The patient is a 62-year-old with a history of mitral valve prolapse and regurgitation (MR). The patient has no symptoms of chest pain or shortness of breath. The patient had been very active until 8 months ago, jogging on a treadmill daily for 30 minutes at 5.0 mph, but after sustaining a knee injury has not been able to exercise. The most physical activity the patient can presently do is walking up one flight of stairs.
PMHx: mitral valve prolapse, hypercholesterolemia, hypertension, normal renal function
Medications: simvastatin 20 mg, lisinopril 20 mg
PE: BP- 120/76 mmHg, pulse- 70 regular, RR-12
Heart: RRR with 3/6 holosystolic blowing murmur hear best at the apex with radiation to axilla. No RV heave. JVP- normal
Lungs: Clear
Extremities: no edema
ECG: normal sinus rhythm
Laboratory data (6 months ago): BNP 80 pg/ml
Echocardiogram (6 months ago): Bilateral mitral valve prolapse with severe MR, effective regurgitant orifice area (EROA = 0.42 cm2), ejection fraction 65 %, left ventricular end systolic dimension (LVESD) 32 mm, systolic pulmonary artery pressure (SPAP) 25 mmHg,
Laboratory data (presently): BNP 170 pg/ml
Echocardiogram (presently): EROA = 0.44 cm2, ejection fraction 65%, LVESD 36 mmHg, SPAP 40 mmHg
Tranesophageal Echocardiogram confirms severe MR and demonstrates prolapse of both leaflets with central MR
An experienced cardiothoracic surgeon in mitral valve repair has reviewed that case and describes the case as moderately complex with a estimated 60-70% chance for repair.
The correct answer is: 1. Perform left and right heart catheterization and perform MV surgery
The indications for surgery for asymptomatic severe MR are controversial. The ACC/AHA recommendations for MV surgery for severe asymptomatic MR include ejection fraction < 60% (Class I), LVESD > 40 mm (Class I), SPAP > 50 mmHg (Class IIa), or the development of new atrial fibrillation (Class IIa).(1) This differs slightly from the European Society of Cardiology recommendations that surgery is indicated when the LVESD > 45 mm.(2) There are no randomized data to support any of these recommendations, but are based on historical control studies that demonstrate that these factors are independently associated with worse outcomes in patients with asymptomatic severe MR. For example, LVESD > 40 mm is associated with post-operative LV dysfunction and higher mortality.(3,4)
The determination of the optimal time for MV surgery for severe MR can at times be a clinical challenge. To ascertain if a patient is truly symptomatic can be difficult, especially in the presence of co-morbidities such as pulmonary disease. The measurement of the severity of mitral regurgitation can be technically challenging. The intra-observer variability for the echocardiographic estimation of the degree of MR and LV function can be significant even with experienced cardiologists.(5)
Several studies have investigated the relationship between natriuretic peptides (NPs) and MR.(6-11) Detaint(9) studied 124 patients with varying degrees of MR. In a multivariate analysis B-type natriuretic peptide (BNP) was associated with LVESD, SPAP and the development of symptoms or atrial fibrillation. Also, along with ejection fraction and ERO, BNP was independently associated with mortality. Klaar(7) investigated 87 patients with asymptomatic severe MR. The primary endpoint was the development of symptoms or LV dysfunction. The only independent predictors of the primary endpoint were BNP (hazard ratio= 4.68) and SPAP (hazard ratio=1.05). Pizarro(8) studied 269 patients with severe asymptomatic MR and followed them for approximately 3 years. The primary combined endpoint was symptoms, LV dysfunction, or death. Independent predictors of the primary endpoint were BNP > 105 pg/ml, LVESD, and EROA. BNP elevation was the most predictive of adverse events (OR= 4.6). Additional studies are needed to determine the appropriate absolute cut-points, or changes over time that would impact medical decisions in severe asymptomatic MR.
Our patient did not meet current ACC/AHA guidelines for mitral valve surgery. The rationale for proceeding with repair was the increase in SPAP over 6 months, which was magnified by the increase in BNP over the same time. In this case, the patient underwent a successful MV repair, and had only trivial regurgitation on follow-up 1 year later.
References
- Bonow, R.O., et al., 2008 focused update incorporated into the ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to revise the 1998 guidelines for the management of patients with valvular heart disease). Endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. J Am Coll Cardiol 2008; 52:e1-142.
- Vahanian, A., et al., Guidelines on the management of valvular heart disease: The Task Force on the Management of Valvular Heart Disease of the European Society of Cardiology. Eur Heart J 2007; 28:230-68.
- Borow, K.M., et al., End-systolic volume as a predictor of postoperative left ventricular performance in volume overload from valvular regurgitation. Am J Med 1980; 68:655-63.
- Wisenbaugh, T., Skudicky, D., and Sareli, P., Prediction of outcome after valve replacement for rheumatic mitral regurgitation in the era of chordal preservation. Circulation
- Thomas, N., et al., Intraobserver variability in grading severity of repeated identical cases of mitral regurgitation. Am Heart J 2008; 156:1089-94.
- Potocki, M., et al., Relation of N-terminal pro-B-type natriuretic peptide to symptoms, severity, and left ventricular remodeling in patients with organic mitral regurgitation. Am J Cardiol 2009; 104:559-64.
- Klaar, U., et al., Prognostic value of serial B-type natriuretic peptide measurement in asymptomatic organic mitral regurgitation. Eur J Heart Fail 2011; 13:163-9.
- Pizarro, R., et al., Prospective validation of the prognostic usefulness of brain natriuretic peptide in asymptomatic patients with chronic severe mitral regurgitation. J Am Coll Cardiol 2009; 54:1099-106.
- Detaint, D., et al., B-type natriuretic peptide in organic mitral regurgitation: determinants and impact on outcome. Circulation 2005; 111:2391-7.
- Watanabe, M., et al., Is measurement of plasma brain natriuretic peptide levels a useful test to detect for surgical timing of valve disease? Int J Cardiol 2004; 96:21-4.
- Sutton, T.M., et al., Plasma natriuretic peptide levels increase with symptoms and severity of mitral regurgitation. J Am Coll Cardiol 2003; 41:2280-7.