Publications (21)83.87 Total impact
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Article: Protective Role of Vascular Smooth Muscle Cell PPARγ in Angiotensin II-induced Vascular Disease.
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ABSTRACT: AIMS: Vascular PPARγ activation improves vascular remodeling and endothelial function in hypertensive rodents. The goal of this study was to determine that vascular smooth muscle cell (VSMC) PPARγ exerts a vascular protective role beyond its metabolic effects.Methods and ResultsWe generated a model of adult inducible VSMC-specific PPARγ inactivation to test the hypothesis that PPARγ counteracts Ang II-induced vascular remodeling and endothelial dysfunction. Inducible VSMC PPARγ mice were generated by crossing PPARγ floxed mice with mice expressing a tamoxifen-inducible Cre recombinase smooth muscle (sm) myosin heavy chain promoter control. Eight-to-ten week old smPPARγ(-/-) and control mice were infused with a nonpressor dose of Ang II for 7d. Blood pressure was unaffected. Mesenteric arteries showed eutrophic remodeling in Ang II-infused control mice and hypertrophic remodeling in Ang II-infused smPPARγ(-/-) mice. Endothelium-dependent relaxation to acetylcholine was reduced in smPPARγ(-/-) mice and further impaired by Ang II infusion, and was unaffected by an inhibitor of NO synthase, suggesting a defect of NO-mediated relaxation. SmPPARγ deletion increased the sensitivity to Ang II-induced contraction. SmPPARγ(-/-) mice exhibited enhanced Ang II-induced vascular NADPH oxidase activity and adhesion molecule ICAM-1 and chemokine MCP-1 expression. The antioxidant superoxide dismutase 3 (Sod3) expression was decreased by smPPAR deletion. Ang II infusion increased expression of CD3δ and decreased adiponectin in perivascular adipose tissue of smPPARγ(-/-) mice. CONCLUSION: Inducible PPARγ inactivation in VSMCs exacerbated Ang II-induced vascular remodeling and endothelial dysfunction via enhanced vascular oxidative stress and inflammation, revealing the protective role of VSMC PPARγ in angiotensin II-induced vascular injury.Cardiovascular research 12/2012; · 5.80 Impact Factor -
Article: Seasonal and monthly variation in occurrence of hypertensive urgency.
Internal and Emergency Medicine 11/2012; · 2.06 Impact Factor -
Article: Plasma levels of matrix metalloproteinases and their inhibitors in hypertension: a systematic review and meta-analysis
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ABSTRACT: Background: Hypertension is a major cause of cardiovascular remodeling. In the cardiovascular system, the remodeling of the extracellular matrix is controlled by the matrix metalloproteinases (MMPs) and the tissue inhibitors of MMPs (TIMPs). The aim of this meta-analysis is to elucidate the behavior of plasma MMP and TIMP levels in hypertension and their relationship to cardiovascular remodeling. Methods: MEDLINE and EMBASE databases were searched up to July 2011. Studies were considered eligible if they provided values of plasma MMPs and TIMPs in hypertensive patients. Given the high variability of the plasma biomarker values among studies, the standardized mean difference (SMD) was calculated. Results: Ten studies provided plasma MMP-9; the SMD between 778 hypertensive patients and 669 controls was 1.95 units (P < 0.05). Thirteen studies provided plasma TIMP-1; the SMD between 851 hypertensive patients and 646 normotensive individuals was 1.92 units (P < 0.01). Three studies investigated whether plasma TIMP-1 predicted left ventricular (LV) remodeling; the SMD between 92 hypertensive patients with and 88 hypertensive patients without LV hypertrophy was 5.81 units (P < 0.05). As for diastolic heart failure (HF), five studies provided data for plasma MMP-2; the SMD between 321 hypertensive patients with and 334 hypertensive patients without HF was 2.36 units (P < 0.01). The heterogeneity among studies was high. Conclusions: These results suggest that MMP-2, MMP-9 and TIMP-1 may have a role as biomarkers of cardiovascular remodeling in hypertension. If these results are confirmed in prospective clinical studies, they could provide new tools to stratify cardiovascular risk in hypertensive patients.Journal of Hypertension 12/2011; 30(1):3–16. · 4.02 Impact Factor -
Article: Plasma levels of matrix metalloproteinases and their inhibitors in hypertension: a systematic review and meta-analysis.
