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Dive into the research topics where Agnese Milandri is active.

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Featured researches published by Agnese Milandri.


Circulation | 2014

Left Ventricular Structure and Function in Transthyretin-Related Versus Light-Chain Cardiac Amyloidosis

Candida Cristina Quarta; Scott D. Solomon; Imran Uraizee; Jenna Kruger; Simone Longhi; Marinella Ferlito; Christian Gagliardi; Agnese Milandri; Claudio Rapezzi; Rodney H. Falk

Background— Immunoglobulin amyloid light-chain (AL)-related cardiac amyloidosis (CA) has a worse prognosis than either wild-type (ATTRwt) or mutant (ATTRm) transthyretin (TTR) CA. Detailed echocardiographic studies have been performed in AL amyloidosis but not in TTR amyloidosis and might give insight into this difference. We assessed cardiac structure and function and outcome in a large population of patients with CA and compared findings in TTR and AL-related disease. Methods and Results— We analyzed 172 patients with CA (AL amyloidosis, n=80; ATTRm, n=36; ATTRwt, n=56) by standard echocardiography and 2-dimensional speckle-tracking imaging-derived left ventricular (LV) longitudinal (LS), radial, and circumferential strains. Despite a preserved LV ejection fraction (55±12%), LS was severely impaired in CA. Standard measures of LV function and speckle-tracking imaging worsened as wall thickness increased, whereas apical LS was preserved regardless of the pathogenesis of CA and the degree of wall thickening. Compared with ATTRm and AL amyloidosis, ATTRwt was characterized by greater LV wall thickness and lower ejection fraction. LS was more depressed in both ATTRwt and AL amyloidosis (−11±3% and −12±4%, respectively, P=0.54) than in ATTRm (−15±4%, P<0.01 versus AL amyloidosis and ATTRwt). TTR-related causes were favorable predictors of survival, whereas LS and advanced New York Heart Association class were negative predictors. Conclusions— In patients with CA, worsening LV function correlated with increasing wall thickness regardless of pathogenesis. Patients with ATTRwt had a statistically greater wall thickness but lesser mortality than those with AL amyloidosis, despite very similar degrees of LS impairment. This paradox suggests an additional mechanism for LV dysfunction in AL amyloidosis, such as previously demonstrated light-chain toxicity.


Heart Failure Reviews | 2015

Cardiac amyloidosis: the great pretender

Claudio Rapezzi; Massimiliano Lorenzini; Simone Longhi; Agnese Milandri; Christian Gagliardi; Ilaria Bartolomei; Fabrizio Salvi; Mathew S. Maurer

Cardiac amyloidosis (CA) is often misdiagnosed because of both physician-related and disease-related reasons including: fragmented knowledge among different specialties and subspecialties, shortage of centres and specialists dedicated to disease management, erroneous belief it is an incurable disease, rarity of the condition, intrinsic phenotypic heterogeneity, genotypic heterogeneity in transthyretin-related forms and the necessity of target organ tissue histological diagnosis in the vast majority of cases. Pitfalls, incorrect beliefs and deceits challenge not only the path to the diagnosis of CA but also the precise identification of aetiological subtype. The awareness of this condition is the most important prerequisite for the management of the risk of underdiagnoses and misdiagnosis. Almost all clinical, imaging and laboratory tests can be misinterpreted, but fortunately each of these diagnostic steps can also offer diagnostic “red flags” (i.e. highly suggestive findings that can foster the correct diagnostic suspicion and facilitate early, timely diagnosis). This is especially important because outcomes in CA are largely driven by the severity of cardiac dysfunction and emerging therapies are aimed at preventing further amyloid deposition.


Jacc-cardiovascular Imaging | 2014

Identification of TTR-Related Subclinical Amyloidosis With 99mTc-DPD Scintigraphy

Simone Longhi; Pier Luigi Guidalotti; Candida Cristina Quarta; Christian Gagliardi; Agnese Milandri; Massimiliano Lorenzini; Luciano Potena; Ornella Leone; Ilaria Bartolomei; Francesca Pastorelli; Fabrizio Salvi; Claudio Rapezzi

We have previously documented that 99mTc-3,3-diphosphono-1,2-propanodicarboxylic acid (99mTc-DPD) has a high affinity for transthyretin (TTR)-infiltrated myocardium, allowing a differential diagnosis with light-chain cardiac amyloidosis [(1)][1] and other non-amyloidotic cardiomyopathies with a


Amyloid | 2012

New pathological insights into cardiac amyloidosis: implications for non-invasive diagnosis.

