Francesca Tarantini

University of Florence, Florens, Tuscany, Italy

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Publications (65)220.57 Total impact

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    ABSTRACT: Atrial fibrillation (AF) is the most common arrhythmia in elderly people, yet oral anticoagulation is underused in the aged. We tried to determine whether new oral anticoagulants (NOA) have greater psychological tolerability than warfarin.
    Aging clinical and experimental research. 06/2014;
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    ABSTRACT: Abstract Aim: In AL amyloidosis, the importance of right ventricle (RV) involvement has recently been underlined and its role in predicting prognosis has been emphasized. Little is known about the relationship between RV involvement, N-terminal pro-brain natriuretic peptide (NT-proBNP) and troponin levels. Aim of our study was to clarify the relationship between NT-proBNP and troponin and RV involvement and analyze their independent value as predictors of RV dysfunction. Methods and Results: We examined 76 consecutive patients with biopsy-proven AL amyloidosis. Each patient received complete clinical evaluation, troponin I, NT-proBNP assay and comprehensive echocardiographic evaluation. Considering a tricuspidal annulus plane systolic excursion (TAPSE) value <16 mm, 23 patients (30%) presented RV systolic dysfunction, whereas 53 (70%) did not. Patient with reduced TAPSE had thicker left ventricle (LV) walls and RV free walls, reduced LV fractional shortening, impaired LV diastolic function and worse LV and RV myocardial performance index. For RV dysfunction the best predictive value for NT-proBNP was identified as 2977 ng/l with sensitivity and specificity of 87% and 84%, respectively; best cut-off for troponin I was identified as 0.085 ng/l, with sensitivity and specificity of 85% and 90% respectively. At multivariable logistic regression analysis, both NT-proBNP and troponin I emerged as independent predictors of RV dysfunction presence but troponin appears to have a higher predictive power. Conclusion: Our study demonstrated that cut-off values of 2977 ng/ml for NT-proBNP and 0.085 ng/l for troponin were able to identify a subgroup of AL patients with RV dysfunction. Troponin I is more accurate and seems to be the best biohumoral marker of RV dysfunction.
    Amyloid: the international journal of experimental and clinical investigation: the official journal of the International Society of Amyloidosis 02/2014; · 2.51 Impact Factor
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    ABSTRACT: FGF applied as a single growth factor to quiescent mouse fibroblasts induces a round of DNA replication, however continuous stimulation results in arrest in the G1 phase of the next cell cycle. We hypothesized that FGF stimulation induces the establishment of cell memory, which prevents the proliferative response to repeated or continuous FGF application. When a 2-5 day quiescence period was introduced between primary and repeated FGF treatments, fibroblasts failed to efficiently replicate in response to secondary FGF application. The establishment of "FGF memory" during the first FGF stimulation did not require DNA synthesis, but was dependent on the activity of FGF receptors, MEK, p38 MAPK and NFκB signaling, and protein synthesis. While secondary stimulation resulted in strongly decreased replication rate, we did not observe any attenuation of morphological changes, Erk1/2 phosphorylation and cyclin D1 induction. However, secondary FGF stimulation failed to induce the expression of cyclin A, which is critical for the progression from G1 to S phase. Treatment of cells with a broad range histone deacetylase inhibitor during the primary FGF stimulation rescued the proliferative response to the secondary FGF treatment suggesting that the establishment of "FGF memory" may be based on epigenetic changes. We suggest that "FGF memory" can prevent the hyperplastic response to cell damage and inflammation, which are associated with an enhanced FGF production and secretion. "FGF memory" may present a natural obstacle to the efficient application of recombinant FGFs for the treament of ulcers, ischemias and wounds. J. Cell. Biochem. © 2013 Wiley Periodicals, Inc.
    Journal of Cellular Biochemistry 12/2013; · 3.06 Impact Factor
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    ABSTRACT: Epicardial adipose tissue (EAT) is a visceral fat that fulfills two important functions: lipid-storage and secretion of adipokines with pro-inflammatory and pro-atherogenic properties. It has been suggested that EAT may affect the pathogenesis of atherosclerosis and the clinical course of coronary artery disease (CAD). In patients with obesity, diabetes and metabolic syndrome, the epicardial adipose tissue is enlarged. Little is known about the role of EAT in left ventricular dysfunction. Aim of this study was to evaluate the ability of insulin resistance to predict EAT thickness in patients with significant CAD and systolic dysfunction.
