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Leonella Pasqualini

Publications and source records attributed to Leonella Pasqualini.

13 recordsLinked to original sources
PubMed2005

Paraoxonase-1 activity modulates endothelial function in patients with peripheral arterial disease.

Human serum paraoxonase-1 (PON1) is thought to play a role in the favorable vascular effects of high-density lipoproteins, mainly through a reduction in low-density lipoprotein oxidation. Endothelial dysfunction, characterized by an impaired capacity of the arteries to dilate in response to a number of stimuli, represents the earliest stage of atherosclerosis. We performed the present study in 37 patients with peripheral arterial disease, with the aim of investigating the influence of PON1 Q192R polymorphism and activity on peripheral endothelial function, evaluated as brachial-artery flow-mediated vasodilation (FMV). Patients with the R allele (QR or RR genotype, n=19) had significantly higher PON1 activity [408 U/mL (309-456) versus 180 U/mL (141-243), p<0.001] and greater brachial FMV (5.7+/-3.9% versus 3.0+/-2.8%, p<0.001) than those with Q allele (QQ genotype, n=18). In the whole population, PON1 activity showed a direct relation to brachial FMV (r=0.46, p=0.004). In a multivariate linear regression analysis, the only independent predictors of brachial FMV were PON1 activity (beta=0.40, p=0.008), brachial-artery diameter (beta=-0.39, p=0.01) and male sex (beta=-0.27, p=0.04). These finding support the importance of PON1 activity as a modulating factor of the endothelial function.

Aged↗
PubMed2004

Prognostic significance of isolated, non-specific left ventricular repolarization abnormalities in hypertension.

OBJECTIVE: Clinicians are often confronted with the incidental finding of isolated minor, non-specific repolarization changes on the electrocardiogram (ECG) in hypertensive patients. The aim of this study was to investigate the prognostic significance of such changes. DESIGN: Prospective, observational study. METHODS: A total of 1970 hypertensive patients without prevalent cardiovascular disease were followed for up to 9.1 years (mean 4.7 years). Patients with ECG abnormalities including ischaemia, previous infarction, bundle branch block, atrial fibrillation and ventricular pre-excitation were excluded. Patients were divided into three groups: normal left ventricular (LV) repolarization (n = 1355); minor repolarization changes (n = 504); and typical LV strain (n = 111). RESULTS: During follow-up, 78 patients developed new-onset ischaemic heart disease. The event rates were 0.50, 1.28 and 3.08 per 100 patient-years in the groups with normal repolarization, minor changes, and typical LV strain, respectively (P < 0.001). After adjustment for the effect of age, sex, diabetes, serum cholesterol, smoking, LV hypertrophy and 24-h pulse pressure, the risk for developing coronary events was higher in patients with minor repolarization changes (hazard ratio 2.07, 95% confidence interval 1.23-3.47; P < 0.01) or LV strain (hazard ratio 4.00, 95% confidence interval 2.09-7.65; P < 0.001) than in patients with normal repolarization (reference category). Population-attributable risks were 21 and 14%, respectively. Minor ST-T changes also retained an adverse prognostic value among patients without LV hypertrophy (hazard ratio 1.90, 95% confidence interval 1.08-3.33; P = 0.026). CONCLUSION: We have identified minor, non-specific LV repolarization changes as a novel, independent risk factor for ischaemic heart disease in patients with uncomplicated hypertension.

Adult↗
PubMed2003

Effect of body weight changes on 24-hour blood pressure and left ventricular mass in hypertension: a 4-year follow-up.

