Complications
Patients at increased risk can be identified by clinical and echocardiographic features and require vigilant follow-up.[25] Increased risk of developing severe mitral regurgitation (MR) is associated with male sex, age greater than 45 years, elevated BMI, hypertension (HTN), left ventricular (LV) enlargement, LV dysfunction, and thickened mitral valve leaflets.[5][6][40][41][42] Only a small number of patients develop severe primary mitral regurgitation. Most patients are asymptomatic, and no specific therapy is required. Atrial fibrillation or indicators of haemodynamic compromise, such as LV dysfunction or pulmonary HTN, are more typically associated with severe primary MR in MVP patients.
Patients with severe primary MR may warrant early consideration for surgical intervention, even when asymptomatic.
The correlation between palpitations and MVP is complex and incompletely understood. MVP is found to be associated with malignant ventricular arrhythmias and sudden cardiac arrest in up to 4% of individuals. Myocardial fibrosis and presence of MAD are found to be additional risk markers for ventricular arrhythmia.[30] Evaluation of palpitations or syncope should mirror the workup in patients without MVP, including evaluation with Holter or ambulatory event monitoring to rule out significant arrhythmias.
Studies have reported increased prevalence of several ECG abnormalities in MVP patients, including ST-T changes, QT prolongation, and presence of accessory pathways. This, however, is controversial, as other studies found no difference in the prevalence of these ECG changes compared with the general population.
MVP is considered the most common cardiovascular condition predisposing to infective endocarditis, even though the absolute incidence of this complication in the MVP population is extremely low (estimated at 0.02% per year).[42]
Factors associated with increased risk include male sex, age over 45 years, presence of mitral regurgitation, and leaflet thickening greater than 5 mm.[5][36][37][52]
Morbidity and mortality are significant with a 5-year incidence of death or mitral valve surgery estimated to be 60%.[53]
Routine antibiotic prophylaxis before procedures is not required, as the risk of endocarditis is low and there are few data to show that antibiotic prophylaxis reduces the risk of subsequent endocarditis.[33] Situations where prophylaxis may be indicated include those where endocarditis may pose a greater than normal risk such as prior history of endocarditis.
Treatment of infective endocarditis generally involves a prolonged course of tailored antimicrobial therapy and in certain cases surgical intervention. According to ESC guidelines, a nuanced interpretation of echocardiographic findings, such as the vigilant detection of vegetations, abscesses, or new partial dehiscence of prosthetic valves, which are pivotal in diagnosing infective endocarditis in MVP patients.[33] The ESC guidelines advocate for the inclusion of advanced imaging techniques, such as positron emission tomography-computed tomography and cardiac magnetic resonance imaging, to identify infective endocarditis indicators, especially in complex MVP cases where traditional echocardiography may not suffice.[33]
This is a rare complication of MVP, occurring in less than 2% of patients during long-term follow-up with an estimated yearly rate of 0.004%.[6][54] The aetiology is uncertain but is thought to be related to ventricular arrhythmia.
Factors associated with increased risk include the familial form of MVP, severe MR, mitral annular disjunction (MAD), and impaired LV systolic function.[6][28][54]
While a considerable number of ventricular arrhythmias can be attributed to LV systolic dysfunction resulting from severe MR, life-threatening arrhythmias, and sudden cardiac death have also been reported in patients with MVP who present with no or only mild MR.[28]
Asymptomatic patients with evidence of severe mitral regurgitation should be vigorously followed up.
Holter or event monitor should be done for symptoms of palpitations. Indications for electrophysiological testing are similar to those of the general population, including aborted sudden cardiac death, recurrent syncope of unknown cause, or symptomatic or sustained ventricular tachycardia.
There is disagreement as to whether MVP can cause strokes. The proposed mechanism is embolism formation due to release of platelet-fibrin thrombi from the leaflet surface. Patients with MVP who have strokes tend to have risk factors such as older age (>50 years), severe mitral regurgitation, atrial fibrillation, and thickened valve leaflets.[6][44] Data suggest a yearly event rate of 0.7%.[45]
MVP should rarely be considered the sole source of stroke. Anticoagulation is used in appropriate patients.
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