Functional and structural markers of atherosclerosis in human immunodeficiency virus-infected patients.

OBJECTIVES: We investigated functional and structural markers of atherosclerosis in human immunodeficiency virus (HIV)-infected patients in relation to the presence of the metabolic syndrome (MS). BACKGROUND: Antiretroviral combination therapy in HIV has been associated with cardiovascular risk factors that cluster in the MS. METHODS: Thirty-seven HIV-infected patients underwent assessment of flow-mediated vasodilation (FMD), aortic pulse-wave velocity (PWV), and carotid intima-media thickness (IMT). Age-matched type 2 diabetic patients (n = 13) and healthy controls (n = 14) served as reference groups. RESULTS: Fifteen HIV-infected patients (41%) fulfilled the National Cholesterol Education Program criteria of the MS. The FMD was similarly impaired in HIV-infected patients without the MS (MS- group) and the diabetic patients (5.1 +/- 0.4% and 4.9 +/- 0.6%, respectively) compared with controls (8.8 +/- 0.7%). The HIV-infected patients with the MS (MS+ group) had even more impaired FMD (2.5 +/- 0.3%). Carotid IMT was similarly increased in the MS+ group and the diabetic patients compared with the other groups. Aortic PWV was increased in the diabetic patients only. In HIV-infected patients, FMD was related to metabolic parameters, whereas aortic PWV and IMT were related to parameters of HIV infection, time on antiretroviral combination therapy, inflammatory (C-reactive protein and leukocytes) and metabolic parameters. CONCLUSIONS: The data of the present study suggest an increased cardiovascular risk in HIV-infected patients, even in the absence of clustering of metabolic risk variables. The presence of the MS in HIV is associated with even more advanced atherosclerotic changes. Presumably, both HIV infection and antiretroviral therapy may promote atherosclerosis through mechanisms involving endothelial cells, either directly or indirectly via metabolic risk factors.     

Atherosclerosis in HIV-positive patients

Worldwide, human immunodeficiency virus (HIV) infection is one of the main health subjects. Even, the human immunodeficiency virus primarily effects the immune system, HIV infection also has an impact on other organs. Cardiovascular manifestations in HIV-infected patients could occur by the HI-virus itself or by opportunistic infections. Reports of myocardial infarction in young HIV-infected patients, who received protease inhibitors, have raised concerns about premature arteriosclerosis and coronary artery disease in this population. In the pre-protease inhibitor era, autopsy reports were the first to describe an association between coronary artery disease and HIV infection. Long-term antiretroviral therapy, including protease inhibitors, significantly reduced mortality, morbidity and revolutionized the care of HIV-infected patients. However, class-specific metabolic side effects, such as elevated total cholesterol and triglyceride levels and insulin resistance, have been described. These metabolic alterations of antiretroviral therapy impair the cardiovascular risk profile of HIV-infected patients. Even epidemiological studies found no significant effect of antiretroviral treatment type on coronary heart disease or myocardial infarction, an increase of arteriosclerosis in HIV-infected patients is suspected. Recent results of autopsy studies and analyses of endothelial function in patients with HIV infection described an effect of HIV and antiretroviral therapy on premature arteriosclerosis. The present article gives an overview about arteriosclerosis and coronary events in HIV-infected patients and the impact of antiretroviral therapy.     

Relation between renal function within the normal range and central and peripheral arterial stiffness in hypertension

