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Biomedical subjects

G Tripepi

Publications and source records attributed to G Tripepi.

29 records · Page 2Linked to original sources
PubMed1998

Nocturnal hypoxemia, night-day arterial pressure changes and left ventricular geometry in dialysis patients.

It is well established that nocturnal hypoxemia in sleep apnea causes an inversion of the circadian arterial pressure rhythm and triggers nocturnal hypertension. Since sleep apnea is very frequent in dialysis patients, we hypothesized that nocturnal hypoxemia may be a factor that contributes to alter the 24-hour arterial pressure profile in these patients. To test the hypothesis 32 dialysis patients underwent 24-hour blood pressure (BP) monitoring and continuous monitoring of arterial O2 saturation during the night-time. Hemodialysis patients were studied during the non-dialysis day. All patients underwent an echocardiographic study. Thirteen patients had no episode of nocturnal hypoxemia (group I), 7 had at least one episode overnight but less than 2 episodes/hr (group II) and 12 had > or = 2 episodes/hr (group III). The average daytime systolic pressure was similar in the three groups. However, the average nocturnal systolic pressure fell in the first group (-2.5 +/- 4.2%) and rose in the second (+2.0 +/- 3.6%) and in the third (+3.9 +/- 2.2%) group (one way ANOVA, P < 0.005). The relative wall thickness of the left ventricle (RWT) was significantly (P < 0.05) higher in group III than in group I, and in the aggregate (N = 32) there was an inverse relationship between average nocturnal SaO2 and RWT (r = -0.43, P = 0.015). The proportion of patients with concentric remodeling or concentric hypertrophy was higher (P = 0.05) in the group with a more severe degree of nocturnal hypoxemia (group III, 8 of 12) than in the other two groups (group I, 3 of 13; group II, 2 of 7). Nocturnal hypoxemia is associated with the "non-dipping" arterial pressure profile in dialysis patients. Disturbed respiratory control during the night may represent an important cardiovascular risk factor in dialysis patients.

Adolescent↗
PubMed1997

The heart rate response pattern to dialysis hypotension in haemodialysis patients.

BACKGROUND: Hypotension during haemodialysis may be caused by the activation of a cardiovascular reflex causing abrupt sympathetic withdrawal, vasodilatation and bradycardia (bradycardic hypotension). However, the frequency of this type of hypotension is undefined and it is unclear whether or not it underlies a peculiar predisposition to vasodepressor syncope. OBJECTIVE: To assess the prevalence of bradycardic hypotension and to test the hypothesis that dialysis patients are predisposed to vasodepressor syncope. RESULTS: Sixty hypotensive episodes were recorded in 20 patients (> or = 2 episodes in 15 patients). Heart rate increased in 35 episodes, did not change in 19 episodes and decreased in six episodes. The HR response pattern to hypotension was reproducible in 10 patients (always tachycardia, 6; always unchanged heart rate 4). Patients developing bradycardic hypotension (n = 5) all had an erratic HR response to hypotension (i.e. bradycardia preceded or followed by tachycardia or by no HR change) and were characterized either by the typical haemodynamic pattern of hypovolaemia (predialysis hypotension, tachycardia and low TBW) or by being treated with a very high UF rate (> 0.3 ml/kg/min). Post-dialysis echocardiography showed that the LVEDD was less (one-tailed P = 0.055) in patients with bradycardic hypotension than in those with tachycardic responses or with unchanged HR. On tilt testing (after dialysis) three of 11 (27%) dialysis hypotensive patients developed bradycardic hypotension. This proportion was identical to that expected in healthy subjects and in control patients without syncope. CONCLUSIONS: Tachycardia is the more frequent heart rate response to dialysis hypotension in uraemic patients. Bradycardic hypotension in dialysis patients is associated with a haemodynamic profile indicating a more severe degree of cardiovascular underfilling. Bradycardic hypotension probably represents a physiological response to hypovolaemia rather than the expression of a peculiar predisposition to vasodepressor syncope.

Adult↗
PubMedDate not supplied

Plasma concentration of asymmetrical dimethylarginine and mortality in patients with end-stage renal disease: a prospective study.

