INTRODUCTION — Mitral valve prolapse (MVP) is a common disease of the mitral valve. The clinical and anatomic characteristics of patients with MVP are heterogeneous. Although most patients with MVP have mild, trivial, or no mitral regurgitation (MR) [1], MVP is the most common cause of primary moderate or severe MR that requires intervention [2] in resource-abundant countries [3]. In resource-limited countries, rheumatic mitral valve disease is more common. (See "Clinical manifestations and diagnosis of rheumatic heart disease", section on 'Mitral regurgitation'.)
The definition, classification, pathophysiology, and diagnosis of MVP will be reviewed here.
Other aspects of MVP are discussed separately:
●(See "Nonarrhythmic complications of mitral valve prolapse" and "Arrhythmic complications of mitral valve prolapse".)
●(See "Management of chronic primary mitral regurgitation".)
●(See "Acute mitral regurgitation in adults".)
DEFINITION — MVP is a cause of primary mitral regurgitation (MR; caused by disease of one or more valve components, including leaflets, chordae tendineae, papillary muscles, or annulus) rather than secondary/functional MR (caused by disease of the left ventricle [LV]) [4,5]. (See "Clinical manifestations and diagnosis of chronic mitral regurgitation", section on 'Identifying the cause of MR'.)
MVP is diagnosed clinically based on echocardiography showing diffuse redundancy and thickening of the mitral valve leaflets with systolic motion of one or both leaflets beyond the plane of the mitral annulus into the left atrium, with or without associated MR. Echocardiographic criteria for MVP are described below. (See 'Imaging definition of MVP' below.)
EPIDEMIOLOGY — Using the currently accepted definition of MVP, its prevalence in the general population is estimated to be 0.6 to 3 percent. The Framingham Heart Study reported an overall prevalence of 2.4 percent [6]. Individuals with classic MVP (leaflet thickness ≥5 mm; 1.3 percent) and nonclassic MVP (leaflet thickness <5 mm; 1.1 percent) had similar age and sex distributions. In another population-based study (Cardia), the prevalence of MVP in 4136 young adults was only 0.6 percent [7]. In a Canadian study of 972 patients, MVP prevalence was similar in three ethnic groups (2.7 percent in South Asian, 3.1 percent in European, and 2.2 percent in Chinese) [8]. MVP patients were leaner and had a greater degree of mitral regurgitation (MR) than the general population [6,7]. Because MVP is a progressive lesion, anatomically [9] and physiologically in terms of MR severity [10], these prevalence differences are generally interpreted as age-related, with higher prevalence in older cohorts.
MVP may be slightly more common in females than in males. In the Framingham study, there was a nonsignificant trend toward a female preponderance among those with MVP (59.5 versus 52.7 percent in those without MVP) [6]; in the larger Olmsted county study, 64 percent of individuals with MVP were females [11].
Reports published early in the development of echocardiography suggested high MVP prevalence, 4 to 10 percent, and even close to 20 percent in selected populations [12-14]. These early reports are now considered inaccurate because echocardiographic criteria for diagnosis were not yet fully developed and lacked specificity.
CLASSIFICATION — MVP is classified as either primary (caused by abnormal mitral leaflet tissue in the absence of an identifiable connective tissue disease; may be sporadic or familial) or secondary (associated with an identifiable disorder such as Marfan syndrome or congenital heart disease) (table 1).
Primary MVP — Primary MVP can be sporadic or familial. It may present as an isolated lesion or accompanied by cardiac and/or extracardiac findings.
Sporadic or familial — While most cases of primary MVP are sporadic, familial cases of classic (diffuse myxomatous) MVP also occur [15-19]. Multiple genetic loci for MVP have been identified [20,21]. A large genome-wide association study identified 16 loci associated with MVP; candidate genes for MVP included genes linked to transforming-growth-factor beta (TGF-β), cardiomyopathy, or cytoskeletal physiology [21]. This genetic heterogeneity matches the morphologic and clinical heterogeneity of MVP.
The most common reported transmission pattern for MVP is autosomal dominant with incomplete penetrance [20]. The prevalence in first-degree relatives is relatively high, ranging from 30 to 50 percent [22,23].