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ABSTRACT: Hypertension is a major cause of cardiovascular remodeling. In the cardiovascular system, the remodeling of the extracellular matrix is controlled by the matrix metalloproteinases (MMPs) and the tissue inhibitors of MMPs (TIMPs). The aim of this meta-analysis is to elucidate the behavior of plasma MMP and TIMP levels in hypertension and their relationship to cardiovascular remodeling. MEDLINE and EMBASE databases were searched up to July 2011. Studies were considered eligible if they provided values of plasma MMPs and TIMPs in hypertensive patients. Given the high variability of the plasma biomarker values among studies, the standardized mean difference (SMD) was calculated. Ten studies provided plasma MMP-9; the SMD between 778 hypertensive patients and 669 controls was 1.95 units (P < 0.05). Thirteen studies provided plasma TIMP-1; the SMD between 851 hypertensive patients and 646 normotensive individuals was 1.92 units (P < 0.01). Three studies investigated whether plasma TIMP-1 predicted left ventricular (LV) remodeling; the SMD between 92 hypertensive patients with and 88 hypertensive patients without LV hypertrophy was 5.81 units (P < 0.05). As for diastolic heart failure (HF), five studies provided data for plasma MMP-2; the SMD between 321 hypertensive patients with and 334 hypertensive patients without HF was 2.36 units (P < 0.01). The heterogeneity among studies was high. These results suggest that MMP-2, MMP-9 and TIMP-1 may have a role as biomarkers of cardiovascular remodeling in hypertension. If these results are confirmed in prospective clinical studies, they could provide new tools to stratify cardiovascular risk in hypertensive patients.Journal of hypertension 11/2011; 30(1):3-16. · 4.02 Impact Factor -
Article: OSA, metabolic syndrome and CPAP: effect on cardiac remodeling in subjects with abdominal obesity.
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ABSTRACT: We evaluated whether obstructive sleep apnoea (OSA) and continuous positive airway pressure (CPAP) treatment influence left ventricular (LV) remodelling independently of abdominal obesity and metabolic syndrome (MetS). Cardiorespiratory examination, 24-h BP monitoring and echocardiogram were performed in overweight/obese patients with increased abdominal adiposity and symptoms suggesting OSA : OSA/MetS (n.50), OSA/noMetS (n.22), noOSA/MetS (n.29), noOSA/noMets (n.16). The evaluation was repeated in 41 patients after ≥18 months of CPAP. Despite similar age, gender, BMI and 24-h BP, the 2 groups with MetS had greater LV remodelling (LV hypertrophy and diastolic dysfunction) than the 2 groups without MetS. From multiple regression analysis independent determinants for LV mass were MetS, 24-h systolic BP and age, for LV diastolic function were LV mass index, MetS and age. After CPAP, the 20 patients with decreased body weight showed diastolic BP decrease, LV hypertrophy regression and diastolic function improvement, whereas, despite similar respiratory improvement, BP and LV parameters were unchanged in the 21 patients with body weight unchanged/increased. In patients with increased abdominal adiposity, LV remodelling is not associated to OSA per se; chronic CPAP treatment does not influence LV remodelling whose regression is mainly linked to body weight decrease.Respiratory medicine 11/2011; 106(1):145-52. · 2.33 Impact Factor -
Article: Inactivation of endothelial proprotein convertase 5/6 decreases collagen deposition in the cardiovascular system: role of fibroblast autophagy.
