MR severity is determined by a combination of several echo parameters well delineated in the ACC/AHA/ASE and European guideline documents [2, 3]. These include anatomy of mitral leaflets and supporting apparatus, size, geometry and function of left ventricle and left atrium, size and function of right ventricle and pulmonary artery pressure. Severity of MR is assessed by qualitative, semiquantitative as well as quantitative methods. These include eyeball assessment of MR jet area within the left atrium estimating percent of left atrium occupied by the MR jet, contour and direction of MR jet, vena contracta width of MR jet, continuous-wave (CW) Doppler intensity, the shape of the transmitral regurgitant jet velocity curve, effective orifice area (ERO), regurgitant volume (RV), regurgitant fraction (obtained by using the proximal isovelocity surface area (PISA) method or quantitative Doppler flow measurements) [4], Criteria for severe MR include vena contracta width of $\ge$7 mm, ERO of $\ge$0.4 cm${}^2$, regurgitant volume of $\ge$60 mL and regurgitant fraction of $\ge$50%. Volumetric measurements provide a better assessment as conventional color Doppler parameter may overestimate its severity on a single image [5]. Earlier ACC/AHA guidelines reduced the cut off for EROA for severe functional MR to $\le$0.2 cm${}^2$ based on outcome studies that have shown poor prognosis in patients with ERO $\ge$0.2 cm${}^2$ [5], however the most recent ACC/AHA guidelines suggest the same EROA ($\ge$0.4 cm${}^2$) for severe MR of functional and degenerative etiology [3].

These criteria are generally more reliable in central jets. Pulmonary artery systolic pressure, mitral inflow E wave velocity and pulmonary vein flow pattern are other helpful parameters. Systolic pulmonary vein reversal (Fig. 1) is highly specific for severe MR but is not very sensitive. Discrepancy may occur between MR ERO and RV in mitral valve prolapse in early stages of MR where non holosystolic MR jet duration and hence regurgitant volume are smaller than the PISA derived EROA which does not account for the duration of MR jet. 2D vena contracta width may be unreliable in eccentric jets, however direct measurement of regurgitant orifice can be done using 3D color Doppler vena contracta area which may allow better quantitation of MR in central as well as eccentric MR jets [5] as well as in patients with multiple MR jets in whom PISA quantitation by adding multiple jets has not be validated and in whom continuity equation cannot be performed [6].

Symptom onset is a distinctive point in developmental history of MR and also starting point for intervention. Because symptoms develop gradually, patients may fail to recognize or ignore symptoms. In patients with chronic MR, exercise echocardiography [7, 8] or exercise invasive hemodynamics may unmask exertional symptoms in asymptomatic patients. Exercise echocardiography can also be helpful when there is discrepancy between MR severity and clinical symptoms such as in patients with moderate MR. In such patients, MR and filling pressures may become significantly worse with exercise helping to demonstrate MR as the cause of the patient’s dyspnea. Among asymptomatic patients with severe MR, signs of LV remodeling and systolic dysfunction are reflected by LVESD $\ge$40 mm or LVEF 60% which are indications for mitral valve repair [3] provided a $>$90% success rate for mitral valve repair can be predicted operatively [9, 10]. The results of mitral valve repair are superior to the results of mitral valve replacement even in elderly patients [11, 12, 13] if the repair is performed at surgery centers having high surgical volume. Patients with significant MR are often not referred for surgical management [14]. Twenty-year outcome status post pre mitral repair vs. replacement for moderate to severe or severe degenerative MR showed that mitral valve repair has lower mortality than after replacement [15]. Twenty-year survival was also better after mitral valve repair than after replacement (46% vs. 23%) [15]. Mitral valve (MV) repair has been shown to be superior than replacement in patient subsets on the basis of age, sex, or any stratification criteria [15].

Elevated natriuretic peptide levels provide objective evidence of increased preload to provide an adequate cardiac output in patients with chronic severe MR and may be helpful in making treatment decisions [16]. Repair should also be considered first, with other causes of severe MR, such as papillary muscle rupture, infective endocarditis, and cleft mitral valve. Complex and extensive repair is needed for anterior and/or bileaflet primary mitral valve disease [17, 18].

Degenerative MR is the most common cause of mitral valve repair and is caused by valvular or chordal degeneration and systolic excessive leaflet movement defined by a prolapse in left atrium $\ge$2 mm, or flail leaflet which can affect one or both leaflets and one or multiple scallops [1] (Fig. 1A–D).

