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NCT Number: NCT05209776

Local Inflammation in Arrhythmogenic Right Ventricular Cardiomyopathy

The understanding of ARVC pathophysiology remains incomplete. Several clues indicate that disease progression is mediated through inflammation. The present study aim to document the feasibility of detecting the potential presence of intracardiac local inflammatory components in patients with ARVC.

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Key information

Conditions

Arrhythmogenic Right Ventricular Dysplasia Bone Diseases Bone Diseases, Developmental Camurati-Engelmann Syndrome Cardiomyopathies Cardiovascular Abnormalities Cardiovascular Diseases Congenital Abnormalities Congenital, Hereditary, and Neonatal Diseases and Abnormalities Genetic Diseases, Inborn Heart Defects, Congenital Heart Diseases Inflammation Musculoskeletal Diseases Osteochondrodysplasias Pathologic Processes Pathological Conditions, Signs and Symptoms

Age range

18 year–99 year

Sex eligibility

All sexes

Study type

Interventional

Phase

Not applicable

Primary location

Toulouse University Hospital Center

Toulouse, France

Location status: Recruiting

Location contact

Audrey TOMASIK

CONTACT

[email protected]

5 61 77 85 97 ext. +33

Maxime BENEYTO

SUB_INVESTIGATOR

Philippe MAURY

PRINCIPAL_INVESTIGATOR

About this study

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a heritable condition characterized by right ventricular (RV) dilatation/dysfunction and malignant ventricular arrhythmias. The understanding of ARVC pathophysiology remains incomplete. Several clues indicate that disease progression is mediated through inflammation. First, presence of subepicardial late gadolinium enhancement sharing the same characteristics as the ones found in myocarditis is common on cardiac magnetic resonance imaging (CMR). Second, clinical pathology findings of inflammatory infiltrates of mononuclear cells are frequent and correlate to the extent and severity of ARVC. Finally, from a biological standpoint, the exploratory study conducted by Campian et al. has shown an exaggerated humoral inflammatory response in peripheral blood whilst anti-desmoglein-2 antibodies (targeting a component of the desmosome) emerge as a sensitive and specific biomarker for ARVC. As specific treatments for ARVC are currently lacking, a better understanding of the humoral pathophysiology of the disease could unlock new therapeutic targets. We recently demonstrated that collecting local cardiomyocytes was feasible through irrigated ablation catheters in patients with ARVC. These steerable catheters may easily map the whole right ventricle and locate endocardial or epicardial scars. Aspiration of local blood or cellular material through the inner lumen of the catheter once pressed on the parietal wall may be an interesting technique for retrieving local inflammation markers.

Who can participate

Healthy volunteers accepted: No

Only the study team can determine whether someone qualifies for participation.

Inclusion criteria

  • For cases:
  • Arrhythmogenic right ventricular dysplasia diagnosed (according to 2010 Task Force Criteria)
  • Admitted for right ventricle electrophysiologic mapping
  • For controls * Admitted for ablation procedures (accessory pathway, atrial flutter) on otherwise healthy hearts.

Exclusion criteria

  • Diagnostic of systemic chronic inflammatory disease
  • Presence of possible or proven cardiac involvement of an inflammatory disease, an acute or chronic infectious disease.
  • Taking immunosuppressant or immunomodulating medications

Treatment and study plan

Peripheral immunological assessment on venous blood

Biological

Peripheral immunological assessment carried out as part of the research, on venous blood at the puncture point necessary for the electrophysiological examination: 1 heparin tube and 1 EDTA tube

Immunological assessment carried out on intracardiac material

Biological

Immunological assessment carried out as part of the research, on intracardiac material taken during the electrophysiological examination: 1 EDTA tube

Primary outcomes

  1. Identify the inflammatory components by C-reactive protein

    Time frame: 24 months

    Rate of C-reactive protein in the blood

  2. Identify the inflammatory components by interleukine1

    Time frame: 24 months

    Rate of interleukin 1 beta in the blood

  3. Identify the inflammatory components by onterleukine6

    Time frame: 24 months

    Rate of interleukin 6 in the blood

  4. Identify the inflammatory components by interleukine10

    Time frame: 24 months

    Rate of interleukin 10 in the blood

  5. Identify the inflammatory components by Tumor Necrosis Factor

    Time frame: 24 months

    Rate of Tumor Necrosis Factor alpha in the blood

  6. Identify the inflammatory components by Transforming Growth Factor

    Time frame: 24 months

    Rate of Transforming Growth Factor beta in the blood

Study contacts

Contact information is provided by the study sponsor or research team.

Maxime BENEYTO

CONTACT

[email protected]

Philippe MAURY, MD

CONTACT

[email protected]

5 61 32 34 70 ext. +33

Sponsors and collaborators

Lead sponsor

University Hospital, Toulouse

Other

Registry information

Acronym: LI-ARVC

Important dates

Study start
2022
Primary completion
2027
Study completion
2027
First posted
Jan 27, 2022
Registry last updated
Jun 1, 2026

OpenTrials presents study information sourced from ClinicalTrials.gov. The official registry record should be consulted for the latest information.

View the official ClinicalTrials.gov record (opens in a new tab)

This listing is for discovery and informational purposes only. It is not medical advice, does not guarantee that a study is recruiting, and does not determine eligibility. Contact the study team and a qualified healthcare professional when considering participation.

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