BACKGROUND: Few data are available on the long-term effects of weight loss on 24-h blood pressure (BP) and left ventricular mass in overweight hypertensive patients. METHODS: A total of 181 never-treated overweight hypertensive subjects (body mass index, 25 to 39 kg/m(2), office BP 145/94 +/- 12/7 mm Hg) had 24-h BP monitoring and echocardiography twice, at baseline and after 3.8 +/- 2 years (minimum 1 year). None of the subjects received antihypertensive drugs during the follow-up. Main outcome measures were changes in 24-h BP and in left ventricular mass. RESULTS: Percent change in body weight had a direct relationship with 24-h BP changes (r = 0.35 and 0.31 for systolic and diastolic BP, respectively; both P <.001). The associations with office BP changes (r = 0.13, P =.10 for systolic BP; r = 0.15, P =.06 for diastolic BP) were significantly weaker (both P <.01, z test). The patients who lost weight during follow-up (n = 106) had a significantly lower increase in 24-h BP (+0.6 +/- 9/ +0.2 +/- 6 v +4.9 +/- 9/ +2.7 +/- 7 mm Hg for systolic/diastolic BP, both P <.01) and in left ventricular mass (-3 +/- 30 g v +9 +/- 32 g, P <.02) than the remaining subjects. In a multiple linear regression, a 10% weight loss independently predicted a 4.3/3.8 mm Hg decrease in 24-h systolic/diastolic BP. CONCLUSIONS: Long-term weight loss determines a sustained BP reduction during the 24 h and a decrease in left ventricular mass in overweight hypertensive subjects. The relation of weight loss with ambulatory BP changes is closer than that with office BP.

Adult↗
PubMed2003

Early vascular damage in primary hypoalphalipoproteinemia.

The relationship between hypoalphalipoproteinemia (hypoalpha), a metabolic disorder characterized by reduced high-density lipoprotein (HDL) cholesterol levels, and atherosclerotic disease is not completely understood. We investigated arterial functional and structural changes in 19 subjects with hypoalpha (HDL cholesterol < or = 0.7 mmol/L for men and < or = 0.8 mmol/L for women; 13 men; 47 +/- 7 years) and in 21 healthy control subjects (11 men; 46 +/- 13 years). Brachial-artery flow-mediated vasodilation (FMV) and intima-media thickness (IMT) of the carotid and femoral arteries were determined in all subjects. FMV was significantly lower in hypoalpha than in controls (5.6% +/- 4.3% v 8.2% +/- 2.7%; P <.05). IMT was greater in hypoalpha than in controls at both the internal carotid (0.83 +/- 0.1 mm v 0.69 +/- 0.1 mm) and superficial femoral level (0.83 +/- 0.2 mm v 0.68 +/- 0.1 mm; both P <.05). FMV had a positive correlation with HDL cholesterol (r =.42, P =.06) and a negative one with triglycerides (r = -0.38, P =.01). An inverse relationship was found between HDL cholesterol and internal carotid and superficial femoral IMT (r = -0.64 and r = -0.60, respectively; P <.01 for both) and a positive one between triglycerides and internal carotid and superficial femoral IMT (r =.53 and r =.47, P <.05). In a multivariate regression analysis, brachial FMV was predicted by HDL cholesterol and brachial diameter (beta =.42 and -0.43, respectively; both P <.05). HDL cholesterol was the only significant predictor of internal carotid and superficial femoral IMT (beta = -0.45 and -0.49, respectively; both P <.05). In conclusion, subjects with primary hypoalpha, without overt cardiovascular disease, are characterized by an impaired endothelial function and by an increase in large-artery IMT.

Adult↗
PubMed2003

Plasma C-reactive protein in subjects with hypo/hyperalphalipoproteinemias.

