaneously their capacity to predict high cardiovascular risk and subclinical atherosclerosis in a primary prevention population. METHODS: In 723 asymptomatic men, we measured apoB, non-HDLC, and LDLC, and we determined concomitantly coronary heart disease (CHD) risk equivalent defined by National Cholesterol Education Program guidelines, ultrasound-assessed extra-coronary plaques at multiple sites, and electron beam computed tomography-assessed high coronary calcium. RESULTS: Odds ratios (95% confidence interval) per standard deviation of apoB, non-HDLC, and LDLC of having: (i) CHD risk equivalent were 1.90 (1.53-2.37), 1.78 (1.43-2.21), 1.47 (1.19-1.81); (ii) extra-coronary plaques were 1.37 (1.16-1.61), 1.31 (1.11-1.56), 1.19 (1.01-1.39); (iii) high coronary calcium were 1.35 (1.09-1.68), 1.33 (1.07-1.64), 1.26 (1.01-1.39), respectively. Risk factors and treatment did not confound the above associations, except triglycerides for which adjustment weakened the risk predictions of lipids and annihilated lipids differences in predicting CHD risk equivalent and atherosclerosis markers. CONCLUSIONS: ApoB was the best predictor, non-HDLC the second best predictor, and LDLC the poorest predictor of high cardiovascular risk and subclinical extra-coronary and coronary atherosclerosis, and triglycerides participated to these differences.

Plasma cGMP and large artery remodeling in asymptomatic men.

cGMP regulates vascular smooth muscle tone and arterial wall response to proliferative signals. We determined plasma cGMP and carotid artery intima-media thickness (IMT) and diameter in 84 asymptomatic men submitted to investigation of their cardiovascular risk profiles. Plasma cGMP was positively associated with IMT (P<0.01) and diameter (P<0.05), independently of coexisting risk factors. These associations were reinforced in the subgroup of subjects with high-sensitivity C-reactive protein level or multiple atherosclerotic plaques. A positive relationship existed between diameter and IMT (P<0.01) and disappeared after cGMP adjustment. This suggests a link between cGMP pathway and arterial wall geometry that is revealed by vascular injury conditions and may participate in early large artery remodeling.

Large artery wall thickening and its determinants under antihypertensive treatment: the IMT-INSIGHT study.

BACKGROUND: Calcium antagonists retard progression of intima-media thickness (IMT), but whether this retardation covers heterogeneous individual patient responses of IMT change is unknown. METHODS: Hypertensive patients treated for 4 years with nifedipine (n = 115) or coamilozide (n = 127) underwent ultrasound measurements of carotid IMT at baseline, 4 months later, and then every year. RESULTS: A histogram of individual slopes of IMT change (least square regression of IMT to time) during treatment identified three categories of slopes according to the 20th and 80th percentiles of distribution: lower, intermediate and higher percentiles of IMT slope; the proportion of categories of IMT slope differed between treatments (P < 0.05), due to a more frequent lower slope percentile under nifedipine (27%) than under coamilozide (14%); within-group differences between IMT slope categories were: (i) increased baseline IMT associated with lower IMT slope percentile in nifedipine group (P < 0.001) and (ii) more frequent carotid plaque associated with higher IMT slope percentile in both treatment groups (P < 0.05). Analysis of overall patients showed that IMT slope was associated negatively with nifedipine treatment (P < 0.01) and baseline IMT (P < 0.001) and positively with carotid plaque (P < 0.01); the relationship between IMT slope and baseline IMT was negative under nifedipine and flat under coamilozide, and the presence of plaque reset both relationships towards a higher IMT slope; the between-treatment difference in IMT slope was different between tertiles of baseline IMT (P = 0.016). CONCLUSIONS: The differences in IMT slope between nifedipine and coamilozide increase with increasing baseline IMT.

[The vascular smooth muscle of great arteries: local control site of arterial buffering function?]. / El músculo liso vascular de las grandes arterias: ¿sitio de control local de la función de amortiguamiento arterial?