Chronic kidney disease is accompanied by increased large-artery stiffness, but the relation between glomerular filtration rate within the reference range and central or peripheral arterial stiffness has been understudied. The link between renal function and arterial stiffness was assessed in 305 patients with never-treated essential hypertension (men: 58%; age: 48+/-11 years, blood pressure: 151/95+/-20/11 mm Hg), free from overt cardiovascular disease and with serum creatinine values <1.4 mg/dL (men) and <1.2 mg/dL (women), who underwent noninvasive aortic and upper-limb pulse wave velocity (PWV) determination. Aortic PWV was strongly related to age (r=0.55; P<0.001), whereas upper-limb PWV had a weaker nonlinear relation with age (beta=1.392; P<0.001 for age; beta=-1.312; P<0.001 for age squared) and a weak relation with aortic PWV (r=0.22; P<0.001). Glomerular filtration rate (GFR), estimated according to the Mayo clinic equation for healthy subjects, was inversely correlated with large-artery stiffness, as assessed by aortic PWV (r=-0.34; P<0.001), and with peripheral artery stiffness, as assessed by upper-limb PWV (r=-0.25; P<0.001). In a multivariate linear regression, aortic PWV was independently predicted by age (beta=0.48; P<0.001), mean arterial pressure (beta=0.14; P=0.013), and GFR (beta=-0.13, P=0.029). Upper-limb PWV was predicted by GFR (beta=-0.24; P<0.001) and mean arterial pressure (beta=0.20; P<0.001). We conclude that, in hypertensive patients with normal renal function, an inverse relationship exists between GFR and stiffness of both central elastic and peripheral muscular arteries. These relations are in part independent from the effect of several confounders, including age, sex, and blood pressure values.     

Prognostic application of arterial stiffness: task forces

Epidemiologic and clinical studies have shown that increased pulse pressure is an independent cardiovascular risk factor in general population. Pulse pressure is determined by combined effects of cardiac factors (stroke volume) and the arterial stiffness. Arterial stiffness can be more directly evaluated by several measurements including the measure of pulse wave velocity (PWV). Aortic PWV, a marker of aortic stiffness, has been shown to be a strong independent predictor of cardiovascular and all cause mortality in patients with end-stage renal disease (ESRD) on hemodialysis as well as in patients with essential hypertension and older subjects over 80 years. Local arterial stiffness assessment, namely carotid distensibility was also shown to predict cardiovascular risk, both in ESRD patients and in renal transplant recipients. Furthermore, it has been shown in a therapeutic trial that the lack of aortic PWV attenuation despite significant drug-induced reduction in mean blood pressure was a significant predictor of cardiovascular death in subjects with ESRD. These results support the hypothesis that measurement of aortic PWV could then help, not only in risk assessment strategies, but also in risk reduction strategies by monitoring arterial stiffness under different pharmacologic regimens. The drug-related reduction of aortic PWV could then give prognostic information, additionally to blood pressure reduction. Aortic stiffness measurements could serve as an important tool in identifying ESRD patients at higher risk of cardiovascular disease. The ability to identify these patients would lead to better risk stratification and earlier and more cost-effective preventive therapy.     

Arterial stiffness and osteoporosis in chronic obstructive pulmonary disease

RATIONALE: Chronic obstructive pulmonary disease (COPD) is associated with an increased risk of cardiovascular events and osteoporosis. Increased arterial stiffness is an independent predictor of cardiovascular disease. OBJECTIVES: We tested the hypothesis that patients with COPD would have increased arterial stiffness, which would be associated with osteoporosis and systemic inflammation. METHODS: We studied 75 clinically stable patients with a range of severity of airway obstruction and 42 healthy smoker or ex-smoker control subjects, free of cardiovascular disease. All subjects underwent spirometry, measurement of aortic pulse wave velocity (PWV) and augmentation index, dual-energy X-ray absorptiometry, and blood sampling for inflammatory mediators. MEASUREMENTS AND MAIN RESULTS: Mean (SD) aortic PWV was greater in patients, 11.4 (2.7) m/s, than in control subjects, 8.95 (1.7) m/s, p < 0.0001. Inflammatory mediators and augmentation index were also greater in patients. Patients with osteoporosis at the hip had a greater aortic PWV, 13.1 (1.8) m/s, than those without, 11.2 (2.7) m/s, p < 0.05. In patients, aortic PWV was related to age (r = 0.63, p < 0.0001) and log(10) IL-6 (r = 0.31, p < 0.01), and inversely to FEV(1) (r = -0.34, p < 0.01). The strongest predictors of aortic PWV in all subjects were age (p < 0.0001), percent predicted FEV(1) (p < 0.05), mean arterial pressure (p < 0.05), and log(10) IL-6 (p < 0.05). CONCLUSIONS: Increased arterial stiffness was related to the severity of airflow obstruction and may be a factor in the excess risk for cardiovascular disease in COPD. The increased aortic PWV in patients with osteoporosis and the association with systemic inflammation suggest that age-related bone and vascular changes occur prematurely in COPD.     

