D.BASEM ELSAID ENANYLECTURER OF CARDIOLOGY

AINSHAMS UNIVERSITY

Mitral regurge

ETIOLOGY

--Primary MR:-Mitral valve prolapse is the most common in developed countries and is also called "degenerative" or myxomatous mitral valve disease. (valve prolapse of 2 mm or more above the mitral annulus, as seen in the parasternal long-axis view).The most common cause of chronic primary MR in developed countries is mitralvalve prolapse, which has a wide spectrum of etiology and presentation. Younger populations present withsevere myxomatous degeneration with gross redundancy of both anterior and posterior leaflets and the chordalapparatus (Barlow’s valve). Alternatively, older populations present with fibroelastic deficiency disease, inwhich lack of connective tissue leads to chordal rupture. The differentiation between these 2 etiologies hasimportant implications for operative intervention.-Infective endocarditis. -Trauma, which can cause ruptured chordae and acute MR. -Rheumatic heart disease is uncommon in developed countries but continues to constitute a significant burden in the rest of the world. Although rheumatic valve disease often results in MR in the first two decades of life, mitral stenosis (MS) and mixed MS/MR are more often seen in adults.

-Anorectic drug combinations that are no longer available and prolonged use of certain other drugs, such as ergotamine, pergolide, and cabergoline, which may induce MR by a mechanism similar to that with anorectic drugs {Serotonin stimulates fibroblast growth and fibrogenesis}-Congenital due, for example, to a valve cleft.-Mitral annular calcification is a common finding in older adults that is often associated with mild to moderate MR-Rupture of a papillary muscle in the setting of an acute myocardial infarction

--Secondary (functional) MR:-Ischemic heart disease.-Left ventricular systolic dysfunction.-Hypertrophic cardiomyopathy.

Because MR is only 1 component of the disease (severe LV dysfunction, coronary disease, or idiopathic myocardial disease are the others), restoration of mitral valve competence is not by itself curative; thus, the best therapy for chronic secondary MR is much less clear than it is for chronic primary MR. The data are limited, and there is greater difficulty in defining the severity of MR in patients with secondary MR than in those with primary MR. In patients with secondary MR, adverse outcomes are associated with a smaller calculated effective regurgitant orifice compared to primary MR due to multiple reasons. The MR will likely progress due to the associated progressive LV systolic dysfunction and adverse remodeling. In addition, there is an underestimation of effective regurgitant orifice area by the 2-dimensional echocardiography derived flow convergence method due to the crescentic shape of the regurgitant orifice. There are the additional clinical effects of a smaller amount of regurgitation in the presence of compromised LV systolic function and baseline elevated filling pressures.

AHA 2014

CLINICAL MANIFESTATIONS

--Patients with isolated mild to moderate MR are asymptomatic, since there is little volume overload--Even with severe MR, most patients remain asymptomatic until there is left ventricular failure, pulmonary hypertension, or the onset of atrial fibrillation--Exertional dyspnea and fatigue, palpitation symptomatic heart failure with pulmonary congestion and edema.{often irreversible due to the long standing MR}--Thromboembolism, hemoptysis, and right-sided heart failure do occur, but are less common than with mitral stenosis--IEC

PHYSICAL EXAMINATION

--Bounding pulse, However, the pulse pressure is normal--Leftward displacement of the apical impulse; it is usually brisk or hyperdynamic--Thrill and an S3 may be palpable

CARDIAC AUSCULTATION

--Heart sounds:-S1 is diminished, reflecting failure of the mitral leaflets to close properly.-Wide splitting of S2 is common because the decrease in left ventricular ejection time results in an early A2. Furthermore, if pulmonary artery hypertension is present, P2 will be increased and delayed, further widening the splitting of S2.-The augmented flow rate across the mitral valve orifice into a dilated left ventricle produces an S3 gallop, which becomes particularly prominent if left ventricular failure occurs.

--Murmurs:-Most cases, the murmur is holosystolic, commencing immediately after S1 and continuing up to and sometime beyond and obscuring A2, a result of the persistent pressure gradient between the left ventricle and atrium after aortic valve closure.-Best over the apex, radiating to the axilla and when very loud may often radiate to the back. It is most often blowing and high pitched in quality.-Loudness of the murmur correlates even less well with severity in secondary (functional) MR-Moderate to severe acute MR is often silent or associated with only a soft murmur due to equalization of left ventricular and left atrial pressures

-Isometric hand grip is carried out by asking the patient to lock the cupped fingers of both handsinto a grip and then trying to pull them apart. The resulting increase in peripheral vascularresistance intensifies MR (and ventricular septal defect) while softening instead AS (and aorticsclerosis). Hence, a positive hand grip argues strongly in favor of MR.

