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Matteo Pirro

Publications and source records attributed to Matteo Pirro.

34 records · Page 2Linked to original sources
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↗
PubMed2004

Attenuation of inflammation with short-term dietary intervention is associated with a reduction of arterial stiffness in subjects with hypercholesterolaemia.

BACKGROUND: Increased arterial stiffness has been found in patients with chronic high-grade inflammatory diseases. Whether mitigation of low-grade systemic inflammation, through a low-cholesterol/low-saturated fat diet, may have a role in improving arterial stiffness is still untested. DESIGN: We investigated whether variations in blood lipids and plasma C-reactive protein induced by low-cholesterol/low-saturated fat diet are associated with variations in large-artery stiffness in hypercholesterolaemia. METHODS: Thirty-five patients with primary hypercholesterolaemia and 15 normal control subjects were recruited for the study. Hypercholesterolaemic patients followed an 8-week low-cholesterol/low-saturated fat diet (30% total fat, 5% saturated fat, cholesterol <200 mg/daily). Anthropometric characteristics, blood lipids, plasma C-reactive protein and arterial stiffness were measured at baseline and after the diet. RESULTS: Arterial stiffness and C-reactive protein levels were higher in hypercholesterolaemic patients than in controls. Significant reductions in body weight (2 kg, 3%), plasma total cholesterol (13.4 mg/dl, 5.3%), low-density lipoprotein cholesterol (11.2 mg/dl, 6.4%), C-reactive protein (0.7 mg/l, 39%) and arterial stiffness (from 8.9+/-2.0 to 8.1+/-1.9 m/s, 11%) were achieved among hypercholesterolaemic patients after the 8-week diet (P<0.05 for all). Bivariate correlations and multivariate analysis showed reduction in arterial stiffness after short-term diet to be associated with reduction of plasma C-reactive protein levels (r=0.59, beta=0.38, P<0.05 for both). CONCLUSIONS: Short-term low-cholesterol/low-saturated fat diet in hypercholesterolaemia may be effective in improving large artery stiffness, likely through the mitigation of low-grade systemic inflammation.

Arteries↗
PubMed2003

Effect of plasma C-reactive protein levels in modulating the risk of coronary heart disease associated with small, dense, low-density lipoproteins in men (The Quebec Cardiovascular Study).

This purpose of this study was to investigate how plasma C-reactive protein (CRP), a nonspecific acute-phase reactant, modulates the risk of coronary heart disease (CHD) associated with the small, dense, low-density lipoprotein (LDL) phenotype. LDL particle size and plasma CRP were measured in the Quebec Cardiovascular Study cohort of 2,025 men free of CHD at baseline, among whom 103 had a first CHD event during a 5-year follow-up period. Plasma CRP levels were measured using the Behring Latex-Enhanced (highly sensitive) CRP assay. LDL particle size phenotype was characterized using 2% to 16% polyacrylamide gradient gel electrophoresis. There were weak but significant associations between plasma CRP levels and features of LDL size, such as the proportion of LDL with a diameter <255 A (r = 0.09, p <0.001) and LDL peak particle size (r = -0.09, p <0.001). Variations in plasma CRP levels modulated the risk of CHD associated with small LDL peak particle size (relative risk 4.3 vs 2.5 in men with high vs low plasma CRP levels, respectively) and with an elevated proportion of LDL <255 A (relative risk 6.6 vs 3.0). Thus, increased plasma CRP levels further elevate the risk of CHD associated with having small, dense LDL particles.

Age Distribution↗
PubMed2003

Effects of atorvastatin on electrophoretic characteristics of LDL particles among subjects with heterozygous familial hypercholesterolemia.

The effects of the HMG CoA reductase inhibitor atorvastatin on electrophoretic characteristics of LDL particles were evaluated in 46 patients (28 males and 18 females) with heterozygous familial hypercholesterolemia (FH) aged 20-61 carrying either a negative or a defective LDL receptor gene mutation. Following a 6 week drug-free baseline period, FH heterozygotes were treated with atorvastatin (median dose: 20 mg/day, range 10-80 mg/day)) for 6 months to maintain their plasma LDL-cholesterol concentrations between 4.0 and 5.0 mmol/l. Atorvastatin treatment significantly reduced plasma total cholesterol, LDL-cholesterol and triglyceride levels and increased plasma HDL-cholesterol. Furthermore, atorvastatin treatment significantly increased LDL peak particle diameter (LDL-PPD) by 0.5% (from 255.0+/-6.2 to 256.4+/-5.5 A, P=0.004) and reduced the absolute concentration of cholesterol among small (<255 A) and large (>260 A) LDL particles by 35% (P<0.001). Changes in LDL-PPD and plasma triglyceride levels were inversely correlated (R=-0.34; P=0.02). Stepwise multiple linear regression analyses showed that 41.6% of the variation in the LDL-PPD response to atorvastatin was attributable to the initial LDL-PPD (14.4%, P=0.003), the apo E polymorphism (12.4%, P=0.02), the nature of the LDL receptor gene mutation (9.6%, P=0.01) and change in triglyceride levels (5.2%, P=0.04). Moreover, the reduction in the cholesterol content of LDL <255 A was directly correlated with the daily dosage of atorvastatin (P=0.05). Results of the present study showed that atorvastatin alters significantly LDL heterogeneity in patients at high risk of coronary heart disease (CHD) such as FH heterozygotes. These results also suggest that genetic and metabolic factors may be important determinants of atorvastatin-induced changes of LDL particle size and distribution among FH heterozygotes.