BACKGROUND: The plasma concentration of asymmetrical dimethylarginine (ADMA), an inhibitor of nitric-oxide synthase, which has been linked to endothelial dysfunction and atherosclerosis in the general population, is raised in patients with end-stage renal disease and could contribute to the high cardiovascular risk in patients with chronic renal failure. We investigated the relation between cardiovascular risk factors and plasma ADMA concentration in a cohort of haemodialysis patients (n=225), and tested the predictive power of ADMA for mortality and cardiovascular outcomes. METHODS: Patients had standard dialysis three times a week. We accurately recorded cardiovascular events over a mean follow-up of 33.4 months (SD 14.6); these events were reviewed by a panel of physicians. We identified correlates of plasma ADMA by univariate and multivariate analyses. FINDINGS: On univariate analysis, ADMA concentration in plasma was directly related to concentrations of fibrinogen and L-arginine in plasma, duration of dialysis treatment, and serum cholesterol concentration, and was inversely related to serum albumin concentration. On multivariate analysis, only plasma fibrinogen (p=0.0001) and serum albumin (p=0.04) concentrations were independently related to plasma ADMA concentration (multiple r=0.44, p=0.0001). 83 patients died, 53 (64%) by cardiovascular causes. In a Cox's proportional-hazards model, plasma ADMA ranked as the second factor predicting overall mortality (hazard ratio 1.26, 95% Cl 1.11-1.41, p=0.0001) and cardiovascular events (1.17, 1.04-1.33, p=0.008). INTERPRETATION: In haemodialysis patients, plasma ADMA is a strong and independent predictor of overall mortality and cardiovascular outcome. These findings lend support to the hypothesis that accumulation of ADMA is an important risk factor for cardiovascular disease in chronic renal failure.

Arginine↗
PubMedDate not supplied

Smoking, blood pressure and serum albumin are major determinants of carotid atherosclerosis in dialysis patients. CREED Investigators. Cardiovascular Risk Extended Evaluation in Dialysis patients.

AIM: To investigate the relationship between carotid atherosclerosis and some major cardiovascular risk factors in uremic patients on chronic dialysis. METHODS: A cross-sectional study was carried out in 119 unselected dialysis patients (89 on hemodialysis and 30 on chronic ambulatory peritoneal dialysis, CAPD). Fasting blood sampling for serum lipids, albumin, hemoglobin, and echo-colour-Doppler evaluation of common carotid arteries were performed in all patients (during the non-dialysis day in hemodialysis patients). In hemodialysis patients BP was measured before and after dialysis; in CAPD patients home BP values were recorded during the month before the study day. RESULTS: Ninety-five patients had at least one plaque and 57 had at least four plaques. Thirty-eight had mild and eleven severe carotid stenosis. In multiple regression models, the mean internal diameter of carotid arteries was explained (R=0.52, P=0.0001) by systolic pressure (r=0.39), serum cholesterol (r=-0.28), age (r=0.27) and smoking (r=0.24) while the degree of carotid stenosis was predicted (R=0.39, P=0.0001) by age (r=0.36) and smoking (r=0.25). The number of atherosclerotic plaques was explained (R=0.51, P=0.0001) by age (r=0.36), smoking (r=0.25) and pulse pressure (r=0.20), serum albumin just failing to reach statistical significance (P = 0.06). However, serum albumin was a significant and independent predictor of the number of atherosclerotic plaques (r=-0.26) in hemodialysis patients (n=89). Sex, diabetes, Kt/V, duration of dialysis treatment, hemoglobin, serum calcium and phosphate did not add any predictive power to the models. CONCLUSIONS: In dialysis patients arterial pressure and smoking are associated with carotid atherosclerosis. Serum albumin appears to serve as an independent predictor of carotid atherosclerosis.

Arteriosclerosis↗
PubMedDate not supplied

Renal endothelin-1 is linked to changes in urinary salt and volume in essential hypertension. Salt Sensitivity Group of the Italian Society of Hypertension.

METHODS: We investigated the influence of salt intake on urinary and plasma endothelin-1 (ET-1) in 55 patients who entered a two-week double-blind, randomised, crossover study comparing a 50 mMol/day salt intake and 150 mMol/day. Twenty-four-hour ET-1 excretion and plasma ET-1 were measured by RIA on pre-extracted samples. RESULTS: In the whole cohort (n=55), changes in urinary ET-1 were related to salt excretion (r=0.28, P=0.04) and urinary volume (r=0.47, P=0.0001). In a multivariable model, changes in PRA, plasma aldosterone, blood pressure and heart rate did not add any predictive power to salt excretion with regard to urinary ET-1 variations. The relationship between urinary volume and urinary ET-1 was stronger than that of urinary sodium with ET-1 excretion because sodium was excluded from the multivariable model when urinary volume was introduced. Changes in urinary ET-1 were unrelated to mean blood pressure changes (P=0.66). Changes in plasma ET-1 were unaffected by changes in salt intake (P=0.58) but were strongly related to those in PRA (r= -0.45, P=0.01) and plasma aldosterone (r= -0.53, P=0.002). CONCLUSIONS: The renal excretion of ET-1 is influenced by changes in salt intake and appears largely independent of the blood pressure response to salt. Changes in urinary volume which accompany variations in salt excretion play an important role in this response. Since urinary ET-1 reflects its renal synthesis, our data support the notion that renal ET-1 plays a role in the regulation of sodium balance in patients with mild hypertension.