    12/2013; 80(4):170-6.
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    ABSTRACT: Atrial fibrillation (AF) is the most frequent arrhythmia in elderly patients. Aims of this study were to evaluate the predictors of arterial stiffness after external cardioversion (ECV) of AF and to establish whether a link exists between vascular properties and left atrial diameter (LAD). We studied 33 patients (age 73 ± 12 years). After 5 h from ECV of persistent AF, an echocardiogram was recorded and arterial stiffness was evaluated with cardio-ankle vascular stiffness index (CAVI). In multivariate analysis (R = 0.538, p = 0.006), CAVI (mean 9.60 ± 1.63) increased with age (p = 0.018) and with an AF length ≤3 months (p = 0.022). LAD was significantly related to CAVI (p = 0.007) even after adjustment for interventricular septum thickness (p = 0.018) (R = 0.574, p = 0.002). In patients with AF, immediately after ECV, arterial stiffness is associated with age and AF length, and could represent an important factor for left atrium remodeling and, therefore, for AF maintenance.
    Aging - Clinical and Experimental Research 11/2013; · 1.01 Impact Factor
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    ABSTRACT: Patients affected by coronary artery disease (CAD) have a high prevalence of depressive disorders. It has been suggested that depressive symptoms significantly reduce exercise stress test performance in CAD patients, whereas their influence on functional capacity tests, such as the 6-minute walking test (6WT), has been less investigated. The aim of this study was to evaluate the correlation between depressive symptoms and 6WT in patients with CAD and the role of age on this relationship. We enrolled 148 CAD patients. Global functional capacity was measured with 6WT and the presence of depressive symptoms with the 30-item Geriatric Depression Scale (GDS). GDS score was analysed as a continuous variable or categorized as depression absent (score <10), probable (10-14), or present (≤15). A significant inverse correlation was observed between GDS score and distance walked at 6WT. Patients positive for depressive symptoms (probable or present) had a significantly worse performance compared to those with GDS score <10. In multivariable analysis adjusted for indexes of cardiovascular disease severity and comorbidity, the presence of depressive symptoms proved to be an independent predictor of distance walked at 6WT; the predictivity of depressive symptoms on 6WT was age dependent. Depressive symptoms negatively affect 6WT performance among older CAD subjects. Non-cardiovascular parameters, such as psycho-affective disorders, must be taken into account for the interpretation of 6WT performance in old age.
    European journal of preventive cardiology. 06/2013;
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    ABSTRACT: Prostate cancer is still the second cause of cancer-related death among men. Although patients with metastatic presentation have an ominous outcome, the vast majority of PCs are diagnosed at an early stage. Nonetheless, even among patients with clinically localized disease the outcome may vary considerably. Other than androgen sensitivity, little is known about which other signaling pathways are deranged in aggressive, localized cancers. The elucidation of such pathways may help to develop innovative therapies aimed at specific molecular targets. We report that in a hormone-sensitive prostate cancer cell line, LNCaP, Notch3 was activated by hypoxia and sustained cell proliferation and colony formation in soft agar. Hypoxia also modulated cellular cholesterol content and the number and size of lipid rafts, causing a coalescence of small rafts into bigger clusters; under this experimental condition Notch3 migrated from the non-raft into the raft compartment where it co-localized with the γ-secretase complex. We also looked at human prostate cancer biopsies and found that expression of Notch3 positively correlated with Gleason score and with expression of carbonic anhydrase IX, a marker of hypoxia. In conclusion, hypoxia triggers the activation of Notch3 which, in turn, sustains proliferation of prostate cancer cells. Notch3 pathway represents a promising target for adjuvant therapy in patients with prostate cancer. © 2013 Wiley Periodicals, Inc.
