**2.2 Etiology**

Competence of the TV depends on the integrity of all its components (leaflets, TVA and subvalvular apparatus). The dysfunction of any of these structures can cause TR and we can differentiate two types according to the mechanism of the valve insufficiency:

	- Left-side HF with either preserve or not preserve left ventricular ejection fraction: ischemic heart disease, hypertension, dilated cardiomyopathy, mitral or aortic valvular disease… leading to increased left atrial pressure and postcapillary PH.
	- Precapillary PH and/or primary RV dysfunction.
	- Atrial fibrillation (AF).

From a physiopathological perspective, all these disorders are closely related to each other and frequently two or more of them can coexist in the same patient. In fact, all of them end in a common pathway characterized by progressive TVA dilatation, RV dilatation and dysfunction, and TV leaflet tethering. These changes increase the TR regurgitation, thus, worsening RV adverse remodeling that further impairs the coaptation gap of TV leaflets [19]. Moreover, systemic congestion and


#### **Table 1.**

*Causes of primary tricuspid regurgitation. CHD: congenital heart disease, ICD: implantable cardiac devices; EMB: endomyocardial biopsy.*

chronic neuro-hormonal activation also contribute to this self-perpetuating mechanism that, if untreated, conducts to irreversible end-stage right HF.
