[{"data":1,"prerenderedAt":-1},["ShallowReactive",2],{"health-study-detail:100651831":3},{"organization":4,"armGroups":7,"interventions":10,"overallOfficials":15,"centralContacts":24,"locations":29,"responsibleParty":50,"collaborators":54,"id":56,"slug":57,"hasResults":58,"nctId":59,"briefTitle":60,"officialTitle":61,"acronym":62,"eligibilityCriteria":63,"healthyVolunteers":58,"sex":64,"minAge":65,"maxAge":10,"enrollmentInfo":66,"targetDuration":10,"studyType":69,"phases":10,"briefSummary":70,"conditions":71,"keywords":77,"overallStatus":32,"whyStopped":10,"lastUpdateSubmitDate":96,"lastUpdatePostDateStruct":97,"startDateStruct":100,"completionDateStruct":102,"leadSponsor":104,"locationsCount":105},{"fullName":5,"class":6},"University of Messina","OTHER",[8,12],{"label":9,"type":10,"description":11,"interventionNames":10},"ATTR-CA Patients",null,"Patients with wild-type or hereditary transthyretin cardiac amyloidosis (ATTR-CA) diagnosed according to current European recommendations and followed at the University Hospital G. Martino, Messina. Participants will undergo clinical, laboratory, echocardiographic, hepatic ultrasound, liver elastography, and coagulation assessments at baseline and during follow-up.",{"label":13,"type":10,"description":14,"interventionNames":10},"Hypertrophic Phenotype Controls","Age-matched patients with non-amyloid hypertrophic phenotype cardiomyopathy serving as a control population. Participants will undergo the same clinical, laboratory, echocardiographic, hepatic, and coagulation evaluations as the ATTR-CA group.",[16,20],{"name":17,"affiliation":18,"role":19},"Gianluca Di Bella, MD, PhD","University of Messina and AOU Policlinico G. Martino","STUDY_CHAIR",{"name":21,"affiliation":22,"role":23},"Luigi Colarusso, MD, PhD Candidate","AOU Policlinico G. Martino","PRINCIPAL_INVESTIGATOR",[25],{"name":21,"role":26,"phone":27,"phoneExt":10,"email":28},"CONTACT","+390902212341","luigi.colarusso@polime.it",[30],{"facility":31,"status":32,"city":33,"state":34,"zip":35,"country":36,"countryCode":37,"cosmosGeoPoint":38,"geoPoint":43,"contacts":44},"AOU Policlinico G. Martino, UOC Cardiologia con UTIC","RECRUITING","Messina","Sicily","98124","Italy","IT",{"type":39,"coordinates":40},"Point",[41,42],15.55256,38.19394,{"lat":42,"lon":41},[45,46,49],{"name":21,"role":26,"phone":27,"phoneExt":10,"email":28},{"name":47,"role":48,"phone":10,"phoneExt":10,"email":10},"Roberto Licordari, MD, PhD","SUB_INVESTIGATOR",{"name":21,"role":23,"phone":10,"phoneExt":10,"email":10},{"type":23,"investigatorFullName":51,"investigatorTitle":52,"investigatorAffiliation":53,"oldNameTitle":10,"oldOrganization":10},"Gianluca Di Bella","MD, PhD","Azienda Ospedaliera Universitaria Policlinico \"G. Martino\"",[55],{"name":53,"class":6},"100651831","liver-and-coagulation-disorders-in-cardiac-transthyretin-amyloidosis-100651831",false,"NCT07766135","Liver and Coagulation Disorders in Cardiac Transthyretin Amyloidosis","Liver and Coagulation Disorders in Cardiac Transthyretin Amyloidosis (ATTR-CA): New Horizons in Disease Staging and Follow-Up","LICA2025","Inclusion Criteria:\n\n* Written informed consent obtained prior to study participation.\n* Diagnosis of wild-type or hereditary transthyretin cardiac amyloidosis (ATTR-CA) according to current European recommendations.\n* Ability to comply with study procedures and follow-up visits.\n\nExclusion Criteria:\n\n* Age younger than 18 years.\n* Severe liver dysfunction due to causes other than amyloidosis.\n* Inability to comply with study procedures because of language barriers, cognitive impairment, or severe psychiatric disorders.\n* Comorbidities associated with life expectancy less than 12 months.\n* Active alcohol or substance abuse.\n* For coagulation analyses: congenital coagulation disorders, thrombotic disorders, active malignancy, or sepsis.\n* Pregnancy or breastfeeding.","ALL","18 Years",{"count":67,"type":68},70,"ESTIMATED","OBSERVATIONAL","Transthyretin cardiac amyloidosis (ATTR-CA) is a progressive infiltrative cardiomyopathy caused by the deposition of misfolded transthyretin protein within the myocardium. Current disease staging and follow-up strategies mainly rely on cardiac biomarkers and renal function; however, the systemic nature of ATTR suggests that additional organ involvement may provide valuable prognostic information.\n\nThe purpose of this prospective observational study is to investigate liver dysfunction and coagulation abnormalities in patients with wild-type or hereditary ATTR-CA and to evaluate their potential role as novel markers of disease severity and progression. Patients with ATTR-CA will be compared with an age-matched control population with non-amyloid hypertrophic cardiomyopathy.\n\nClinical, laboratory, echocardiographic, hepatic ultrasound, liver stiffness, and coagulation parameters will be assessed at baseline and during follow-up. The study will also evaluate changes in these parameters after 6 and 12 months of treatment with tafamidis.\n\nThe results may improve the understanding of cardio-hepatic interactions in ATTR-CA and identify new tools for disease staging and longitudinal monitoring.",[72,73,74,75,76],"Transthyretin (TTR) Amyloid Cardiomyopathy","Cardiac Amyloidosis","Cardiomyopathies","Wild-Type Transthyretin Cardiac Amyloidosis","Hereditary Transthyretin Amyloidosis (ATTRv)",[78,79,73,80,81,82,83,84,85,86,87,88,89,90,91,92,93,94,95],"ATTR","ATTR-CA","Transthyretin Amyloidosis","Tafamidis","Acoramidis","Liver Stiffness","Fibroscan","Liver Dysfunction","Hepatic Congestion","Coagulation Disorder","Hemostasis","Cardiohepatic Syndrome","Biomarkers","Disease Staging","Echocardiography","Heart Failure","Wild-Type ATTR","Hereditary ATTR","2026-08-10",{"date":98,"type":99},"2026-08-14","ACTUAL",{"date":101,"type":99},"2026-01-30",{"date":103,"type":68},"2028-01",{"name":5,"class":6},1]