Pre or intraoperative communication between echocardiographer and the surgeon regarding MV pathology is key to successful MV repair. Surgeon’s view of the MV can be effectively reproduced with the en face real time view on 3D image of the MV (real time or with reconstruction). The aortic valve (AV) can be seen in the 12 o’clock position, left atrial appendage is visualized in the 9 o’clock position, and the coronary sinus is at the 3 o’clock position [19, 20]. Automation advances in 3D imaging allow rapid reproduction of this view.

Besides prolapsing or flail scallops, MR jet may also originate between individual scallops. This occurs more commonly between the posterior leaflet through cleft like indentations that sometimes extend to the mitral annulus. This origin of MR can be very difficult to diagnose on 2D TTE or TEE (Fig. 2A–C). 3D color Doppler further assists in confirming jet origin at the site of suspected leaflet pathology/ies including presence of mitral valve cleft like indentation/s. Presence of calcification on the annulus and leaflets and in the subvalvular apparatus further assists surgeon in planning repair [21]. Visualization of the valve from the LV perspective adds further information on leaflet morphology, coaptation and regurgitant site/s particularly if jet originates from mitral valve clefts. Optimal visualization of the MR jets using real-time 3D TEE leads direct guidance for catheter movement and positioning of the implanted device(s) capturing the opposing sides of anterior and posterior mitral leaflet scallops during catheter based MV interventional procedures [22].

As opposed to degenerative MR, mitral valve leaflets in secondary MR may be normal but MR results from leaflet mal-coaptation due to a dilated mitral annulus as in dilated cardiomyopathy or due to tenting of mitral leaflets due to LV infarct remodeling causing outward displacement of papillary muscles and tethering of chordae attached to these papillary muscles. Mal-coaptation may be along the entire mitral leaflet coaptation plane mostly in functional MR (Fig. 3A–C) or localized to some scallops commonly seen at the P3 scallop of the mitral valve in the presence of a remodeled infero-posterior myocardial infarction causing tethering of the chordae to P3 scallop (ischemic MR).

In a study evaluating surgical mitral valve repair with echo-guidance, repair was successful in 99% of degenerative, 97% of myopathic, and 84% of inflammatory mitral valve disease [23]. Concordance of echo findings with surgical findings increased the chances of successful repair by 2D TEE (98% vs. 57%) and 3D TEE (100% vs. 94%) [24]. Another study found global LV reverse remodeling after 5 years of successful MV repair [24].

The tricuspid annulus is comprised of a fibrous ring where the leaflets are attached. The tricuspid annulus area is 8~12 cm${}^2$ and is about 20% bigger than the mitral annulus.

In adults TR is most commonly secondary (or functional), with normal leaflets and chords. Dilatation of the right atrium and RV with dilation of the tricuspid annulus is the most cause of secondary TR [32] (Fig. 4A–C). In an echocardiographic review of patients without primary tricuspid valve disease [33], severe TR was associated with higher pulmonary artery systolic pressure (PASP), atrial fibrillation, right atrial and RV enlargement, LV dysfunction, and primary mitral valve disease. In patients with concomitant mitral valve disease, TR is referred to as functional and is considered to be caused by filling pressure elevation in left heart, resulting in eventually tricuspid annular dilation and the tethering of tricuspid leaflets induced by RV enlargement [34, 35, 36]. This may also be true in patients with late TR after left side valve surgery [37]. Secondary TR in patients with right ventricular pressure and/or volume overload is caused by annular dilatation and increased tricuspid leaflet tethering [2].

Marked right atrial enlargement in atrial fibrillation with dilated tricuspid annulus and annular dynamics results in “atrial functional TR”. Moderate or severe TR was associated with most of these factors, as well as presence of an RV pacemaker lead, older age, and female sex. Primary pulmonary parenchymal diseases that elevate PASP and pulmonary arterio-venous disorders such as pulmonary embolism and primary pulmonary hypertension are other causes. Although TR severity was associated with higher PASP, many patients with pulmonary hypertension had only mild TR (65% of patients with PASP 50 to 69 mmHg and 46% with PASP $\ge$70 mmHg).

