Reported diagnosis of previous asthma in a sample of the Italian general population.

In this cross-sectional study we describe the prevalence and characteristics of subjects who self-reported a diagnosis of previous asthma in a sample of the Italian general population. We chose a wide age range (3-69 yrs) in order to obtain data over a large spectrum of the population. Interviews were conducted in 1,038 subjects by trained physicians using a modified version of the American Thoracic Society and National Heart & Lung Institute--Division of Lung Disease questionnaire proposed in 1978 (ATS-DLD-78). 791 subjects underwent skin prick tests for 7 common aeroallergens; 422 subjects underwent spirometry and 212 methacholine challenge tests. Cumulative prevalence of asthma was 7.9% (82/1038). Previous asthma (PA) was reported by 29 (35.4%) of the subjects, who said they had been but were no longer asthmatic; 65.5% of these claimed that PA had developed at or before the age of 14 yrs. No significant differences emerged in sex, age, family and personal history of atopy, and size of skin test reaction in subjects with PA compared to those with current asthma (CA). Although the difference was not statistically significant, the latter tended to be lifetime nonsmokers while subjects with PA were more often current smokers. Age at onset of asthma was significantly higher in subjects with CA than in subjects with PA (24.6 +/- 20 yrs vs. 12.0 +/- 15.0 yrs, p = 0.005). Bronchial hyperreactivity was present in 37.5% of subjects with PA, while forced expiratory volume in 1 sec (FEV1) was within normal limits in all. In conclusion, in this sample of the Italian population, PA was reported by about 1/3 of the asthmatic subjects, most of whom were atopic. Lung function was within normal limits in all, but bronchial hyperreactivity persisted in 1/3 subjects.

Cardiac and carotid structure in patients with established hypertension and white-coat hypertension.

AIM: The introduction of ambulatory blood pressure monitoring in the clinical practice has defined a new subgroup of hypertensive patients called white-coat hypertensives. It has been reported that white-coat hypertensives have less cardiac involvement than established hypertensive patients. This study was designed to examine the extent of cardiac and vascular involvement in patients with white-coat hypertension and established hypertension. PATIENTS AND METHODS: We studied 82 patients with mild essential hypertension, never previously treated, using 24-h ambulatory blood pressure monitoring and an echocardiographic and vascular ultrasonographic study. Left ventricular dimensions and mass were obtained according to the Penn convention. The intima-media thickness of the posterior wall of both common carotid arteries was measured 5, 10 and 20 mm caudally to the flow-divider and the average value was used for analysis. RESULTS: Of the 82 patients, 31 (mean +/- SD age 35 +/- 10 years) had average 24-h systolic/diastolic blood pressure values of below 132/85 mmHg (white-coat hypertensives) and 51 (aged 42 +/- 2 years) had a consistently elevated diastolic blood pressure. Both groups had similar body surface area (1.82 +/- 0.22 versus 1.81 +/- 0.22 m2), sex distribution (20 males and 11 females versus 32 males and 19 females), duration of hypertension, metabolic parameters and smoking habit. The 24-h ambulatory blood pressure monitoring values were, by definition, significantly higher in established hypertensives than in white-coat hypertensives (142 +/- 10/94 +/- 6 versus 127 +/- 6/79 +/- 4 mmHg, P<0.001). The left ventricular mass index and intima-media thickness were significantly higher in the established hypertensives (112 +/- 17 g/m2, 0.67 +/- 0.11 mm, respectively) than in the white-coat hypertensives (98 +/- 18 g/m2, 0.58 +/- 0.09 mm; P<0.001 for both). CONCLUSIONS: The prevalence of left ventricular hypertrophy and cardiac remodeling was significantly more frequent in established hypertensives (51%) compared to white-coat hypertensives (19%). These confirm that structural changes in the left ventricle in white-coat hypertensives are more limited than in established hypertensives and show that in white-coat hypertensives there is significantly less involvement of the conductance vessels than in established hypertensives.

[Cardiac and vascular morphology in patients with "white-coat hypertension": echocardiographic and ultrasonographic study]. / Caratteristiche strutturali cardiache e vascolari nei soggetti con "white coat hypertension": studio echocardiografico ed ultrasonografico.

