Mitral regurgitation

Mitral regurgitation

Other names	Mitral insufficiency
Anesthetic relevance	High
Anesthetic management
Specialty	Cardiology
Signs and symptoms
Diagnosis	Echocardiogram
Treatment	Surgical repair or replacement
Article quality
Editor rating	In development
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Mitral regurgitation (MR), also known as mitral insufficiency, is a condition in which a portion of the left ventricular stroke volume flows retrograde through the mitral valve back into the left atrium during systole. MR can be chronic—where the body develops compensatory mechanisms to maintain adequate perfusion—or acute resulting in a sudden drop in cardiac output and often precipitating cardiogenic shock. MR is the most common valvular heart condition worldwide. There is increasing recognition of the benefits of early intervention even in asymptomatic disease and a number of a technologies are both in use and in development in addition to surgical valve repair or replacement.

Anesthetic implications

The anesthetic implications of mitral regurgitation differ between acute and chronic disease. Acute mitral regurgitation often results in a mainly resuscitative effort to stabilize the patient to ultimately tolerate definitive treatment. The cornerstone of anesthetic management of chronic disease is hemodynamic control.

Preoperative optimization

It has been shown that patients with mitral regurgitation who have minimal symptoms prior to surgery incur less morbidity and mortality from surgical correction than those with moderate to severe symptoms, suggesting that early intervention is preferred. Patients with signs and symptoms of heart failure should be medically optimized prior to surgery.

Intraoperative management

The objective of intraoperative management is to maintain adequate forward flow by controlling the regurgitant fraction (see Pathophysiology section). Regurgitant fraction increases with afterload as systemic vascular resistance opposes forward flow. Goal systolic blood pressure should range from 100-120 or within 20% of their baseline blood pressure.

Heart rate affects the fraction of the time the heart spends in diastole. As the heart fills in diastole, bradycardia can increase filling time and further worsen the volume work required of the left ventricle. A normal to fast heart rate is preferred, although significant tachycardia may not allow for sufficient filling time and may instead result in hypotension.

Euvolemia should be targeted and the use of intraoperative transesophageal echocardiography (TEE) could be considered to monitor a patient's volume status.

Excessive use of medications that decrease contractility should be avoided. In patients with severe MR who require inotropic support, milrinone or dobutamine are preferred because of their vasodilating effects.

Management of well-compensated mitral regurgitation during induction is actually made somewhat easier by the fact that induction often causes vasodilation and tachycardia. However, patients with severe chronic MR with advanced LV dysfunction or patients with acute MR have significantly disturbed hemodynamics which complicate their management. It is worth noting that such patients may be at increased risk of intraoperative awareness if their tenuous hemodynamics require judicious use of anesthetics.

Postoperative management

The principles of intraoperative management apply also to the postoperative state.

Related surgical procedures

• Mitral valve repair or replacement
• MitraClip
• TAVR in Mitral Position
• Mitral Cinch

Pathophysiology

The mitral valve apparatus consists of the valve annulus, two leaflets, chordae tendoneae and papillary muscles. Proper forward flow depends on precise choreography of the annulus during contraction. Incoordination of any of these components of the annulus compromises the integrity of the valve and can result in mitral regurgitation. MR resulting from defects in the structure of the valve annulus itself is referred to as primary mitral regurgitation. Secondary mitral regurgitation results from left atrial or ventricular dilation that stretches the valve annulus and prevents proper approximation of the valve leaflets. The most common etiologies of MR are listed in Table 1.

During left ventricular contraction, the pressure in the left ventricle exceeds left atrial pressure and a portion of the stroke volume flows along this pressure gradient back through an incompetent mitral valve. Consequently, the flow through the left ventricular outflow tract (LVOT) necessarily decreases. The split in flow can be calculated by the regurgitant fraction (RF)

$RF={\frac {\mathsf {regurgitant\,volume}}{\mathsf {stroke\,volume}}}={\frac {SV_{LV}-SV_{forward}}{SV_{LV}}}$

where SV_LV is left ventricular stroke volume and SV_forward is the stroke volume delivered through the LVOT. The regurgitant fraction is affected by the diameter of the mitral valve defect, the pressure gradient between the left ventricle and atrium, the systemic vascular resistance, the left atrial compliance and the duration of regurgitation during systole.

The change in flow dynamics has consequences for both the left atrium and ventricle. The left atrium experiences higher filling volume and pressure due to the addition of the regurgitant flow to the normal return from the pulmonary veins. The left ventricle must also perform greater volume work to offset the regurgitant fraction and maintain adequate cardiac output and to accommodate filling from an overfilled atrium. In chronic disease, the heart adapts its stroke volume via the Frank-Starling mechanism. Over time the architecture of the left atrium and ventricle will change to increase the compliance of the chamber and allow for higher filling volumes without a commensurate rise in filling pressures. However, such an adaptation is limited and as the disease progresses the ability of the heart to maintain normal filling pressures will be overcome and lead to heart failure. In acute MR such as that which might result from a sudden rupture of a papillary muscle, the compliance of the left atrium does not have time to adapt and a sudden rise in left atrial filling pressure is transmitted backward to the pulmonary vasculature resulting in flash pulmonary edema.