Metabolic syndrome and age-related progression of aortic stiffness.

Aortic stiffness measured from pulse wave velocity (PWV) was studied during a six-year period in a population of subjects with zero to three and more cardiovascular (CV) factors involving hypertension, body mass index, dyslipidemia, hypertriglyceridemia, and hyperglycemia. During the follow-up, the increase in PWV was significantly higher in subjects with three and more CV risk factors (i.e., in subjects with metabolic syndrome) than in subjects with zero, one, or two factors, even after adjustments for confounding factors. Metabolic syndrome involves an increased progression of arterial stiffness with age and, thus, favors premature senescence. OBJECTIVES: The purpose of the study was to evaluate whether a clustering of metabolic risk factors might accelerate the progression of arterial stiffness with age in subjects with metabolic syndrome (MS). BACKGROUND: Arterial stiffness is increased in MS, but the genetic and environmental factors that might influence its progression are unknown. METHODS: Four hundred seventy-six subjects were classified at baseline according to their number of cardiovascular (CV) risk factors (from zero to three and more), after adjustment for smoking habits. The CV risk factors were: hypertension, body mass index, dyslipidemia, hypertriglyceridemia, and hyperglycemia, classified according to traditional criterions. Subjects were followed for six years and had, at the beginning and end of the survey, determinations of blood pressure (BP), heart rate (HR), and aortic pulse wave velocity (PWV). RESULTS: At baseline, BP, HR, plasma creatinine, and PWV were significantly higher (p < 0.001) in the group with three and more CV risk factors than in groups with zero to two risk factors. During the follow-up, the increase in PWV, but not in pulse pressure, was significantly higher (p < 0.01) in the group with three and more risk factors (i.e., metabolic syndrome) than in other groups. Results were unmodified after adjustments for age, gender, baseline values, drug treatment, smoking habits, and mean arterial pressure. CONCLUSIONS: Metabolic syndrome is associated with an increased progression of aortic stiffness with age, supporting premature senescence in these patients.     

Central artery pulse pressure in end-stage renal disease: the roles of aortic diameter, aortic stiffness and wave reflection

In elderly subjects and patients with end-stage renal disease (ESRD), carotid pulse pressure (PP) is an independent and significant predictor of cardiovascular (CV) risk. Whereas in the elderly carotid diameter, but not carotid stiffness, is an associated CV risk factor, an opposite CV risk pattern was observed in ESRD patients that was associated with stiffness. Whether in ESRD patients arterial diameter, stiffness or both are involved in the mechanism(s) of increased carotid PP has never been investigated. Nondiabetic ESRD patients (n = 144) were compared with 57 control subjects matched for age, sex and mean blood pressure, but with higher brachial and carotid PP. Noninvasive echo-Doppler techniques and pulse wave velocity (PWV) and pulse wave analysis were used to evaluate cardiac and carotid arterial structures and functions using multiple stepwise regressions. In controls, carotid PP was associated only with stroke volume, arterial wave reflections and aortic PWV, but not aortic diameter. In ESRD patients, it was associated with wave reflections, aortic PWV, stroke volume and higher aortic diameter. In ESRD patients and controls, elevated carotid PP mainly reflected increased aortic PWV and earlier wave reflections. Aortic diameter had an impact only on ESRD patients, where it compensated for enhanced aortic stiffness and the more pronounced effect of reflected waves. This hemodynamic profile differs consistently from that in elderly subjects of the general population and selectively influences CV risk and drug treatment.     

