Claudio Passino

Fondazione Toscana Gabriele Monasterio, Pisa, Tuscany, Italy

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Publications (234)900.31 Total impact

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    ABSTRACT: Chronic kidney disease is associated with sympathetic activation and muscle abnormalities, which may contribute to decreased exercise capacity. We investigated the correlation of renal function with peak exercise oxygen consumption (V̇O2) in heart failure (HF) patients.Methods and Results:We recruited 2,938 systolic HF patients who underwent clinical, laboratory, echocardiographic and cardiopulmonary exercise testing. The patients were stratified according to estimated glomerular filtration rate (eGFR). Mean follow-up was 3.7 years. The primary outcome was a composite of cardiovascular death and urgent heart transplantation at 3 years. On multivariable regression, eGFR was predictor of peakV̇O2(P<0.0001). Other predictors were age, sex, body mass index, HF etiology, NYHA class, atrial fibrillation, resting heart rate, B-type natriuretic peptide, hemoglobin, and treatment. After adjusting for significant covariates, the hazard ratio for primary outcome associated with peakV̇O2<12 ml·kg(-1)·min(-1)was 1.75 (95% confidence interval (CI): 1.06-2.91; P=0.0292) in patients with eGFR ≥60, 1.77 (0.87-3.61; P=0.1141) in those with eGFR of 45-59, and 2.72 (1.01-7.37; P=0.0489) in those with eGFR <45 ml·min(-1)·1.73 m(-2). The area under the receiver-operating characteristic curve for peakV̇O2<12 ml·kg(-1)·min(-1)was 0.63 (95% CI: 0.54-0.71), 0.67 (0.56-0.78), and 0.57 (0.47-0.69), respectively. Testing for interaction was not significant. Renal dysfunction is correlated with peakV̇O2. A peakV̇O2cutoff of 12 ml·kg(-1)·min(-1)offers limited prognostic information in HF patients with more severely impaired renal function. (Circ J 2015; 79: 583-591).
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    ABSTRACT: Left ventricular (LV) fibrosis, assessed by late gadolinium enhancement (LGE) at cardiac magnetic resonance imaging (MRI), is a marker of LV remodeling, and holds prognostic value in nonischemic dilated cardiomyopathy (NICM). Galectin-3 has been shown to participate in tissue fibrogenesis and to be a prognosticator in heart failure. Our aim was to investigate the relationships between galectin-3 circulating level and myocardial fibrosis at MRI in patients with NICM. One-hundred-fifty patients were enrolled (males 73%; age 58, SD 14years), with a NICM diagnosis according to the World Health Organization criteria. All patients underwent a comprehensive clinical assessment and biohumoral characterization, including galectin-3 assay, and cardiac MRI, with LGE assessment of fibrosis. Median galectin-3 value was 14.4ng/mL (IQR 11.7-19.0ng/mL), and LGE was detected in 106 (71%) patients. Patients with LGE had higher galectin-3 than those without (15.4, 11.8-21.0, vs 13.1, 11.7-16.4ng/mL, p=0.006). Among univariate predictors of LGE presence (galectin-3, male sex, disease duration, arterial hypertension, left and right ventricular ejection fraction, left ventricular stroke volume), galectin-3 maintained its predictive value at multivariate analysis, together with sex, hypertension, disease duration and right ventricular ejection fraction. At receiver operating characteristic analysis the optimal galectin-3 cut-off for LGE prediction was 14.6ng/mL (AUC 0.651, sensitivity 57%, specificity 73%). Galectin-3 is associated with LGE-assessed myocardial replacement fibrosis in patients with NICM. These results support the hypothesis that galectin-3 is involved in cardiac fibrosis and remodeling in NICM, and that its assay may help to select subgroups at higher risk. Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.