    International Journal of Cancer 06/2013; · 6.20 Impact Factor
  • Alessandra Pratesi, Francesca Tarantini, Mauro Di Bari
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    ABSTRACT: Tropism and efficiency of skeletal muscle depend on the complex balance between anabolic and catabolic factors. This balance gradually deteriorates with aging, leading to an age-related decline in muscle quantity and quality, called sarcopenia: this condition plays a central role in physical and functional impairment in late life. The knowledge of the mechanisms that induce sarcopenia and the ability to prevent or counteract them, therefore, can greatly contribute to the prevention of disability and probably also mortality in the elderly. It is well known that skeletal muscle is the target of numerous hormones, but only in recent years studies have shown a role of skeletal muscle as a secretory organ of cytokines and other peptides, denominated myokines (IL6, IL8, IL15, Brain-derived neurotrophic factor, and leukaemia inhibitory factor), which have autocrine, paracrine, or endocrine actions and are deeply involved in inflammatory processes. Physical inactivity promotes an unbalance between these substances towards a pro-inflammatory status, thus favoring the vicious circle of sarcopenia, accumulation of fat - especially visceral - and development of cardiovascular diseases, type 2 diabetes mellitus, cancer, dementia and depression, according to what has been called "the diseasome of physical inactivity".
    Clinical Cases in Mineral and Bone Metabolism 01/2013; 10(1):11-4.
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    ABSTRACT: BACKGROUND: Several peptides, named adipokines, are produced by the adipose tissue. Among those, adiponectin (AD) is the most abundant. AD promotes peripheral insulin sensitivity, inhibits liver gluconeogenesis and displays anti-atherogenic and anti-inflammatory properties. Lower levels of AD are related to a higher risk of myocardial infarction and a worse prognosis in patients with coronary artery disease. However, despite a favorable clinical profile, AD increases in relation to worsening heart failure (HF); in this context, higher adiponectinemia is reliably related to poor prognosis. There is still little knowledge about how certain metabolic conditions, such as diabetes mellitus, modulate the relationship between AD and HF.We evaluated the level of adiponectin in patients with ischemic HF, with and without type 2 diabetes, to elucidate whether the metabolic syndrome was able to influence the relationship between AD and HF. RESULTS: We demonstrated that AD rises in patients with advanced HF, but to a lesser extent in diabetics than in non-diabetics. Diabetic patients with reduced systolic performance orchestrated a slower rise of AD which began only in face of overt HF. The different behavior of AD in the presence of diabetes was not entirely explained by differences in body mass index. In addition, NT-proBNP, the second strongest predictor of AD, did not differ significantly between diabetic and non-diabetic patients. These data indicate that some other mechanisms are involved in the regulation of AD in patients with type 2 diabetes and coronary artery disease. CONCLUSIONS: AD rises across chronic heart failure stages but this phenomenon is less evident in type 2 diabetic patients. In the presence of diabetes, the progressive increase of AD in relation to the severity of LV dysfunction is hampered and becomes evident only in overt HF.
    Cardiovascular Diabetology 12/2012; 11(1):151. · 4.21 Impact Factor
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    ABSTRACT: During the last decades the older patients who are candidates for surgery have grown esponentially due to the increase in life expectancy and the surgery technique improvement. Despite this, the mortality remains high and our ability to predict the surgery outcomes continues to be low in the elderly. The main reason is related to different difficulties; we are unable to differentiate properly the chronological from the biological age, and the current surgery and cardiology risk scores are poorly geriatric-oriented. We must underline how the measure of comorbidity during the preoperative evaluation is often limited to a simple count of comorbid conditions, without a more detailed assessment of their severity. On the other hand different comorbidity scores have been validated in geriatric populations showing a good correlation with prognosis, such as the Index of Coexisting Disease-ICED or the Geriatric Index of Comorbidity-GIC. Our predictive deficiency about the outcomes is linked to poor attention for identifying the frail patients that are already at high risk of disability. Recently, the evaluation of frailty is a key target for geriatric medicine, and geriatricians have developed various methods for measuring this parameter and suggesting the physical performance indexes as a reliable surrogate of frailty. Surrogate frailty measures, such as the "gait speed" or the "Short Physical Performance Battery-SPPB" seem to be the valid tools for evaluating older surgery patients due to their simplicity and short administration time. We think that the future challenge will be their widespread use in this specific clinical setting.
    Monaldi archives for chest disease = Archivio Monaldi per le malattie del torace / Fondazione clinica del lavoro, IRCCS [and] Istituto di clinica tisiologica e malattie apparato respiratorio, Università di Napoli, Secondo ateneo 09/2012; 78(3):129-37.
