In mechanical prosthetic valves, color Doppler is the mainstay in identifying, localizing, and grading the severity of regurgitation. The knowledge of the specific model and type of the prosthetic valve we are facing is mandatory. At the same time, it’s important to keep in mind that regurgitation of a prosthetic valve can be physiologic. There are two different types of physiologic regurgitations: The first is the closure volume, that is, the volume of blood pulled back by the closure of the occluders and is confined just after the valve closure; the second is the lavage volume that consists in the blood flow that passes between the occluders and the prosthetic ring throughout the closing state of the valve and is functional to the correct washing of the valve elements. A caged ball valve realizes small and variable jets along the whole circumference of the ball. A tilting disk valve presents jets, one at each side of the occluder; in the bileaflet valve, we can see three regurgitant jets: one central and two near the hinges; making a distinction from perivalvular leakages could be very difficult [4].

Pathologic intra-valvular regurgitation could be secondary to the blockage of an occluder in opening position due to thrombosis, vegetation, or pannus, that is, a fibrous overgrowth of the endocardial tissue over the valve elements. When facing a perivalvular or suspected perivalvular regurgitation, we are called to distinguish a lavage volume passing near the hinges of the occluders from an anomalous regurgitation due to an initial prosthetic valve detachment. Pathologic perivalvular regurgitations are bigger than physiologic ones and show an extensive aliasing. Grading criteria are the same of regurgitation in native valves although the eccentricity and the valve masking phenomenon could make a purely quantitative approach misleading [6].

Regarding biologic prosthetic valve, physiologic regurgitation rarely occurs 2 years before the implant, but when present has a central origin, a short length, and low velocities without aliasing. It is important to bear in mind that biologic stentless valves could present physiologic central regurgitation also just after the implant. Pathologic regurgitations of different origin, direction, and nature, either intra- or perivalvular, can occur due to calcific degeneration and endocarditis that could damage a biologic valve even more frequently than a native one.

Prosthetic valve detachment is the most dramatic complication that should be monitored after the recognition of a true perivalvular regurgitation. It is commonly due to an infective endocarditis, frequently with an early onset within 1 year from the implant and related to the implant itself. The infective process disrupts the sewing ring directly generating a perivalvular regurgitation or creating a periprosthetic aneurysm that could be silent until its emptying, when a loss of tissue occurs and the valve anchorage is lost. Beside regurgitation that could range from moderate to severe leading to heart failure manifestations, we can see the rocking movement of the valve that is a sign of a more extensive detachment with a more urgent indication to surgery. The most dreadful consequence is prosthetic valve embolization.

On the opposite side, we can face prosthetic valve obstruction generating valve stenosis of different severity [3]. In this setting, knowing the exact type (mechanical, single disk, bileaflet or biologic, stented/stentless, etc.), model, and dimension of the valve is of paramount importance because the normal values reported by the manufacturers differ in relation to these factors. Moreover, it is essential, at every follow-up, to know the early post-implant gradient values in order to avoid an incorrect diagnosis of prosthetic valve dysfunction. In mechanical valves, the obstruction could be suspected in the presence of a gradient higher than expected for the specific prosthesis. Sometimes the cause is evident such as the presence of a voluminous mass (thrombus or vegetation) occupying space and then reducing the effective orifice area or blocking an occluder in close position; sometimes the cause consists of a small pathologic process that interferes with the hinges that is not directly visible with 2D echocardiography. In those cases, we must look for an anomalous or incomplete opening of the occluders, although it is often difficult to see without the use of fluoroscopy.