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ABSTRACT: Proprotein convertase (PC) 5/6 belongs to a family of secretory proteases involved in proprotein proteolysis. Several studies suggest a role for PC5/6 in cardiovascular disease. Because lethality at birth of mice lacking PC5/6 precluded elucidation of its function in the adult, we generated mice in which the gene of PC5/6 (pcsk5) is specifically inactivated in endothelial cells (ecKO), which are viable and do not exhibit overt abnormalities. In order to uncover the function of PC5/6 in the cardiovascular system, the effect of ecKO was studied in aging mice. In 16 to 18-month-old ecKO mice, the left ventricle (LV) mass, media cross-sectional area of aorta and coronary arteries, and media-to-lumen ratio of mesenteric arteries were decreased. The LV presented decreased diastolic function, and mesenteric arteries showed decreased stiffness. Collagen was decreased in the LV myocardial interstitium and perivascularly in coronary arteries and aorta. Cardiovascular hypotrophy likely develops with aging, since no significant changes were observed in 2-month-old ecKO mice. Fibroblasts, as a source of collagen in myocardium and vasculature, may play a role in the decrease in collagen deposition. Fibroblasts co-cultured with ecKO endothelial cells showed decreased collagen production, decreased insulin-like growth factor (IGF)-1/Akt/mTOR signaling, and enhanced autophagic activation. PC5/6 inactivation in endothelial cells results in cardiovascular hypotrophy associated with decreased collagen deposition, decreased LV diastolic function, and vascular stiffness, suggesting a trophic role of endothelial PC5/6 in the cardiovascular system, likely mediated by IGF-1/Akt/mTOR signaling and control of autophagy.Journal of Molecular Medicine 06/2011; 89(11):1103-11. · 4.67 Impact Factor -
Article: Mthfr deficiency induces endothelial progenitor cell senescence via uncoupling of eNOS and downregulation of SIRT1.
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ABSTRACT: Hyperhomocysteinemia (HHcy) has been shown to induce endothelial dysfunction in part as a result of enhanced oxidative stress. Function and survival of endothelial progenitor cells (EPCs, defined as sca1(+) c-kit(+) flk-1(+) bone marrow-derived cells), which significantly contribute to neovascularization and endothelial regeneration, depend on controlled production of reactive oxygen species (ROS). Mice heterozygous for the gene deletion of methylenetetrahydrofolate reductase (Mthfr(+/-)) have a 1.5- to 2-fold elevation in plasma homocysteine. This mild HHcy significantly reduced the number of circulating EPCs as well as their differentiation. Mthfr deficiency was also associated with increased ROS production and reduced nitric oxide (NO) generation in Mthfr(+/-) EPCs. Treatment of EPCs with sepiapterin, a precursor of tetrahydrobiopterin (BH(4)), a cofactor of endothelial nitric oxide synthase (eNOS), significantly reduced ROS and improved NO production. mRNA and protein expression of eNOS and the relative amount of eNOS dimer compared with monomer were decreased by Mthfr deficiency. Impaired differentiation of EPCs induced by Mthfr deficiency correlated with increased senescence, decreased telomere length, and reduced expression of SIRT1. Addition of sepiapterin maintained cell senescence and SIRT1 expression at levels comparable to the wild type. Taken together, these results demonstrate that Mthfr deficiency impairs EPC formation and increases EPC senescence by eNOS uncoupling and downregulation of SIRT1.AJP Heart and Circulatory Physiology 12/2010; 300(3):H745-53. · 3.71 Impact Factor -
Article: Endothelial nitric oxide synthase uncoupling and perivascular adipose oxidative stress and inflammation contribute to vascular dysfunction in a rodent model of metabolic syndrome.
