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AIM: The aim of this paper was to assess short and long term prognostic value of the OESIL risk score (ORS), a risk stratification rule for syncope which consider abnormal ECG, age > 65, history of cardiovascular diseases, lack of prodromal symptoms to identify patients at higher risk of mortality (ORS≥2) to be admitted. METHODS: This is a prospective cohort study in which syncopal recurrences, readmission for other reasons, major therapeutic procedures, cardiovascular events, death for any reason, were assessed in a group of 200 syncopal patients at both 1 month and 1 year after discharge from an Emergency Department Observation Unit. RESULTS: Multinomial logistic regression analysis showed that ORS ≥2 is not associated with any endpoint, except major procedures. Conversely, ORS≥3 was a strong predictor of at least 1 adverse event within 1 month and severe outcomes within 1 year, particularly for non-syncopal readmission (P<0.005), major procedures (P<0.002), cardiovascular events (P<0.023), and death for any cause (P<0.022). CONCLUSION: Our patient group was significantly older than the ORS derivation cohort (72.4±15.1 vs. 59.5±24.3 yrs) and mostly above the age considered as 1 point in the ORS, so it is rather understandable that only a more restrictive cut-off might be advantageous for identifying high risk patients. On the evidence of a progressive ageing of patients presenting at the EDs, we suggest to use a ³3 ORS threshold when deciding for admission.

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This study was performed in 28 patients with mild to moderate hypertension, classified as being either salt sensitive or salt resistant on the basis of the percent decrement in mean arterial blood pressure (MAP) seen 7 days after daily salt intake was decreased from 220 to 30 mmol/L. Ten patients had a percent decrease of MAP > 10% and were defined as being salt sensitive. Salt resistance was defined as a percent decrease in MAP of < 3% and eight patients satisfied this criterion. Both plasma glucose and insulin concentrations following a 75-g oral glucose challenge were significantly higher after the high-salt diet in the salt-sensitive patients. Furthermore, there were correlations of marginal statistical significance between the decrease in MAP after the low-salt diet and the plasma glucose (r = 0.32, P < .10) and insulin (r = 0.38, P < .06) responses to oral glucose. These data are consistent with the view that there is an association between resistance to insulin-mediated glucose disposal and salt sensitivity in patients with high blood pressure.

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Six renal transplant recipients, six uninephrectomized patients and six normal subjects were subjected to the physiological manoeuvre of head-out water immersion (WI), in order to compare changes in electrolyte and humoral responses known to occur in healthy individuals with those arising as a result of renal denervation in the transplant recipients. The denervated, transplanted kidneys of the six patients were able to maintain a sodium excretory response to WI identical to that obtained in the controls (from 121 +/- 18 to 236 +/- 29 mumol/min, p < 0.005 vs 113 +/- 17 to 213 +/- 18 mumol/min, p < 0.005, respectively). Kidney transplant patients were also characterized by a preserved suppression of renin-aldosterone system (from 1.2 +/- 0.2 to 0.5 +/- 0.1 ng/ml/h, p < 0.03 and 12 +/- 1.0 to 7.0 +/- 1.0 ng/dl, p < 0.005, respectively) and stimulation of atrial natriuretic peptide (from 84 +/- 15 to 153 +/- 25 pg/ml, p < 0.05) to central hypervolemia by water immersion. The present study, while confirming the ability of the denervated kidney to handle sodium normally, also suggests that atrial natriuretic peptide could assume a crucial role in regulating renin secretion.

