Blood pressure changes after high- and low-salt diets: are intermittent arm measures and beat-by-beat finger measures equivalent?

The assessment of sodium sensitivity requires to measure the difference in mean arterial pressure (MAP) at the end of sodium-loading (SLoad) and sodium-depletion (SDepl) maneuvers with an arm-cuff manometer. Aim of this study is to evaluate whether MAP measuring devices based on the volume-clamp method at the finger can also be used for assessing sodium sensitivity. Sixty-eight normotensive volunteers underwent SLoad and SDepl diets in random order. MAP was simultaneously measured at the end of each diet with arm (Spacelabs 90207) and finger (Portapres model-2) cuff devices. The sodium sensitivity was assessed as the difference in MAP at the end of SLoad and SDepl diets (ΔMAP), and as salt-sensitivity index (SSI; SSI = ΔMAP divided by the difference in urinary-sodium-excretion rate at the end of the diets). Discrepancies between finger and arm-cuff devices in ΔMAP or SSI were evaluated by Bland and Altman analysis. Even if discrepancies between devices had null-fixed bias, results showed a significant proportional bias and large limits of agreement (between -25 and 25 mm Hg for ΔMAP, between -196 and 180 mm Hg mol(-1) per day for SSI). The SSI distribution over the group was larger, flatter and less symmetric if derived from finger-cuff rather than arm-cuff devices, and this influenced substantially the identification of salt-sensitive individuals. Therefore, the response of MAP to SLoad/SDepl diets and consequently the assessment of the salt-sensitivity condition depends importantly on the measurement site, and brachial measures should be preferred for consistency with literature and normative data.

Stress-ECG vs. CT coronary angiography for the diagnosis of coronary artery disease: a "real-world" experience.

PURPOSE: This study aimed to evaluate the diagnostic accuracy of stress electrocardiogram (ECG) and computed tomography coronary angiography (CTCA) for the detection of significant coronary artery stenosis (> or =50%) in the real world using conventional CA as the reference standard. MATERIALS AND METHODS: A total of 236 consecutive patients (159 men, 77 women; mean age 62.8+/-10.2 years) at moderate risk and with suspected coronary artery disease (CAD) were enrolled in the study and underwent stress ECG, CTCA and CA. The CTCA scan was performed after i.v. administration of a 100-ml bolus of iodinated contrast material. The stress ECG and CTCA reports were used to evaluate diagnostic accuracy compared with CA in the detection of significant stenosis > or =50%. RESULTS: We excluded 16 patients from the analysis because of the nondiagnostic quality of stress ECG and/or CTCA. The prevalence of disease demonstrated at CA was 62% (n=220), 51% in the population with comparable stress ECG and CTCA (n=147) and 84% in the population with equivocal stress ECG (n=73). Stress ECG was classified as equivocal in 73 cases (33.2%), positive in 69 (31.4%) and negative in 78 (35.5%). In the per-patient analysis, the diagnostic accuracy of stress ECG was sensitivity 47%, specificity 53%, positive predictive value (PPV) 51% and negative predictive value (NPV) 49%. On stress ECG, 40 (27.2%) patients were misclassified as negative, and 34 (23.1%) patients with nonsignificant stenosis were overestimated as positive. The diagnostic accuracy of CTCA was sensitivity 96%, specificity 65%, PPV 74% and NPV 94%. CTCA incorrectly classified three (2%) as negative and 25 (17%) as positive. The difference in diagnostic accuracy between stress ECG and CTCA was significant (p<0.01). CONCLUSIONS: CTCA in the real world has significantly higher diagnostic accuracy compared with stress ECG and could be used as a first-line study in patients at moderate risk.

Autonomic cardiovascular regulation in quiescent ulcerative colitis and Crohn's disease.

