"Atriogenic Tricuspid Selected, Omics Profile, Multimodality Imaging and Clinical Outcomes" (ATOMIC)

Institute of Hospitalization and Scientific Care (IRCCS)

Status: Active, not recruiting

Conditions: Tricuspid Valve Insufficiency

Study type: Observational

Funder types: Other

Identifiers

NCT05724225

4424

Details and patient eligibility

About

The aim of our study is to investigate the molecular mechanisms underlying remodeling of the tricuspid valve apparatus in patients with ITF and isolated AF, in comparison with patients with ITF from right ventricular remodeling, patients with atriogenic MI and left ventricular remodeling. To achieve these aims, markers obtained from cardiovascular imaging methods, such as 3D echocardiogram, and biomarkers isolated from the peripheral blood of the study participants will be considered.

Full description

Advances in echocardiography and, in particular, the development of three-dimensional echocardiography have allowed a more accurate analysis of the morphology of the tricuspid valve and a detailed understanding of the mechanisms underlying its insufficiency. From a clinical point of view, ITF is divided into a primary form, less frequent (8-10%), caused by primary alterations of the tricuspid valve apparatus, acquired or congenital, and in a "functional" form, the most frequent, conventionally associated in most cases with coexisting pathologies of the left heart or primitive pathologies of the right heart. More recently, long-lasting persistent atrial fibrillation (AF) has been associated with the development of ITF in the presence of structurally normal valve leaflets, preserved right ventricular size and function, and right atrial dilatation. This form of ITF, defined as "atrial functional", could benefit from a different therapeutic management compared to the classic form, more commonly caused by right ventricular dilatation and dysfunction ("ventricular functional" IT). However, not all patients with AF and tricuspid annulus dilatation develop valvular insufficiency and, on the other hand, with the same valvular annulus dilatation and right atrial size, the prevalence of severe IT forms is extremely variable.

This could depend on different adaptive mechanisms implemented by the valve leaflet tissue that lead to their growth or not in response to atrial remodeling and valve annulus dilatation, representing a key factor in the development and progression of the disease. Atriogenic ITF. If confirmed, these observations could lead to a better prognostic classification and different therapeutic perspectives for patients with AF at risk of developing forms of severe ITF and congestive heart failure.

Enrollment: 60 estimated patients

Sex: All

Ages: 18 to 80 years old

Volunteers: Accepts Healthy Volunteers

Inclusion criteria

• Admitted to the Department of cardiological, neurological and metabolic sciences of the San Luca hospital with a diagnosis of persistent atrial fibrillation

Exclusion criteria

• Patient aged <18 years;
• Pregnancy;
• Chronic inflammatory diseases;
• Autoimmune diseases;
• Tumor diseases;
• Chronic renal failure with eGFR < 30 mL/min;

Trial design

60 participants in 6 patient groups

First group with atrial fibrillation disease

Description:

10 Atrial fibrillation(AF), predominant right atrial dilatation with at least moderate IT

Second group with atrial fibrillation disease and tricuspid insufficiency

Description:

10 AF, predominantly right atrial dilatation without TI (or TI no more than mild)

Third group with AF and mitral insufficiency

Description:

10 AF, predominantly left atrial dilatation with at least moderate MI

Fourth group with atrial fibrillation and IM

Description:

10 AF, predominantly left atrial dilatation without MI (or no more than mild MI)

Fifth group with tricuspid insufficiency

Description:

10 IT at least moderate to right ventricular remodeling in patients with pulmonary hypertension

Sixth group with mitral insufficiency

Description:

10 MI at least average from left ventricular remodeling from left ventricular dysfunction