Ornella Leone; Simone Longhi; Candida Cristina Quarta; Teresa Ragazzini; Lucilla Badiali De Giorgi; Ferdinando Pasquale; Luciano Potena; Luigi Lovato; Agnese Milandri; Giorgio Arpesella; Claudio Rapezzi

Background: Knowledge of the patterns of myocardial amyloid accumulation could improve the interpretation of electrocardiographic, echocardiographic and magnetic resonance imaging findings of amyloidosis. We assessed the extent and pattern of myocardial amyloid infiltration in explanted or autopsied hearts of patients with cardiomyopathy related to acquired monoclonal immunoglobulin light-chain (AL) or hereditary transthyretin (TTR) related amyloidosis (ATTR). Methods: We analyzed nine explanted/autopsied hearts from patients with AL (n = 4) and ATTR (n = 5) cardiac amyloidosis. For each heart, a biventricular histological macrosection was obtained at mid-ventricular level and analyzed with both inspective and computer-assisted histologic and histomorphometric analysis aimed in particular at quantifying muscle cells, fibrosis and amyloid infiltration. Results: The extent of amyloid infiltration of the left ventricle (LV) ranged from 45 to 76% (median [interquartile range (IQR)] = 57% [51–64]) of the overall surface. Although LV trabecular and subendocardial were the most infiltrated layers (45–94%, median [IQR] = 73% [67–84] and from 44 to 71%, median [IQR] = 57% [49–59], respectively), intra- and inter-patient heterogeneity was high. Three main patterns of amyloid infiltration of the LV were identified: diffuse (five cases), mainly subendocardial (two cases), and mainly segmental (two cases). The extent of amyloid infiltration of the right ventricle ranged from 48 to 93% (median [IQR] = 61% [59–83]); contributions of parietal and trabecular layers ranged from 32 to 99% (median [IQR] = 63% [47–88]) and from 49 to 93% (median [IQR] = 74% [64–79]), respectively. Conclusions: In amyloidotic cardiomyopathy, amyloid deposition is highly heterogeneous. Different patterns of infiltration are identifiable, including diffuse, mainly segmental and mainly subendocardial. Awareness of this variability can help the interpretation of ECGs, echocardiograms and magnetic resonance imaging.


Jacc-cardiovascular Imaging | 2012

Defining the Diagnosis in Echocardiographically Suspected Senile Systemic Amyloidosis

Candida Cristina Quarta; Pier Luigi Guidalotti; Simone Longhi; Cinzia Pettinato; Ornella Leone; Alessandra Ferlini; Elena Biagini; Francesco Grigioni; Maria Letizia Bacchi-Reggiani; Massimiliano Lorenzini; Agnese Milandri; Angelo Branzi; Claudio Rapezzi

Senile systemic amyloidosis (SSA) is a cardiomyopathy mainly affecting elderly men due to intramyocardial deposition of wild-type (nonmutant) transthyretin (TTR) ([1][1]). Since the heart is the only involved organ, SSA—which requires endomyocardial biopsy (EMB) for a definite diagnosis—is often


European Heart Journal | 2017

Clinical characteristics of wild-type transthyretin cardiac amyloidosis: disproving myths

Esther González-López; Christian Gagliardi; Fernando Dominguez; Cristina Candida Quarta; F. Javier de Haro-del Moral; Agnese Milandri; Clara Salas; Marta Cobo-Marcos; Massimiliano Lorenzini; Enrique Lara-Pezzi; Serena Foffi; Luis Alonso-Pulpón; Claudio Rapezzi; Pablo García-Pavía

Aims Wild-type transthyretin amyloidosis (ATTRwt) is mostly considered a disease predominantly of elderly male, characterized by concentric LV hypertrophy, preserved LVEF, and low QRS voltages. We sought to describe the characteristics of a large cohort of ATTRwt patients to better define the disease. Methods and results Clinical findings of consecutive ATTRwt patients diagnosed at 2 centres were reviewed. ATTRwt was diagnosed histologically or non-invasively (LV hypertrophy ≥12 mm, intense cardiac uptake at 99mTc-DPD scintigraphy and AL exclusion). Mutations in TTR were excluded in all cases. The study cohort comprised 108 patients (78.6 ± 8 years); 67 (62%) diagnosed invasively and 41 (38%) non-invasively. Twenty patients (19%) were females. An asymmetric hypertrophy pattern was observed in 25 (23%) patients. Mean LVEF was 52 ± 14%, with 39 patients (37%) showing a LVEF < 50%. Atrial fibrillation (56%) and a pseudo-infarct pattern (63%) were the commonest ECG findings. Only 22 patients fulfilled QRS low-voltage criteria while 10 showed LV hypertrophy on ECG. Although heart failure was the most frequent profile leading to diagnosis (68%), 7% of individuals presented with atrioventricular block and 11% were diagnosed incidentally. Almost one third (35; 32%) were previously misdiagnosed. Conclusion The clinical spectrum of ATTRwt is heterogeneous and differs from the classic phenotype: women are affected in a significant proportion; asymmetric LV hypertrophy and impaired LVEF are not rare and only a minority have low QRS voltages. Clinicians should be aware of the broad clinical spectrum of ATTRwt to correctly identify an entity for which a number of disease-modifying treatments are under investigation.


