Mitral regurgitation natural history
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2]; Varun Kumar, M.B.B.S.; Lakshmi Gopalakrishnan, M.B.B.S.; Mohammed A. Sbeih, M.D. [3]
Overview
Mitral regurgitation results in chronic volume overload of the left ventricle, leading initially to compensatory eccentric hypertrophy and ventricular dilation that maintain forward stroke volume[1] The natural history of mitral regurgitation (MR) may follow one of two patterns, acute or chronic. Chronic MR can be either compensated or decompensated. The natural history and prognosis of MR depend on the underlying etiology and the degree of severity of the valvular abnormality. Mild MR is associated with few if any complications. However, when severe, MR may lead to development of pulmonary edema, pulmonary hypertension, and right heart failure.
Natural History
The natural history of MR may follow one of two patterns, acute or chronic. In acute MR, the volume and pressure overload in the left atrium is transmitted backward into the pulmonary vasculature leading to sudden onset of dyspnea, PND, orthopnea and rales.Chronic mitral regurgitation produces increased left ventricular preload and reduced afterload, resulting in a compliant dilated ventricle with increased end-diastolic volume and stroke volume[1]. Chronic MR can be either compensated or decompensated.During the chronic compensated phase of mitral regurgitation, adaptive enlargement of the left ventricle and left atrium helps maintain forward cardiac output and reduces pulmonary congestion. Patients are often asymptomatic with normal exercise tolerance, and this phase may persist for many years. Left ventricular dilation with eccentric hypertrophy preserves systolic function, and the left ventricular ejection fraction typically remains >60%[1]. Over time, however, progressive ventricular dysfunction may develop, marking transition to the chronic decompensated phase of mitral regurgitation. Once the patient transitions into the decompensated phase, there may not be recovery of left ventricular funtion following operative repair or replacement of the mitral valve. The decompensated stage is defined on the basis of a decompensated ventricular function. At this stage, the patients are at risk for a poor results of valve replacement. Recognition of mitral regurgitation prior to the onset of myocardial dysfunction is critical because irreversible myocardial injury may occur before the development of symptoms[1].
Complications
Chronic volume overload in mitral regurgitation leads to structural remodeling of the left ventricle and left atrium, predisposing patients to complications such as atrial fibrillation, pulmonary hypertension, and right-sided heart dysfunction[1]. Persistent left atrial volume overload results in left atrial enlargement and atrial fibrosis, which increases the risk of atrial fibrillation[2]. In addition, elevated left atrial pressures may lead to pulmonary hypertension, which can progressively contribute to right ventricular dysfunction[3].
Prognosis
Patients with asymptomatic chronic severe MR have a high likelihood of developing symptoms or left ventricular dysfunction over the course of 6 to 10 years.[4][5][6] The incidence of sudden death in asymptomatic patients with normal left ventricular function varies widely among studies.
The prognosis is poor in patients with severe symptomatic MR with an estimated eight year survival rate of only 33% in the absence of surgical intervention. Heart failure and sudden death due to ventricular arrhythmia are common causes of death.[7]
Among subjects with severe MR due to a flail posterior mitral leaflet, 90% of patients are either dead or require mitral valve surgery by 10 years with a mortality rate of 6% to 7% per year. However, the risk of death is higher in those patients with a left ventricular ejection fraction <60% or with NYHA functional class III–IV symptoms.[4][8]
Severe symptoms are associated with a poor outcome after mitral valve repair or replacement. Postoperative survival rates in patients with NYHA functional class III–IV symptoms at 5 and 10 years are 73 ± 3% and 48 ± 4% respectively, compared to 5 and 10 years survival rates of 90 ± 2% and 76 ± 5% respectively among patients with NYHA functional class I/II symptoms before surgery.[8]
In a long-term retrospective study, 198 patients with an effective orifice area >40 mm² had a risk of cardiac death of 4% per year during a mean follow-up period of 2.7 years.[5]
Acute MR with cardiogenic shock is associated with an operative mortality of 80%.
References
- ↑ 1.0 1.1 1.2 1.3 1.4 Gaasch WH, Meyer TE. Left ventricular response to mitral regurgitation: implications for management. Circulation. 2008 Nov 25;118(22):2298-303. doi: 10.1161/CIRCULATIONAHA.107.755942. PMID: 19029478.
- ↑ Eguchi K, Ohtaki E, Matsumura T, Tanaka K, Tohbaru T, Iguchi N, Misu K, Asano R, Nagayama M, Sumiyoshi T, Kasegawa H, Hosoda S. Pre-operative atrial fibrillation as the key determinant of outcome of mitral valve repair for degenerative mitral regurgitation. Eur Heart J. 2005 Sep;26(18):1866-72. doi: 10.1093/eurheartj/ehi272. Epub 2005 Apr 21. PMID: 15845559.
- ↑ Barbieri A, Bursi F, Grigioni F, Tribouilloy C, Avierinos JF, Michelena HI, Rusinaru D, Szymansky C, Russo A, Suri R, Bacchi Reggiani ML, Branzi A, Modena MG, Enriquez-Sarano M; Mitral Regurgitation International DAtabase (MIDA) Investigators. Prognostic and therapeutic implications of pulmonary hypertension complicating degenerative mitral regurgitation due to flail leaflet: a multicenter long-term international study. Eur Heart J. 2011 Mar;32(6):751-9. doi: 10.1093/eurheartj/ehq294. Epub 2010 Sep 8. PMID: 20829213.
- ↑ 4.0 4.1 Ling LH, Enriquez-Sarano M, Seward JB, Tajik AJ, Schaff HV, Bailey KR, Frye RL (1996). "Clinical outcome of mitral regurgitation due to flail leaflet". The New England Journal of Medicine. 335 (19): 1417–23. doi:10.1056/NEJM199611073351902. PMID 8875918. Retrieved 2011-03-06. Unknown parameter
|month=ignored (help) - ↑ 5.0 5.1 Enriquez-Sarano M, Avierinos JF, Messika-Zeitoun D, Detaint D, Capps M, Nkomo V, Scott C, Schaff HV, Tajik AJ (2005). "Quantitative determinants of the outcome of asymptomatic mitral regurgitation". The New England Journal of Medicine. 352 (9): 875–83. doi:10.1056/NEJMoa041451. PMID 15745978. Retrieved 2011-03-06. Unknown parameter
|month=ignored (help) - ↑ Rosenhek R, Rader F, Klaar U, Gabriel H, Krejc M, Kalbeck D, Schemper M, Maurer G, Baumgartner H (2006). "Outcome of watchful waiting in asymptomatic severe mitral regurgitation". Circulation. 113 (18): 2238–44. doi:10.1161/CIRCULATIONAHA.105.599175. PMID 16651470. Retrieved 2011-03-06. Unknown parameter
|month=ignored (help) - ↑ Delahaye JP, Gare JP, Viguier E, Delahaye F, De Gevigney G, Milon H (1991). "Natural history of severe mitral regurgitation". European Heart Journal. 12 Suppl B: 5–9. PMID 1936025. Retrieved 2011-03-06. Unknown parameter
|month=ignored (help) - ↑ 8.0 8.1 Tribouilloy CM, Enriquez-Sarano M, Schaff HV, Orszulak TA, Bailey KR, Tajik AJ, Frye RL (1999). "Impact of preoperative symptoms on survival after surgical correction of organic mitral regurgitation: rationale for optimizing surgical indications". Circulation. 99 (3): 400–5. PMID 9918527. Retrieved 2011-03-06. Unknown parameter
|month=ignored (help)