Other types of murmurs

--Posterior leaflet involved (due to prolapse or chordal rupture), the murmur may radiate anteriorly toward the sternum and is heard well at the base. This type of murmur is often confused with aortic stenosis but does not radiate to the carotid arteries.--Mid to late systolic murmur, harsh in quality, is often heard when the MR is due to prolapse or papillary muscle displacement (previously known as papillary muscle dysfunction)==mitral valve prolapse (MVP) murmur?It is an MR murmur—hence, loudest at the apex, mid to late systolic in onset (immediately following the click), and usually extending all the way into the second sound (A2). In fact, it often has a crescendo shape that peaks at S2. It is usually not too loud (never greater than 3/6), with some musical features that have been variously described as whoops or honks (as in the honking of a goose). Indeed, musical murmurs of this kind are almost always due to MVP.--Infrequently, the large diastolic volume across the mitral valve produces an early diastolic murmur--Mitral valve prolapse, a mid systolic click (correlating with the maximal prolapse and tension on the chordae) may be heard and the murmur may start in mid to late systole--MR due to dilatation of the valvular annulus, the murmur often diminishes in intensity or disappears as the heart failure is treated and left ventricular function improves-- Maneuvers that decrease venous return and reduce the left ventricular volume cause the systolic click to occur earlier (move toward S1) and the murmur to be of longer duration (although it is often fainter). On the other hand, those maneuvers that increase venous return or afterload cause the click to occur later (move toward S2) and the murmur to be abbreviated

Electrocardiogram

--Left atrial enlargement--Left ventricular hypertrophy--Pulmonary artery hypertension right ventricular hypertrophy, which includes a tall R wave in V1 or V2 with R/S ratio >1

Chest radiograph

--Cardiomegaly, resulting from enlargement of the left ventricle {cardiac silhouette to be displaced towards the left chest wall and the chamber becomes globular} and left atrium {straightening of the left heart border with the appearance of a double density and elevation of the left main stem bronchus}--Right ventricle is usually normal in size, unless there is pulmonary hypertension.--Lung fields are usually clear unless congestive heart failure is present. --Calcification of the mitral valve annulus may be seen.

Echocardiogram

--If image quality is suboptimal, transesophageal imaging is recommended --Severity of MR:-Severe chronic MR does NOT exist (with rare exceptions) without clear evidence of left atrial or left ventricular enlargement

AHA 2014

Mitral:EROA= regurg V/VTI mr jetRegurge V=vol transmitral (CSA mitral annulusX VTI mitral annulus)-

vol transaortic (CSA lvotX VTI lvot) Regurg fraction=rgeurge V/vol transmitral

--Cause of MR:Intraoperative TEE is indicated to establish the anatomic basis for chronic primary MR (stages C and D) and to guide repair . (Level of Evidence: B)

TEE is indicated for evaluation of patients with chronic primary MR (stages B to D) in whom noninvasive imaging provides nondiagnostic information about severity of MR, mechanism of MR, and/or status of LV function. (Level of Evidence: C)

-Mitral valve prolapse, there is posterior movement of the leaflets (hammocking) into the left atrium during systole. Either one or both leaflets may prolapse to variable degrees. In addition, the leaflets are thickened and redundant-Rheumatic heart disease, there is significant thickening of the leaflets and some evidence of commissural fusion or chordal shortening-Endocarditis, vegetations are present, typically on the atrial side of the mitral valve leaflets-Perforated mitral valve leaflet is present, an MR jet can be seen passing through the leaflet-Chordal or papillary muscle rupture is present, the movement of the leaflets is markedly exaggerated and the ruptured chord or papillary muscle is seen in the left atrium in systole-Ischemic MR restricted leaflet motion, particularly of the posterior leaflet, resulting in inadequate apposition of the leaflets, often called "tenting" or "tethering"

--contrast angiography of the left ventricle is generally avoided at the time of catheterization in patients with acute MR because of the contrast load in an already compromised patient--Fup / 6-12 m according to severity