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    ABSTRACT: Background and Aims: Atrial fibrillation (AF) is the most frequent sustained arrhythmia of elderly patients, in whom it determines an increase in morbidity and mortality. Aim of this study was to assess age-related differences in the characteristics, management and prognosis of patients with AF in European cardiology practices. Methods: The Euro Heart Survey on AF was an observational study sponsored by the European Society of Cardiology. Patients were enrolled between 2003 and 2004 in 182 hospitals of 35 countries. For the purposes of this study, they were categorized into three age-groups: <65 (N=2124), 65-80 (N=2534) and >80 years (N=671). Follow-up was closed in 2005. Results: Compared with general population estimates, patients >80 years were underrepresented in the Euro Heart Survey. The oldest patients were less likely to be enrolled by university or specialized centers, to receive extensive diagnostic testing, and to receive oral anticoagulation despite a worse stroke risk profile. Furthermore, the oldest patients less often received rhythm control therapy, even when presenting with palpitations and non-permanent AF. During 1 year follow-up, elderly patients more often suffered a myocardial infarction, new onset heart failure and major bleedings. They had higher all-cause and cardiovascular mortality. Conclusions: Elderly patients with AF are less often referred to the cardiologist and, based on current guidelines, are inadequately studied and treated, compared to younger counterparts. Education on evidence based management and the design of randomized controlled trials specifically targeting the elderly, should improve the management and prognosis of this frail segment of the AF population.
    Aging - Clinical and Experimental Research 05/2012; · 1.01 Impact Factor
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    ABSTRACT: The mechanisms of nonclassical export of signal peptide-less proteins remain insufficiently understood. Here, we demonstrate that stress-induced unconventional export of FGF1, a potent and ubiquitously expressed mitogenic and proangiogenic protein, is associated with and dependent on the formation of membrane blebs and localized cell surface exposure of phosphatidylserine (PS). In addition, we found that the differentiation of promonocytic cells results in massive FGF1 release, which also correlates with membrane blebbing and exposure of PS. These findings indicate that the externalization of acidic phospholipids could be used as a pharmacological target to regulate the availability of FGF1 in the organism.
    Journal of Cellular Biochemistry 03/2012; 113(3):956-66. · 3.06 Impact Factor
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    ABSTRACT: Chronic heart failure (HF) is characterised by a neurohormonal dysfunction associated with chronic inflammation. A role of metabolic derangement in the pathophysiology of HF has been recently reported. Adiponectin, an adipose-tissue-derived cytokine, seems to play an important role in cardiac dysfunction. We investigated the variation of circulating adiponectin in patients with coronary artery disease (CAD), with or without HF, in order to identify its independent predictors. A total of 107 outpatients with CAD were enrolled in the study and divided into three groups: CAD without left ventricular systolic dysfunction (group 1); CAD with left ventricular dysfunction without HF symptoms (group 2) and CAD with overt HF (group 3). Plasma adiponectin was determined by enzyme-linked immunosorbent assay. Adiponectin concentrations increased progressively from group 1 (7.6 ± 3.6 ng ml⁻¹) to group 2 (9.1 ± 6.7 ng ml⁻¹) and group 3 (13.7 ± 7.6 ng ml⁻¹), with the difference reaching statistical significance in group 3 versus 1 and 2 (p < 0.001). A multivariable model of analysis demonstrated that the best predictors of plasma adiponectin were body mass index, N-terminal pro-brain natriuretic peptide and high-density lipoprotein cholesterol. However, even after adjusting for all three independent predictors, the increase of adiponectin in group 3 still remained statistically significant (p = 0.015). Our data confirm the rise of adiponectin in overt HF. The levels of circulating adipokine seem to be mainly predicted by the metabolic profile of patients and by biohumoral indicators, rather than by clinical and echocardiographic indexes of HF severity.