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.     

Increased pulse wave velocity and shortened pulse wave propagation time in young patients with rheumatoid arthritis

BACKGROUND: Rheumatoid arthritis (RA) is a systemic immune and inflammatory disease associated with excess cardiovascular morbidity and mortality. Pulse wave velocity (PWV) is an index of arterial stiffness and a marker of cardiovascular events. OBJECTIVE: To investigate arterial stiffness using carotid-femoral (aortic) PWV measurements in young patients with RA. PATIENTS AND METHODS: Eight patients (aged 21 to 34 years, seven women, mean RA duration 13.8+/-12.6 months) with RA according to the criteria of the American College of Rheumatology, and eight age- and sex-matched control subjects (aged 22 to 34 years, seven women) were recruited. Aortic PWV was determined using an automatic device, the Complior (Complior Colson, France), which allowed on-line pulse wave recording and automatic calculation of PWV. RESULTS: The carotid-femoral PWV, systolic blood pressure and heart rate were higher in young patients with RA than in sex- and age-matched control subjects (P=0.03, P=0.02 and P=0.002, respectively). In the young patients with RA, pulse wave propagation time between measurement sites was significantly shorter than in the control group (P=0.02). There were no significant differences in the sex, age, body mass index, waist to hip ratio, diastolic blood pressure, mean blood pressure or pulse pressure between the two groups (P=1.00, P=0.71, P=0.20, P=0.66, P=0.55, P=0.07 and P=0.11, respectively). CONCLUSION: The carotid-femoral PWV is increased and pulse wave propagation time is decreased in young patients with RA. Measurements of carotid-femoral PWV may provide a simple and noninvasive technique for identifying patients at increased risk of vascular disease.     

Arterial stiffness and cardiovascular risk factors in a population-based study

OBJECTIVE: To determine the relationships between pulse wave velocity (PWV), an estimate of arterial distensibility and cardiovascular risk factors. DESIGN: This cross-sectional population-based study was carried out from 1995 to 1997 to investigate these relationships. POPULATION AND METHODS: Some 993 subjects, aged 35-64 years (52.7% men), living in the south-west of France, were randomly selected from electoral rolls and participated in a cross-sectional study. Medical examinations were performed by specially trained medical staff. Carotid-femoral PWV was measured using a semiautomatic device (Complior, Garges les Gonesse, France). The relationships between PWV and risk factors were assessed, first in subjects not treated with hypolipidaemic, antidiabetic and antihypertensive drugs and then in treated subjects. In subjects not treated for cardiovascular risk factors, age, gender, systolic blood pressure (SBP) and heart rate (P< 0.001) were the variables significantly associated with PWV. In treated patients, age (P < 0.01), SBP (P < 0.001), heart rate (P < 0.001), apolipoprotein B (P< 0.05) and the number of treated cardiovascular risk factors (P< 0.05) were positively correlated with PWV. CONCLUSION: This study shows that, in a sample of subjects at high risk, the cumulative influence of risk factors, even treated, is an independent determinant of arterial stiffness. These results suggest that PWV may be used as a relevant tool to assess the influence of cardiovascular risk factors on aortic stiffness in high-risk patients.     