AHA2014:Class IIa1. Exercise hemodynamics with either Doppler echocardiography or cardiac catheterization is reasonable in symptomatic patients with chronic primary MR where there is a discrepancy between symptoms and the severity of MR at rest (stages B and C) . (Level of Evidence: B)2. Exercise treadmill testing can be useful in patients with chronic primary MR to establish symptom status and exercise tolerance (stages B and C). (Level of Evidence: C)

PHYSICAL ACTIVITY AND EXERCISE

--2006 ACC/AHA guidelines concluded that there are no exercise restrictions in asymptomatic patients who are in sinus rhythm and have normal left ventricular and left atrial dimensions and a normal pulmonary artery pressure--Mild left ventricular enlargement can participate in low and moderate static and all dynamic competitive sports--Severe MR and definite left ventricular enlargement, pulmonary hypertension, or any reduction in left ventricular systolic function at rest should not participate in any competitive sports-- AF who are treated with long-term anticoagulation therapy should not engage in sports with any for bodily contact or risk of trauma

Medical treatment

--USE OF VASODILATORS:-Asymptomatic patients:There are no published studies that support the hypothesis that vasodilator therapy is beneficial in asymptomatic patients with chronic MR. In addition, the administration of vasodilators in patients with normal LV function might limit the development of symptoms due to increasing LV dysfunction, thereby masking an indication for surgery. Thus, with some exceptions (eg, the hypertensive patient), vasodilators are not recommended for use in asymptomatic patients with chronic MR due to primary valve disease

-Symptomatic patients:--In primary MR (eg, myxomatous or rheumatic), the therapeutic goal should be a reduction in systolic pressure. Thus, a beta blocker, diuretic, hydralazine, or calcium channel blocker should be used. {medical therapy is not a substitute for surgical intervention in patients with chronic symptomatic MR}.--Chronic vasodilator therapy is indicated in symptomatic patients who are not candidates for surgery. The evidence of benefit is best in patients with secondary (functional) MR due to left ventricular dysfunction--Several studies confirm a beneficial effect of acute vasodilator therapy in patients with chronic MR. Intravenous nitroprusside, for example, decreases left ventricular end-diastolic pressure and volume while increasing forward stroke volume and cardiac index. Also Hydralazine.

--ANTICOAGULATION:-Mitral annular calcification, which is often associated with MR, increases the risk of embolism, even in the absence of atrial fibrillation.-2008 ACCP guidelines that anticoagulation with warfarin (target INR 2.5, range 2.0 to 3.0) is indicated in patients with rheumatic mitral valve disease who have a history of systemic embolism, left atrial thrombus, or paroxysmal or chronic atrial fibrillation, left atrial diameter >55 mm and rheumatic mitral valve disease-Recurrent systemic embolism despite adequate anticoagulation, the addition of aspirin (75 to 100 mg/day) is suggested or higher target INR (target INR 3.0, range 2.5 to 3.5-Data are lacking to support the use of direct thrombin inhibitors in patients with valve disease and atrial fibrillation.

--ENDOCARDITIS PROPHYLAXIS:-No longer recommended when patients with mitral valve disease (in the absence of prosthetic repair or replacement)

AHA 2014

The patient and family should be sufficientlyeducated by the Heart Valve Team about all alternatives for treatment so that their expectations can be met as fully as possible using a shared decision-making approach.

Heart Valve Centers of Excellence

1) are composed of experienced healthcare providers withexpertise from multiple disciplines; 2) offer all available options for diagnosis and management, including complex valve repair, aortic surgery, and transcatheter therapies; 3) participate in regional or national outcomeregistries; 4) demonstrate adherence to national guidelines; 5) participate in continued evaluation and quality improvement processes to enhance patient outcomes; and 6) publicly report their available mortality and successrates.

Mechanical or bioprosthetic

--Mechanical valves have the disadvantage of requiring lifelong warfarin therapy, while bioprosthetic valves have the disadvantage of limited durability due to valve degeneration, particularly in patients under age 65--2006 ACC/AHA guidelines when valve replacement:-Bioprosthetic valves are recommended in patients who cannot or will not take warfarin or have a clear contraindication to warfarin therapy.-Among patients who can take warfarin, the weight of evidence supports the following approach:--A mechanical valve in patients under age 65 who have long-standing AF.--A bioprosthetic valve in patients ≥65 years of age.--Among patients under age 65 who are in sinus rhythm, patient preference plays a central role in the choice of valve. The guidelines suggested that a bioprosthetic valve should only be considered after a detailed discussion with the patient of the risks of warfarin therapy compared to the likelihood of repeat valve replacement in the future