Adult↗
PubMedDate not supplied

Pentosidine, carotid atherosclerosis and alterations in left ventricular geometry in hemodialysis patients.

OBJECTIVE: To assess the relationship between advanced glycation end products (AGE) and cardiovascular damage in end-stage renal diseases. METHODS: Ninety-one hemodialysis patients who had been on dialysis treatment for at least six months were recruited for the study. Each patient underwent echocardiography and an echo-color Doppler study of the carotid arteries. We measured plasma pentosidine and related it to intima media thickness, atherosclerotic plaques and parameters of left ventricular geometry. RESULTS: Pentosidine was higher in patients treated by low-flux dialysis (31.0+/-16.6 pmol/mg protein) than in those treated by high-flux dialysis (25.4+/-7.6 pmol/mg protein), but this difference was of marginal statistical significance (P=0.08). On multivariate analysis, plasma IgG (beta=0.24, P=0.02) was the only independent correlate of plasma pentosidine. Intima media thickness and the number of atherosclerotic plaques were unrelated to plasma pentosidine. Mean wall thickness (beta=0.18, P<0.05), relative wall thickness (beta=0.20, P<0.05) and left ventricular end-diastolic volume (beta= -0.23, P<0.01) were independently related to plasma pentosidine. CONCLUSIONS: Pentosidine, a reliable marker of "carbonyl stress", is unrelated to intima media thickness and to the number of atherosclerotic plaques, but it is related to alterations in heart geometry. These data suggest that the effect of carbonyl stress on the cardiovascular system is complex and that the effects of AGE on the heart may be dissociated from those on the arterial system.

Arginine↗
PubMedDate not supplied

[Hyperaldosteronism and simultaneous pheocromocytoma: a puzzle case].

Pheochromocytoma and primary hyperaldosteronism are well-known causes of hypertension. It was recently reported that their frequency in the hypertensive population is 0.1-0.2% and 3-15%, respectively. We describe the case study of a patient with severe hypertension (200/100 mmHg) and the coexistence of pheochromocytoma and primary hyperaldosteronism attributable to adrenal hyperplasia. The originality of this clinical report is that the patient presented a pheochromocytoma in the left adrenal gland and hyperplasia of the contralateral adrenal gland. The simultaneous presence of pheochromocytoma and primary hyperaldosteronism in the same patient is probably due to either genetic predisposition or to specific environmental risk factors for these adrenal diseases.

Adrenal Gland Neoplasms↗
PubMedDate not supplied

[Kaplan-Meier analysis].

Kaplan-Meier analysis is largely used in nephrology to estimate a population survival curve from a sample. If patients are followed-up until death, the survival curve can be estimated simply by computing the fraction survival at each time point. Kaplan-Meier analysis allows the estimation of survival over time, even when patients drop out or are studied for different lengths of time. In Kaplan-Meier analysis, the comparison between two survival curves is made by the log-rank test.

Data Interpretation, Statistical↗
PubMedDate not supplied

Leptin in end stage renal disease (ESRD): a link between fat mass, bone and the cardiovascular system.

Adipose tissue is now considered an important system operating strictly in concert with other systems. The adipocyte is the main producer of two pleiotropic compounds, leptin and adiponectin, modulating inflammation and having multiple effects in disparate organs including the cardiovascular and the central nervous system. Leptin has disparate influences on various physiologic and organ systems including glucose homeostasis, hematopoiesis and the reproductive and cardiovascular systems and is a crucial hormone for the regulation of food intake and body weight. Peripherally, leptin modulates insulin sensitivity and high leptin triggers insulin resistance and vice versa. Obesity, a situation where circulating leptin attains very high levels is accompanied by increased bone mass, a phenomenon which may depend on direct stimulation of osteoblasts by leptin. However in animal models the stimulating effect of leptin on the osteoblast is counterbalanced by a strong inhibitor effect on bone formation in the central nervous system. Two recent studies reported an inverse link between leptin, bone mass and PTH in dialysis patients suggesting that leptin may be implicated in low bone turnover in these patients, likely by a mechanism involving the central nervous system. Leptin induces vascular calcifications in vitro. In uremic man leptin is unrelated to valvular calcifications but predicts incident cardiovascular events in overweight and obese dialysis patients. Leptin seems to be a relevant player in the emerging connection between bone and cardiovascular alterations in patients with end stage renal disease.

Adipose Tissue↗