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ABSTRACT: The metabolic syndrome represents a constellation of cardiovascular risk factors that promote the development of cardiovascular disease. Oxidative stress is a mediator of endothelial dysfunction and vascular remodeling. We investigated vascular dysfunction in the metabolic syndrome and the oxidant mechanisms involved. New Zealand obese (NZO) mice with metabolic syndrome and New Zealand black control mice were studied. NZO mice showed insulin resistance and increased visceral fat and blood pressure compared with New Zealand black mice. Mesenteric resistance arteries from NZO mice exhibited increased media:lumen ratio and media cross-sectional area, demonstrating hypertrophic vascular remodeling. Endothelium-dependent relaxation to acetylcholine, assessed by pressurized myography, was impaired in NZO mice, not affected by N(G)-nitro-l-arginine methyl ester, inhibitor of endothelial NO synthase, and improved by the antioxidant Tempol, suggesting reduced NO bioavailability and increased oxidative stress. Dimer:monomer ratio of endothelial NO synthase was decreased in NZO mice compared with New Zealand black mice, suggesting endothelial NO synthase uncoupling. Furthermore, vascular superoxide and peroxynitrite production was increased, as well as adhesion molecule expression. Perivascular adipose tissue of NZO mice showed increased superoxide production and NADPH oxidase activity, as well as adipocyte hypertrophy, associated with inflammatory Mac-3-positive cell infiltration. Vasoconstriction to norepinephrine decreased in the presence of perivascular adipose tissue in New Zealand black mice but was unaffected by perivascular adipose tissue in NZO mice, suggesting loss of perivascular adipose tissue anticontractile properties. Our data suggest that this rodent model of metabolic syndrome is associated with perivascular adipose inflammation and oxidative stress, hypertrophic resistance artery remodeling, and endothelial dysfunction, the latter a result of decreased NO and enhanced superoxide generated by uncoupled endothelial NO synthase.Hypertension 10/2009; 54(6):1384-92. · 6.21 Impact Factor -
Article: Role of the renin-angiotensin system in vascular inflammation.
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ABSTRACT: Angiotensin (Ang) II, the main effector of the renin-angiotensin system (RAS), is one of the major mediators of vascular remodeling in hypertension. Besides being a potent vasoactive peptide, Ang II exerts proinflammatory effects on the vasculature by inducing integrins, adhesion molecules, cytokines and growth and profibrotic mediators through activation of redox-sensitive pathways and transcription factors. Clinical findings suggest that inflammation participates in the mechanisms involved in the pathophysiology of hypertension and its complications. Antagonists of the RAS have been shown to exert cardiovascular protection, in part through their vascular anti-inflammatory effects. However, further studies are needed to better understand whether inflammatory biomarkers might be clinically useful for cardiovascular risk stratification and whether targeting inflammation pharmacologically will improve cardiovascular outcomes beyond blood pressure reduction. The present review addresses recent findings regarding the pathophysiology of vascular inflammation in hypertension, focusing specifically on the role of Ang II.Trends in Pharmacological Sciences 08/2008; 29(7):367-74. · 10.93 Impact Factor -
Article: Effects of dual blockade of Renin-Angiotensin system on concentric left ventricular hypertrophy in essential hypertension: a randomized, controlled pilot study.
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ABSTRACT: The renin-angiotensin system (RAS) plays a major role in promoting left ventricular (LV) remodeling in essential hypertension. We designed a controlled, randomized pilot study aimed to test the hypothesis that the dual RAS blockade with angiotensin-converting enzyme (ACE) inhibitor (ACEi) + angiotensin II receptor blocker (ARB) can be more effective in decreasing LV hypertrophy and improving diastolic function than a largely employed association such as ACEi + calcium-antagonist (Ca-A). Twenty-four never-treated hypertensive patients with LV concentric hypertrophy were randomized to ramipril + candesartan or ramipril + lercanidipine. Before and after the 6-month treatment they underwent a 24-h blood pressure (BP) monitoring and echocardiographic examination. At baseline, age, body mass index (BMI), 24-h BP, and LV morpho-functional parameters were similar between the two groups. The 6-month treatment induced in both groups a significant decrease of 24-h BP, septal and posterior wall thickness, and LV mass index (LVMi) (ACEi + ARB 155 +/- 19 to 122 +/- 17 g/m(2), P < 0.0001; ACEi + Ca-A 146 +/- 18 to 127 +/- 20 g/m(2), P < 0.0001). Systolic function remained unchanged; LV diastolic parameters increased significantly in both groups. The extent of 24-h BP decrease was similar between the two groups (-13.3/16.3% vs. -12.3/15.8%, P = 0.63/P = 0.71), whereas the decrease of LV mass (-22% vs. -12.8%, P < 0.005) and the improvement of diastolic function were greater in ACEi + ARB group. In comparison with ACEi + Ca-A, ACEi + ARB treatment showed a greater antiremodeling effect, that can be reasonably ascribed to a BP-independent effect of the dual RAS blockade.American Journal of Hypertension 02/2008; 21(2):231-7. · 3.18 Impact Factor -
Article: Masked hypertension in type 2 diabetes mellitus. Relationship with left-ventricular structure and function.