    Nutrition, metabolism, and cardiovascular diseases: NMCD 03/2012; 22(3):292-9. · 3.52 Impact Factor
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    ABSTRACT: OBJECTIVES: The aim of this study was to evaluate resistin levels in patients with coronary artery disease (CAD) with or without chronic heart failure, in order to define its independent predictor. METHODS: One hundred and seven outpatients with CAD were enrolled in the study and divided into three groups: CAD without left-ventricular systolic dysfunction (group 1); CAD with left-ventricular dysfunction without heart failure symptoms (group 2); CAD with overt heart failure (group 3). Plasma resistin was determined by ELISA. RESULTS: Resistin progressively increased from group 1 (10.7 ± 5.0 ng/ml) to groups 2 (11.8 ± 5.8 ng/ml) and 3 (17.0 ± 6.8 ng/ml), with the difference reaching statistical significance in group 3 versus groups 1 and 2 (P = 0.001). A multivariable model of analysis demonstrated that the best predictor of plasma resistin level was the estimated glomerular filtration rate (P < 0.001), indicating that reduction of kidney function was the main cause of the adipokine increase observed in patients with CAD and overt heart failure. CONCLUSIONS: Our data confirm the rise of resistin plasma levels previously described in patients affected by chronic heart failure; however, in our study, this relationship seemed to be mediated mainly by the level of kidney function, and only partially by the severity of ventricular dysfunction.
    Journal of Cardiovascular Medicine 01/2012; · 2.66 Impact Factor
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    ABSTRACT: Prostate carcinoma is among the most common causes of cancer-related death in men, representing 15% of all male malignancies in developed countries. Neuroendocrine differentiation (NED) has been associated with tumor progression, poor prognosis, and with the androgen-independent status. Currently, no successful therapy exists for advanced, castration-resistant disease. Because hypoxia has been linked to prostate cancer progression and unfavorable outcome, we sought to determine whether hypoxia would impact the degree of neuroendocrine differentiation of prostate cancer cells in vitro. RESULTS: Exposure of LNCaP cells to low oxygen tension induced a neuroendocrine phenotype, associated with an increased expression of the transcription factor neurogenin3 and neuroendocrine markers, such as neuron-specific enolase, chromogranin A, and β3-tubulin. Moreover, hypoxia triggered a significant decrease of Notch 1 and Notch 2 mRNA and protein expression, with subsequent downregulation of Notch-mediated signaling, as shown by reduced levels of the Notch target genes, Hes1 and Hey1. NED was promoted by attenuation of Hes1 transcription, as cells expressing a dominant-negative form of Hes1 displayed increased levels of neuroendocrine markers under normoxic conditions. Although hypoxia downregulated Notch 1 and Notch 2 mRNA transcription and receptor activation also in the androgen-independent cell lines, PC-3 and Du145, it did not change the extent of NED in these cultures, suggesting that androgen sensitivity may be required for transdifferentiation to occur. CONCLUSIONS: Hypoxia induces NED of LNCaP cells in vitro, which seems to be driven by the inhibition of Notch signaling with subsequent downregulation of Hes1 transcription.
    Molecular Cancer Research 12/2011; 10(2):230-8. · 4.35 Impact Factor
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    ABSTRACT: Studies have suggested that micronutrient deficiency has some role in the progression of chronic heart failure (CHF). Oral supplementation with coenzyme Q(10) (CoQ(10)) and creatine may reduce mitochondrial dysfunction that contributes to impaired physical performance in CHF. We conducted a randomized, double-blind, placebo-controlled trial to determine the effect of a mixture of water-soluble CoQ(10) (CoQ(10) terclatrate; Q-ter) and creatine on exercise tolerance and health-related quality of life. Exercise tolerance was measured as total work capacity (kg·m) and peak oxygen consumption (VO(2), mL/min/kg), both from a cardiopulmonary exercise test. Health-related quality of life was measured by the Sickness Impact Profile (SIP) in CHF secondary to left ventricular systolic dysfunction (left ventricular ejection fraction ≤ 35%). After baseline assessment, 67 patients with stable CHF were randomized to receive Q-ter 320 mg + creatine 340 mg (n = 35) or placebo (n = 32) once daily for 8 weeks. At multivariate analysis, 8-week peak VO(2) was significantly higher in the active treatment group than in the placebo group (+1.8 ± 0.9 mL/min/kg, 95% CI: 0.1-3.6, P < 0.05). No untoward effects occurred in either group. This study suggests that oral Q-ter and creatine, added to conventional drug therapy, exert some beneficial effect on physical performance in stable systolic CHF. Results may support the design of larger studies aimed at assessing the long-term effects of this treatment on functional status and harder outcomes.