A less common X-linked recessive form seems to be related to filamin A mutations, and results in a rare form of multivalvular myxomatous degeneration (X-linked myxomatous valvular dystrophy) [24,25]. In affected males, this disease is characterized by myxomatous degeneration of the mitral valve frequently associated with aortic valve degeneration. Female carriers can also exhibit valvular degeneration, but this is usually less severe.
Associated findings
●Associated valve findings – Some patients with primary MVP have other valvular abnormalities (tricuspid valve in up to 40 to 50 percent of patients and aortic valve in 10 to 20 percent) [26-28].
●Nonsyndromic or syndromic – Primary MVP is classified as nonsyndromic when extracardiac manifestations are absent and syndromic when extracardiac manifestations are present. Additional extracardiac manifestations include von Willebrand syndrome [16] (eg, thoracic skeletal abnormalities such as pectus excavatum [15,29]) and hypomastia [30]. The latter two associations suggest that MVP may be related to a linked mesenchymal dysplasia, although hypomastia may also be a simple reflection of patients’ lean body habitus.
Morphology of primary MVP — While primary MVP presents with a great diversity of lesions, the macro-alterations are often categorized as "classic" or "nonclassic." It is important to distinguish between these forms, as the complexity of surgical repair increases with the extent of mitral valve involvement by myxomatous degeneration.
●Classic – At one end of the spectrum is "classic" (also known as Barlow disease or diffuse myxomatous) MVP, characterized by markedly thickened (≥5 mm) and diffusely redundant myxomatous leaflet tissue with prolapse of most of the segments of both leaflets, severe mitral annular enlargement, and elongated (rarely ruptured) chords (figure 1 and movie 1A-B) [31].
A subset of patients with classic MVP have mitral annular disjunction, an abnormality of the mitral annulus fibrosus resulting in a systolic gap between the insertion of the posterior mitral leaflet and the basal inferolateral myocardium (movie 2). This disjunction commonly occurs in patients with advanced classic disease [32] and is associated with progressive development of ventricular arrhythmias and LV dilation [33]. (See "Arrhythmic complications of mitral valve prolapse".)
●Nonclassic – At the other end of the spectrum is "nonclassic" disease, known as fibroelastic deficiency, first described by Carpentier [34], which can be seen in up to 40 percent of patients requiring mitral valve repair. It usually affects individuals over the age of 60 and is characterized by involvement of a single segment (most commonly P2 scallop), with thin (<5 mm thickness) and somewhat redundant leaflets, ruptured chords, and mild mitral annular enlargement (figure 1 and movie 3A-B). The flail segment is thickened and myxomatous in a very localized manner. This MVP type is often associated with cleft-like indentations separating posterior mitral scallops [35] that may affect the quality of mitral repair.
●Forme fruste Barlow disease – This is an intermediate form between classic and nonclassic disease.
Secondary MVP associated with connective tissue disorders — MVP is more prevalent in patients with Marfan syndrome, MASS phenotype (associated with MVP and myopia, as well as aorta, skin, and skeletal features), Ehlers–Danlos syndrome, osteogenesis imperfecta, and pseudoxanthoma elasticum [20,36]. Among patients with Marfan syndrome, mitral valve prolapse occurs more frequently in patients with FBN1 mutations as compared with those with TGFBR2 mutations (eg, 45 and 21 percent [37]). (See "Genetics, clinical features, and diagnosis of Marfan syndrome and related disorders".)
Secondary MVP associated with congenital heart disease — MVP has also been found in as many as 15 percent of patients with Ebstein anomaly [38]. This suggests a role for LV deformation in creating mitral imbalance and prolapse despite a structurally normal mitral valve. (See "Clinical manifestations and diagnosis of Ebstein anomaly".)
Flail leaflet without myxomatous degeneration — A number of other diseases are associated with imbalance of the mitral valve complex, leading to prolapse and flail of the mitral valve. Infective endocarditis causes destructive lesions, and ruptured chordae may ensue, leading to flail mitral leaflet(s).
●Myocardial infarction – Myocardial ischemia is not a cause of MVP, but myocardial infarction with papillary muscle rupture causes one or both leaflets to prolapse in the left atrium, often with a muscle tip attached.
●Trauma – Similarly, blunt chest trauma with rupture of chordae or papillary muscle can cause a flail mitral leaflet. Acute rheumatic fever may cause prolapse by true elongation of the valvular tissue, but subsequent tissue retraction makes the occurrence of prolapse due to chronic rheumatic heart disease exceptional unless there is a ruptured chord.
