Prucalopride differs from other 5-HT4 agonists such as tegaserod and cisapride, which at therapeutic concentrations also  interact with other receptors (5-HT1B/D and the cardiac human ether-a-go-go K+ or hERG channel respectively) and this may account for the adverse cardiovascular events that have resulted in the restricted availability of these drugs. Clinical trials evaluating the effect of prucalopride on QT interval and related adverse events have not demonstrated significant differences compared with placebo. Pharmacokinetics
Prucalopride is rapidly absorbed (Cmax attained 2–3 hours after single 2 mg oral dose) and is extensively distributed. Metabolism is not the major route of elimination. In vitro, human liver metabolism is very slow and only minor amounts of metabolites are found. A large fraction of the active substance is excreted unchanged (about 60% of the administered dose in urine and at least 6% in feces). Renal excretion of unchanged prucalopride involves both passive filtration and active secretion. Plasma clearance averages 317 ml/min, terminal half-life is 24–30 hours, and steady-state is reached within 3–4 days. On once daily treatment with 2 mg prucalopride, steady-state plasma concentrations fluctuate between trough and peak values of 2.5 and 7 ng/ml, respectively.In vitro data indicate that prucalopride has a low interaction potential, and therapeutic concentrations of prucalopride are not expected to affect the CYP-mediated metabolism of co-medicated medicinal products. Approval
In the European Economic Area, prucalopride was originally approved for the symptomatic treatment of chronic constipation in women in whom laxatives fail to provide adequate relief.
Severe TR may be suspected if right ventricular enlargement is seen on chest x-ray, and other causes of this enlargement are ruled out.Definitive diagnosis is made by echocardiogram, which is capable of measuring both the presence and the severity of the TR, as well as right ventricular dimensions and systolic pressures. Management
Medical
Medical therapy of Tricuspid regurgitation consists of diuretics, but as the disease progresses, they become inefficient. Surgical
Indications for surgical fixation of tricuspidal issues include organic lesion(s) in the valve or severe functional regurgitation. During open heart surgery for another issue (e.g. mitral valve), fixing the tricuspid valve may be considered, but medical consensus is unclear. Some argue that even mild to moderate tricuspid regurgitation should be addressed, while others take a more conservative approach. Infective endocarditis or traumatic lesions are other indications.Surgical options include annuloplasty or replacement of the valve. Adding a rigid prosthetic ring aims to decrease the diameter of the valve and stabilize it. Another annuloplasty modality is the "De Vega technique", in which the valve diameter is decreased by two sutures placed around the periphery of the valve. In cases of severe organic lesions of the valve, such as endocarditis, the valve may be excised. Tricuspid valve replacement with either a mechanical valve or a bioprosthesis may be indicated depending on the patient. Mechanical prostheses can cause thromboembolic phenomena, while bioprostheses may degenerate with use.