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Alain P Guerin

Publications and source records attributed to Alain P Guerin.

12 recordsLinked to original sources
PubMed2004

Arterial stiffness and function in end-stage renal disease.

Cardiovascular disease is a major cause of mortality in patients with end-stage renal disease, with damage to arteries as a major contributing factor. Arterial stiffness is a factor associated with high systolic and pulse pressure in these patients and is a strong independent factor associated with morbidity and mortality. Arterial stiffness is one of the principal factors opposing left ventricular ejection. The appropriate term to define the arterial factor(s) opposing left ventricular ejection is aortic input impedance. Aortic input impedance depends on TPR, arterial distensibility, and wave reflections. Distensibility defines the capacitive properties of arterial stiffness, whose role it is to dampen pressure and flow oscillations and to transform pulsatile flow and pressure in arteries into a steady flow and pressure in peripheral tissues. Stiffness is the reciprocal value of distensibility. These parameters are blood pressure dependent; arteries become stiffer at high pressure. While distensibility provides information about the elasticity of the artery as a hollow structure, the elastic incremental modulus characterizes the properties of the arterial wall biomaterials independent of vessel geometry. Alternatively, arterial distensibility can be evaluated by measuring pulse wave velocity, which increases with the stiffening of arteries. Arterial stiffening increases left ventricular afterload and alters the coronary perfusion. With increased pulse wave velocity, the wave reflections affects the aorta during systole, which increases systolic pressures and myocardial oxygen consumption and decreases diastolic blood pressure and coronary flow. The arterial stiffness is altered primarily in association with increased collagen content and alterations of extracellular matrix and calcification of the arterial wall. The arterial stiffening estimated by changes in aortic pulse wave velocity and intensity of wave reflections are independent predictors of survival in end-stage renal disease and in the general population. Improvement of arterial stiffening could be obtained by antihypertensive treatments as observed with calcium-channel blockers and angiotensin-converting enzyme inhibitors. Angiotensin-converting enzymes inhibitors increase AC and reduce wave reflections. It has been shown that reversibility of aortic stiffening and use of angiotensin-converting enzyme inhibitors had a favorable independent effect on survival in hypertensive patients with advanced renal disease.

Aorta↗
PubMed2004

Arterial calcifications and bone histomorphometry in end-stage renal disease.

Arterial calcification (AC) is a common complication of end-stage renal disease (ESRD). The mechanisms responsible are complex, including disturbances of mineral metabolism and active expression of various mineral-regulating proteins. An inverse relationship between AC and bone density has been documented in uremic patients. In the study presented here, which included 58 patients with ESRD on hemodialysis (HD), bone-histomorphometry characteristics were compared with the AC scores (0 to 4) determined according to the number of arterial sites with calcifications. Patients with AC scores of 0 (no calcifications), or 1 or 2 (mild calcifications) had similar serum parathyroid hormone levels and bone histomorphometry, with larger osteoclast resorption, higher osteoclast numbers, and larger osteoblastic and double tertracycline-labeled surfaces. In contrast, patients with high AC scores (3 and 4) were characterized by lower serum parathyroid hormone, low osteoclast numbers and osteoblastic surfaces, smaller or absent double tetracycline-labeled surfaces, and high percentages of aluminum-stained surfaces. According to multivariate analysis, AC score was positively associated with age (P < 0.0001), daily dose of calcium-containing phosphate binders (P = 0.009), and bone aluminum-stained surfaces (P = 0.037), and an inverse correlation was observed with osteoblastic surfaces (P = 0.001). A high AC score is associated with bone histomorphometry suggestive of low bone activity and adynamic bone disease. These findings suggest that therapeutic interventions associated with excessive lowering of parathyroid activity (parathyroidectomy, excessive calcium or aluminum load) favor lower bone turnover and adynamic bone disease, which could influence the development and progression of AC.

Aluminum↗
PubMed2004

Forearm reactive hyperemia and mortality in end-stage renal disease.