BACKGROUND: In inflammatory bowel diseases, changes in autonomic enteric regulation may also affect neural cardiovascular control. However, while cardiac autonomic modulation has been shown to be impaired in active ulcerative colitis, the occurrence of cardiovascular autonomic alterations, also in the quiescent phase of inflammatory bowel diseases, is still a matter of debate. The aim of our study was thus to explore the features of cardiovascular autonomic regulation in ulcerative colitis and Crohn's disease during their remission phase. MATERIALS AND METHODS: Autonomic cardiovascular control was evaluated by time- and frequency-domain indexes of spontaneous heart rate and blood pressure variability and by assessing the baroreflex heart rate control (sequence technique) in 26 patients with ulcerative colitis, in 26 patients with Crohn's disease and in 23 healthy controls. RESULTS: The groups were matched for age, gender and body mass index. They had similar blood pressure mean levels and variability. By contrast, mean heart rate, its overall variability (standard deviation), and baroreflex sensitivity were lower in ulcerative colitis patients than in controls. Moreover, all indexes related to cardiac vagal control were significantly lower in ulcerative colitis patients with respect not only to controls but also to Crohn's disease patients. CONCLUSIONS: Cardiac vagal control is impaired in quiescent ulcerative colitis only, and not in Crohn's disease, while in both bowel diseases vascular control appears preserved. Since cardiovagal modulation seems related to anti-inflammatory mechanisms, the reduced parasympathetic cardiac regulation in apparently quiescent ulcerative colitis suggests that such systemic derangement is accompanied by local subclinical inflammations, even in the absence of clinically active inflammatory processes.

Coronary artery anomalies: incidence, pathophysiology, clinical relevance and role of diagnostic imaging.

Conventional coronary angiography is the gold standard for the diagnosis of coronary artery anomalies. Coronary anomalies are relatively rare findings in patients undergoing conventional coronary angiography for suspected obstructive coronary artery disease. Recently, the increasing performance of diagnostic techniques, such as electron beam tomography (EBT), magnetic resonance (MR) and, more recently, multislice computed tomography (MSCT), has enabled their application to cardiac imaging. MSCT, in particular, has a prominent role in coronary imaging due to its spatial and temporal resolution and three-dimensional capabilities. We report the incidence and pathophysiology of coronary artery anomalies based on the capabilities of recent diagnostic tools with the aim of improving an accurate and noninvasive diagnostic approach.

Non-invasive assessment of coronary artery stent patency with multislice CT: preliminary experience.

PURPOSE: To evaluate the diagnostic accuracy of multislice computed tomography coronary angiography (MSCT-CA) in the detection of in-stent restenosis. MATERIALS AND METHODS: Forty-two patients (33 male, 9 female, mean age 58+/-8 years) previously subjected to percutaneous implantation of coronary stent with suspected in-stent restenosis, underwent a 16-row MSCT (Sensation 16, Siemens) examination. The average time between stent implantation and MSCT-CA was 7.4+/-5.3 months. The following scan parameters were used: collimation 16x0.75 mm, rotation time 0.42 s, feed 3.0 mm/rot., kV 120, mAs 500. After administration of iodinated contrast material (Iomeprol 400 mgI/ml, 100 ml at 4 ml/s) and bolus chaser (40 ml of saline at 4 ml/s) the scan was completed in <20 s. All segments with a stent were assessed by two observers in consensus and were graded according to the following scheme: patent stent, in-stent intimal hyperplasia (IIH) (lumen reduction <50%), in-stent restenosis (ISR) (=/>50%), in-stent occlusion (ISO) (100%). Consensus reading was compared with coronary angiography. RESULTS: Forty-seven stents were assessed (16 in the right coronary artery; 4 in the left main; 22 in the left anterior descending; 5 in the circumflex). In 7 (17%) stents there was ISR (3) or ISO (4), and in 4 (10%) stents there was IIH. The sensitivity and negative predictive values for the detection of ISO were 80% and 98%, respectively, while for the detection of ISR+ISO they were 50% and 89%, respectively. CONCLUSIONS: Although the results are encouraging, the follow-up of stent patency with MSCT-CA does not show a diagnostic accuracy suitable for clinical implementation.