Amyloid | 2012

Cardiac involvement in hereditary-transthyretin related amyloidosis

Claudio Rapezzi; Simone Longhi; Agnese Milandri; Massimiliano Lorenzini; Christian Gagliardi; Ilaria Gallelli; Ornella Leone; Candida Cristina Quarta

Hereditary transthyretin-related amyloidosis remains a widely underdiagnosed condition, owing to its extreme phenotypic variability: the clinical spectrum of the disease ranges from an almost exclusive neurologic involvement to strictly cardiac manifestations. This heterogeneity is linked to several factors including specific transthyretin mutations, geographic distribution and endemic vs. non-endemic aggregation type. The existence of exclusively or predominantly cardiac phenotypes makes the recognition of the disease very challenging since it can mimic other more common causes of left ventricular “hypertrophy”. Assessment of such patients should include an active search for possible red flags that can indicate the correct final diagnosis.


Journal of Nuclear Cardiology | 2017

Does the etiology of cardiac amyloidosis determine the myocardial uptake of [18F]-NaF PET/CT?

Christian Gagliardi; Elena Tabacchi; Rachele Bonfiglioli; Stefania Diodato; Cristina Nanni; Pierluigi Guidalotti; Massimiliano Lorenzini; Filippo Lodi; Agnese Milandri; Claudio Rapezzi; Stefano Fanti

Cardiac amyloidosis (CA) leads to variable degrees of myocardial infiltration with a final echocardiographic phenotype of “hypertrophy.” Although many non-invasive imaging techniques (MRI, CT, scintigraphy, PET) are useful, the definitive diagnosis is still based on myocardial histology. We explored the possible role of [18F]-NaF PET/CT in the diagnosis of this disease in two cases with wild-type (ATTRwt) or mutant (ATTRm) Ile68Leu transthyretin (TTR)-related CA.


Clinical Nuclear Medicine | 2015

Etiology of amyloidosis determines myocardial 99mTc-DPD uptake in amyloidotic cardiomyopathy.

Simone Longhi; Rachele Bonfiglioli; Laura Obici; Christian Gagliardi; Agnese Milandri; Massimiliano Lorenzini; Pier Luigi Guidalotti; Giampaolo Merlini; Claudio Rapezzi

Tc-DPD (Tc-3,3-diphosphono-1,2-propanodicarboxylic acid) has a high affinity for transthyretin (TTR)-infiltrated myocardium, allowing a differential diagnosis with light chain cardiac amyloidosis and other nonamyloidotic cardiomyopathies with a hypertrophic phenotype, in which myocardial tracer uptake is low or absent. Myocardial bone tracer uptake in the rarer forms of amyloidosis (eg, apolipoprotein-related) has been rarely studied. We present 4 cases of cardiac amyloidosis that underwent Tc-DPD scintigraphy; myocardial DPD uptake was present in patients with ATTR, wtTTR and apolipoprotein AI and negative in cases with AL and apolipoprotein AII-related disease.


Journal of the American College of Cardiology | 2012

A SIMPLE VOLTAGE/MASS INDEX IMPROVES DIAGNOSIS OF CARDIAC AMYLOIDOSIS: AN ELECTROCARDIOGRAPHIC AND ECHOCARDIOGRAPHIC STUDY OF 570 PATIENTS WITH LEFT VENTRICULAR HYPERTROPHY

Candida Cristina Quarta; Stefano Perlini; Simone Longhi; Alessandra Berardini; Francesco Musca; Francesco Salinaro; Laura Obici; Agnese Milandri; Pamela Gallo; Christian Gagliardi; Elena Biagini; Francesca Mingardi; Chiara Pazzi; Giampaolo Merlini; Claudio Rapezzi

Amyloidotic cardiomyopathy (AC) can mimic other diseases with left ventricular (LV) hypertrophy, including hypertrophic cardiomyopathy (HCM) and hypertensive heart disease (HHD). Low QRS voltage on ECG provides valuable clues for the non-invasive suspicion of AC. However its sensitivity is limited

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