Mitral valve replacement versus repair

--In most patients, mitral valve repair at experienced surgical centers is the preferred approach because of both functional and survival benefits compared to valve replacement {It preserves the patient's native valve, avoids the risk of chronic anticoagulation or prosthetic valve failure ,,, Preservation of the mitral chordal apparatus better postoperative left ventricular function ---chordal preservation can also be attained during mitral valve replacement---}--Patients should not participate in sports that are associated with a risk of bodily contact or trauma that might disrupt the repair--Rate of late recurrent MR following mitral valve repair is as high as 28 percent redo only 3%*Degree of MR may have limited importance compared with the underlying cardiovascular disease*Almost one-half of patients died within five years*Surgeons may be reluctant to perform a repeat operation in this older, high-risk population

--Unlike the aortic valve, the mitral valve serves to do more than just direct forward cardiac flow. The mitral valve is also an integral part of the LV, coordinating LV contraction and maintaining LV shape. When the valve is destroyed at the time of surgery, there is a precipitous fall in LV function postoperatively, which does not occur when the valve apparatus is conserved--The use of the maze procedure or radiofrequency or cryoablation as an adjunct to mitral valve repair or replacement is an effective approach to reduce the incidence of postoperative AF

--The 2005 ACC/AHA heart failure guidelines note that the effectiveness of mitral valve repair or replacement for severe secondary mitral regurgitation in refractory end-stage HF is not established.--The 2006 Heart Failure Society of America (HFSA) practice guidelines note that isolated mitral valve repair or replacement for severe mitral regurgitation secondary to ventricular dilatation in the presence of severe LV systolic dysfunction is not generally recommended.--The 2006 International Society for Heart and Lung Transplantation (ISHLT) guidelines for cardiac transplant candidates note that isolated mitral valve repair (not associated with revascularization or ventricular restoration) should not be routinely performed in patients with advanced LV dysfunction and HF

PERCUTANEOUS REPAIR

--Under investigation--Techniques include direct and indirect annuloplasty approaches and an implantable clip.--The MitraClip provides a noninvasive means of mitral valve repair, superior safety and similar improvements in clinical outcomes, but its efficacy in reducing mitral regurgitation is somewhat limited {EVEREST II trial}--European 2012:The percutaneous mitral clip procedure may be considered inpatients with symptomatic severe secondary MR despite optimalmedical therapy (including CRT if indicated), who fulfil the echocriteria of eligibility, are judged inoperable or at high surgical riskby a team of cardiologists and cardiac surgeons, and who have alife expectancy greater than 1 year (recommendation class IIb)-- Despite the lack of evidence, a combination of low-dose aspirin and a thienopyridine is used early after TAVI and percutaneous edge-to-edge repair, followed by aspirin or a thienopyridine alone

AHA 2014

IConcomitant mitral valve repair or MVR is indicated in patients with chronic severe (or moderate IIb)primary MR undergoing cardiac surgery for other indications. (Level of Evidence: B)IIbTranscatheter mitral valve repair may be considered for severely symptomatic patients (NYHA class III to IV) with chronic severe primary MR (stage D) who have favorable anatomy for the repair procedure and a reasonable life expectancy but who have a prohibitive surgical risk because of severe comorbidities and remain severely symptomatic despite optimal GDMT for HF. (Level of Evidence: B)

Other valvular lesions

--When either stenosis or regurgitation is predominant, management follows the recommendations concerning the predominant VHD--Interaction between the different valve lesions ex. associated MR may lead to underestimation of the severity of AS--Indications for intervention are based on global assessment ofthe consequences of the different valve lesions, i.e. symptomsor presence of LV dilatation or dysfunction--The decision to intervene on multiple valves should take intoaccount the extra surgical risk--The choice of surgical technique should take into account thepresence of the other VHD.

Noncardiac surgery

--Asymptomatic patients with severe MR or AR and preserved LV function, non-cardiac surgery can be performed safely. --The presence of symptoms or LV dysfunction should lead to consideration of valvular surgery, but this is seldom needed before non-cardiac surgery. --If LV dysfunction is severe (EF <30%), non-cardiacsurgery should only be performed if strictly necessary, after optimization of medical therapy for HF.----Control heart rate (particularly in MS), to avoid fluid overload as well as volume depletion and hypotension (particularly in AS)

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