    International Journal of Cardiology 02/2015; 184C:96-100. DOI:10.1016/j.ijcard.2015.02.008 · 6.18 Impact Factor
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    ABSTRACT: Two new immunoassay methods for aldosterone assay using automated platforms recently became available into market. The main aim of the present study is to evaluate the analytical performance of these automated direct immunoassay methods, and also to compare their analytical characteristics to those of the most popular RIA and EIA methods used in an Italian External Quality Assessment (EQA) study. In this study analytical performances of two aldosterone immunoassays using the IDS iSYS and DiaSorin LIAISON fully automated platforms, were evaluated. Results obtained with the two platforms in EDTA plasma samples of healthy subjects and patients were compared with those obtained by RIA and EIA methods used in the Italian EQA scheme, named Immunocheck study. The two automated methods showed similar analytical performances: LoD 83.9 vs 92.2pmol/L, LoQ 104.4 vs 111.1pmol/L, respectively; moreover, the within-run and total imprecision values showed CV% between 8.1 and 14.1 for samples with 180.8 and 387.2pmol/L concentration for both methods. There was a close linear regression between methods, however we found a significant proportional bias between LIAISON and iSYS methods. The EQA samples results obtained with these two methods were highly correlated to the consensus mean values. Our data indicate that aldosterone values measured with the two automated methods actually show better reproducibility, shorter laboratory Turn Around Time (TAT) and require less "hands on labor" compared to RIA and EIA immunoassays. However, in our study significant bias was observed in result comparison, this means that translating aldosterone concentration in clinical information an appropriate definition of reference ranges for each method is mandatory. Copyright © 2015. Published by Elsevier B.V.
    Clinica Chimica Acta 02/2015; 444. DOI:10.1016/j.cca.2015.01.028 · 2.76 Impact Factor
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    ABSTRACT: Arterial hypertension is a main determinant of arterial remodelling and atherosclerosis. Coronary artery calcium score and carotid intima-media thickness are recognized indices of vascular remodelling. Established biohumoral markers for the diagnosis of atherosclerosis are still lacking in asymptomatic subjects with hypertension. We aimed to test the association of plasma N-terminal pro B-type natriuretic peptide concentrations with either coronary artery calcium score or carotid intima-media thickness in asymptomatic hypertensive subjects. We conducted a case-control study on 436 hypertensi.ve and 436 age/sex-matched normotensive subjects from the population of the Montignoso HEart and Lung Project, a community-based study of asymptomatic general population ≥45 years. Subjects underwent N-terminal pro B-type natriuretic peptide measurement, echocardiography and evaluation of coronary artery calcium score and carotid intima-media thickness. Hypertensive subjects had higher median coronary artery calcium score (60 (interquartile range, 30-112) vs. 15 (interquartile range 3-70) Agatson units, p = 0.007), carotid intima-media thickness (8.6 (interquartile range 7.5-9.1) vs. 7.9 (7.1-8.4) µm, p < 0.001) and indexed left ventricular mass (101 (interquartile range 82-126) vs. 87 (63-91) mg/m2, p = 0.03) than controls, with no differences in left ventricular ejection fraction, diameters, E/E', left atrial area. N-terminal pro B-type natriuretic peptide concentrations were higher in hypertensive subjects with either coronary artery calcium score (p = 0.008) or carotid intima-media thickness >75th (p < 0.006) percentile and highest in combined coronary artery calcium score/carotid intima-media thickness >75th percentile (p = 0.021). In multivariable analysis, N-terminal pro B-type natriuretic peptide independently predicted either coronary artery calcium score or carotid intima-media thickness >75th percentile, but only in hypertensive subjects (odds ratio = 1.87, 95% confidence interval 1.30-2.74, p = 0.001 and odds ratio = 1.99, 95% confidence interval 1.43-2.76, p = 0.001). In asymptomatic subjects with hypertension, N-terminal pro B-type natriuretic peptide is a marker of hypertension-mediated preclinical vascular disease. © The European Society of Cardiology 2015 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav.
    European Journal of Preventive Cardiology 02/2015; DOI:10.1177/2047487315569675 · 2.68 Impact Factor
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    ABSTRACT: The aim of this review article is to give an update on the state of the art of the immunoassay methods for the measurement of B-type natriuretic peptide (BNP) and its related peptides. Using chromatographic procedures, several studies reported an increasing number of circulating peptides related to BNP in human plasma of patients with heart failure. These peptides may have reduced or even no biological activity. Furthermore, other studies have suggested that, using immunoassays that are considered specific for BNP, the precursor of the peptide hormone, proBNP, constitutes a major portion of the peptide measured in plasma of patients with heart failure. Because BNP immunoassay methods show large (up to 50%) systematic differences in values, the use of identical decision values for all immunoassay methods, as suggested by the most recent international guidelines, seems unreasonable. Since proBNP significantly cross-reacts with all commercial immunoassay methods considered specific for BNP, manufacturers should test and clearly declare the degree of cross-reactivity of glycosylated and non-glycosylated proBNP in their BNP immunoassay methods. Clinicians should take into account that there are large systematic differences between methods when they compare results from different laboratories that use different BNP immunoassays. On the other hand, clinical laboratories should take part in external quality assessment (EQA) programs to evaluate the bias of their method in comparison to other BNP methods. Finally, the authors believe that the development of more specific methods for the active peptide, BNP1–32, should reduce the systematic differences between methods and result in better harmonization of results.