Pulse wave velocity is increased in patients with transient myocardial ischemia

OBJECTIVE: We have recently shown that mean pulse pressure is higher in patients with transient myocardial ischemia. Pulse pressure elevation might be an important consequence of increased arterial stiffness. The aim of this study was to prove if arterial stiffness is changed in patients with transient myocardial ischemia who bear a high cardiovascular risk. Additionally we investigated whether arterial stiffness or wave reflection is the best indicator for transient myocardial ischemia. Aortic pulse wave velocity (PWV) is a measure of arterial stiffness, and augmentation index (AIx) an indication of arterial wave reflection. Both are indicators for cardiovascular risk. METHODS: PWV (carotid-femoral) and AIx (SphygmoCor) were assessed in 74 hypertensive patients. Transient myocardial ischemia was detected using an ST-triggered 24-h ambulatory blood pressure monitoring device. RESULTS: ST-segment depressions were recorded in 30 of 74 patients. There were no significant differences with regard to age, mean arterial pressure, systolic blood pressure, diastolic blood pressure or heart rate. PWV was seen to be higher in patients with transient myocardial ischemia (10.6 versus 9.5 m/s, P = 0.036). There was no significant difference in AIx between the two groups. PWV (r = 0.36, P = 0.002) but not AIx correlated with pulse pressure. CONCLUSIONS: PWV is higher in hypertensive individuals (age > 60 years) with transient myocardial ischemia, suggesting that PWV is an indicator of increased cardiovascular risk. Although AIx is known to be associated with several cardiovascular diseases, it was not seen to be associated with silent myocardial ischemia. Our results suggest that the clinical significance of parameters of arterial stiffness and arterial wave reflection change with age, with a higher clinical importance of PWV indicated in patients over the age of 60.     

Validity of pulse pressure and augmentation index as surrogate measures of arterial stiffness during beta-adrenergic stimulation

OBJECTIVE: Increased arterial stiffness is a determinant of cardiovascular mortality. Pulse wave velocity (PWV) is a direct measure of arterial stiffness. Aortic augmentation index (AI) and pulse pressure (PP) are surrogate measures of arterial stiffness. Both PWV, AI and PP increase with cardiovascular risk factors. The aim of this study was to test the validity of AI and PP as surrogate measures of arterial stiffness compared with PWV, during beta-adrenergic stimulation with Isoprenaline (Iso). DESIGN AND METHODS: A total of 41 healthy volunteers entered a randomized, double-blind, placebo-controlled, cross-over study. In random order, subjects were given intravenous infusion in equal volume of Iso 8 microg/kg per min (dissolved in glucose 5%) and placebo (glucose 5%). A wash-out period of 25 min was observed between the infusions. Measurements included blood pressure (BP), heart rate (HR), PWV, and AI. PWV were determined using complior (Complior, Artech-Medical, Paris, France). AI and aortic PP were obtained from pulse wave analysis of radial applanation tonometry, using transfer function (SphygmoCor Windows software). RESULTS: Baseline AI increased (P < 0.05) with aging, a lower height and a larger diastolic BP (DBP). Iso increased (P < 0.0001) HR, brachial SBP, brachial and aortic PP as compared with placebo. In contrast, Iso decreased (P < 0.05) AI, brachial DBP, peripheral PWV, but not aortic PWV. Decrease of AI induced by Iso was not related to PWV. In stepwise multiple regression changes in HR, brachial SBP and DBP were independent determinants of AI response to Iso (r = 0.78, P < 0.0001). CONCLUSIONS: Our findings show that AI and PP fail as surrogate measures of arterial stiffness during beta-adrenergic stimulation.     

Gestational age and birth weight in relation to aortic stiffness in healthy young adults: two separate mechanisms?