Primary tricuspid valve disease was found in 10 percent of patients with severe TR [38]. Iatrogenic or acquired TV diseases such as endocarditis, pacemaker/ICD leads, ruptured chords or flail leaflets in myxomatous tricuspid valve disease, chordal rupture from repeated right heart biopsies as in heart transplant recipients, and chest trauma are common causes of TR. It may result from mechanical causes that impair closure, such as scar formation or thrombus on the leads, although the perforation or laceration of the valve leaflets is another cause of TR. Lead impingement, lead adherence, and lead entanglement are TR causing pathophysiologies [39]. Another mechanism is asynchrony, which occurs with abnormal right ventricle activation caused by pacemaker [40, 41]. One study showed 5 of 41 (12%) of patients having tricuspid valve leaflet perforation or impingement by the PPM or ICD lead detected on the initial TTE [39]. Pacemaker or ICD leads causing damage to the tricuspid valve may result in severe symptomatic TR and may not be well visualized by TTE.

TR is often observed following orthotopic cardiac transplantation with a prevalence ranging from 67% to 85% in echocardiographic series [42]. Damage to the valve apparatus during endomyocardial biopsy could account for the high prevalence of TR in these patients [43]. TR may be caused directly by anatomic disruption of the valve apparatus, such as torn leaflet or ruptured chordae tendinea; and excessive leaflet motion is associated with severe prolapse or flail valve [44, 45]. With longer follow-up duration, the severity and clinical impact of TR worsens. TR can potentially exert hemodynamic stress on the right ventricle, which then undergoes morphologic remodeling that leads to chamber dilation. This may worsen right-sided atrioventricular coupling geometrically and hemodynamically that in turn causes more TR [45].

Marantic endocarditis in connective tissue disease, Ebstein anomaly, carcinoid syndrome, and drug-induced disease (combined use of the anorectic drugs, fenfluramine and phentermine, or the dopamine agonist pergolide) are other etiologies of primary TR.

Examples of valvular injury directly from implantable cardioverter-defibrillator lead placement (Fig. 5A–C) or a permanent pacemaker (Fig. 6A–C) or endomyocardial biopsy in cardiac transplant recipients (Fig. 7A,B) are shown.

Congenital heart disease such as intracardiac shunts at atrial or ventricular level and anomalous pulmonary venous return cause RV volume and pressure overload causing RV enlargement and dilated tricuspid annulus. RV outflow obstruction such as in the pulmonic valve or pulmonary artery stenosis, tetralogy of Fallot and systemic right ventricle facing systemic afterload result in RV enlargement, hypertrophy, systolic dysfunction and increase in RV systolic pressure with resultant TR. Other causes include Epstein anomaly and primary RV dysfunction due to RV infarct and RV cardiomyopathies.

I Dilation of aortic root/ascending aorta: (a) sinotubular junction and ascending aorta, (b) sinuses and ST junction, (c) ventriculo-arterial dilation at the aortic annulus resulting in aortic leaflet malcoaptation.

II Aortic cusp prolapse/perforation: endocarditis, aortic dissection (Figs. 8, 9)

III Restrictive Valve Disease:

a. Degenerative—Calcification of aortic leaflets with aging

b. Congenital—Bicuspid aortic valve

c. Rheumatic

TTE is an essential first diagnostic tool and is frequently sufficient to assess the presence and severity of AR [60]. Besides an assessment of the aortic valve and aortic root anatomy to determine the etiology of the regurgitation, assessment of AR should include evaluation of LV size, geometry, and function [5]. In chronic AR, TTE is essential in monitoring the changes in LV geometry (LV size and LV volume increase) and function (progressive worsening LV function) due to the prolonged LV volume overload. LV dilatation, particularly with preserved LV function, is a supportive sign of significant AR and becomes more specific excluding other causes of LV volume overload (e.g., in athletes, anemia). In severe acute AR, the LV is not dilated, and the LV end-diastolic pressure increase may cause the MV premature closure, best documented with an M-mode.

Ratio of AR jet width to the LVOT width of $\ge$65% (Fig. 9), vena contracta of AR jet ($\ge$0.6 cm), effective regurgitant orifice area of $\ge$0.3 cm${}^2$ (Fig. 8), regurgitant volume of $\ge$60 mL by PISA method [or continuity equation], density of AR jet Doppler velocity similar to aortic valve forward flow, pressure half time of AR jet 200 ms (Fig. 9C), diastolic flow reversal in the abdominal aorta and pan-diastolic flow reversal in the proximal thoracic aorta with time velocity integral of $>$15 cm (Fig. 9D), are all used as criterial for severe AR. Importantly no one criterion is diagnostic and an integrative approach using multiple methods should be used to arrive at a conclusion on AR severity. LV enlargement should be present in patients with chronic severe AR.