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ABSTRACT: To evaluate in type 2 diabetes mellitus the relationship between masked hypertension (MH) and left ventricular (LV) morpho-functional characteristics. Using 24-hour BP monitoring and echocardiography, we evaluated 71 type 2 diabetic patients, without overt cardiac disease and never treated with antihypertensive drugs: 45 normotensive subjects with clinic BP <130/85 mmHg and 26 sustained hypertensives (SH)(clinic BP > or = 140 and/or 90 mmHg and 24-hour BP > or =125 and/or 80 mmHg), matched for age, gender, BMI and duration of diabetes with clinically normotensive patients. MH was diagnosed with clinic BP <130/85 mmHg and 24-hour BP > or =125 and/or 80 mmHg. Among clinically normotensive patients, 21 (47%) had MH and 24 were true normotensive (NT, 24-hour BP <125/80 mmHg). LV mass increased from NT to MH to SH (p < 0.001); the parameters of LV diastolic function were similar between MH and SH and significantly lower than in NT. In type 2 diabetic patients with clinic BP <130/85 mmHg, MH is frequent and is associated with LV remodelling characterized by increased myocardial mass and preclinical impairment of LV diastolic function; the remodelling is qualitatively and for some aspects also quantitatively similar to that found in sustained hypertensive patients. Therefore it would be useful to look for MH in diabetic subjects with clinic BP <130/85 mmHg, who, following the guidelines, are not entitled to antihypertensive treatment: the finding of MH could identify a subgroup of patients at higher cardiovascular risk and therefore needing a prompt antihypertensive treatment.American Journal of Hypertension 11/2007; 20(10):1079-84. · 3.18 Impact Factor -
Article: Family history of hypertension influences left ventricular diastolic function during chronic antihypertensive therapy.
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ABSTRACT: Genetic factors play an important role in linking insulin resistance and hypertension, also influencing insulin sensitivity changes during antihypertensive treatment. This study was aimed to evaluate whether genetic predisposition to hypertension can also influence left ventricular (LV) changes during antihypertensive treatment. We enrolled 36 never-treated hypertensives: 18 with both parents hypertensive (F+) and 18 with both parents normotensive (F-), matched for age, gender, and body mass index (BMI). The patients were evaluated twice, before and after 2.5 years of treatment with enalapril. At both evaluations the patients underwent: 24-h blood pressure (BP) monitoring, LV echocardiogram, and oral glucose tolerance test, with measurements of glucose and insulin levels. At basal evaluation the two groups were not different with regard to gender, age, BMI, 24-h BP, and fasting glucose; glucose metabolic clearance rate was significantly lower in F+. The LV mass index was similar between the groups, whereas diastolic parameters were significantly lower in F+. At second evaluation, 24-h BP and LV mass were decreased to the same extent in both groups; glucose metabolic clearance rate significantly increased in F- and remained unchanged in F+. The improvement of LV diastolic function, found in both group, was significantly greater in F-. Genetic predisposition to hypertension, in addition to affecting insulin sensitivity, influences LV functional changes during antihypertensive treatment. Despite a similar extent of 24-h BP and LV mass decrease, F+ patients showed no changes in insulin sensitivity and a smaller improvement in LV diastolic function than F-.American Journal of Hypertension 05/2007; 20(4):410-5. · 3.18 Impact Factor -
Article: Angiotensin-converting enzyme inhibitors influence left ventricular mass and function independently of the antihypertensive effect.