BACKGROUND: Impaired vascular development due to intrauterine growth retardation and postnatal-induced vascular damage by an unfavorable cardiovascular risk profile may both cause stiffer arteries in later decades. METHODS: Of 524 young adults, participating in the Atherosclerosis Risk in Young Adults (ARYA) study, data on birth characteristics were obtained from the original medical records of the Municipal Health Service and the extent of aortic stiffness was assessed using carotid-femoral pulse wave velocity (PWV). RESULTS: The PWV showed an inverse trend with gestational age (linear regression coefficient (beta) = -0.07 m/sec per 1 week; P =.064) whereas it was positively related to birth weight (beta = 0.33 m/sec per 1 kg; P =.020), adjusted for blood pressure (BP), gender, age, and each other. After exclusion of the 26 prematurely born infants, the association with gestational age was attenuated (beta = -0.03 m/sec per 1 week; P =.582), whereas the relation with birth weight hardly changed (beta = 0.30 m/sec per 1 kg; P =.041). In an analysis in which we excluded the 26 subjects with diabetic mothers the birth weight-PWV relation was attenuated (beta = 0.21 m/sec per 1 kg; P =.169). CONCLUSIONS: Our findings suggest that prematurity drives the relation of gestational age and PWV, whereas risk of impaired glucose tolerance drives the relation of birth weight and PWV. We hypothesized that two separate mechanisms might be involved in the development of arterial stiffness in healthy young adults.     

Isolated systolic hypertension is characterized by increased aortic stiffness and endothelial dysfunction

Isolated systolic hypertension is associated with increased cardiovascular risk. It is thought to result from large artery stiffening, which is determined by structural components within the vasculature but also by functional factors including NO and endothelin-1. We hypothesized that endothelial dysfunction would account for increased arterial stiffness in patients with isolated systolic hypertension. The aim of this study was to investigate the relationship between endothelial function and arterial stiffness in these patients along with control subjects. We studied 113 subjects: 35 patients with isolated systolic hypertension (mean age+/-SD: 68+/-6 years), 30 age-matched control subjects (65+/-5 years), and 48 young control subjects (37+/-9 years). Aortic pulse wave velocity (PWV) was derived by sequential carotid/femoral waveform recordings. Conduit artery endothelial function was determined by flow-mediated dilatation. Aortic PWV was higher (9.65+/-2.56 m/s versus 8.26+/-0.85 m/s; P=0.009), and flow-mediated dilatation was lower (2.67+/-1.64% versus 4.79+/-3.1%; P=0.03) in patients with isolated systolic hypertension compared with age-matched control subjects. Similarly, aortic PWV was also higher, and flow-mediated dilatation lower, in older versus young control subjects (8.26+/-0.85 m/s versus 7.09+/-1.01 m/s and 4.79+/-3.1% versus 6.94+/-2.7%; P=0.004 for both). Overall, aortic PWV correlated inversely with flow-mediated dilatation (r=-0.3; P=0.001), which remained significant after adjustment for confounding factors (P=0.01). Patients with isolated systolic hypertension have higher aortic PWV and decreased endothelial function compared with age-matched control subjects. Our results suggest that endothelial function contributes significantly to increased arterial stiffness in patients with isolated systolic hypertension and with age.     

Diabetes mellitus and renal failure: effects on large artery stiffness

Diabetes mellitus and end-stage renal disease are two pathologic entities associated with increased cardiovascular risk. Several studies have shown that arterial stiffness is increased in both cases and contributes to the increased risk. In order to determine the effect of diabetes and renal failure on arterial stiffness, we conducted a case-control study. One hundred and twenty-two diabetic patients were compared to 122 non-diabetic patients matched to the study group for sex, age, mean arterial pressure, number and localisation of the atherosclerotic alterations. Arterial stiffness was assessed by automatic measurement of the aortic pulse wave velocity (PWV) and by measuring the peripheral and carotid pulse pressure (PP) and reflected waves through analysis of the pulse wave using the principle of applanation tonometry. Aortic PWV was significantly higher in the diabetic subgroup as well as PP at the peripheral and central levels for the same age and mean arterial pressure. In addition, renal failure was independently associated with an increased aortic PWV but not PP in the general population. Independent of the degree of renal failure, a fall in the glomerular filtration rate was also associated with increased aortic PWV. No interaction was noted between renal failure and diabetes mellitus. In conclusion, this study shows that diabetic patients have higher arterial stiffness compared to non-diabetic ones having one or more cardiovascular risk factors, manifested by increased aortic PWV and PP. In addition, renal failure, irrespective of its degree and independent of diabetes mellitus, is associated with increased aortic PWV but not PP.     