Adult↗
PubMed2003

Mechanisms of high-density lipoprotein cholesterol effects on the endothelial function in hyperlipemia.

High-density lipoprotein-cholesterol (HDL-c) has a favorable influence on the endothelial function, but the mechanisms of this protective action are not fully understood. We studied lipid parameters, soluble adhesion molecules (vascular cell adhesion molecule-1 [VCAM-1], intercellular adhesion molecule [ICAM-1], E-selectin) oxidized low-density lipoproteins (LDL), and brachial-artery flow-mediated vasodilation (FMV) in 184 hyperlipemic patients (90 men, age 54 +/- 10 years, waist/hip circumference ratio 0.89 +/- 0.07, LDL-cholesterol [LDL-c] 4.9 +/- 1.3 mmol/L, triglycerides 1.8 +/- 0.9 mmol/L, HDL-c 1.3 +/- 0.5 mmol/L) after excluding those with current smoking, diabetes, hypertension, and vascular diseases. Patients were divided into 2 groups on the basis of HDL-c levels: < 1.03 mmol/L (n = 53) v >or= 1.03 mmol/L (n = 131). Patients with low HDL-c showed significantly lower LDL-c (P <.05), higher triglycerides (P <.001), higher body mass index (P <.02), lower FMV (3.7% +/- 2.0% v 4.9% +/- 3.4%, P <.002), higher VCAM-1 (1,195 +/- 395 ng/mL v 984 +/- 303 ng/mL, P <.01), and higher ICAM-1 (406 +/- 78 ng/mL v 364 +/- 68 ng/mL, P <.01). E-selectin and oxidized LDL showed no significant differences. In a multivariate age, oxidized LDL and brachial artery diameter predicted a lower FMV, while HDL-c was an independent predictor of a greater FMV (P =.003). Increasing levels of VCAM-1 and ICAM-1 were predicted by lower HDL-c, while higher oxidized LDL predicted higher VCAM-1 (P <.05). Our data suggest that in hyperlipemic subjects free of cardiovascular disease low HDL-c negatively modulates endothelial function through a lack of oxidation inhibition and a concomitant overexpression of adhesion molecules.

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

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

Plasma free fatty acid levels and the risk of ischemic heart disease in men: prospective results from the Québec Cardiovascular Study.

Insulin resistance, through numerous related disturbances in glucose and lipoprotein-lipid metabolism, is associated with an increased risk of ischemic heart disease (IHD). The purpose of the present study was to examine the relationship between increased plasma free fatty acid (FFA) concentrations, as a feature of the insulin resistance syndrome, and the risk of IHD in men. Analyses were carried out in a nested, case-control sample of men selected from a population of 2103 individuals without IHD at baseline among whom 114 developed IHD during a 5-year follow-up period. Incident IHD cases were matched with controls for age, body mass index, smoking habits and alcohol intake. Analyses were performed while excluding (88 cases and 98 controls) and including (103 cases and 99 controls) patients with type 2 diabetes. Among non-diabetic individuals, elevated plasma FFA concentrations (3rd tertile of the distribution) yielded a twofold increase in the risk of IHD (odds ratio [OR] 2.1, P=0.05) compared with lower plasma FFA levels (lowest tertile) after adjusting for non-lipid risk factors. Further adjustment for insulin, triglycerides, apolipoprotein B, HDL cholesterol and small dense LDL attenuated significantly the relationship between plasma FFA concentrations and the risk of IHD. High plasma FFA levels showed no synergism with selected features of the insulin resistance syndrome in determining the risk of IHD. Inclusion of diabetic subjects in the study did not improve FFA independent prognostic value to the risk of IHD. These results suggest that elevated plasma FFA concentrations are associated with an increased risk of IHD. However, a single fasting measurement of plasma FFA levels does not appear to improve our ability to predict IHD onset in men when information on other risk factors is considered.

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↗