BACKGROUND: Reports on the general population indicated that decreased endothelial-mediated vasodilation has a prognostic impact on cardiovascular (CV) morbidity and mortality. Flow-dependent vasodilation of conduit arteries and ischemia-induced forearm reactive hyperemia are impaired in end-stage renal disease (ESRD). Whether deterioration of vasodilator function in ESRD patients has a prognostic impact has not been documented. The aim of this study was to determine whether the impaired forearm postischemic vasodilation is an independent predictor of mortality in ESRD patients, independently from CV end-organ damages, which are usually associated with decreased vasodilatory response. METHODS: Common carotid artery intima-media thickness (CCA-IMT), aortic stiffness (pulse wave velocity-PWV), and LV mass (LVM) were determined for 78 stable ESRD patients on hemodialysis. Forearm postischemic vasodilation [flow debt repayment (FDR)] was measured by venous plethysmography. All-cause mortality served as the outcome variable over a median follow-up of 60 +/- 27 months. RESULTS: Twenty-four deaths occurred (16 of CV origin). According to Cox regression adjusted for age, CCA-IMT, LVM, and PWV, all-cause mortality was independently associated with decreased FDR (RR 0.69 for every 10% increase; 95% CI 0.56-0.85; P= 0.0006) and increased aortic PWV (RR 1.16 for 1 m/s increase; 95% CI 1.04-1.29; P= 0.0091). CONCLUSION: Our data indicate that lower postischemic forearm reactive hyperemia is associated with all-cause mortality of ESRD patients, independently of the presence of end-organ damage such as LVH or arteriosclerosis.

Adolescent↗
PubMed2003

Aortic pulse wave velocity index and mortality in end-stage renal disease.

BACKGROUND: Aortic pulse wave velocity (PWV) is a strong independent predictor of overall and cardiovascular mortality in patients with end-stage renal disease (ESRD). Nevertheless, because age, blood pressure, heart rate, and gender are strong determinants of both arterial stiffness and mortality, the individual relevance of PWV measurements remains controversial. METHODS: A cohort of 242 patients with ESRD undergoing hemodialysis was studied for a mean (+/- SD) duration of 78 +/- 46 months. At entry, together with standard clinical and biochemical analyses, PWV was measured using Doppler ultrasonography. On the basis of a nomogram established on 469 nonuremic subjects, a theoretical value of PWV was determined in ESRD patients according to their age, blood pressure, gender, and heart period. The PWV index (measured PWV - theoretical PWV) was then calculated for each individual ESRD patient. RESULTS: Based on Cox analysis, the PWV index, but neither pulse pressure nor cardiac mass, was a strong and independent predictor of both cardiovascular and overall mortality, together with age and time on dialysis before inclusion. Patients with positive (versus negative) PWV index had a twofold adjusted risk of mortality during the follow-up. Per each 1 meter/second PWV index increment, we observed a 34% (crude) and a 14% (adjusted) increase in both cardiovascular and overall mortality (P < 0.02 for all). CONCLUSION: In ESRD patients, the calculation of a PWV index provides information about cardiovascular and overall mortality risk with high predictive power, showing that PWV measurements provide discriminatory prognostic power over and above conventional cardiovascular risk factors.

Adult↗
PubMed2003

Inflammation, arteriosclerosis, and cardiovascular therapy in hemodialysis patients.

BACKGROUND: Aortic stiffness and left ventricular hypertrophy (LVH) are predictors of mortality in hemodialysis (HD) patients. Attenuation of arterial stiffness and regression of LVH had a favorable effect on survival in these patients, but this favorable effect was observed in less than 50% of patients, the rest being resistant to therapeutical interventions. The aim of this study was to analyze the factors associated with this resistance to treatment. METHODS: 138 patients on HD were studied during a follow-up survey. From entry until the end of follow up, the changes of aortic pulse wave velocity (PWV) and of LV mass were measured in response to treatment with antihypertensive drugs and erythropoietin, together with measurements of blood chemistry, including high-sensitive C-reactive protein (CRP). Patients with decreased aortic PWV were considered to be responders (N = 68), the others to be nonresponders (N = 70). RESULTS: Nonresponders were older (P < 0.05) and had persistently higher systolic blood pressure (BP) and pulse pressure. Responders were treated more frequently with an ACE inhibitor (P < 0.001), and had lower serum CRP (P < 0.01). The baseline PWV, as well as the changes of PWV and LV mass during the follow-up were significantly and independently correlated with serum CRP level (P < 0.001). According to logistic regression after adjustment for age, gender, diabetes, history of CVD, and the nonspecific cardiovascular risk factors, the improvement of aortic stiffness and LV hypertrophy was positively associated with prescription of ACE inhibitor (P < 0.0001), and negatively with the serum CRP level (P < 0.01). CONCLUSION: These results indicate that in HD patients, the presence of low-grade inflammation decreases the efficiency of cardiovascular therapeutic interventions and participates in the persistence of cardiovascular hemodynamic overload.