Hypoalphalipoproteinemia (Hypo-A), a lipid disorder characterized by low high-density lipoprotein (HDL)-cholesterol (HDL-C) levels, is frequently associated with an increased risk of suffering future coronary heart disease (CHD). Conversely, hyperalphalipoproteinemia (Hyper-A) is a characterized by high HDL-C concentrations and is possibly associated with longevity and protection against CHD. Whether plasma C-reactive protein (CRP) level, an emerging marker of CHD risk, may be influenced by either extremely low or high HDL-C concentrations is yet to be determined. Plasma levels of lipids and CRP have been measured in 52 middle-aged men and women, clinically free of CHD, including 20 subjects with Hypo-A, 12 with Hyper-A, and 20 healthy normolipemic age-matched controls. CRP levels were the highest in Hypo-A [0.22 mg/dL (interquartile range, 0.15 to 0.44)], the lowest in Hyper-A [0.03 mg/dL (0.02 to 0.07)], and intermediate in the control group [0.10 mg/dL (0.05 to 0.20)]. Differences in plasma CRP concentrations were significant between Hypo-A and the other 2 groups, as well as between Hyper-A and controls. Plasma CRP levels showed a particularly strong correlation with plasma HDL-C concentrations (r = -.66, P <.001). In multivariate models, HDL-C represented the only significant predictor of circulating levels of CRP. In conclusion, in subjects with Hypo-A or Hyper-A, HDL-C levels may account for plasma CRP variations independent of other potential cardiovascular risk factors.

Adult↗
PubMed2003

Increased C-reactive protein concentrations in never-treated hypertension: the role of systolic and pulse pressures.

OBJECTIVE: To test whether the plasma concentration of C-reactive protein (CRP), a sensitive marker of systemic inflammation, is increased in patients with newly diagnosed, never-treated hypertension and whether blood pressure and its pulsatile component, pulse pressure, are correlated with plasma CRP concentration independently of a consistent number of cardiovascular risk factors. DESIGN: Cross-sectional study in a hospital outpatient hypertension clinic. METHODS: A total of 135 newly diagnosed, never-treated patients with hypertension and 40 healthy matched non-hypertensive controls underwent office and 24-h blood pressure measurement and blood sampling for determination of plasma CRP and serum lipid concentrations. RESULTS: Plasma CRP concentration was greater in hypertensive individuals (1.85 mg/l, interquartile range 0.74-3.64) than in control individuals (1.01 mg/l, interquartile range 0.67-1.88; P = 0.02). In the entire population, CRP had a significant direct association with office systolic blood pressure and pulse pressure, but not with diastolic blood pressure. Among hypertensive patients, plasma CRP was related to 24-h systolic blood pressure (r = 0.28, P < 0.01) and pulse pressure (r = 0.32, P < 0.01), but not to diastolic blood pressure (r = 0.12, P > 0.2). CRP was also directly associated with body mass index (r = 0.25, P < 0.01), serum low-density lipoprotein cholesterol (r = 0.21, P = 0.03) and serum triglycerides (r = 0.21, P = 0.03). In the multivariate analysis, systolic blood pressure and pulse pressure, but not diastolic blood pressure, were significant predictors of plasma CRP concentration when a consistent number of cardiovascular risk factors was controlled for simultaneously. CONCLUSIONS: Systolic blood pressure and pulse pressure, but not diastolic blood pressure, are predictors of plasma C-reactive protein concentrations in patients with newly diagnosed, never-treated hypertension, irrespective of the potential proinflammatory action of traditional cardiovascular risk factors.

Adult↗
PubMed2003

Capillary rarefaction and abnormal cardiovascular reactivity in hypertension.