Diastolic blood pressure is an important determinant of augmentation index and pulse wave velocity in young,healthy males

Pulse wave velocity (PWV) and augmentation index are widely used measures of arterial stiffness. The purpose of this study was to evaluate the role of blood pressure as a determinant of both indices independent of potentially confounding factors including gender, age and cardiovascular disorders. A total of 77 young, healthy subjects were investigated under resting conditions. Augmentation index was derived by pulse wave analysis using carotid applanation tonometry. PWV was determined from pressure tracing over the carotid and femoral artery. The relations between stiffness markers and haemodynamic parameters were analysed by simple (r) and multiple (beta) regression analysis. Using simple regression analysis, augmentation index was correlated to age (r=0.292, P=0.0105), diastolic blood pressure (DBP, r=0.483, P<0.0001), mean arterial blood pressure (MAP, r=0.381, P=0.0007), pulse pressure (r=-0.414, P=0.0002) and total peripheral resistance (r=0.266, P=0.0204). After multiple regression analysis, augmentation index remained significantly correlated only to DBP (beta=0.347, P=0.0051). Using simple regression analysis, PWV was correlated to age (r=0.304, P=0.0067), systolic blood pressure (r=0.280, P=0.0129). DBP (r=0.455, P<0.0001), MAP (r=0.446, P&<0.0001) and heart rate (r=0.348, P=0.0018). After multiple regression analysis, PWV remained correlated only to age (beta=0.218, P=0.0422) and DBP (beta=0.4105, P=0.0316). In summary, DBP is an important determinant of augmentation index and PWV in young, healthy males. Further studies are needed to characterize the impact of blood pressure on arterial stiffness in other populations including females and older subjects.     

Augmentation index and central aortic stiffness in middle-aged to elderly individuals

BACKGROUND: Increased aortic stiffness contributes to systolic hypertension and increased cardiovascular risk. The augmentation index (AI), ie, the percentage of central pulse pressure attributed to reflected wave overlap in systole, was proposed as a noninvasive indicator of increased arterial stiffness. We evaluated this hypothesis by investigating relations between AI and other direct measures of aortic stiffness. METHODS: Tonometric carotid- and femoral-pressure waveforms, Doppler aortic flow, and aortic-root diameter were assessed in 123 individuals with uncomplicated systolic hypertension and 29 controls of comparable age and sex. Carotid-femoral pulse-wave velocity (PWV) was assessed from the carotid-femoral time delay and body-surface measurements. Aortic PWV was assessed from the ratio of the upstroke of carotid pressure and aortic flow velocity and was used to calculate proximal aortic compliance as [aortic area]/[1.06 x (aortic PWV)(2)]. RESULTS: Partial correlations (adjusted for age, sex, presence of hypertension, height, weight, and systolic ejection period) showed no association between AI and carotid-femoral PWV (R = -0.05, P = .54). The AI was significantly though weakly related directly with aortic compliance (R = 0.21, P = .012) and inversely with aortic PWV (R = -0.198, P = .017). However, higher stiffness (lower compliance and higher PWV) was associated with lower AI. CONCLUSIONS: Increased AI is not a reliable surrogate for increased aortic stiffness. Decreasing AI with decreasing compliance (increasing aortic stiffness) may be attributable to impedance matching and reduced wave reflection at the interface between the aorta and the muscular arteries.     