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ABSTRACT: In our retrospective study, we evaluated whether ACE inhibitors can influence left ventricular (LV) morphofunctional characteristics in essential hypertension independently of the antihypertensive effect. We studied 21 hypertensive patients (group 1) before and after at least 18 months of treatment with ACE inhibitors that did not induce any blood pressure (BP) reduction; as a control group, we evaluated 19 hypertensive patients (group 2) not treated with antihypertensive drugs during the same period. At baseline, the 2 groups, neither one previously treated with antihypertensive drugs, were not significantly different with regard to sex, age, body mass index, 24-hour BP, and heart rate; LV mass index was similar between the groups, whereas LV diastolic indices were significantly lower in group 1. At the second evaluation, body mass index, 24-hour BP, and heart rate were unchanged in both groups; LV mass index was significantly decreased in group 1 and increased in group 2. LV diastolic parameters were significantly improved in group 1, whereas in group 2, diastolic function was significantly deteriorated. In conclusion, our clinical study shows that ACE inhibitors can induce LV hypertrophy regression and improvement of diastolic function also in the absence of any antihypertensive effect.Journal of Cardiovascular Pharmacology 12/2006; 48(5):207-11. · 2.29 Impact Factor -
Article: Metabolic syndrome and morphofunctional characteristics of the left ventricle in clinically hypertensive nondiabetic subjects.
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ABSTRACT: The study was aimed to evaluate the impact of the metabolic syndrome on left ventricular (LV) structure and function in nondiabetic patients, never treated with antihypertensive or lipid-lowering drugs. Eighty-eight patients, with recent finding of clinic BP >140 or 90 mm Hg, underwent 24-h blood pressure (BP) monitoring, echocardiogram, evaluation for metabolic syndrome (Adult Treatment Panel III criteria). Metabolic syndrome was diagnosed in 38 subjects (43.2%) (metabolic syndrome+). Age, gender, 24-h systolic and diastolic BP were similar between metabolic syndrome+ and metabolic syndrome- groups, whereas body mass index, clinic and 24-h heart rate, fasting glycemia, and triglycerides were significantly higher and HDL-cholesterol lower in metabolic syndrome + subjects. The prevalence of sustained hypertension (24-h BP >125 or 80 mm Hg) was similar between the two groups. Relative wall thickness and LV mass were significantly greater in the metabolic syndrome+ group, also after correction for body mass index. The LV systolic function was similar between the two groups, whereas all the parameters of diastolic function, but the mitral E/A ratio, were significantly lower in the metabolic syndrome+ group. From multiple regression analysis the main independent determinant of LV mass index was the presence of metabolic syndrome, followed by the 24-h systolic BP. Nondiabetic patients with metabolic syndrome showed more pronounced alterations of LV geometry and function compared with subjects without metabolic syndrome. These greater preclinical myocardial abnormalities were not accounted for by difference in age, gender, or 24-h BP and can be reasonably ascribed to the interplay of the metabolic syndrome components, making the metabolic syndrome in itself a relevant clinical problem, possibly a cardiovascular disease equivalent, that deserves aggressive treatment.American Journal of Hypertension 02/2006; 19(2):199-205. · 3.18 Impact Factor -
Article: Isolated office hypertension: a 3-year follow-up study.
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ABSTRACT: The study aimed to evaluate, over a 3-year period, the progression towards sustained hypertension and left ventricular (LV) changes in patients with isolated office (IO) hypertension (office BP>140 and/or 90 mmHg, daytime BP<130/80 mmHg). After 3 years from the basal evaluation, 38 subjects with basal normal BP and 42 subjects with basal IO hypertension underwent a second 24-h BP monitoring and echocardiography; 19 patients of the basal IO hypertension group were not revaluated because they had already developed ambulatory hypertension and were on antihypertensive treatment. At the second evaluation, the 38 normotensive subjects had unchanged BP and LV parameters; 25 IO hypertensives have developed sustained hypertension. Considering them together with the 19 patients already treated, 72% of 61 IO hypertensives developed ambulatory hypertension over a 3-year period. The patients who subsequently developed hypertension differed from the group who did not only for lower basal values of LV diastolic parameters; all the patients with basal LV hypertrophy and/or preclinical diastolic impairment subsequently developed sustained hypertension. In conclusion, IO hypertensive patients show a high rate of progression towards sustained hypertension. Basal LV hypertrophy and/or preclinical diastolic dysfunction were the only markers of a greater risk of becoming hypertensives.Blood Pressure 02/2005; 14(5):298-305. · 1.43 Impact Factor -
Article: Body mass index is associated with the development of the post-thrombotic syndrome.