●Other causes of ruptured chordae – Other diseases, such as hypertrophic cardiomyopathy, myxomas, or prominent mitral annular calcifications, may also cause ruptured chordae and thereby cause leaflet prolapse. While mitral regurgitation (MR) in these cases is technically due to leaflet prolapse, the diagnosis is usually obvious from the clinical presentation and echocardiographic findings, and not associated with myxomatous degeneration of the leaflets.
By severity
●Severity of prolapse – MVP is classified by severity of the abnormal movement of the valve. The leaflets are described as billowing when the tips of leaflets remain in the LV, versus flail when the tip(s) of one (or both) leaflets prolapses into the left atrium.
●Severity of MR – The degree of MR accompanying MVP can range from none, trivial, or mild to progressive (moderate) to severe (table 2). Quantification of the severity of MR associated with MVP is essential for clinical decision making [39]. (See 'Quantifying MR' below and "Clinical manifestations and diagnosis of chronic mitral regurgitation", section on 'Identifying the severity of MR'.)
PATHOPHYSIOLOGY — Anatomically, the mitral valve is formed by a long and narrow anterior leaflet and a shorter and wider posterior leaflet occupying a larger portion of the annular circumference (figure 2). Thus, when the mitral valve is closed, it appears from the atrial side as the "mitral smile" with two leaflets and two commissures (anterolateral and posteromedial). The leaflets' bases are attached to the annulus and their tips to the chordae, which join the papillary muscles.
In both primary MVP and secondary MVP associated with connective tissue disorders, the pathologic process may involve the entire mitral valvular complex (leaflets, chordae, mitral annulus). The hallmark macroscopic valvular lesion of MVP is excessive mitral leaflet tissue leading to folding and hooding affecting one or more segments of one or both leaflets [40,41]. The chordae are elongated, have reduced strength, and may rupture [42]. The annulus is typically dilated and frequently separated from its normal myocardial support [43], causing annular expansion in systole which further accentuates the mitral regurgitation (MR). In contrast, the papillary muscles are usually normal in structure. Thus, MVP is physiologically heterogeneous, with various combinations of leaflet, chordal, and annular alterations yielding insufficient leaflet apposition, resulting in MR.
Histologically, the characteristic myxomatous lesion is proliferation of the spongiosa of the mitral valve leaflets, with mucopolysaccharide deposits and excessive water content causing leaflet thickening and redundancy. The collagen composition is altered, with a marked increase in type III collagen [41]; elastin fibers appear fragmented [42]. Focal accumulation of activated valvular interstitial cells and increased expression of matrix metalloproteinases suggest that abnormal tissue remodeling is responsible for the disease [44].
Qualitative histologic analysis cannot differentiate between classic MVP (Barlow disease) and nonclassic MVP (fibroelastic deficiency) [45]. However, a more elaborate semiquantitative analysis shows different patterns, with more myxomatous infiltration, collagen proliferation, and elastic fiber lesions in Barlow disease and Marfan syndrome than in fibroelastic deficiency. (See 'Morphology of primary MVP' above.)
CLINICAL MANIFESTATIONS — Symptoms do not reliably indicate MVP [46]. Most patients are diagnosed based on auscultatory findings that lead to evaluation by echocardiography or on echocardiography ordered for other unrelated reasons.
MVP syndrome — MVP syndrome is a term previously used to describe a constellation of symptoms and conditions associated with MVP including chest pain, palpitations, dyspnea, exercise intolerance, dizziness, lean body habitus, and anxiety disorders [6,47]. However, many reports of associations were limited by inadequate control groups and use of insufficiently stringent diagnostic criteria for MVP (see 'Imaging definition of MVP' below). Among the previously reported clinical correlates of MVP, only the association with lower body mass index than controls has been reproducibly associated with MVP [6,47,48]. A study comparing 281 individuals with MVP with 65 individuals without MVP found that presence of MVP was not independently associated with psychoemotional status [48].
Symptoms — Most patients with MVP are asymptomatic. Symptoms in patients with MVP usually are due either to significant mitral regurgitation (MR) or to a cardiac arrhythmia.
The majority of patients with MVP (approximately 75 percent) have mild, trace, or no MR; severe MR is uncommon (occurring in approximately 4 percent) [1]. Severe MR can cause heart failure with associated dyspnea and fatigue or may cause asymptomatic progressive LV enlargement.