Adult↗
PubMed2002

Iron therapy, advanced oxidation protein products, and carotid artery intima-media thickness in end-stage renal disease.

BACKGROUND: Increased common carotid artery intima-media thickness (CCA-IMT) is a marker of early atherosclerosis. Low-grade inflammation is associated with the pathogenesis of atherosclerosis. Low-grade inflammation and increased CCA-IMT are observed in end-stage renal disease (ESRD). Oxidative stress is involved in uremia-related inflammation. Advanced oxidation protein products (AOPP) are markers of oxidant-mediated protein damage in ESRD. Intravenous iron given to patients on hemodialysis (HD) might induce oxidative stress. We investigated the relationships between AOPP, iron therapy, and CCA-IMT in stable HD patients. METHODS AND RESULTS: Plasma AOPP and blood chemistry, including iron status, were analyzed in a cohort of 79 ESRD patients on HD. Measurements of CCA-IMT and CCA diameter, as assessed by B-mode ultrasonography, were obtained in 60 patients. AOPP levels were elevated in ESRD patients, and in univariate (r=0.42, P<0.0001) and multivariate analyses (r=0.38, P<0.001), they correlated with serum ferritin and with the intravenous iron dose received during the 12 months preceding the study (ferritin, P<0001; AOPP, P<0.01). Univariate and multivariate analyses identified the AOPP concentration as being significantly associated with CCA-IMT (P=0.0197) and CCA wall-to-lumen ratio (r=0.560, P<0.0001). Independently of AOPP concentration, cumulative iron dose was positively related to CCA-IMT (P=0.015) in patients <60 years. CONCLUSION: In ESRD patients, CCA-IMT and CCA wall-to-lumen ratio were associated with plasma AOPP, serum ferritin, and the annual intravenous iron dose administered. These findings support the concept of a role of oxidative stress in the early atherosclerosis of ESRD patients, which may be increased by the usually recommended doses of intravenous iron.

Biomarkers↗
PubMed2002

Central pulse pressure and mortality in end-stage renal disease.

Damage of large arteries is a major factor in the high cardiovascular morbidity and mortality of patients with end-stage renal disease (ESRD). Increased aortic pulse wave velocity (PWV) and brachial pulse pressure (PP) are the principal arterial markers of cardiovascular mortality described in these patients. Whether central (carotid) PP and brachial-carotid PP amplification may predict all-cause (including cardiovascular) mortality has never been investigated. A cohort of 180 patients with ESRD who were undergoing hemodialysis was studied between January 1990 and March 2000. The mean duration of follow-up was 52+/-36 months (mean+/-SD). Mean age at entry was 51.5+/-16.3 years. Seventy deaths occurred, including both cardiovascular and noncardiovascular fatal events. At entry, patients underwent carotid PP measurements (pulse wave analysis), echocardiography, and aortic PWV (Doppler ultrasonography), together with standard clinical and biochemical analyses. On the basis of Cox analyses, after adjustment of age, time on dialysis before inclusion, and previous cardiovascular events, 3 factors emerged as predictors of all-cause mortality: carotid PP, brachial/carotid PP, and aortic PWV. Adjusted hazard ratios for 1-SD increments were 1.4 (1.1 to 1.8) for carotid PP, 0.5 (0.3 to 0.8) for brachial/carotid PP, and 1.3 (1.0 to 1.7) for PWV. Brachial blood pressure, including PP, had no predictive value for mortality after adjustment. These results provide the first direct evidence that in patients with ESRD, the carotid PP level and, mostly, the disappearance of PP amplification are strong independent predictors of all-cause (including cardiovascular) mortality.

Adolescent↗
PubMed2002

Prognostic significance of arterial stiffness measurements in end-stage renal disease patients.

PURPOSE OF REVIEW: As epidemiological and clinical studies have shown that damage of large arteries is a major contributory factor to the high cardiovascular morbidity of patients with end-stage renal disease, such a population is particularly appropriate for analysis the impact of arterial stiffness on cardiovascular risk assessment and reduction strategies. RECENT FINDINGS: Aortic pulse wave velocity, 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 on hemodialysis. Local arterial stiffness assessment, namely carotid distensibility was also shown to predict cardiovascular risk, both in end-stage renal disease patients and in renal transplant recipients. Furthermore, it was shown in a therapeutic trial that the lack of aortic pulse wave velocity attenuation, despite significant drug-induced reduction in mean blood pressure, was a significant predictor of cardiovascular death in subjects with end-stage renal disease. These results support the hypothesis that measurement of aortic pulse wave velocity could help, not only in risk assessment strategies, but also in risk reduction strategies by monitoring arterial stiffness under different pharmacological regimens. The drug-related reduction of aortic pulse wave velocity could then give prognostic information, in addition to blood pressure reduction. SUMMARY: Aortic stiffness measurements could serve as an important tool in identifying end-stage renal disease 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.