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ABSTRACT: Post-thrombotic syndrome (PTS) is a chronic complication of deep vein thrombosis (DVT). Little is known about prognostic factors that might identify patients at high risk for the development of PTS. Body mass index (BMI) has been previously reported to be associated to the development of PTS. The aim of this study was to assess the association between BMI and other anthropometric parameters and PTS in a general population of DVT patients. In a prospective cohort study, 83 consecutive patients with objective diagnosis of DVT underwent physical examination. BMI was recorded at baseline and at 12 months, and waist circumference was recorded at 12 months to assess individual patterns of body fat distribution. The presence of PTS at 12 months was ascertained using a validated clinical scale. Sixty-three patients (75.9%) were overweight or obese at 12 months, 60 (72.3%) had a weight gain over 1 year. Twenty patients developed PTS (24.1%). Mean BMI was significantly higher in patients who developed PTS than in patients who did not (29.6 and 27.2 Kg/m(2), respectively, p = 0.022). A BMI of > 28 Kg/m(2) predicted early onset of PTS (OR 3.54, 95% CI 1.07-12.08, p = 0.017). Neither patterns of fat distribution nor weight gain in 1 year were correlated with PTS (p = 0.918 and p = 0.775, respectively). BMI is significantly correlated with the development of PTS. Patients with DVT should be encouraged to avoid weight gain. Reducing patient weight might be an important strategy to prevent PTS.Thrombosis and Haemostasis 02/2003; 89(2):305-9. · 5.04 Impact Factor -
Article: The initial phase of oral anticoagulation with warfarin in outpatients with deep venous thrombosis.
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ABSTRACT: Patients with deep venous thrombosis (DVT) treated out of hospital usually start warfarin with the recommended 5 mg loading dose and have their International Normalized Ratio (INR) test performed every 2-3 days. Thus, achievement of the therapeutic range may be more difficult than for inpatients, possibly resulting in extended duration of low molecular weight heparin (LMWH) treatment. We retrospectively examined the charts of 55 DVT outpatients (mean age, 61.4 years; 30 males) to assess the actual duration of LMWH treatment and to identify predictors of a slow achievement of the INR range. Thirty patients (54.4%) reached the therapeutic INR range and stopped LMWH within 7 days, and 25 patients (45.6%) had to continue for an average of 10.5 days. The latter group was significantly younger than the former (57 and 65 years, respectively; P = 0.039). Patients younger than 60 years old had an odds ratio for an extended treatment of 4.92 (P = 0.0057). Algorithms with different loading doses of warfarin according to age should be proposed for outpatient treatment of DVT.Blood Coagulation and Fibrinolysis 02/2003; 14(1):11-4. · 1.24 Impact Factor -
Article: Weight gain after acute deep venous thrombosis: a prospective observational study.
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ABSTRACT: The onset of acute disorders often results in a significant reduction in physical exercise, thus predisposing to further increase in body weight. Weight gain is strongly associated with an increase in metabolic and cardiovascular risk factors. The aim of this study was to assess weight changes occurring after an episode of acute deep venous thrombosis (DVT). To compare the prevalence of overweight and obesity at baseline and 6 months after acute DVT, and to compare weight changes between patients with DVT treated in hospital or at home over a similar time frame, we evaluated 72 patients (mean age 59.8+/-15.3 years, 34 men and 38 females) with objectively diagnosed DVT. Body mass index (BMI) was recorded at baseline and at 6 months; waist circumference was recorded at 6 months to assess individual patterns of body fat distribution. At baseline, BMI was 27.6+/-4.6 kg/m(2). Overweight and obesity were observed in 33 (45.8%) and 19 (26.4%) patients, respectively. After 6 months, BMI was 28.7+/-5.0 kg/m(2). The prevalence of overweight and obesity was 44.4% and 32%, respectively; visceral pattern of body fat distribution was found in 64.8% of overweight or obese patients. Mean weight gain was 7.12%; inpatients (n=42) showed a higher weight gain than outpatients (n=30) (8.6% and 4.9%, respectively, p=0.046). We observed a significant weight gain after acute DVT. This weight gain was more marked in hospitalised patients than in outpatients. Our findings suggest that weight control should be considered in all patients with acute DVT.Thrombosis Research 02/2003; 109(1):31-5. · 2.44 Impact Factor -
Article: Thrombosis prophylaxis in medical patients: a retrospective review of clinical practice patterns.