Some patients with MVP develop atrial fibrillation or other arrhythmias and present with palpitations. MVP is associated with a risk of ventricular arrhythmias and sudden cardiac death.
MVP may first be diagnosed in a patient with endocarditis who presents with fever and bacteremia [49]. (See 'Complications' below.)
Physical examination
Cardiac examination — The most common auscultatory features of mitral valve prolapse are the nonejection click (single or multiple) and the murmur of MR. The click is thought to be caused by snapping of the mitral chordae during systole when the valve bows into the atrium. The click is mobile, meaning its timing varies with maneuvers that change the LV volume, occurring earlier in systole with sitting, standing, or other interventions that reduce ventricular size, or later with those interventions that increase chamber size such as squatting (movie 4 and movie 5) [50]. (See "Auscultation of heart sounds", section on 'Midsystolic click'.)
Some patients with MVP have tricuspid valve prolapse, which also produces a midsystolic click. The interval between S1 and the tricuspid valve click generally increases following inspiration or raising the legs or other maneuvers that increase right ventricular volume. (See "Auscultation of heart sounds", section on 'Midsystolic click'.)
When present (see 'Symptoms' above), the murmur of MR with MVP is late-systolic, particularly early in the disease course. The position of maximal intensity and radiation pattern vary with the direction of the jet (anteriorly-directed jets can be heard over the entire precordial area, while posteriorly directed jets are typically best heard at the apex and radiate towards the axilla and the back). With severe prolapse or a flail leaflet, the murmur is holosystolic and indistinguishable in pitch from other causes of MR, but often will remain maximum at mid-late systole. With long-standing severe MR, the LV apical impulse is displaced laterally, and clinical findings of LV dysfunction (gallop sounds) and pulmonary hypertension (loud P2 component) may be present. (See "Auscultation of cardiac murmurs in adults" and "Physiologic and pharmacologic maneuvers in the differential diagnosis of heart murmurs and sounds".)
With acute severe MR (as may result from chordal rupture), the cardiac impulse is hyperdynamic but normal in location unless there has been preceding chronic MR. The murmur of acute MR may be early systolic, midsystolic, or holosystolic and is generally soft and low-pitched, ending before A2. (See "Auscultation of cardiac murmurs in adults".)
Limited data are available on the diagnostic accuracy of auscultation for MVP, particularly when limited to studies using current echocardiographic diagnostic criteria. Identification of a mobile systolic click by an expert observer may be a highly sensitive finding (88 and 100 percent) with fair specificity (66 and 73 percent) [51,52]. In contrast, in a study of 147 patients referred for echocardiography for suspected MVP, identification of a systolic click by a referring clinician had a sensitivity of 52 percent and specificity of 68 percent for MVP [53]. Of note, auscultatory manifestations are highly variable [50]. This, together with inconsistent clinical examination skills among clinicians and variable auscultatory and echocardiographic criteria used to diagnose MVP, likely explains the conflicting observations on the accuracy of auscultatory findings in MVP.
General examination — Observation of the general appearance and body habitus is usually the first step in the physical examination. In most patients with MVP, the general examination reveals no specific findings suggestive of MVP. Patients with MVP tend to have a lower body mass index than controls [6,7].
Some patients with primary MVP have noncardiac findings ("syndromic MVP") including skeletal abnormalities and/or other findings of connective tissue disorders. Skeletal abnormalities associated with MVP include narrow anteroposterior chest diameter, scoliosis and loss of kyphosis of the thoracic spine, and pectus excavatum deformity, although the data on the frequency of these abnormalities in patients with MVP are limited [15,29,54].
Other physical findings are observed in patients with secondary MVP with connective tissue disorders or other causes of mitral valve disease. (See 'Secondary MVP associated with connective tissue disorders' above and 'Flail leaflet without myxomatous degeneration' above.)
Complications — Additional clinical findings are caused by complications of MVP including severe MR, infective endocarditis (which may be accompanied by worsening MR), and arrhythmias. (See "Nonarrhythmic complications of mitral valve prolapse" and "Arrhythmic complications of mitral valve prolapse".)
As discussed separately, a potential association between MVP and stroke or transient ischemic attack has been explored, but a causal relationship has not been established. (See "Nonarrhythmic complications of mitral valve prolapse", section on 'Transient ischemic attacks and cerebral vascular accidents'.)
