Is there a place for duplex screening of brachial artery in haemodialysis patients with vascular access?

BACKGROUND: Vascular access (VA) stenosis with subsequent thrombosis remains one of the major causes of morbidity and hospitalization in haemodialysis patients. The present cross-sectional study was planned in order to analyze the usefulness of brachial artery duplex ultrasound for detection and prediction of vascular access stenoses. METHODS: Color duplex ultrasound (Apogée Cx200, sectorial probe 7.5 MHz) was used to obtain the anatomical pattern of the VA and flow velocity waveforms of the brachial artery in 77 non-selected VA (47 Ciminio-Brescia fistulae and 30 PTFE grafts). In each VA, the resistance index (RI), the mean blood flow rate (Q) and the blood flow ratio index (QI) (QI = VA flow rate/contralateral flow rate) were calculated at the level of the brachial artery. The sensitivity and specificity of these brachial Doppler parameters were calculated for the detection of VA stenosis. In normal VA, positive (PPV) and negative predictive (NPV) values were calculated for the development of clinical stenotic complications 3 months post ultrasound examination. RESULTS: Thirteen of the 77 VA (17%) were identified as stenosed by duplex ultrasound and confirmed by fistulography and/or during surgical exploration. The best screening tests for VA stenosis detection were a QI threshold < 4.0 with a sensitivity and specificity of 69 and 69% and an RI > 0.55 with a sensitivity and specificity of 62 and 66%, respectively. In the VA considered as normal by ultrasound, the prediction of subsequent stenosis within three months post-ultrasound examination gave a PPV of only 18% and 19% for RI and QI, respectively. NPV for RI and QI were 90% and 88%. CONCLUSIONS: While Doppler ultrasound is a useful non-invasive test for the detection of prevalent VA stenosis, our results do not confirm that abnormal brachial Doppler flow parameters can predict short term development of VA stenosis.

Impaired contraction and relaxation in skin resistance arteries from patients with congestive heart failure.

OBJECTIVE: The aim was to determine the pharmacological reactivity of human small resistance arteries in patients with cardiac failure. METHODS: Small arteries (< 300 microns internal diameter) were removed from gluteal skin biopsy specimens and mounted in a double myograph for isometric force recording. RESULTS: Arteries from six patients with congestive heart failure contracted to only 65% of the maximum response recorded in nine arteries from normal volunteers when activated by potassium chloride (124 mM), noradrenaline (1 microM), or both. The lesser contraction in congestive heart failure vessels with no significant shift in sensitivity (EC50) was also observed in concentration-response studies with noradrenaline, angiotensin I, and angiotensin II. The concentration-contraction curves for serotonin showed only 40% of the maximum contractility to K+ in normal arteries, and this ratio was similar in congestive heart failure arteries. Normal arteries precontracted with noradrenaline (1 microM) relaxed in response to sodium nitroprusside, calcitonin gene related peptide, and the endothelium dependent agonist acetylcholine; in congestive heart failure vessels there was a marked loss of the relaxation response only to acetylcholine. CONCLUSIONS: These results suggest that in chronic congestive heart failure skin resistance arteries have impaired contraction responses probably independent of any receptor down regulation. The loss of endothelium dependent vasodilatation to acetylcholine suggests that EDRF release is impaired. These changes may well play an important role in the disturbances of peripheral vascular function associated with heart failure.

Atrial natriuretic factor and autonomic nervous system function in man.

To delineate a possible interaction of atrial natriuretic peptide ANF-(99-126) with autonomic nervous system function in humans, a spectrum of indices were assessed in 10 healthy young men during a 90 min iv administration of a) synthetic ANF-(99-126) 50 micrograms bolus followed by 0.025 micrograms.kg-1.min-1, b) the potent vasodilator sodium nitroprusside (SNP) 0.35 micrograms.kg-1. min-1, or c) vehicle 0.9% NaCl40 ml and 20% albumin 5 ml, in random sequence. Plasma immunoreactive ANF (irANF) rose from 32 to 1700 pg.ml-1 during the ANF-(99-126) infusion and was stable during SNP or vehicle. Infusion of ANF-(99-126) and SNP, but not vehicle, decreased diastolic blood pressure (BP) on average by -9 and -7.5%, respectively; systolic BP was largely unchanged. Heart rate (HR, + 15 and 12%) or plasma norepinephrine (NE) rose similarly during ANF-(99-126) and SNP infusions, and the systolic BP response to orthostasis was similar (-18 mmHg). The following autonomic indices did not differ significantly after the 3 infusions: responses of HR and NE to orthrostasis; reflex bradycardic response to phenylephrine (PE)-induced rise in systolic BP (+ 20 mmHg); responses of BP to hyperventilation, PE, or 3 min of sustained handgrip; and beat-to-beat variation (R-R interval) during deep breathing. The immediate orthostatic HR response (30/15 R-R interval ratio) fell similarly during infusion of ANF-(99-126) or nitroprusside. The findings indicate that in healthy men the function of the autonomic nervous system is not notably impaired by high circulating ANF levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Antihypertensive contribution of sodium depletion and the sympathetic axis during chronic angiotensin II converting enzyme inhibition.