    Clinical Cardiology 04/2011; 34(4):211-7. · 1.83 Impact Factor
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    ABSTRACT: FGF1, a widely expressed proangiogenic factor involved in tissue repair and carcinogenesis, is released from cells through a non-classical pathway independent of endoplasmic reticulum and Golgi. Although several proteins participating in FGF1 export were identified, genetic mechanisms regulating this process remained obscure. We found that FGF1 export and expression are regulated through Notch signaling mediated by transcription factor CBF1 and its partner MAML. The expression of a dominant negative (dn) form of CBF1 in 3T3 cells induces transcription of FGF1 and sphingosine kinase 1 (SphK1), which is a component of FGF1 export pathway. dnCBF1 expression stimulates the stress-independent release of transduced FGF1 from NIH 3T3 cells and endogenous FGF1 from A375 melanoma cells. NIH 3T3 cells transfected with dnCBF1 form colonies in soft agar and produce rapidly growing highly angiogenic tumors in nude mice. The transformed phenotype of dnCBF1 transfected cells is efficiently blocked by dn forms of FGF receptor 1 and S100A13, which is a component of FGF1 export pathway. FGF1 export and acceleration of cell growth induced by dnCBF1 depend on SphK1. Similar to dnCBF1, dnMAML transfection induces FGF1 expression and release, and accelerates cell proliferation. The latter effect is strongly decreased in FGF1 null cells. We suggest that the regulation of FGF1 expression and release by CBF1-mediated Notch signaling can play an important role in tumor formation.
    Journal of Cellular Physiology 02/2011; 226(11):3064-75. · 4.22 Impact Factor
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    ABSTRACT: Metabolic and neurodegenerative disorders have a growing prevalence in Western countries. Available epidemiologic and neurobiological evidences support the existence of a pathophysiological link between these conditions. Glucagon-like peptide 1 (GLP-1), whose activity is reduced in insulin resistance, has been implicated in central nervous system function, including cognition, synaptic plasticity, and neurogenesis. We review the experimental researches suggesting that GLP-1 dysfunction might be a mediating factor between Type 2 diabetes mellitus (T2DM) and neurodegeneration. Drug treatments enhancing GLP-1 activity hold out hope for treatment and prevention of Alzheimer's disease (AD) and cognitive decline.
    Experimental Diabetes Research 01/2011; 2011:281674. · 1.89 Impact Factor
  • International journal of cardiology 12/2010; 145(3):550-2. · 6.18 Impact Factor
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    ABSTRACT: Cognitive decline and heart failure frequently coexist in the elderly. Although an epidemiologic association may partially explain this finding, cerebral hypoperfusion and cardioembolism have been advocated as pathophysiological links. The aim of the present study was to evaluate the relationship between mild cognitive decline and exercise capacity in older outpatients with chronic heart failure (CHF). We studied 80 elderly outpatients with stable CHF, mainly of ischemic etiology, assessing total exercise capacity with the 6-minute walking test (6MWT) and global cognitive function with the Mini Mental State Examination (MMSE). CHF severity, emotional status, comorbidity, disability and disease-specific quality of life were also determined at the time of enrollment. A positive association was observed between the distance walked at 6MWT and MMSE score, even after adjusting for demographic parameters, indexes of CHF severity, comorbidities, level of disability, and quality of life. An easy and reliable measure of cardiovascular global performance is independently associated with cognitive function in older outpatients affected by CHF. In the context of global aging, this observation emphasizes the importance of a comprehensive assessment, encompassing a standard, brief and reliable cognitive evaluation, in elderly CHF outpatients.
    Aging clinical and experimental research 08/2010; 22(4):308-13. · 1.01 Impact Factor

Publication Stats

1k Citations
220.57 Total Impact Points


  • 2000–2014
    • University of Florence
      • Dipartimento di Chirurgia e Medicina Traslazionale (DCMT)
      Florens, Tuscany, Italy
  • 2007–2013
    • Azienda Ospedaliero Universitaria Careggi
      Firenzuola, Tuscany, Italy
  • 1998–2012
    • Maine Medical Center Research Institute
      Scarborough, Maine, United States
  • 2003
    • National Institute on Aging
      • Clinical Research Branch (CRB)
      Baltimore, Maryland, United States