Severe mitral regurgitation — While MVP represents the most common cause of severe primary MR in resource-abundant countries [55], only a minority of patients with MVP ultimately develop symptomatic severe MR due to profound leaflet prolapse and/or chordal rupture with one of the following presentations:
●Insidious worsening – With chronic severe MR, most patients remain asymptomatic for years and the development of symptoms is generally insidious with time or at the onset of atrial fibrillation. The most common symptom of severe MR is dyspnea. Fatigue is a much less specific symptom and thus less likely to improve after surgery. (See "Clinical manifestations and diagnosis of chronic mitral regurgitation" and "Pathophysiology and natural history of chronic mitral regurgitation".)
●Acute heart failure – A less common presentation is the chordal rupture syndrome whereby acute severe MR causes sudden dyspnea, chest pressure, and often rapidly progressive pulmonary edema. Hypotension and other signs of shock occur in rare cases. (See "Acute mitral regurgitation in adults".)
●Subacute deterioration – When acute MR progression is superimposed upon chronic MR, patients may present subacutely with progressive dyspnea.
Infective endocarditis — Fever and other symptoms of infective endocarditis are uncommon presenting symptoms of MVP, as discussed separately. (See "Nonarrhythmic complications of mitral valve prolapse", section on 'Infective endocarditis' and "Clinical manifestations and evaluation of adults with suspected left-sided native valve endocarditis".)
Arrhythmias — Some patients with MVP may present with palpitations due to atrial or ventricular arrhythmias, although the risk caused by these arrhythmias in most patients with MVP is low [49]. However, severe ventricular arrhythmias are associated with excess mortality [49], and a subset of patients of MVP are at risk for sudden cardiac death [56,57], as discussed separately. (See "Arrhythmic complications of mitral valve prolapse".)
DIAGNOSIS AND EVALUATION
General approach — MVP should be suspected in patients with a nonejection click (single or multiple) with or without a systolic murmur of mitral regurgitation (MR). Evaluation for MVP is also indicated for adults with one or more first-degree relatives with MVP. Given the time course of development and progression of MVP and MR, these may develop later in life though absent during youth.
All patients with known or suspected valvular heart disease should undergo careful history, physical examination, and transthoracic echocardiogram (TTE) [4,5].
Diagnostic evaluation for patients with MVP and a suspected connective tissue disorder is discussed separately. (See "Genetics, clinical features, and diagnosis of Marfan syndrome and related disorders", section on 'Diagnosis of MFS' and "Clinical manifestations and diagnosis of Ehlers-Danlos syndromes".)
Echocardiography — MVP is diagnosed on TTE, although transesophageal echocardiographic (TEE) imaging may be needed in certain situations (eg, inadequate acoustic windows on TTE). Echocardiography provides information not only about the presence (or absence) of MVP but also allows a comprehensive evaluation of the subvalvular structures, assessment of MR, and identification of hemodynamic consequences.
Two-dimensional and three-dimensional TEE are important for planning for transcatheter or surgical intervention, as discussed separately. (See "Management of chronic primary mitral regurgitation".)
Imaging definition of MVP — The current imaging definition of MVP is systolic billowing of any portion of one or both mitral leaflets ≥2 mm above the annular plane into the left atrium in a long-axis view (parasternal or apical three-chamber) (image 1) [26]. Two-dimensional features associated with MVP are disruption or elongation of mitral leaflets, chordae, or papillary muscles, and enlargement of the annular diameter.
The abnormal movement of MVP has been challenging to define given the saddle shape of the mitral annulus, which is accentuated in systole due to displacement of the annulus at the commissures towards the ventricular apex [58,59]. Thus, in the apical four-chamber view, the leaflets may appear posterior to the annulus, even in healthy subjects [60,61]. These observations, published in the late 1980s, led to a change in the accepted echocardiographic view for identification of MVP from "any view" to "a (three-chamber) long-axis view."
Simple override of the anterior leaflet (ie, the anterior leaflet passing behind the posterior leaflet in systole without crossing the annulus plane as commonly seen in ischemic MR due to tethering of the posterior mitral leaflet) should be distinguished from MVP, as management of this condition differs from that for MVP.
Since diagnostic criteria for MVP have evolved, the literature on MVP must be reviewed with care. Many studies of MVP have design flaws due to inadequate controls and/or insufficiently stringent criteria for MVP. In addition, patients previously misdiagnosed with MVP require appropriate evaluation and counseling.