    Critical Reviews in Clinical Laboratory Sciences 12/2014; DOI:10.3109/10408363.2014.987720 · 7.00 Impact Factor
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    Revista portuguesa de cardiologia: orgao oficial da Sociedade Portuguesa de Cardiologia = Portuguese journal of cardiology: an official journal of the Portuguese Society of Cardiology 11/2014; 33(12). DOI:10.1016/j.repc.2014.06.007 · 0.53 Impact Factor
  • Clinical Chemistry and Laboratory Medicine 11/2014; 53(5). DOI:10.1515/cclm-2014-0873 · 2.96 Impact Factor
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    ABSTRACT: Renin-angiotensin-aldosterone system (RAAS), participated by kidney, liver, vascular endothelium, and adrenal cortex, and counter-regulated by cardiac endocrine function, is a complex endocrine system regulating systemic functions, such as body salt and water homeostasis and vasomotion, in order to allow the accomplishment of physiological tasks, such as orthostasis, physical and emotional stimuli, and to react towards the hemorrhagic insult, in tight conjunction with other neurohormonal axes, namely the sympathetic nervous system, the endothelin and vasopressin systems. The systemic as well as the tissue RAAS are also dedicated to promote tissue remodeling, particularly relevant after damage, when chronic activation may configure as a maladaptive response, leading to fibrosis, hypertrophy and apoptosis, and organ dysfunction. RAAS activation is a fingerprint of systemic arterial hypertension, kidney dysfunction, vascular atherosclerotic disease, and is definitely an hallmark of heart failure, which rapidly shifts from organ disease to a disorder of neurohormonal regulatory systems. Chronic RAAS activation is an indirect or direct target of most effective pharmacological treatments in heart failure, such as beta-blockers, inhibitors of angiotensin converting enzyme, angiotensin receptor blockers, direct renin inhibitors, and mineralocorticoid receptor blockers. Biomarkers of RAAS activation are available, with different feasibility and accuracy, such as plasma renin activity, renin, angiotensin II, and aldosterone, which all accompany the increasing clinical severity of heart failure disease, and are well recognized prognostic factors, even in patients with optimal therapy. Polymorphisms influencing the expression and activity of RAAS pathways have been recognized as clinically relevant biomarkers, likely influencing either the individual clinical phenotype, or the response to drugs. This solid, growing evidence strongly suggests the rationale for the use of biomarkers of the RAAS activation, as a guide to tailor individual therapy in the current practice, and their implementation as a rule-in marker for future trials on novel drugs in the heart failure setting. Copyright © 2014 Elsevier B.V. All rights reserved.
    Clinica Chimica Acta 10/2014; 443. DOI:10.1016/j.cca.2014.10.031 · 2.76 Impact Factor
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    ABSTRACT: Objective The atherosclerotic plaque that is vulnerable to rupture and to superimposed thrombosis is mainly represented by a thin-cap fibroatheroma with or without ulceration/thrombosis and inflammatory infiltrates. Total serum gamma-glutamyltransferase (GGT) activity is an independent predictor for cardiovascular events. Four GGT fractions have been identified in plasma and only one of them (b-GGT) in atherosclerotic plaques, but the possible role of GGT in plaque pathophysiology has not been assessed yet. We investigated the relationships between plaque b-GGT activity and the histological features of plaque vulnerability. Methods and Results Plaque GGT activity was investigated in 65 patients undergoing carotid endarterectomy; plaques were histologically characterized and immunostained for GGT. Intra-plaque total and fractional GGT activity was determined by a cost-effective test of molecular size exclusion chromatography, and compared with histological markers of plaque vulnerability. Plaque cholesterol content was also measured by chromatography. b-GGT was the only fraction detected within the atherosclerotic plaques and intra-plaque b-GGT activity correlated to plaque cholesterol content (r = 0.667, P < 0.0001), plasma b-GGT and f-GGT fractions (r = 0.249; r = 0.298, both P < 0.05). Higher b-GGT activity was found in thin-cap fibroatheromas and it was associated to histological markers of vulnerable plaques, i.e. larger necrotic areas, greater macrophage infiltration and higher cholesterol content (P<0.05). Conclusions intra-plaque b-GGT activity correlates with the histological markers of vulnerable plaque and with plasma b-GGT in human carotid atherosclerosis; these data support the possible role of b-GGT in clinically significant atherosclerotic disease.