Diagnostic accuracy of 16-row multislice CT angiography in the evaluation of coronary segments.

PURPOSE: To evaluate the diagnostic accuracy of 16-row multislice spiral computed tomography coronary angiography (16-MSCT-CA) for the non-invasive assessment of significant coronary artery stenosis. MATERIALS AND METHODS: We enrolled 40 patients (36 male, aged 59+/-11 yrs) with suspected obstructive coronary artery disease and a heart rate <65 bpm during the scan. The 16-MSCT-CA (Sensation 16, Siemens, Forchheim, Germany) was performed with electrocardiographically-gated technique after the intravenous administration of 100 ml of iodinated contrast material followed by a saline bolus chaser. The scan parameters were: collimation 16 x 0.75 mm, rotation time 0.42 s, feed/rot. 3 mm (pitch 0.25), 120 kVp, 500 mAs. All coronary segments = or >2 mm in diameter were evaluated by two independent observers for the presence of significant coronary artery stenosis (= or >50%). Consensus reading was compared to quantitative coronary angiography. RESULTS: The average heart rate was 55+/-6 bpm. Of the 428 segments of = or >2.0 mm diameter 92 were significantly diseased. Without exclusion of any branches (428), the sensitivity, specificity, positive, and negative predictive values to identify = or >50% obstructed segments were 95.7% (88/92), 95.8% (322/336), 86.3% (88/102), and 98.8% (322/326), respectively. No occluded left main, left anterior descending, circumflex or right coronary artery segments remained undetected. CONCLUSIONS: 16-MSCT-CA in a selected low-heart-rate patient population provides high diagnostic accuracy in the evaluation of significant coronary artery stenosis.

Potassium depletion and salt sensitivity in essential hypertension.

To evaluate the actual role of potassium depletion on blood pressure, 11 hypertensive patients were placed on a 10-day isocaloric diet providing a daily potassium intake of either 18 or 80 mmol, with each subject serving as his or her own control; the intake of sodium (220 mmol/day) and other minerals was kept constant. On day 11 each patient was also subjected to central volume expansion by water immersion associated with either normal or low potassium intake. After a 10-day period of low potassium intake, systolic blood pressure increased (P < 0.02) by 5 mm Hg, whereas serum potassium decreased (P < 0.001) by 0.9 mmol/L; no significant changes in urinary sodium and a marked increase in urinary calcium excretion (P < 0.001) were found during the 10-day low potassium intake. PRA (P < 0.02) and plasma aldosterone (P < 0.04) concentrations also decreased during low potassium intake in hypertensive patients. Even though an identical natriuretic response was found during the water immersion experiments with either high or low potassium in the whole hypertensive group, the evaluation of hypertensive subjects in relation to salt sensitivity enabled us to disclose pronounced differences in the natriuretic and calciuretic response. In fact, although an impaired natriuretic ability and moderate calcium loss were particularly found during water immersion in those hypertensive subjects exhibiting a lower salt sensitivity index, a predominant calcium depletion appeared to be the most important consequence of potassium depletion in the hypertensive subjects with a higher salt sensitivity index. By confirming that potassium depletion may exacerbate essential hypertension, our data also suggest that not only sodium restriction, but also potassium and calcium supplementation, could be particularly advisable in salt-sensitive hypertensive patients.

Association between salt sensitivity and insulin concentrations in patients with hypertension.

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.

The renin-aldosterone system and renal function in kidney transplantation.

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.

Escape from the sodium-retaining effects of mineralocorticoids: is there a role for dopamine?