BACKGROUND: The introduction of ambulatory blood pressure (ABPM) in the clinical practice has defined a new subgroup of hypertensive patients (pts) called "white coat" hypertensive pts. It has been reported that white coat hypertensive pts have less cardiac involvement than established hypertensive pts. This study was designed to examine the extent of cardiac and vascular involvement in pts with white coat hypertension and established hypertension. METHODS: Fifty-four previously never treated pts with mild or moderate hypertension underwent a 24h ABPM and an echocardiographic and vascular ultrasonographic study in order to assess left ventricular anatomical parameters and the intima-media thickness of common carotid arteries. Left ventricular dimensions and mass were obtained according to Penn convention. The intima-media thickness of the far wall of both common carotid arteries was measured at 5, 10 and 20 mm caudally to the flow-divider; the average values were considered. RESULTS: Twenty-eight pts (age 43 +/- 8 years) had an average daytime ABPM below 140/90 mm Hg ("white coat") and 26 pts (age 46 +/- 10) had a consistently elevated diastolic blood pressure. Both groups had similar office blood pressure (152 +/- 9/101 +/- 7 vs 155 +/- 10/103 +/- 6 mm Hg) body surface mass (1.79 +/- 0.23 vs 1.86 +/- 0.21 mq), sex (18M/20F vs 18M/8F), duration of hypertension, glycolipidic parameters and smoking habit. The daytime ABPM was (by definition) significantly higher in established hypertensive pts than in white coat hypertensive pts (145 +/- 11/97 +/- 4 vs 129 +/- 7/83 +/- 5 mm Hg, p < 0.001). Left ventricular mass index and intima-media thickness resulted significantly greater in established (119 +/- 1.7 g/m2; 0.70 +/- 0.11 mm) than in white coat hypertensive pts (99 +/- 16 g/m2; 0.60 +/- 0.1 mm, p < 0.002). The prevalence of left ventricular hypertrophy and cardiac remodeling was more frequent in established hypertensive pts (53%) compared to white coat hypertensive pts (7.7%). CONCLUSION: The results of our study confirm that structural changes of left ventricle in white coat hypertensive pts are more limited than in established hypertensive pts and for the first time show that in white coat hypertensive pts the involvement of the conductance vessels is significantly lower than in established hypertensive pts.

Vasopressin release and water metabolism in patients with cirrhosis.

Water retention is a complication in many patients with cirrhosis, usually attributed to excessive release of arginine vasopressin. To investigate the responsiveness of arginine vasopressin to osmotic and non-osmotic stimuli and its relationship to free water excretion, we studied 19 patients with cirrhosis under three different conditions: 45 min with legs raised to 60 degrees, to expand the central blood volume; infusion of 1000 ml of 0.45% saline solution to reduce plasma osmolality; and rapid injection of 50 ml of 2 M NaCl to increase plasma osmolality. Both expansion of central blood volume and decrease of plasma osmolality significantly reduced plasma vasopressin levels (from 2.1 +/- 0.6 to 1.39 +/- 0.3 pg/ml, p < 0.04; and from 1.09 +/- 0.25 to 0.41 +/- 0.13 pg/ml, p < 0.0001). The changes in free water excretion differentiated two subgroups of patients during each test: excretors and non-excretors. In the excretors, increased free water excretion was associated with suppressed vasopressin levels (below 0.5 pg/ml) and normal renal function. In the non-excretors, inability to improve free water excretion was associated with high vasopressin levels or with reduced distal delivery of the glomerular filtrate, except in some cases where vasopressin levels had fallen below 0.5 pg/ml and renal function was normal. For these cases the presence of other vasopressin-independent antidiuretic mechanisms is conceivable. The injection of hypertonic saline solution caused significant rises in plasma osmolality (from 287 +/- 1.9 to 292 +/- 1.6 mmol/kg, p < 0.05) and in plasma vasopressin levels (from 1.13 +/- 0.29 to 2.86 +/- 0.52 pg/ml, p < 0.05). These results suggest that vasopressin release in patients with cirrhosis is normally responsive to osmotic and non-osmotic stimuli, although our results show a lower theoretical osmolar threshold for suppression of vasopressin release in non-excretors than in excretors (276 vs 284 mmol/kg).

Mechanisms responsible for sympathetic activation by cigarette smoking in humans.