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It has been demonstrated that an exaggerated natriuretic response to central hypervolaemia is not necessarily associated with hypertension; many hypertensive subjects manifest either an appropriate or a blunted natriuresis in response to ECFV expansion attained by head-out water immersion. In this study, we tested the hypothesis that an underlying condition of salt-sensitivity may explain the heterogeneity of the natriuretic response of essential hypertension. Both salt-sensitivity tests and 2h water-immersion studies were randomly performed in 18 untreated essential hypertensives under a selected and controlled diet. Salt-sensitivity was defined as a significant drop in mean arterial pressure of 10% or greater, calculated as the difference between the average of the 25 readings under the high and the low salt period. Water immersion did result in a significant natriuretic and calciuretic response in the whole hypertensive group (n = 18, p < 0.001 and p < 0.05, respectively), while the examination of the individual excretion disclosed either exaggerated and appropriate or blunted urinary response. When the hypertensive group was classified in relation to salt-sensitivity, the greater fall in mean arterial pressure during low salt diet (salt-sensitivity) was associated with the more pronounced natriuretic response during water immersion (r = -0.66, p < 0.003). An identical correlation (r = -0.58, p < 0.01) was also found between changes in mean arterial pressure (low salt diet) and urinary calcium excretion (water immersion) in the same hypertensives. The water immersion-induced suppression of plasma aldosterone and the increase in plasma atrial natriuretic peptide did result from comparable magnitude in the salt-sensitive and in salt-resistant subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

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To evaluate the actual role of extracellular fluid volume (ECFV) expansion per se in modulating the rate of urinary calcium excretion, a thermoneutral water immersion (WI) study was conducted in 10 normal subjects and 30 patients with essential hypertension. Central hypervolemia by 2 hours of WI caused a significant diuretic and natriuretic response (P < .005) in normal subjects; no significant changes were detected in urinary calcium and magnesium excretion. WI provoked either an appropriate or exaggerated natriuresis (P < .001) in 21 hypertensive patients; these subjects also exhibited a highly positive correlation between urinary sodium and calcium excretion during WI (P < .001). In the remaining nine hypertensive patients, WI produced a significant diuretic response, but a barely discernible (P = NS) natriuresis (inappropriate response). These subjects also exhibited a significant reduction of urinary calcium (P < .001) and magnesium (P < .01) excretion. The data indicate that (1) volume expansion per se may have a role in regulating calcium excretion in hypertensive subjects; (2) a calcium leak may be attributable to a close relationship between urinary sodium and calcium metabolism, and causally related to a disturbance of sodium and volume homeostasis in hypertension.

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Fourteen subjects with untreated essential hypertension were subjected to 2-h water immersion (WI) study. They were then randomly assigned to two distinct oral antihypertensive regimens with either calcium-channel blocker nifedipine (group 1, n = 7) or the angiotensin-converting enzyme (ACE) inhibitor lisinopril (group 2, n = 7). Three months later, a WI study identical to the first was repeated in the same hypertensive subjects. In group 1, treatment with nifedipine gastrointestinal therapeutic system (30 mg daily) significantly enhanced the natriuretic response to volume expansion by WI (peak value 405 +/- 82 mumol/min during WI plus nifedipine vs. 291 +/- 52 mumol/min during WI alone, p < 0.05). In group 2, treatment with lisinopril (20 mg daily) was associated with a blunted natriuretic response to volume expansion by WI (peak value 189 +/- 54 mumol/min during WI plus lisinopril vs. 320 +/- 53 mumol/min during WI alone; p < 0.025). A significant direct correlation between urinary sodium excretion (delta UNa V) and mean arterial pressure (delta MAP) was noted during WI plus nifedipine. Each long-term drug treatment was associated with a decrease in BP and hormonal changes of the same magnitude. Our data suggest that calcium antagonists could act as "diuretic agents" capable of counteracting the antinatriuretic effect of reduced renal perfusion pressure.

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Water immersion to the neck is able to provoke a profound suppression of the renin-angiotensin system in several clinical conditions associated with hyper-reninaemia. Both hyper-reninaemia and secondary aldosteronism have sometimes been described in phaeochromocytoma. We report on two patients, with surgically proven phaeochromocytoma, in whom water immersion, performed before surgery, failed to induce any significant change in plasma renin activity.

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