Mitral regurgitation (MR) refers to the dysfunction of the valve, where it allows blood to flow ‘backwards’ i.e. to re-enter the left atrium during systole. It has a number of causes, due to the complex nature of normal mitral valve functioning.
A good way of remembering the causes of mitral regurgitation is to consider the different factors that contribute to the successful function of the valve:
Left ventricle (papillary muscles in particular)
Some classification systems may differentiate it purely into primary (related to the valve) or secondary (related to extra-valvular causes).
Another very important classification of MR is whether it is acute or chronic. Patients with chronic disease may be able to undergo some compensatory changes, whereas acute valve failure can result in significant CVS dysfunction.
The disturbance of these factors can lead to impaired valve function.
Rheumatic heart disease
Post MI papillary muscle rupture
LV dilatation (e.g. myocarditis)
Hypertrophic cardiomyopathy (functional)
Myxomatous degeneration of the valve leaflets or chordae tendineae is the most common cause of mitral valve prolapse (though it may not cause MR). This is often idiopathic, but can be associated with a number of connective tissue diseases: Marfan syndrome, Ehlers-Danlos syndrome, SLE.
The pathophysiological consequences of MR can be considered based on the physiological consequences, and need differentiating between acute and chronic.
Acute MR can be a significant event e.g. following acute papillary muscle rupture post-MI. Valve failure results in the left ventricle pumping blood into the left atrium. There is loss of ‘forward’ stroke volume and cardiac output. There is also simultaneous overload of the pulmonary circulation, which can lead to acute pulmonary oedema, and right sided heart failure. The consequences can thus be biventricular failure, respiratory failure, cardiogenic shock, or just sudden death.
More chronic MR results in dilatation of the LA due to the increased backward flow of blood into it. This dilatation can be quite notable and often results in the development of AF, but often serves to reduce the pressure. In the chronic disease, there is therefore usually enough compensation to prevent significant back-pressure on the pulmonary circulation, and thus pulmonary oedema is rare unless the MR is severe. The consequence of this regurgitation is that a degree of the cardiac output is ‘recirculated’ - being sent back into the LA before reentering the LV during the next cardiac cycle. The consequence of this is that the LV becomes increasingly volume loaded The (mal)adaptation of the LV in response is to dilate. To some degree this preserves forward stroke volume (as per the Frank-Starling hypothesis) and is compensatory. However, increased dilatation can proceed to worsen the MR, and there can be progression to LV systolic failure, as the LV decompensates. In most cases this is a late feature of MR, and the ejection fraction of the LV can actually be increased.
The main differentiation will be between acute and chronic MR.
As noted above, acute MR will frequently be poorly tolerated. The clinical presentation could be one of the following clinical syndromes:
Severe pulmonary oedema
There may be accompanying features of a causative pathology e.g. chest pain of acute MI, signs of infective endocarditis.
Chronic MR may present very insidiously. The presentation will often be of a cardiac failure syndrome, as compensatory mechanisms begin to fail. Investigation of atrial fibrillation may also lead to its discovery.
Clinical signs may include the pansystolic murmur of MR. This classically is best heart in the ‘mitral area’ of the precordium and radiates to the left axilla.
Echocardiography The essential investigation in the diagnosis. Although the grading of severity is challenging (see below) a lot of useful information can be gained from transthoracic echo. Assessment of LV function is challenging with echo, as the regurgitation makes the LV look better than it actually is. An LV ejection fraction of 70% should be considered as normal in patients with MR.
ECG An ECG should be performed to look for AF (a common consequence) and for features of IHD (a common aetiology).
Bloods Routine blood tests may be indicated in the assessment of the presenting pathology. A plasma BNP can be useful in diagnosing heart failure pathology. A low BNP is also an encouraging prognostic sign in patients with MR.
Chest X-Ray This may be undertaken in the assessment of the initial presentation. In acute MR there may be features of pulmonary oedema. In chronic disease, left atrial and ventricular enlargement may be visible.
Grading the severity of MR is challenging. Images from transoesophageal echocardiography remain the gold-standard, though images from transthoracic echo may be used if they are of sufficient quality. Several different measurement are used to help with the grading: Regurgitant fraction:
Mild - <30%
Moderate - 30-49%
Severe - >50%
Regurgitant orifice area (cm^2):
Mild - <0.2
Moderate - 0.20-0.39
Severe - >0.4
Regurgitant volume (ml/beat):
Mild - <30
Moderate - 30-50
Severe - >60
Management can be considered in terms of medical and surgical management. The concerns that may guide management are:
Risk of progressive LV dysfunction - a feature of the maladaptive processes with MR
Risk of sudden death - an uncommon but recognised feature of MR (quoted at 1.8%/year)
These risks mean that correction of MR is often seen as important, even in asymptomatic disease. In cases where there are no identifiable adverse effects, close follow up may be an options, but regular assessment is needed.