    Atherosclerosis 10/2014; 237(1). DOI:10.1016/j.atherosclerosis.2014.09.028 · 3.97 Impact Factor
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    ABSTRACT: Background Cardiac involvement in systemic amyloidosis is caused by the extracellular deposition of misfolded proteins, mainly immunoglobulin light chains (AL) or transthyretin (ATTR), and may be detected by cardiovascular magnetic resonance (CMR). The aim of this study was to measure myocardial extracellular volume (ECV) in amyloid patients with a novel T1 mapping CMR technique and to determine the correlation between ECV and disease severity.Methods Thirty‐six patients with biopsy‐proven systemic amyloidosis (mean age 70±9 years, 31 men, 30 with AL and six with ATTR amyloidosis) and seven patients with possible amyloidosis (mean age 64±10 years, six men) underwent comprehensive clinical and CMR assessment, with ECV estimation from pre‐ and post‐contrast T1 mapping. Thirty healthy subjects (mean age 39±17 years, 21 men) served as the control group.ResultsAmyloid patients presented with left ventricular (LV) concentric hypertrophy with impaired biventricular systolic function. Cardiac ECV was higher in amyloid patients (definite amyloidosis, 0.43±0.12; possible amyloidosis, 0.34±0.11) than in control subjects (0.26±0.04, P < 0.05); even in amyloid patients without late gadolinium enhancement (0.35±0.10), ECV was significantly higher than in the control group (P < 0.01). A cut‐off value of myocardial ECV >0.316, corresponding to the 95th percentile in normal subjects, showed a sensitivity of 79% and specificity of 97% for discriminating amyloid patients from control subjects (area under the curve of 0.884). Myocardial ECV was significantly correlated with LV ejection fraction (R2=0.16), LV mean wall thickness (R2=0.41), LV diastolic function (R2=0.21), right ventricular ejection fraction (R2=0.13), N‐terminal fragment of the pro‐brain natriuretic peptides (R2=0.23) and cardiac troponin (R2=0.33).Conclusion Myocardial ECV was increased in amyloid patients and correlated with disease severity. Thus measurement of myocardial ECV represents a potential non‐invasive index of amyloid burden for use in early diagnosis and disease monitoring.This article is protected by copyright. All rights reserved.
    Journal of Internal Medicine 10/2014; DOI:10.1111/joim.12324 · 5.79 Impact Factor
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    ABSTRACT: Oxygen uptake at the anaerobic threshold (VO2AT), a submaximal exercise-derived variable, independent of patients' motivation, is a marker of outcome in heart failure (HF). However, previous evidence of VO2AT values paradoxically higher in HF patients with permanent atrial fibrillation (AF) than in those with sinus rhythm (SR) raised uncertainties.