The known physiological adaptation of cardiovascular sensitivity to variations in angiotensin II (Ang II) levels would predict that the blood pressure (BP)-lowering effect of Ang II inhibition might be at least partly counterbalanced by enhanced Ang II reactivity. Therefore, factors other than Ang II inhibition per se may contribute to the antihypertensive mechanisms of angiotensin converting enzyme (ACE) inhibitors. In order to further investigate this, the body sodium-blood volume state as well as the pressor reactivity to infused Ang II or norepinephrine (NE) were assessed in 12 normal subjects and 16 patients with essential hypertension given a placebo, and after 6 weeks of intervention with enalapril (20-40 mg/day). Enalapril produced in both groups similar falls in plasma ACE activity (P less than 0.0001) and upright plasma aldosterone (P less than 0.01), and a rise in plasma renin activity (PRA; P less than 0.05). BP decreased from 156/107 +/- 3/2 (mean +/- s.e.m.) to 142/94 +/- 5/3 mmHg (P less than 0.001) in the hypertensives and from 118/84 +/- 4/2 to 111/73 +/- 4/3 mmHg (P less than 0.01) in the normal subjects. In the hypertensive patients only, the Ang II pressor reactivity relative to Ang II plasma levels during Ang II infusion was increased (P less than 0.01), while the NE pressor reactivity relative to NE plasma levels during NE infusion (P less than 0.01) as well as the exchangeable body sodium (-5%, P less than 0.001) were reduced significantly. Blood and plasma volume, levels of plasma atrial natriuretic factor and catecholamines, and the heart rate and its response to isoproterenol were unchanged in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Stimulation of renin secretion by potassium-channel activation with cromakalim.

The cardiovascular and endocrine profile of cromakalim has been studied in 8 healthy men (age 25 +/- 2 years: means SEM) and its influence on renin release from cultured rat juxtaglomerular cells in vitro has also been examined. According to a double-blind, randomized sequence the subjects received placebo or cromakalim 1 mg as a single daily oral dose for 5 days. Compared to placebo, cromakalim significantly increased plasma renin activity (+ 122%; from 1.73 to 3.87 ng AI.ml-1.h-1), angiotensin II (+ 105%; from 5.1 to 10.5 pg.ml-1), and norepinephrine (+ 61%) levels, and heart rate (+ 8%). Plasma aldosterone, blood pressure and indices of the electrolyte-fluid volume state were unchanged. Cromakalim in vitro stimulated renin release, from 9.9 to 36.5 ng AI.h-1.30 min.mg cell protein, from juxtaglomerular cells. It appears that the presumed K+-channel activator cromakalim increases renin release in vivo at least in part by direct stimulation of renal juxtaglomerular cells.

Studies on acute glucose-induced aldosterone suppression: role of renin-angiotensin system.

Glucose loading is known to cause acute suppression of plasma aldosterone and stimulation of plasma renin activity. The relative contribution of variations in circulating angiotensin II to the regulation of aldosterone secretion following glucose loading was assessed in ten normal subjects. The effects of a standard oral glucose loading test (100 g) on plasma concentrations of glucose, insulin, potassium, aldosterone, renin activity and cortisol were studied (a) under basal conditions, and (b) after inhibition of angiotensin II with the converting enzyme inhibitor captopril (50 mg t.i.d. during 3 days). Under basal conditions the acute increase in plasma glucose and insulin after glucose loading was accompanied by a significant decrease (P less than 0.01) in plasma cortisol and aldosterone and by a significant increase in plasma renin activity (P less than 0.01); plasma potassium was decreased slightly but not significantly. Following captopril treatment preloading plasma renin activity was increased significantly, most probably reflecting an effective reduction of angiotensin II. Glucose loading caused a similar suppression of plasma aldosterone, as observed under basal conditions. This observation suggests that renin activation does not substantially contribute to the acute regulation of plasma aldosterone after an oral glucose load.