Takayasu's arteritis: a cause of prolonged arterial stiffness

OBJECTIVES: Cardiovascular disease is a major cause of mortality and morbidity in patients with Takayasu's arteritis (TA). Increased arterial stiffness is an independent risk factor and predictor of cardiovascular mortality in a variety of diseases. Pulse wave velocity (PWV) and the augmentation index (AI) are used as clinical measurements of arterial stiffness. METHODS: Data are presented from 10 patients with TA and 11 normal controls obtained between 2000 and 2004. Arterial compliance was assessed non-invasively by measurement of PWV, using the Complior system, and calculation of the aortic AI. RESULTS: TA patients (mean age 40.8+/-13.2 yr) were compared with a control group of healthy women from a parallel study (mean age 32.3+/-5.5 yr). The mean carotid-femoral PWV (PWV-CF) was higher in TA patients (P = 0.03). In addition, both aortic AI derived from the radial artery (P = 0.002) and carotid AI (P = 0.03) were higher in TA patients compared with controls. PWV-CF did not correlate with CRP (r = - 0.23, P = 0.23) or ESR (r = - 0.19, P = 0.27). Similar results were obtained for the correlation of carotid-radial PWV with CRP (r = 0.15, P = 0.32) and ESR (r = 0.33, P = 0.14). CONCLUSIONS: Our data show that TA is associated with elevated arterial stiffness in the central aorta, which may persist when the disease is quiescent. These data suggest that PWV represents a means by which cardiovascular risk can be detected and monitored in TA, and highlights the importance of effective management of cardiovascular risk factors in these patients.     

Mortality and morbidity in HIV-infected patients undergoing coronary artery bypass surgery: a case control study

The use of highly active antiretroviral therapy (HAART) in patients with HIV infection has improved survival. This improvement combined with the metabolic effects of treatment has increased cardiovascular risk and the need for cardiac surgery in these patients. We compared morbidity and mortality in HIV-infected patients (cases, n=7) and non-HIV-infected patients (controls, n=21) who underwent isolated coronary artery surgery between 1997 and 2004. The durations of extracorporeal circulation and aortic cross-clamping were shorter in HIV-infected patients (P=.002 and P=.014, respectively). The percentage of patients who experienced complications was similar, at 57.1% in both groups, but there was a slightly higher number of complications per patient in non-HIV-infected individuals. The mean length of total hospitalization was greater in HIV-infected patients (27.1 [13.3] versus 8.8 [5.3] days; P=.003), as was that of postoperative hospitalization (18.2 [15.4] vs 7.9 [4.2] days; P=.08). No HIV-infected patient died or needed a repeat cardiac operation. No progression of the HIV infection was observed. Isolated coronary artery surgery in HIV-infected patients produces good results, and there is no increase in morbidity or mortality. Extracorporeal circulation did not influence disease progression.     

Metabolic syndrome and arterial stiffness: the Health 2000 Survey

Metabolic syndrome and its components have been associated with arterial stiffness and cardiovascular disease. The objective of this study was to examine the independent influences of metabolic syndrome, its components, and other cardiovascular risk factors on arterial stiffness as well as to compare 2 definitions for metabolic syndrome (National Cholesterol Education Program [NCEP] and International Diabetes Federation [IDF]) in their ability to identify subjects with arterial stiffness. The study population consisted of 401 Finnish men and women aged 45 years and older who participated in a substudy of the Finnish population-based Health 2000 Survey. Pulse wave velocity (PWV) measured by whole-body impedance cardiography was used as a marker of elevated arterial stiffness. In multivariate models, systolic blood pressure, age, waist circumference, and fasting blood glucose (P ≤ .001 for all) were independent determinants for PWV. In the models including metabolic syndrome instead of its components, the NCEP and IDF definitions were similarly associated with PWV (P ≤ .01 for both), the other independent determinants being age, sex (P < .001 for both) and plasma C-reactive protein concentration (P = .016 and P = .005 in models containing the NCEP and IDF definitions, respectively). Systolic blood pressure, age, waist circumference, and fasting blood glucose level were independently associated with increased arterial stiffness. Metabolic syndrome determined increased arterial stiffness independently of other known cardiovascular risk factors. The NCEP and IDF definitions did not differ in their ability to identify subjects with increased arterial stiffness.