From:  Emerging insights into tricuspid valve disorders: epidemiology, clinical entities, innovations, and future perspectives

 Classification, pathophysiology, and etiology of tricuspid valve disorders.

CategoryType/SubtypeDescription
ClassificationTRThe most common right-sided valvular lesion in adults, physiological trace to mild TR, is often normal [17, 18].
ClassificationPrimary regurgitationCaused by intrinsic abnormalities such as congenital defects, infective endocarditis, or rheumatic disease [19].
ClassificationSecondary (functional) regurgitationDue to RV dilation or pulmonary hypertension, which pulls valve leaflets apart, impairing closure [19].
ClassificationTSThickened or fused leaflets restrict forward blood flow from RA to RV, often caused by rheumatic disease, carcinoid syndrome, or congenital anomalies [2].
PathophysiologyAnnular dilation and leaflet tetheringThe TA is more likely to dilate with RV enlargement. Annular dilation and leaflet tethering (from RA/RV dilation) impair coaptation and worsen TR [19–21].
PathophysiologySeptal annulus dynamicsThe septal portion of the TA remains relatively fixed and is less affected by RV dilation, contributing to asymmetric distortion [19–21].
EtiologyHeart failure and left-sided diseaseTR usually results from RV dilation caused by pulmonary hypertension, often secondary to left-sided heart disease or lung conditions like emphysema [3].
EtiologyOther causes of TRIncludes trauma, infective endocarditis, rheumatic heart disease, and congenital defects [3].
EtiologyDevice-related TRICD or pacemaker leads can interfere with leaflet coaptation or cause fibrosis and tethering, leading to TR. Often diagnosed late [22].
EtiologyRole of imagingTransesophageal echocardiography and 3DE are essential for detection and grading of device-related TR [22].
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3DE: three-dimensional echocardiography; ICD: implantable cardioverter-defibrillator; RA: right atrium; RV: right ventricle; TA: tricuspid annulus; TR: tricuspid regurgitation; TS: tricuspid stenosis.