BACKGROUND: The pressor and tachycardic effects of cigarette smoking are associated with an increase in plasma catecholamines, suggesting the dependence of these effects on adrenergic stimulation. Whether the stimulation occurs at a central or a peripheral level and whether reflex mechanisms are involved is unknown. METHODS AND RESULTS: In nine normotensive healthy subjects (age, 33.0 +/- 3.5 years, mean +/- SEM), we measured blood pressure (Finapres device), heart rate (ECG), calf blood flow and vascular resistance (venous occlusion plethysmography), plasma norepinephrine and epinephrine (high-performance liquid chromatography assay), and postganglionic muscle sympathetic nerve activity (microneurography from the peroneal nerve) while subjects were smoking a filter cigarette (nicotine content, 1.1 mg) or were in control condition. Cigarette smoking (which raised plasma nicotine measured by high-performance liquid chromatography from 1.0 +/- 0.9 to 44.2 +/- 7.1 ng/mL) markedly and significantly increased mean arterial pressure (+13.2 +/- 2.3%), heart rate (+30.3 +/- 4.7%), calf vascular resistance (+12.1 +/- 4.9%), plasma norepinephrine (+34.8 +/- 7.0%), and plasma epinephrine (+90.5 +/- 39.0%). In contrast, muscle sympathetic nerve activity showed a marked reduction (integrated activity -31.8 +/- 5.1%, P < .01). The reduction was inversely related to the increase in mean arterial pressure (r = -.67, P < .05), but the slope of the relation was markedly less (-54.1 +/- 7.5%, P < .05) than that obtained by intravenous infusion of phenylephrine in absence of smoking. The hemodynamic and neurohumoral changes were still visible 30 minutes after smoking and occurred again on smoking a second cigarette. Sham smoking was devoid of any hemodynamic and neurohumoral effect. CONCLUSIONS: These data support the hypothesis that in humans the sympathetic activation induced by smoking depends on an increased release and/or a reduced clearance of catecholamines at the neuroeffector junctions. Central sympathetic activity is inhibited by smoking, presumably via a baroreceptor stimulation triggered by the smoking-related pressor response. The baroreflex is impaired by smoking, however, indicating that partial inability to reflexly counteract the effect of sympathetic activation is also responsible for the pressor response.

Abnormal hemodynamics and elevated angiotensin II plasma levels in polydipsic patients on regular hemodialysis treatment.

To investigate the cause and the mechanisms responsible of the compulsive thirst and excessive fluid intake observed in many patients on chronic dialysis treatment, we measured plasma antidiuretic hormone (ADH), angiotensin II (Ang II) and some hemodynamic parameters in seven polydipsic and in six normodipsic patients before hemodialysis, at the end of it and several times during the interdialytic interval. Before dialysis we found that ADH was elevated in both groups (6.9 +/- 1.9 vs. 6.9 +/- 1.3 pg/ml, respectively in polydipsics and controls), whereas Ang II was abnormally high only in polydipsics (51 +/- 12 vs. 11 +/- 3 pg/ml, P < 0.01); these patients also had significantly higher heart rate and cardiac indices and lower total peripheral resistances than control patients. Overall these hemodynamic indices were related with Ang II but not with ADH. Ang II rose markedly in polydipsics after dialysis, reaching a peak at the fourth hour after its termination (136 +/- 12 pg/ml) and remained consistently elevated throughout the interdialytic period, whereas in controls Ang II was practically unchanged with respect to baseline. In contrast, ADH had minor and similar modifications in both groups, in whom also the hemodynamic changes were superimposable. Significant correlations were found between the absolute and percent changes of Ang II and those of plasma volume during the interdialytic interval (P < 0.001 for both), and between the individual values of Ang II measured during the whole study and the interdialytic weight gain (P < 0.05). These results demonstrate that polydipsic patients have abnormally high levels of Ang II before and after the hemodialysis-induced volume depletion.(ABSTRACT TRUNCATED AT 250 WORDS)

Reflex vasopressin and renin modulation by cardiac receptors in humans.

