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Dr. M Oppizzi
Dr. Matteo Pisani
Dr. Eustachio Agricola
Although the etiology and mechanism of mitral regurgitation (MR) are key pieces of information for the management of patients with MR, the left ventricular (LV) function/dysfunction remains the most powerful predictor of long term prognosis of patients with severe MR under conservative management and the main factor determining the timing of surgery.
Analysing the natural history of MR caused by flail leaflets, Ling et al. observed an excess mortality (6.3% yearly) in comparison to the expected survival.
Patients with NYHA functional class III or IV displayed a considerable mortality (34% yearly) if not operated upon, but even those in class I or II had a notable mortality (4.1% yearly). Furthermore, they found that the sudden deaths represented a quarter of the deaths occurring under medical treatment with a rate of sudden death of 1.8% per year overall. The main determinants of risk of sudden death are mostly severe symptoms and reduced ejection fraction (EF), but most sudden deaths occurred in patients with no or minimal symptoms and normal LV function (0.8% per year).
In all patients in whom cardiac rhythm was monitored during an episode of sudden death, the underlying mechanism was ventricular tachyarrhythmia. Thus, the complex ventricular arrhythmias may be considered a surrogate of “latent myocardial dysfunction”. Among the echocardiographic parameters proposed to assess LV function in asymptomatic patients with MR, resting EF and the end systolic diameter are the best predictors of long term mortality under conservative management and postoperative residual LV dysfunction. Either an EF < 60% or an end systolic diameter > 45 mm are considered the cut off values demonstrating overt LV dysfunction and should be immediately considered as an indication for surgery.
Unfortunately, EF measurements suffer from interobserver error and are dependent on loading condition. Indeed, during the compensated phase of chronic MR when LV dysfunction develops EF may fall but remains within normal limits due to a reduced afterload. Moreover, an LV systolic diameter >45 mm is rarely seen in asymptomatic MR patients. Therefore, it is often impossible to predict the long-term course even in asymptomatic patients with apparently normal LV function.
Thus, a question still remains: How can the development of LV dysfunction be predicted by a load independent parameter?
Tissue Doppler imaging (TDI) uses the same principles as colour flow Doppler, but by applying standard processing, motion of tissue is displayed in preference to blood flow. Thus, tissue velocity data can be obtained with high temporal and spatial resolution both with pulsed wave tissue Doppler or colour Doppler imaging.
From the apical window it is possible to measure the longitudinal shortening velocities of the single myocardial regions or the mitral annulus that can represent a simple estimate of overall systolic function. Therefore, tissue velocity imaging from the apex has the potential to provide equivalent and perhaps more extensive clinical information more readily and more reproducibly than standard echocardiographic measurements. The measurement of long axis function by TDI is a promising new tool to assess LV function in patients with MR.
TDI systolic indices, such as the systolic velocity and the precontraction/contraction time ratio obtained at of the lateral mitral annulus level, are able to predict postoperative LV function in patients with apparently normal preoperative LV function (EF > 60%, end systolic diameter <45 mm) with a sensitivity of 78% and a specificity of 95%.
Moreover, the measurement of longitudinal function is a marker of contractile reserve as compared with exercise echocardiography. TDI systolic parameters seem to be more sensitive than EF for two reasons: firstly, because TDI indices are relatively preload independent and, secondly, because of the architecture and activation of myocardial fibres.
TDI recordings were made from the ventricular apex assessing the longitudinal function. Indeed, the effects of MR are more relevant on longitudinal motion of subendocardial fibres than short axis function, which is similar to circumferential fibres shortening as measured with conventional parameters. Another advantage compared to the conventional indexes is the high reproducibility of TDI measurements. In this view, TDI assessment may be useful to obtain evidence of subclinical myocardial dysfunction and thereby to significantly improve the timing of surgery.
The assessment of LV function remains a cornerstone for management patients with MR. Patients with EF <60% display an excess mortality as compared to those with EF >60%, but no group at very low risk under medical treatment could be defined. Therefore, in patients with EF <60%, no other information regarding LV function over conventional echocardiographic indexes are necessary and such patients require surgery irrespective of repair or replacement therapy.
In the asymptomatic or minimally symptomatic patients with EF >60%, additive echocardiographic parameters such as TDI systolic indices could be useful to unmask eventual latent myocardial dysfunction. If TDI systolic indices are reduced and if there is a high likelihood of valve repair, these are incentives to perform surgery because of its low risk (perioperative mortality around 1%) and good survival, and not incentives to delay surgery and encounter the risk of more left ventricular dysfunction.
In asymptomatic patients without evidence of latent myocardial dysfunction there is not an indisputable indication for surgery, particularly when the reparability of the valve lesion is not consistent. Thus, in this group of patients - today very limited, a close echocardiographic follow-up is advisable. The drug treatment does not alter the MR prognosis.
Moreover, there is no randomised trial comparing the outcome after early surgery to outcome with medical management. Drugs (ACE-inhibitors, diuretics) can be useful to mitigate symptoms if surgery is contraindicated by intercurrent disease. There is no basis for prophylactic treatment to preserve myocardial function in asymptomatic patients.
The content of this article reflects the personal opinion of the author/s and is not necessarily the official position of the European Society of Cardiology.
1. Ling LH, Enriquez-Sarano M, Seward JB, et al. Clinical outcome of mitral regurgitation due to flail leaflet. N Engl J Med 1996; 335: 1417-1423. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=8875918 2. Grigioni F, Enriquez-Sarano M, Ling LH, et al. Sudden death in mitral regurgitation due to flail leaflet. J Am Coll Cardiol 1999; 34: 2078-2085. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=10588227 3. Stewart WJ. Myocardial factor for timing of surgery in asymptomatic patients with mitral regurgitation. Am Heart J 2003; 146: 5-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12851602 4. Agricola E, Galderisi M, Oppizzi M, et al. Pulsed tissue Doppler imaging detects early myocardial dysfunction in asymptomatic patients with severe mitral regurgitation. Heart 2004; 90: 406-410. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15020516 5. Haluska BA, Short L, Marwick TH. Relationship of ventricular longitudinal function to contractile reserve in patients with mitral regurgitation. Am Heart J 2003; 146: 183-188. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12851629
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