    European Journal of Preventive Cardiology 09/2014; DOI:10.1177/2047487314551546 · 2.68 Impact Factor
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    ABSTRACT: Background Patients with repaired tetralogy of Fallot often present residual hemodynamic abnormalities leading to right ventricular (RV) burden. Semisupine exercise echocardiography (Ex-Echo) is a validated method for diagnosis and prognosis in ischemic and valvular heart diseases and has potential for the evaluation of RV burden, pressure, and function. The aims of this study were to assess the effect of exercise on the right ventricle in adults with repaired tetralogy of Fallot and to identify factors associated with decreased RV function at peak exercise in an observational study. Methods A total of 128 patients with repaired tetralogy of Fallot referred to an outpatient congenital heart disease unit were evaluated by Ex-Echo and conventional clinical and diagnostic examinations (i.e., electrocardiography, transthoracic echocardiography, cardiovascular magnetic resonance, cardiopulmonary exercise testing, and N-terminal pro–brain natriuretic peptide assay). The following Ex-Echo parameters were measured at rest and at peak exercise: tricuspid annular plane systolic excursion, RV pressure, and RV fractional area change (FAC). Results Interpretable images for RV FAC analysis were obtained in 123 of 128 patients. In 91 of 128 with detectable tricuspid valve regurgitation, RV systolic pressure during exercise was evaluated. According to positive or negative RV FAC variation during exercise, 74 patients were respectively defined as “responders” on stress echocardiography and 49 as “nonresponders”; the median percentage change between rest and stress was 13.8% (interquartile range, 5.9% to 26.9%) in responders and −13.5% (interquartile range, −25.4% to −7.4%) in nonresponders. Systolic RV systolic pressure increased in a similar manner in the two groups (65 ± 36% in responders vs 59 ± 39% in nonresponders, P = .45). Tricuspid annular plane systolic excursion increased significantly during peak exercise in responders from 17.2 ± 3.4 mm at rest to 19.7 ± 4.3 mm (P < .0001) but did not in nonresponders (from 16.9 ± 4.7 to 18.1 ± 4.6 mm, P = .20). Left ventricular end-diastolic volume at rest and left ventricular ejection fraction < 50% were related to the lack of increased RV FAC on exercise. Conclusions Ex-Echo is feasible in patients with repaired tetralogy of Fallot and allows the integrated assessment of variation in RV systolic pressure, area, and function during exercise, which usefully complement more conventional indices of hemodynamic burden in these patients. Longitudinal follow-up is needed to better delineate the prognostic value of the results of Ex-Echo.
    Journal of the American Society of Echocardiography 09/2014; 27(12). DOI:10.1016/j.echo.2014.08.006 · 3.99 Impact Factor
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    ABSTRACT: Background: The aim of this study is to determine the 99th upper-reference limit (URL) for cardiac troponin T (cTnT) in Italian apparently healthy subjects. Methods: The reference population was selected from 5 cities: Bolzano (n = 290), Milano (CAMELIA-Study, n = 287), Montignoso (MEHLP-Study, n = 306), Pisa (n = 182), and Reggio Calabria (MAREA-Study, n = 535). Subjects having cardiac/systemic acute/chronic diseases were excluded. Participants to MEHLP project underwent cardiac imaging investigation. High-sensitive cTnT was measured with Cobas-e411 (Roche Diagnostics). Results: We enrolled 1600 healthy subjects [54.6% males; age range 10-90 years; mean (SD): 36.4 (21.2) years], including 34.6% aged <20 years, 54.5% between 20 and 64 years, and 10.9% over 65 years. In the youngest the 99th URL was 10.9 ng/L in males and 6.8 ng/L in females; in adults 23.2 ng/L and 10.2 ng/L; and in elderly 36.8 ng/L and 28.6 ng/L. After the exclusion of outliers the 99th URL values were significantly decreased (P < 0.05) in particular those of the oldest (13.8 ng/L and 14 ng/L). MEHLP participants were divided in healthy and asymptomatic, according to known cardiovascular risk factors (HDL, LDL, glucose, C-reactive protein): the 99th URL of cTnT values of these subgroups was significantly different (19.5 vs. 22.7, P < 0.05). Conclusions: 99th URL of cTnT values was strongly affected by age, gender, selection of subjects and the statistical evaluation of outliers.
    Clinica Chimica Acta 09/2014; 438. DOI:10.1016/j.cca.2014.09.010 · 2.76 Impact Factor
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    ABSTRACT: Ventricular remodeling occurs progressively in untreated patients after large myocardial infarction and in those with cardiomyopathy. The pathologic changes of increased left ventricular (LV) volume and perturbation in the LV chamber geometry involves not only the myocytes, but also non-myocyte cells and the extracellular matrix. Inflammation, fibrosis, neuro-hormonal activation, and ongoing myocardial damage are the mechanisms underlying remodeling. The detection of an ongoing remodeling process by means of biomarkers such as cytokines, troponins, neurohormones, metalloproteinases, galectin-3, ST-2 and others, may hold clinical value and could, to some extent, drive the therapeutical strategy in patients after a myocardial infarction or with heart failure. For this reason, there is an increasing interest in the development of new biomarkers and a great number of laboratory tests have been recently proposed, whose clinical usefulness, however, is not fully established yet.