To investigate the possible role of dopamine, a catecholamine with natriuretic properties, in modulating the escape from the sodium-retaining effects of mineralocorticoids, we submitted six aldosterone-producing adenoma (APA) patients and six low-renin essential hypertensive patients to acute volume expansion by head-out water immersion with or without dopaminergic blockade by metoclopramide. Water immersion alone induced a marked, comparable natriuresis (P < 0.001) in both hypertensive groups where a slight reduction of already suppressed renin-angiotensin system and a marked stimulation of atrial natriuretic peptide was also observed (P < 0.03 and P < 0.002, respectively). Water immersion plus dopaminergic blockade by metoclopramide did not significantly affect the natriuresis observed during water immersion alone in APA patients; conversely, there was a blunted natriuretic response in low-renin hypertensives during water immersion plus metoclopramide, in comparison with that obtained during water immersion alone (P < 0.006). Furthermore, metoclopramide did prevent the suppression of plasma aldosterone levels produced by central volume expansion alone in low-renin hypertensives, although it did not affect plasma aldosterone levels during water immersion in APA patients. Our data suggest that dopaminergic blockade does not counteract the natriuretic ability of the other hemodynamic and humoral mechanisms involved in the escape phenomenon of APA patients, thus casting serious doubt on the possible role of dopamine in mediating the escape from the sodium-retaining effects of mineralocorticoids.

Water immersion and salt-sensitivity in essential hypertension.

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)

Calcium and sodium handling during volume expansion in essential hypertension.

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.

Regulation of sodium excretion in human hypertension: long-term effects of calcium antagonist and angiotensin converting enzyme inhibitor.

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.

Renin-angiotensin system unresponsiveness in phaeochromocytoma.

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.

A new diagnostic test for primary aldosteronism.

Isotonic-isooncotic central volume expansion by head-out water immersion was induced in six aldosterone-producing adenoma subjects and in six patients with idiopathic hyperaldosteronism. Plasma renin activity and plasma aldosterone levels did not significantly change during water immersion while serum cortisol was significantly suppressed (P less than .001) and the aldosterone-cortisol ratio increased (P less than .02) in aldosterone-producing adenoma patients. Water immersion also revealed the failure of plasma aldosterone levels to decrease below 10 ng/dL in these subjects, thus confirming previous results obtained during isotonic saline infusion. Otherwise, plasma renin activity and plasma aldosterone were significantly reduced (P less than .05 and P less than .01 respectively) by water immersion and plasma aldosterone invariably fell below 10 ng/dL in patients with idiopathic aldosteronism. In view of the diagnostic reliability of such a suppression test we conclude that water immersion is suitable for discriminating between the two forms of primary aldosteronism. We therefore suggest its use for assessing renin-aldosterone responsiveness in primary aldosteronism.

Dopaminergic modulation of acute renal effects of nicardipine.

In order to investigate whether dopamine receptors are involved in the acute natriuretic effects of calcium channel blockade, experiments were carried out in humans with uncomplicated essential hypertension. In 8 hypertensives 5 mg intravenous nicardipine produced a large decrease in blood pressure and renal vascular resistance, a slight but significant increase in glomerular filtration rate (GFR) and marked natriuresis. When a second identical experiment was performed in the same subjects with the addition of 10 mg metoclopramide as dopamine blocker, changes in sodium excretion and vascular resistance were the same, but GFR did not increase during nicardipine. In a second set of experiments (n = 5) the same design was used, but nicardipine was infused at a dose of 0.01 mg/kg, ie, seven times less than in previous experiments. Under these conditions, blood pressure, renal vascular resistance and GFR did not change, but significant natriuresis occurred. Natriuresis was almost completely prevented by metoclopramide. In 5 additional hypertensives, metoclopramide alone was infused and 0.01 mg/kg nicardipine was added to the infusion. No change in any parameter was observed. Our findings suggest that the dopaminergic system participates in maintaining or increasing GFR during blood pressure reduction by calcium antagonists, although renal vasodilation and natriuresis are largely independent of dopamine receptor activity. In addition, when low doses of calcium antagonists produce natriuresis in the absence of renal or systemic hemodynamic changes (direct tubular effect), dopamine blockade is able to blunt this effect. This indicates a modulation by dopaminergic receptors of the direct tubular action of calcium antagonists.