INTRODUCTION AND OBJECTIVES: To characterize the viscoelastic properties of the aorta and pulmonary arteries and the effects of vascular smooth muscle activation on arterial buffering function. MATERIAL AND METHOD: Aortic and pulmonary artery pressure and diameter were measured in six anesthetized sheep under baseline conditions, and during arterial hypertension induced by mechanical vascular occlusion (passive), and i.v. phenylephrine (active). Arterial wall elasticity and viscosity were calculated, and buffering function was characterized: a) locally as the viscosity/elasticity ratio, and b) globally for each circuit, as the time-constant of ventricular relaxation. RESULTS: Viscoelasticity was higher in the aorta than in the pulmonary artery (p < 0.05), however, parietal buffering function was similar in both. Global buffering function was highest in the systemic circuit (p < 0.05). During passive hypertension, elasticity was significantly increased with no change in viscosity; this led to a significant reduction in local buffering function, and in global buffering function in each circuit. During active hypertension, viscosity increased (p < 0.05), while local and global buffering functions returned to baseline values. CONCLUSIONS: The viscosity/elasticity ratio was higher in the aorta than in the pulmonary artery, and arterial wall buffering function was similar in both vessels. Systemic global buffering function was higher than pulmonary circuit buffering function. Elasticity depends on intravascular pressure, whereas viscosity is a marker of the degree of smooth muscle activation. Smooth muscle activation may benefit the cardiovascular system by maintaining local and global buffering functions.

El músculo liso vascular de las grandes arterias: ¿sitio de control local de la función de amortiguamiento arterial? / The vascular smooth muscle of great arteries: local control site of arterial buffering function?

Introducción y objetivos. Determinar la viscosidad y elasticidad de las arterias aorta y pulmonar y el efecto de la activación del músculo liso vascular sobre la capacidad de amortiguamiento arterial. Material y método. En 6 ovejas anestesiadas se midieron la presión y el diámetro aórtico y pulmonar, en condiciones basales y de hipertensión: a) pasiva, mediante la oclusión mecánica vascular, y b) activa, mediante fenilefrina intravenosa. Se calcularon la elasticidad y viscosidad parietal y se caracterizó la capacidad de amortiguamiento: a) la parietal, mediante el cociente viscosidad/elasticidad, y b) la global de cada circuito mediante la constante de tiempo de descenso de la presión arterial diastólica. Resultados. La viscoelasticidad aórtica fue mayor que la pulmonar (p < 0,05), mientras que ambas arterias tuvieron un amortiguamiento parietal similar. El circuito sistémico presentó un mayor amortiguamiento global (p < 0,05). Durante la hipertensión pasiva se produjo un aumento significativo de la elasticidad sin cambios en la viscosidad, lo que determinó una reducción significativa del amortiguamiento parietal, mientras que el amortiguamiento global de cada circuito disminuyó significativamente. En la hipertensión activa aumentó la viscosidad (p < 0,05), mientras que el amortiguamiento parietal y global recuperaron los valores basales. Conclusiones. La aorta presentó mayor viscoelasticidad que la arteria pulmonar, con un amortiguamiento parietal similar. El amortiguamiento global sistémico fue mayor que el pulmonar. Mientras que la elasticidad depende de la presión intravascular, la viscosidad es un marcador de la activación muscular. La activación muscular resultaría beneficiosa para el sistema cardiovascular, al mantener las funciones de amortiguamiento parietal y global (AU)

Posible rol del contenido iónico y pH plasmáticos sobre la electroafinidad endotelial / Possible role of plasmatic pH and ionic content on endothelial electroaffinity

La ateroscleroris es un proceso multifactorial de gran complejidad cuyo origen es aún desconnocido. Sin embargo, eventos característicos de su patogénesis dan evidencias de una disminuición de la densidad de carga eléctrica exnibida normalmente por el glicocáliz de los elementos parietales y sanguíneos implicados en este proceso. Las investigaciones más recientes indican que el espesor del glicocáliz endotelial es función no sólo de sus moléculas polianiónicas superficiales, sino tambíén de la composición del fluido sanguíneo. Teniendo en cuenta esta dependencia respecto de la composicón de la sangre, el objetivo de este trabajo fue investigar la influencia de la concentración electrolítica y del pH plasmáticos sobre las propiedades electrocinéticas en la interfase pared arterial - fluido sanguíneo. Para lograr esto se evaluó experimentalmente utilizando segmentos aórticos porcinos, el efecto electrocinético que ejerce sobre el endotelio arterial, el flujo de soluciones de contenido iónico y pH variables. Los resultados indicaron que el aumento del contenido iónico normal del plasma podría afectar las propriedades eléctricas de aquellos elementos, favoreciendo su acercamiento. Así también, el decremento del valor del pH fisiológico reduciría la proporción de molécular polianiónicas contenidas en el glicocáliz de dichos elementos, disminuyendo la repulsión electrostática entre ellos. De esta forma, el desarrollo aterogénico asociado con un aumento de la captación de componentes de la sangre, podría estar relacionado con una alteración de las propiedades electrocinéticas de los elementos parietales y sanguíneos involucrados, provocada por cambios de pH o concentración electrolítica plasmática