Swiss Cardiac Amyloidosis REgistry (Swiss-CARE)

NCT04776824 | Recruiting

• 1 other identifier: 2021-00135
• Study Type: observational
• Target: 300
• Locations: 1 country
• Sites: 7

Brief Summary

Cardiac transthyretin amyloidosis (ATTR), caused by ventricular depositions of misfolded transthyretin, results in an infiltrative cardiomyopathy, progressing from pronounced myocardial wall thickening, diastolic and systolic dysfunction to the development of terminal heart failure. Recently, treatment options for TTR amyloidosis have become available. However costs for therapy are enormous and previous trials were not able to differentiate between patients that might benefit from treatment and those without a need for treatment. the investigators study aims to determine markers, as assessed by cardiac magnet resonance imaging (CMR) feature tracking (FT) and T1- and T2- mapping, that might reliably indicate disease severity and could help to identify patients that might benefit from (ongoing) TTR stabilization treatment.

Conditions

Amyloid Cardiomyopathy

Keywords

Cardiac Amyloidosis; Tafamidis; CMR feature tracking; Strain; T1 and T2 Mapping; Outcomes

Outcome Measures

Primary Outcomes (4)

• LV (left ventricle) and RV (right ventricle) function as assessed by CMR feature tracking as predictor for MACE (major adverse cardiac event)

  Global and regional longitudinal (%), circumferential (%) and radial (%) strain measurements are used to quantify LV and RV function before and after therapy initiation. MACE is defined as a composite of sustained ventricular tachycardia, hospitalization for heart failure and all-cause death.

  5 years

• LV and RV tissue characterization as assessed by T1 and T2 mapping as predictor for MACE

  Global and regional tissue characteristics are assessed by repetitive T1 and T2 mapping (global and regional T1 and T2 time (ms)) before and during therapy. MACE is defined as a composite of major cardiovascular endpoints listed above.

  5 years

• Late gadolinium enhancement as predictor for MACE

  Global and regional myocardial tissue is characterized by gadolinium contrast agent application. The presence and extent (% and total mass (g)) of late gadolinium enhancement is evaluated as a predictor for MACE.

  5 years

• Extracellular volume (ECV) as predictor for MACE

  ECV (%) as a marker of myocardial tissue remodelling is calculated from native and post-contrast T1 mapping and haematocrit before and during therapy.

  5 years

Study Arms (1)

Patients with confirmed amyloidosis

Confirmed diagnosis of amyloidosis w/wo cardiac involvement

Eligibility Criteria

• Age: 18 Years+
• Sex: all
• Healthy Volunteers: No
• Age Groups: Adult (18-64), Older Adult (65+)
• Sampling Method: Non-Probability Sample

Study Population

Confirmed diagnosis of amyloidosis w/wo cardiac involvement

You may qualify if:

• Confirmed diagnosis of amyloidosis w/wo cardiac involvement
• General Consent

You may not qualify if:

• Inability to give consent or existence of a written or documented oral refusal of the data subject.\<18 years of age

Sponsors & Collaborators

• Insel Gruppe AG, University Hospital Bern: lead

Study Sites (7)

USB

Basel, 4031, Switzerland

NOT YET RECRUITING

Department of Cardiology, University Hospital Bern, Inselspital, Bern

Bern, 3010, Switzerland

RECRUITING

HUG

Geneva, 1211, Switzerland

RECRUITING

CHUV

Lausanne, 1011, Switzerland

RECRUITING

LUKS

Lucerne, 6000, Switzerland

RECRUITING

KSSG

Sankt Gallen, 9007, Switzerland

RECRUITING

Stadtspital Triemli

Zurich, 8063, Switzerland

RECRUITING

Biospecimen

Retention: SAMPLES WITHOUT DNA

Genetic testing is a part of the routine diagnostic work-up of TTR amyloidosis patients. Current knowledge suggests that therapy response and clinical outcome may differ in TTR patients suffering from wt-TTR and h-/m-TTR-amyloidosis, respectively. Therefore, the genetic background should also be assessed as part of the registry.

MeSH Terms

Conditions

Amyloid Neuropathies, Familial; Sprains and Strains

Condition Hierarchy (Ancestors)

Heredodegenerative Disorders, Nervous System; Neurodegenerative Diseases; Nervous System Diseases; Amyloid Neuropathies; Peripheral Nervous System Diseases; Neuromuscular Diseases; Genetic Diseases, Inborn; Congenital, Hereditary, and Neonatal Diseases and Abnormalities; Amyloidosis, Familial; Metabolism, Inborn Errors; Metabolic Diseases; Nutritional and Metabolic Diseases; Amyloidosis; Proteostasis Deficiencies; Wounds and Injuries

Study Officials

• Christoph Gräni, MD, PhD

  Department of Cardiology, University Hospital Bern, Inselspital, Bern

  PRINCIPAL INVESTIGATOR

Central Study Contacts

Christoph Gräni, MD, PhD

CONTACT

+41 31 632 4508; christoph.graeni@insel.ch

Moritz Hundertmark, MD, PhD

CONTACT

+41 31 63 2 40 86; moritz.hundertmark@insel.ch

Study Design

• Study Type: observational
• Observational Model: CASE ONLY
• Time Perspective: PROSPECTIVE
• Target Duration: 10 Years
• Sponsor Type: OTHER
• Responsible Party: SPONSOR

Study Record Dates

• First Submitted: February 25, 2021
• First Posted: March 2, 2021
• Study Start: February 22, 2001
• Primary Completion (Estimated): May 1, 2031
• Study Completion (Estimated): May 1, 2031
• Last Updated: May 6, 2025

Record last verified: 2025-05

Data Sharing

• IPD Sharing: Will not share

Locations

CH (7)