Table 1: Common causes of primary and secondary mitral regurgitation

Primary MR	Secondary MR
Degenerative disease (e.g., myxomatous changes, leaflet prolapse)	Ischemic cardiomyopathy
Rheumatic heart disease	Atrial enlargement, atrial fibrillation
Endocarditis	Hypertrophic cardiomyopathy
Irradiation

Signs and symptoms

Acute Mitral Regurgitation

• Dyspnea
• Pulmonary edema (e.g., bibasilar crackles)
• Cardiogenic shock (e.g., hypotension, tachycardia, tachypnea, cool extremities, weakness, altered mental status)
• Left-sided heart failure (e.g., orthopnea, paroxysmal nocturnal dyspnea, peripheral edema, rales)
• Soft, decrescendo murmur

Chronic Mitral Regurgitation

Chronic mitral regurgitation often remains asymptomatic until progression to severe disease.

• Dyspnea
• Fatigue
• Palpitations
• Left-sided heart failure (orthopnea, paroxysmal nocturnal dyspnea, peripheral edema, rales)
• Blowing, holosystolic murmur radiating to the axilla best auscultated at the cardiac apex
• S3 in late disease

Diagnosis

Transthoracic echocardiography (TTE) is the most widely used modality used to diagnose mitral regurgitation. If the image quality of TTE limits the assessment of the relevant anatomy, transesophageal echocardiography (TEE) may be used. With either modality, the diagnosis and assessment of mitral regurgitation consists of an amalgamation of both qualitative and quantitative data to define the specific etiology for a given patient as well as to characterize the severity of the disease.

Briefly, the morphology of the mitral valve apparatus (annulus, leaflets, chordae tendonae, papillary muscles) and left ventricular and atrial size and function should be characterized and color doppler should be used to evaluate the characteristics of the regurgitant jet. Quantification of the regurgitant jet is useful in determining disease severity, although there are a number of limitations inherent in such measurements that make depending on any one value potentially unreliable. At a minimum, effective regurgitant orifice area (EROF), regurgitant volume (RVol) and regurgitant fraction (RF) should be measured. Widely accepted cutoff values are listed in Table 2.

Table 2: Disease classification based on color doppler flow measurements of mitral regurgitation †intermediate values listed here as moderate disease have lower specificity and can be measured in what should be classified as severe disease.

	Mild Disease	Moderate Disease†	Severe Disease
EROF	<0.2 cm2	0.2-0.4 cm2	≥0.4 cm2
RVol	≤30 mL	30-60 mL	≥60 mL
RF	<30%	30-50%	≥50%

Treatment

Medication

Medical management of MR requires identification and treatment of the underlying cause. Otherwise, medical management is the management of heart failure for those with evidence of LV dysfunction (i.e., diuretics, ACE inhibitors, beta blockers as appropriate). Although a reduction in afterload can theoretically reduce the regurgitant fraction, studies have not shown any benefit from prophylactic use of vasodilators.

Surgery

The definitive treatment of mitral regurgitation is surgical or percutaneous. However, within this category there is a number of procedures available and pairing the right patient with the right modality is essential. For severe primary MR, surgical valve repair is the gold standard. Treatment modality of choice for secondary MR is more controversial.

Prognosis

Retrospective studies have shown widely variable survival for MR, ranging from a low of 27% at 5 years to a high of 95% at 20 years. A prospective study by Enriquez-Sarano et al published in the NEJM in 2005 demonstrated a 5-year cardiac mortality rate of 36±9% in patients with severe MR and normal LV function. A 2009 prospective study showed a higher cardiac mortality at 4 years of—55%—for those with severe mitral regurgitation and LV dysfunction. Most recently, a community cohort study of approximately 1300 patients over a 10-year period showed excess death in patients with MR compared versus those without (RR 2.23, 95% CI 2.06–2.41) regardless of LV function. Poor LV function— defined as ejection fraction (EF) <50%—was associated with higher mortality compared to an EF >50%.

Thirty-day post-operative mortality following mitral valve surgery has been reported to be between 2.7-25% with older age being a significant determinant of poor outcome. Compared to mitral valve replacement, mitral valve repair has been shown to have better 10-year survival, although the survival benefit does not appear to hold for patients older than 60 or who require CABG at the time of valve surgery. Transcatheter alternatives to mitral valve surgery comprise a rapidly expanding field and may be promising alternatives for patients who are poor surgical candidates. MitraClip transcatheter repair has been shown to have comparable survival to surgical repair with both approaches showing better outcomes than medical management alone. Studies of transcatheter mitral valve replacement (TMVR) technologies have been limited to small, often industry-sponsored trials. But several higher-quality studies are currently underway including the SUMMIT trial which is comparing Tendyne™ TMVR to MitraClip in patients with moderate-to-severe MR who at prohibitive risk for surgery. SUMMIT is expected to complete by 2027.