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Bruno Pannier

Publications and source records attributed to Bruno Pannier.

23 records · Page 2Linked to original sources
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↗