TEE is usually indicated for assessment of mechanism of AR, exclusion of aortic valve infective endocarditis, measurement of aortic root size and quantitation of AR severity when not feasible by TTE. Both 2D and 3D TEE have shown utility, improving diagnostic accuracy of TTE in AR related condition: infectious or inflammatory endocarditis, isolated aortic root dilatation, or acute aortic dissection [61].

The diagnostic value of 2D and 3D TEE in defining the mechanisms of AR is particularly important for pre-operative evaluation of patients undergoing aortic root surgery, or valve repair or replacement [62].

Common causes of leaflet malfunction causing AR include degenerative leaflet calcifications, and infective endocarditis (Fig. 10), bicuspid aortic valve perforation and rheumatic fever. The causes of AR include Marfan’s syndrome, annulo-aortic ectasia (idiopathic root dilatation) (Fig. 9), aortic dissection, connective tissue disease, and syphilis. The Carpentier classification is also widely used to describe the mechanism of AR [63].

Using 2D biplane, 3D and 3D color Doppler, the exact perpendicular plane to the aortic regurgitation jet can be identified, from which planimetry of the AV coaptation gap as well of the color Doppler vena contracta can be performed [64]. This has been shown to have a good correlation with aortographic grading of AR. When the shape of the regurgitant orifice is nonsymmetric, by using 3D images, invalid geometric assumptions of the vena contracta can be avoided with direct measurement [65]. 3D echocardiographic color Doppler also allows visualization, and measurement of multiple jets and correlated morphologically with surgical findings [65].

Isolated aortic valve perforation can occur post endocarditis or post cardiac surgery [15, 16, 17]. Restriction of aortic valve leaflet motion may occur due to leaflet tethering [18, 19]. Combined use of 2D, color Doppler and 3D TEE may facilitate location and mechanism of AR and can allow valve repair instead of replacement.

The time duration of Doppler flow of subclavian artery into late diastole is reported to be another important parameter for the severity of AR [66].

Aortic stenosis (AS) is commonly combined with AR (in nearly 80% of cases) but the regurgitation is usually only mild or moderate in severity and measures of AS severity are not significantly affected [5]. When severe AR combines with AS, measuring of AS severity remain accurate including maximum velocity, mean gradient, and valve area. However, because of the high transaortic volume flow rate, maximum velocity, and mean gradient are higher than expected for a given valve area [5].

Significant pulmonary valve regurgitation (PR) in adults is generally seen in those with prior history of pulmonic valve surgery for congenital heart disease. PR can also result from significant pulmonary hypertension of any cause.

PR is diagnosed with color Doppler revealing diastolic flow in the RV outflow tract (Fig. 11). In severe PR with normal PA pressures (e.g., primary PR), the color jet has low velocity with laminar flow and the duration of the flow can be misleading, as severe PR may lead to rapid equalization of the RV pressure with diastolic pulmonary artery pressure, and thereby lead to a very short duration of flow [67]. In secondary PR from pulmonary hypertension, the jet is aliased and usually holodiastolic [68]. Severe PR from primary or secondary causes has an intense spectral Doppler signal. Other parameters to assess PR severity include PR jet width: if it occupies $>$50–65% of the RVOT, this suggests severe PR, whereas a narrow jet 25% of the pulmonary annulus suggests mild PR. This may be less reliable in the setting of an eccentric jet which may underestimate the severity of the regurgitation. Another helpful parameter is the pressure half time (PHT). A short PHT, defined as 100 ms)is consistent with severe PR. Early termination of the PR flow would be seen with varying degrees of late diastolic forward flow in the pulmonary artery due to increase in RV pressure relative to the pulmonary artery pressure [69]. However, a short PHT can also be seen in the presence of elevated diastolic intrapulmonary pressures as well as RV diastoldys function [70, 71]. Other quantitative variables such as regurgitant volume and fraction can also be used however the difficulty in measuring the pulmonary annulus size makes these measurements less accurate. Additionally, they have not been validated as they have been with AR.

Severe PR also causes RV dilatation and diastolic flattening of the interventricular septum due to volume overload. A normal RV size suggests the absence of chronic severe PR. Carcinoid disease causes thickening and restriction of tricuspid and pulmonic valves leading to valve stenosis and regurgitation. This leads to turbulent forward flow in systole due to varying degrees of pulmonic stenosis and regurgitation due to incomplete closure of the thickened and restricted valve leaflets (Fig. 12).