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ABSTRACT: The risk of venous thromboembolism in medical patients is comparable to the risk in general surgical patients. Thromboprophylaxis is recommended for specific medical patients, but its use in clinical practice is unknown. We conducted a retrospective review of the charts of consecutive patients discharged from 2 departments of Internal Medicine, one in the teaching hospital of Varese and one in the non-teaching hospital of Angera, Italy, from October to December 2000. We selected the charts of patients with clinical conditions at increased risk of venous thromboembolism requiring thromboprophylaxis according to consensus statements. The use of antithrombotic drugs and contraindications to prophylaxis were documented. We screened a total of 516 charts, 265 in Varese and 251 in Angera and we identified 165 patients (103 and 62, respectively) at risk of venous thromboembolism because of malignancy (53), heart failure (34), stroke (33), acute infections (23), acute respiratory failure (18), acute rheumatic disorders (3), and inflammatory bowel disease (1). Forty-two patients had contraindications to antithrombotic drugs and 11 were already on long-term oral anticoagulant treatment. Among the 112 remaining patients, prophylaxis was prescribed to 52 patients (46.4%), 35 of 60 in Varese (58.3%) and 17 of 52 in Angera (32.7%, p=0.0067). Patients with stroke and heart failure were significantly more likely to receive thromboprophylaxis than other groups of patients. Prophylaxis of venous thromboembolism is underused in medical patients and the proportion of patients receiving antithrombotic drugs varies with the medical condition which precipitated hospital admission. The low rate of usage of prophylaxis suggests that preventable cases of thromboembolism are occurring and that better education of physicians is required to increase the usage of thromboprophylaxis.Haematologica 08/2002; 87(7):746-50; discussion 250. · 6.42 Impact Factor -
Article: Selecting patients for home treatment of deep vein thrombosis: the problem of cancer.
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ABSTRACT: Patients with deep vein thrombosis are selected for home treatment on the basis of their clinical and social condition. Cancer is frequently associated with venous thromboembolism and is often considered an exclusion criterion for outpatient treatment. We investigated the impact of cancer on the outpatient management of venous thrombosis. We performed a prospective, cohort study on consecutive patients with objectively documented deep vein thrombosis. All were assessed for home treatment. Hospital admission was recommended in the presence of common exclusion criteria. All patients were treated with low molecular weight heparin and warfarin. Information on previous, active, or suspected cancer was collected. Recurrent thrombosis, bleeding and mortality were documented at a 3-month follow-up. One hundred patients were included; 72 were entirely treated at home (mean age: 61.2 years). There were 22 patients with known cancer: 12 (55%) were managed as outpatients (16.5% of the outpatient population) and 10 were hospitalized (36% of the inpatient population), 6 because of a poor clinical condition, 4 because further investigation of their malignancy was required. The presence of cancer and the likelihood of poor compliance were the most frequent reasons cited for in-hospital treatment. Overall, event rates at 3 months were comparable to those reported in previous studies in the outpatient population and slightly higher in the inpatient population (recurrent thrombosis 1.5% and 7%; bleeding 5.5% and 10.7%; mortality 4% and 18%, respectively). Cancer was the most common reason cited for in-hospital treatment. Nevertheless, more than half of the patients with known cancer were safely and effectively treated at home.Haematologica 04/2002; 87(3):286-91. · 6.42 Impact Factor
Top co-authors
Top Journals
Institutions
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2009–2012
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Lady Davis Institute for Medical Research
Montréal, Quebec, Canada
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2002–2012
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Università degli Studi dell'Insubria
- Department of Clinical and Experimental Medicine
Varese, Lombardy, Italy -
McMaster University
Hamilton, Ontario, Canada
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2008–2010
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McGill University
- Lady Davis Institute for Medical Research
Montréal, Quebec, Canada
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