OBJECTIVE: To determine the effects of capillary rarefaction on cardiovascular reactivity and microcirculatory functioning in essential hypertension. DESIGN: Hypertension is associated with abnormal cardiovascular reactivity and increased vasoconstriction. Capillary rarefaction amplifies these abnormalities, which modify microcirculatory hemodynamics. Hence this study of the hemorheological pattern and the veno-arteriolar reflex in hypertensive patients and normotensive control subjects. METHODS: Sixty-one men with never-treated essential hypertension and capillary rarefaction (< 80 capillaries per field) and 20 age-matched and sex-matched controls underwent a strenuous cycle ergometer test to monitor, during exercise and recovery, the blood pressure profile and the hemorheological pattern: blood viscosity at low shear, hematocrit and leukocyte counts, soluble P-selectin levels, and red and white blood cell filterability rates. The veno-arteriolar reflex was determined by laser-Doppler flowmetry before exercise and at recovery.RESULTS Hypertensive men with < or = 72 capillaries per field had an abnormal hemorheological profile before exercise. The physiological response to exercise was observed only in the controls and in hypertensives with > or = 73 capillaries per field. Abnormal responses to exercise worsened as capillaries were more rarefied. At recovery, hemorheological parameters in hypertensives with 65-72 capillaries per field returned to baseline, remaining significantly (P < 0.05) different to control values. Variations in the hemorheological pattern in hypertensives with < 64 capillary per field persisted at recovery. The veno-arteriolar reflex followed the same pattern. CONCLUSION: A reduced microvascular network may contribute to abnormal cardiovascular reactivity and to exercise-induced rheological abnormalities in hypertension.

Adult↗
PubMed2003

Prostaglandin E1 improves endothelial function in critical limb ischemia.

Prostaglandin E1 (PGE1) may relieve rest pain and heal ulcers in critical limb ischemia, but its mechanism of action is still incompletely understood. To investigate the effects of PGE1 treatment on endothelial function evaluated as brachial artery flow-mediated vasodilation (FMV) and on soluble adhesion molecule plasma levels (vascular adhesion molecule-1 [sVCAM-1] and intercellular adhesion molecule-1 [sICAM-1]), 12 patients with critical limb ischemia were treated with daily PGE IV infusion (alprostadil 60 microg) for 2 weeks. FMV and plasma sICAM-1 and sVCAM-1 concentrations were determined at baseline, after the first infusion, and after 1 and 2 weeks. Compared with 30 healthy control subjects, patients had higher baseline sVCAM-1 (2.402 +/- 296 ng/ml vs 972 +/- 117 ng/ml) and sICAM-1 levels (464 +/- 51 ng/ml vs 206 +/- 37 ng/ml, both p < 0.05) and lower FMV (1.0 +/- 1.1% vs 5.6 +/- 1.6%, p < 0.05). sICAM-1 concentration progressively decreased with treatment (from 464 +/- 51 ng/ml to 326 +/- 56 ng/ml, 288 +/- 42 ng/ml, and 279 +/- 44 ng/ml after the first dose and, respectively, after 1 and 2 weeks; all p < 0.05). sVCAM-1 showed a reduction after 2 weeks (from 2.402 +/- 296 ng/ml to 1.916 +/- 176 ng/ml; p < 0.05). FMV improved after 1 and 2 weeks (from 1.0 +/- 1.1% to 3.1 +/- 0.6% and 5.2 +/- 2.1%, both p < 0.05). In conclusion, treatment with PGE1 determines a significant improvement in endothelial function in patients with critical limb ischemia.

Aged↗
PubMed2003

The influence of iloprost on blood rheology and tissue perfusion in patients with intermittent claudication.

BACKGROUND: In peripheral vascular disease (PVD), impaired blood viscosity (BV) plays a major role in residual microvascular perfusion. Indeed, during acute leg ischaemia factors influencing microvascular BV include the plasma fibrinogen concentration, red and white blood cell rheology, as well as platelet aggregation and activation. AIM: To assess the effects of Iloprost in patients with PVD. METHODS: The effects of an infusion of a single dose of Iloprost (from 0.5 up to a maximum of 2 ng/kg/min. over 6 hours) in 16 patients with stage II peripheral vascular disease on blood rheology and tissue perfusion were determined in a double-blind placebo-controlled study, using repeated treadmill exercise test to stress leg circulation. Blood viscosity at low shear, soluble P-selectin levels (expression of platelet activation), unfractionated leukocyte and erythrocyte filterability rates, plasma fibrinogen concentration, haematocrit, leukocyte and platelet counts and transcutaneous oxygen pressure (TcPO(2)) were measured in two matched groups of 8 PVD patients before and after Iloprost infusion. RESULTS: Controlled peripheral ischaemia generated an impaired haemorheological profile; Iloprost reduced the impairments in BV and the filterability rates of unfractionated leukocytes and erythrocytes, inhibited platelet activation, and improved erythrocyte deformability. These changes were associated with significant shortening of the TcPO(2) half recovery time (the drop of TcPO(2) occurs because the ischaemic skeletal muscle steals oxygen from the skin), indicating that ischaemic damage had been contained. CONCLUSIONS: Our results show that the infusion of a single dose of Iloprost in patients with PVD is associated with a significant improvement in microvascular functioning