    Clinica Chimica Acta 09/2014; 443. DOI:10.1016/j.cca.2014.09.006 · 2.76 Impact Factor
  • International Journal of Cardiology 08/2014; 176(3). DOI:10.1016/j.ijcard.2014.08.022 · 6.18 Impact Factor
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    ABSTRACT: Aims: We aimed to evaluate the impact of glycometabolic imbalance as assessed by glycosylated haemoglobin [HbA(1c)] on neurohormonal activation and outcome in chronic heart failure (CHF). Methods and results: Nine hundred and twenty CHF patients (65 +/- 12 years, left ventricular ejection fraction 33 +/- 10%, 29% diabetic patients) underwent a thorough humoral and clinical characterization, including HbA(1c), and were then followed up for the endpoint of cardiac death. In the whole population, diagnosis of diabetes resulted in no difference in neurohormonal or echocardiographic data, or in outcome. Conversely, the diabetic patients with HbA(1c) above 7% showed, in comparison to both diabetic patients with HbA(1c) below 7% and non-diabetic individuals, higher plasma renin activity (1.81, 0.48-5.68 vs. 1.23, 0.43-2.8 and 1.29, 0.44-5 ng/ml/h, respectively; P < 0.01 for both), N-terminal pro-brain natriuretic peptide (NT-pro-BNP) (1602, 826-3498 vs. 1022, 500-3543 and 1134, 455-3545 ng/l, respectively; P < 0.01 for both) and worse symptoms with a higher rate of cardiac mortality vs. both diabetic patients with HbA1(c) below 7% and non-diabetic individuals (P < 0.05 for both). In the left ventricular ejection fraction 38-50% tertile (mild left ventricular dysfunction), elevated HbA(1c) was associated with higher NT-pro-BNP and PRA (P < 0.01), and, alongside NT-pro-BNP, resulted the only independent predictor of outcome beyond diagnosis of diabetes. HbA(1c) failed to show up differences in neuroendocrine activation or in outcome in moderate and severe left ventricular dysfunction tertiles. Conclusion: Glycometabolic imbalance, as represented by HbA(1c), is associated with neurohormonal activation and poor prognosis in CHF patients, beyond diabetes. The impact of metabolic derangement on prognosis appears greater at the early stages of CHF, when it might exacerbate neurohormonal activation. Copyright
    Journal of Cardiovascular Medicine 07/2014; DOI:10.2459/JCM.0000000000000159 · 1.41 Impact Factor
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    ABSTRACT: Aims: Refractory hyperaldosteronism is frequently observed in heart failure patients on up-to-date treatment, and holds prognostic value. Our aim was to identify which factors, either genetic or nongenetic, are associated with refractory hyperaldosteronism. Methods: We enrolled 109 consecutive patients with left ventricular systolic dysfunction [left ventricular ejection fraction (LVEF) 32 +/- 10%; 86% males; age 65 +/- 13 years (mean +/- standard deviation)] on optimized adrenergic and renin-angiotensin-aldosterone system (RAAS) antagonism, undergoing clinical and neuroendocrine characterization, and genotyping for six polymorphisms in key RAAS-regulating genes [angiotensinogen (AGT M235T), angiotensin-converting enzyme (ACE-240A>T and I/D), angiotensin II type I receptor (AGTR1 1166A>C), aldosterone synthase (CYP11B2-344C>T) and renin (REN rs7539596)]. Results: Patients with refractory hyperaldosteronism (n = 41, 38%, with plasma concentration >180 ng/l, URL, median 283 ng/l, interquartile range 218-433), when compared with those without (106 ng/l, 74-144; P < 0.001), were not different either for treatment or LVEF, while presented with different AGT M235T genotype distribution (P = 0.047). After adjustment for several humoral, instrumental, functional and therapeutical variables, only plasma renin activity (PRA) (P < 0.001) and potassium (P = 0.027) were independently associated with refractory hyperaldosteronism. Among polymorphisms, only AGT M235T (P = 0.038) was associated with refractory hyperaldosteronism, after adjustment for nongenetic variables. Conclusions: In conclusion, refractory hyperaldosteronism in heart failure may be influenced by AGT M235T polymorphism, among RAAS candidate genes, and by PRA, which may represent, respectively, a constitutive (genotype dependent) and a nongenetic (phenotype-dependent) trigger for aldosterone elevation. Copyright (C) 2015 Wolters Kluwer Health, Inc. All rights reserved.