Medical Management In acute MR, patients are often acutely sick, and any medical management is to act as a bridge to definitive surgical correction of the defect (if possible) The can be considered as similar physiological goals as mentioned in the anaesthetic management. This is to reduce afterload as able to maximise forward flow. Vasodilators e.g. Nitrates can be used for this, and can also help reduce the excess volume loading with some venodilation. However, use may be limited by hypotension. Other options include CVS support with an intra-aortic balloon pump. Pharmacological inotropic support may also be combined with afterload reduction to bridge patients to more definitive therapy
In terms of chronic MR, medical management in the context of normal LV function has not been shown to have any impact on outcome. When the condition has progressed to causing LV dysfunction, then this is generally an indication for surgical management. Medical management will be based on the symptoms that the patient has. Patients who have features of heart failure, are generally managed with the usual medication regime for cardiac failure: ACE inhibitors, beta blockers, and diuretics (including aldosterone antagonists)
Surgical Management The surgical management decisions relating to MR are complex, and guided by the appropriate surgical specialist. In general, they relate to the acuity, consequences and aetiology of the disease.
Primary MR If the aetiology is of a primary cause (i.e. relating to the valve structures) then a surgical approach is clearly more viable. If the patient is asymptomatic and without LV dysfunction, the approach will generally be to not intervene, and continue to follow up. Acute valve lesions are very likely to need repair due to the severe physiological derangement that they precipitate. If the patient is developing complications of the MR, then this is also usually an indication for a repair. These may be: LV dysfunction, AF, signs and symptoms of heart failure, pulmonary hypertension.
Secondary MR When the nature of the dysfunction is secondary to a non-valve problem, the surgical approach is less clear. If there is concomitant CABG surgery being undertaken, then repair of severe MR is generally undertaken. It will sometimes be considered in patients with moderate LV dysfunction, in whom medical treatment has failed. There is often a concern that problems will arise if the underlying cause e.g. ischaemic cardiomyopathy, is not also treated.
Surgical approach Surgical repair of primary MR is generally preferred. It has better intra-operative mortality, reduced impact on LV dysfunction postoperatively, and without the longer term consequences of replacement valves. With secondary MR, repair usually has better short term outcomes, but an increased risk failure in the longer term when compared with valve replacement.
Mitral valve surgery is generally a similar approach to other types of open-heart surgery, with median sternotomy and cardiopulmonary bypass.
Minimally invasive surgery is also an option for these patients. This involves a thoracoscopic approach. CPB is implemented through a peripheral approach, with femoral and jugular lines.
Percutaneous MVR is also a possibility in high risk patients. The Mitraclip involves percutaneously clipping the two valve leaflets together, effectively creating two holes as the MV. Although there is an increased rate of failure compared to normal surgical approaches, it may be a consideration for high risk patients.
Anaesthetists may encounter patients with MR undergoing noncardiac surgery, as well as in preparation for MVR.
Preoperative Preoperative assessment for patients should assess the impact of the MR on the patient, particularly assessing for features of severe disease. In particular, signs and symptoms of pulmonary hypertension, right heart failure, or left ventricular failure, can indicate severe disease.
The investigations discussed above (in assessment) can all provide useful information prior to surgery. Echocardiographic information can be particularly useful, with a focus on both the severity of the MR and the LV function.
Functional status is a particularly important part of the assessment. This may be history led, or more objective functional testing can be performed if time allows e.g. CPET. This can be more useful than echo findings in assessing anesthesia risk. If the patient is asymptomatic and the LV function is not severely impaired (i.e. not <30%) then non-cardiac surgery can generally be performed without increased risk.
Intraoperative The management of MR in patients undergoing anaesthesia can be summarised as aiming to minimise the cardiovascular disturbance of the condition (i.e. maximise cardiac function). Fortunately, many of the effects of anaesthesia actually have some positive physiological effects. A useful mnemonic is - Full, Fast and Forward
Preload The remodelled heart (LV) is often quite preload dependent, as this is the physiological compensatory state that has developed. As such, it is often beneficial to keep patients fairly ‘full’ and optimise their preload. However, it is also important to remember that excessive dilatation can worsen functional MR, so should be avoided.
Rate The heart rate is theoretical better at a faster rate (around 80 - 100 bpm) for patients with MR. Bradycardia can prolong the systolic period and thus allow a greater time for regurgitation to occur. It also prolongs the filling time of the heart during a longer diastole, risking excessive LV distension and worsening functional MR. Sinus rhythm is preferable as it will help ventricular loading, but is less essential than in patients with MS. This has to be balanced against the increased myocardial oxygen demand in patients with IHD.
Afterload Reducing the SVR is important to maximise the ‘forward’ ejection fraction. Excess increases in afterload (e.g. primary alpha 1 receptor agonists) can worsen MR, as the ‘path of least resistance’ for the blood flow will be back through the leaky mitral valve. If vasopressors are needed in anaesthesia, a non pure vasoconstrictor such as ephedrine may be preferable. The use of an intra-aortic balloon pump can be very useful in patients failing with severe MR due to its cardiovascular effects, including an reducing afterload. Both general and neuraxial anaesthesia may have beneficial effects in this regard, as both are associated with a reduction in afterload.
Contractility In patients with a failing LV, some degree of inotropic support may also be needed. Dobutamine and inodilators (milrinone, levosimendan) are options.
Postoperative The principles are similar as to the intraoperative ones. Of note, is that patients following MVR may have an increase in their ‘afterload’, as the low resistance pathway through the MV is now gone. This increased strain on the LV may unmask underlying LV dysfunction, and so patients could be worse postoperatively. In these cases, inotropic/inodilator support, or an IABP are required.