Animal studies have shown that vasopressin secretion is modulated by arterial baroreceptors and cardiopulmonary volume receptors. Whether this is the case also in humans is controversial, however. To determine whether vasopressin is reflexly modulated by cardiac volume receptors, we studied the effect on plasma vasopressin (venous blood, radioimmunoassay) of reducing venous return and left ventricular end-diastolic diameter (echocardiography) by producing a 20-minute lower body negative pressure in 14 healthy subjects (aged 49.3 +/- 3.8 years, mean +/- SEM). The data were compared with those of 14 age-matched heart-transplant recipients, i.e., subjects with cardiac denervation. In healthy subjects, lower body negative pressure at -15 mm Hg caused a modest reduction in left ventricular end-diastolic diameter (-5 +/- 3.4%) and no change in vasopressin, whereas lower body negative pressure at -37.5 mm Hg caused a more marked reduction in left ventricular end-diastolic diameter (-12 +/- 2.5%) and a small, variable, but overall statistically significant (p < 0.05) increase in vasopressin (+145 +/- 46%, p < 0.01). The left ventricular end-diastolic diameter changes induced by the two lower body negative pressure stimuli were similar in heart-transplant recipients, but the vasopressin increase seen with the lower body negative pressure at -37.5 mm Hg was abolished. The marked increase in plasma renin activity and forearm vascular resistance induced by lower body negative pressure in healthy subjects was also abolished or drastically attenuated in heart-transplant recipients.(ABSTRACT TRUNCATED AT 250 WORDS)

Regulation of vasopressin release in moderately severe essential hypertension.

Vasopressin plasma concentrations have been measured in two groups of subjects, 13 moderate essential hypertensive patients without target organ damage and eight control normotensive subjects, before and after the assumption of the upright position, and intravenous infusions of hypotonic saline (0.45% NaCl, 0.25 ml kg-1 min-1 for 1 h) and hypertonic saline (100 mmol NaCl in 50 ml). Plasma vasopressin in recumbent baseline conditions was not significantly different in the two groups. Upright posture and hypertonic challenge augmented, while hypotonic saline reduced plasma vasopressin levels, which were not significantly different between the two groups. Plasma renin activity increased in the upright position, was reduced by administration of hypotonic saline and unaffected by hypertonic saline, with no differences between the hypertensives and normotensives. After hypertonic saline, urinary flow rate and urinary sodium excretion in the hypertensive group increased to values significantly (p less than 0.05) higher than in normotensive subjects. In conclusion our study excludes significant alteration of vasopressin regulation in moderate uncomplicated hypertension. In hypertensives although the response of vasopressin to an osmotic load is preserved, the data suggest that the renal handling of the osmotic load may be altered.

[Evaluation of the effectiveness and safety of Fragmin (Kabi 2165) versus calcium heparin in the prevention of deep venous thrombosis in general surgery]. / Valutazione della efficacia e della tollerabilità di Fragmin (Kabi 2165) rispetto all'eparina calcica nella profilassi della trombosi venosa profonda in chirurgia generale.

Fourty patients who underwent general surgery have been enrolled in a double-blind controlled trial which evaluated the efficacy and safety of Fragmin, a new low molecular weight heparin, chosen to be the 1st OMS International Standard for LMWH. Fragmin 2500 UI anti-Xa once daily and unfractionated heparin 5000 UI twice daily were administered to prevent postoperative deep venous thrombosis. Prophylaxis began two hours before surgery and continued for the next 5 postoperative days. The incidence of isotopic venous thrombosis, thromboembolic disorders and bleeding complications have been evaluated. Results have shown a similar efficacy and safety profile of the two drugs, although Fragmin doses are markedly inferior to unfractionated heparin's. Moreover, Fragmin has the advantage of a single daily administration, with a better patients' compliance and an easier and less expensive nursing care.

Osmoregulation of vasopressin during acute lowering of arterial pressure by clonidine in moderate hypertension.

Hypertonic saline (100 mmol in 50 ml) was injected intravenously over 5 min in two groups of moderate essential hypertensive patients (group 1, n = 13; group 2, n = 6). In group 2, arterial pressure had been lowered by infusion of clonidine (0.3 mg in 100 ml saline), from 186 +/- 8/116 +/- 3 to 146 +/- 9/98 +/- 5 mmHg (mean +/- s.e.m.). The hypertonic stimulus increased the plasma osmolality of all subjects from 288 +/- 1 to 296 +/- 1 mosmol/kg (P less than 0.01). Plasma vasopressin increased from baseline values that were not significantly different (P less than 0.01) in each of the two groups. The increase in plasma vasopressin was significantly greater (P less than 0.05) in the group 2 hypertensives with a reduced arterial pressure (+7.81 +/- 1.79 pg/ml) than in the group 1 untreated hypertensives (+3.15 +/- 1.2 pg/ml). In our study, acute lowering of arterial pressure by clonidine did not significantly change baseline vasopressin, but facilitated osmotically induced vasopressin secretion.