Algorithms↗
PubMed2001

Alterations of left ventricular hypertrophy in and survival of patients receiving hemodialysis: follow-up of an interventional study.

Left ventricular (LV) hypertrophy (LVH) is a risk factor for mortality in patients with end-stage renal disease (ESRD). Whether the attenuation of LVH has a positive effect on survival of patients with ESRD has not been documented. The aim of this study was to determine the effect of parallel treatment of hypertension and anemia on LV mass (LVM) and to determine the effect of LVM changes on survival. A cohort of 153 patients receiving hemodialysis was studied. The duration of follow-up was 54 +/- 37 mo. All patients had echocardiographic determination of LV dimensions and LVM at baseline and regular intervals until the end of the follow-up period. During the study, BP decreased from (mean +/- SD) 169.4 +/- 29.7/90.2 +/- 15.6 to 146.7 +/- 29/78 +/- 14.1 mmHg (P < 0.001), and hemoglobin increased from 8.65 +/- 1.65 to 10.5 +/- 1.45 g/dl (P < 0.001). The LV end-diastolic diameter and mean wall thickness decreased from 56.6 +/- 6.5 to 54.8 +/- 6.5 mm (P < 0.001), and from 10.4 +/- 1.6 to 10.2 +/- 1.6 mm (P < 0.05), respectively. The LVM decreased from 290 +/- 80 to 264 +/- 86 g (P < 0.01). Fifty-eight deaths occurred, 38 attributed to cardiovascular (CV) disease and 20 attributed to non-CV causes. According to Cox analyses after adjustment for age, gender, diabetes, history of CV disease, and all nonspecific CV risk factors, LVM regression positively affected the survival. The hazard risk ratio associated with a 10% LVM decrease was 0.78 (95% confidence interval, 0.63 to 0.92) for all-causes mortality and 0.72 (95% confidence interval, 0.51 to 0.90) for mortality due to CV disease. These results show that a partial LVH regression in patients with ESRD had a favorable and independent effect on patients' all-cause and CV survival.

Adult↗
PubMedDate not supplied

Arterial stiffness: pathophysiology and clinical impact.

The ill effects of hypertension are usually attributed to a reduction in the caliber or the number of arterioles, resulting in an increase in total peripheral resistance (TPR). This definition does not take into account the fact that BP is a cyclic phenomenon with systolic and diastolic BP being the limits of these oscillations. The appropriate term to define the arterial factor(s) opposing LV ejection is aortic input impedance which depends on TPR, arterial distensibility (D), and wave reflections (WR). D defines the capacitive properties of arterial stiffness, whose role is to dampen pressure and flow oscillations and to transform pulsatile flow and pressure in arteries into a steady flow and pressure in peripheral tissues. Stiffness is the reciprocal value of D. These parameters are BP dependent, and arteries become stiffer at high pressure. In to D which provides information about the < > of artery as a hollow structure, the elastic incremental modulus (Einc) characterizes the properties of the arterial wall biomaterials, independently of vessel geometry. As an alternative, arterial D can be evaluated by measuring the pulse wave velocity (PWV) which increases with the stiffening of arteries. Arterial stiffening increases left ventricular (LV) afterload and alters the coronary perfusion. With increased PWV, the WR impacts on the aorta during systole, increasing systolic pressures and myocardial oxygen consumption, and decreasing diastolic BP and coronary flow. The arterial stiffness is altered primarily in association with increased collagen content and alterations of extracellular matrix (arteriosclerosis) as classically observed during aging or in arterial hypertension. The arterial stiffening estimated by changes in aortic PWV and intensity of WR are independent predictors of survival in end stage renal disease (ESRD) and general population. Improvement of arterial stiffening could be obtained by antihypertensive treatmen as observed with the calcium-channel blocker and ACE inhibitors. ACE inhibitors increased AC and reduced WR, and it has been shown that reversibility of aortic stiffening and use of ACE inhbitors had favorable independent effect on survival in hypertensive patients with advanced renal disease.

Arteries↗