    Journal of Cardiovascular Medicine 07/2014; DOI:10.2459/JCM.0000000000000156 · 1.41 Impact Factor
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    ABSTRACT: Diagnosis of heart failure (HF) is not based on a single test, but on a combination of history, physical examination and appropriate investigations. For these reasons, the accuracy of diagnosis by clinical means alone is often inadequate, especially in the early, asymptomatic stages of the HF. Thus, there is an increasing interest in the development of new cardiovascular biomarkers and, consequently, a great number of laboratory tests have recently been proposed for their assay. The aim of this article is to provide a general overview on the biomarkers, recommended by international guidelines, for the diagnosis, risk stratification, and follow-up of patients with HF. Cardiac natriuretic peptides and in particular the B-type related peptides, which are considered to be the first line biomarker for HF by international guidelines, will be discussed with special emphasis.
    Clinica Chimica Acta 06/2014; DOI:10.1016/j.cca.2014.06.003 · 2.76 Impact Factor
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    ABSTRACT: Late Gadolinium Enhancement (LGE) pattern of cardiac amyloidosis (CA) at cardiac magnetic resonance (CMR) examination is absent in approximately 30 % of patients. We tested whether the evaluation of myocardial gadolinium signal intensity (SI) decay (SID) has a higher diagnostic accuracy for CA. CMR was performed in 59 patients with systemic AL amyloidosis (36 males, 69 ± 10 years, mean ± SD), and 20 age/sex-matched healthy controls. LGE images were acquired every minute up to 8 min after gadolinium injection (time of inversion 250 ms). SI regions of interest were plotted in SI/time curves for endocardial (Endo) and epicardial layer of interventricular septum, cavity, and skeletal muscle as reference. SID (a negative exponential function described by the parameter TSID) was expressed as number of heart beats (HB) from each ROI. The typical LGE pattern for CA was detected in 42 patients (Ty-LGE), while 17 showed either absent LGE or an atypical pattern (ATy-LGE). A definite CA diagnosis was confirmed in all Ty-LGE patients and in 10/17 ATy-LGE patients. At ROC analysis Endo-TSID was the most accurate parameter to distinguish Ty-LGE and ATy-LGE patients from controls. A 269 HB threshold (mean + 2 SD Endo-TSID measured in controls) identified 51/52 patients with definite CA diagnosis, with 98 % sensitivity, 93 % specificity, and 96 % diagnostic accuracy. A direct relation was found between the extracellular volume and Endo-TSID in CA patients (r 0.72, 95 % CI 0.37-089, p < 0.001). the analysis of myocardial SID after gadolinium injection improves the accuracy of CMR for CA diagnosis.
    The international journal of cardiovascular imaging 05/2014; 30(6). DOI:10.1007/s10554-014-0436-6 · 2.32 Impact Factor

Publication Stats

3k Citations
900.31 Total Impact Points

Institutions

  • 2009–2015
    • Fondazione Toscana Gabriele Monasterio
      Pisa, Tuscany, Italy
  • 2007–2015
    • Scuola Superiore Sant'Anna
      • Institute of Life Sciences
      Pisa, Tuscany, Italy
  • 2007–2013
    • Scuola Normale Superiore di Pisa
      Pisa, Tuscany, Italy
  • 2001–2010
    • National Research Council
      • Institute of Clinical Physiology IFC
      Roma, Latium, Italy
  • 2003–2009
    • INO - Istituto Nazionale di Ottica
      Florens, Tuscany, Italy
  • 1996–2007
    • University of Pavia
      • Department of Internal Medicine and Therapeutics
      Ticinum, Lombardy, Italy
    • University Hospital of Lausanne
      Lausanne, Vaud, Switzerland
  • 2006
    • New York Medical College
      New York, New York, United States
  • 2003–2006
    • Università di Pisa
      • Department of Clinical and Experimental Medicine
      Pisa, Tuscany, Italy
  • 1997
    • Oxford University Hospitals NHS Trust
      • Department of Cardiovascular Medicine
      Oxford, England, United Kingdom