Blood Viscosity↗
PubMed2002

Prognostic significance of left ventricular diastolic dysfunction in essential hypertension.

OBJECTIVES: We sought to assess the prognostic value of alterations in left ventricular (LV) diastolic function in patients with essential hypertension. BACKGROUND: Alterations in LV diastolic function are frequent in patients with hypertension, even in the absence of LV hypertrophy, but their prognostic significance has never been investigated. METHODS: In the setting of the Progetto Ipertensione Umbria Monitoraggio Ambulatoriale (PIUMA) study, we followed, for up to 11 years (mean: 4.4 years), 1,839 Caucasian hypertensive patients (50 +/- 12 years, 53% men, blood pressure (BP) 156/98 mm Hg) without previous cardiovascular events, who underwent Doppler echocardiography and 24-h BP monitoring before therapy. The early/atrial (E/A) mitral flow velocity ratio was calculated and corrected for age and heart rate (HR). RESULTS: During follow-up, there were 164 major cardiovascular events (2.04 per 100 patient-years). The incidence of cardiovascular events was 2.47 and 1.65 per 100 patient-years in patients with an age- and HR-adjusted E/A ratio below (n = 919) and above (n = 920) the median value, respectively (p < 0.005 by the log-rank test). In Cox analysis, controlling for age, gender, diabetes, cholesterol, smoking, LV mass and 24-h systolic BP (all p < 0.05), a low age- and HR-adjusted E/A ratio conferred an increased risk of cardiovascular events (odds ratio 1.57, 95% confidence interval [CI] 1.11 to 2.18, p < 0.01). A 21% excess risk was found for each 0.3 decrease of the adjusted E/A ratio (95% CI from +2% to +43%; p = 0.03). CONCLUSIONS: Impaired LV early diastolic relaxation, detected by pulsed Doppler echocardiography, identifies hypertensive patients at increased cardiovascular risk. Such association is independent of LV mass and ambulatory BP.

Adult↗
PubMed2002

Increased postprandial lipemia in patients with normolipemic peripheral arterial disease.

METHODS: We evaluated the postprandial lipid metabolism in patients with normolipemic peripheral arterial disease (PAD) after the administration of an oral fat load. Total cholesterol, low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), HDL2 and HDL3 subfractions, triglycerides (TGs), lipoprotein(a), and LDL size were determined at baseline and for 8 hours after the meal. RESULTS: In patients with PAD, TGs increased significantly at the 4th, 6th, and 8th hours postprandially; in control subjects, TGs increased at the 4th and 6th hours. HDL decreased significantly at the 4th, 6th, and 8th hours in patients with PAD and at the 6th hour in control subjects. The magnitude of postprandial lipemia, expressed as "the area under the incremental curve for TGs," was higher in patients with PAD than in control subjects (770 +/- 476 vs 391 +/- 195 mg/dL at 8 hours, P <.05). Multiple-regression analysis showed that baseline TGs were positively related to the magnitude of postprandial lipemia (P =.01) and that LDL size was negatively related (P =.05). CONCLUSIONS: This is the first documentation of postprandial behavior in patients with normolipemic PAD, suggesting the relevance of postprandial lipoprotein metabolism in the pathogenesis of peripheral atherosclerosis.

Aged↗