Quantifying MR — Doppler echocardiographic techniques are used to quantify the severity of MR, as discussed separately (table 2). (See "Echocardiographic evaluation of the mitral valve" and "Clinical manifestations and diagnosis of chronic mitral regurgitation", section on 'Identifying the severity of MR'.)
MR severity should be quantified in all patients with a visual appearance of greater than mild MR on color Doppler to guide assessment of prognosis and management. Quantification includes determination of the effective regurgitant orifice area (EROA) and the regurgitant volume. Quantitative measures of MR are essential predictors of outcome [62], as confirmed in large independent prospective studies [63,64], including in routine clinical practice [39]. (See "Echocardiographic evaluation of the mitral valve", section on 'Quantitative parameters of mitral regurgitation' and "Natural history of chronic mitral regurgitation caused by mitral valve prolapse and flail mitral leaflet".)
It is important to distinguish mid-late (partial) systolic MR (which is generally associated with benign outcomes) from holosystolic MR. Leaflet malcoaptation limited to mid to late systole causes partial systolic MR [65]. With mid-late systolic MR, regurgitation severity will be overestimated based on EROA and jet area; regurgitant volume more accurately measures disease severity.
M-mode not used — M-mode echocardiography should no longer be used in making a diagnosis of MVP. Previously used M-mode criteria for MVP are not reliable because the normal motion of the base of the heart can either mask or mimic true prolapse.
Other imaging
Cardiovascular magnetic resonance — When quantification of MR by echocardiography is uncertain, cardiovascular magnetic resonance (CMR) imaging enables accurate quantification [4].
In addition, MVP can be diagnosed by CMR, and focal late gadolinium enhancement of mitral valve leaflets and papillary muscles has been observed [66]. Studies have shown that the occurrence of ventricular arrhythmias is also associated with mitral annular disjunction diagnosed by CMR [67], as well as ventricular fibrosis diagnosed by late gadolinium enhancement [68]. (See "Clinical utility of cardiovascular magnetic resonance imaging", section on 'Regurgitant valve disease'.)
Left ventricular angiography — Angiography is not used to diagnose MVP. However, in some patients referred for cardiac catheterization, MVP may be incidentally found on LV angiography, showing the displacement of the mitral valve leaflets into the left atrium with late systolic MR. These patients should be further evaluated by echocardiography. In addition, hemodynamic catheterization and LV angiography are used for assessment of MR severity in patients with discordant clinical and echocardiographic findings. (See "Hemodynamics of valvular disorders as measured by cardiac catheterization", section on 'Chronic mitral regurgitation' and "Hemodynamics of valvular disorders as measured by cardiac catheterization", section on 'Acute mitral regurgitation'.)
DIFFERENTIAL DIAGNOSIS — The midsystolic click of MVP should be differentiated from other systolic sounds such as aortic or pulmonary ejection clicks (occurring early in systole, at the foot of the carotid upstroke) and from other cardiac sounds (split first or second heart sounds, pericardial sounds, atrial septal aneurysm clicks). A midsystolic click may be confirmed by maneuvers that alter the timing of the sound, as described separately. (See "Auscultation of heart sounds", section on 'Midsystolic click'.)
Echocardiography accurately distinguishes MVP from other causes of systolic sounds as well as from other causes of mitral regurgitation. (See "Auscultation of heart sounds", section on 'Nonejection systolic sounds' and "Auscultation of heart sounds", section on 'Ejection sounds' and "Clinical manifestations and diagnosis of chronic mitral regurgitation", section on 'Identifying the cause of MR' and "Acute mitral regurgitation in adults", section on 'Echocardiography'.)
MVP with myxomatous disease should be differentiated from other causes of flail mitral valve leaflet, as discussed above. (See 'Flail leaflet without myxomatous degeneration' above.)
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Cardiac valve disease".)
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, “The Basics” and “Beyond the Basics.” The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on “patient info” and the keyword(s) of interest.)
●Basics topic (see "Patient education: Mitral valve prolapse (The Basics)")
SUMMARY AND RECOMMENDATIONS
●Prevalence – The prevalence of mitral valve prolapse (MVP) in the general population is estimated to be 0.6 to 3 percent. This estimate is significantly lower than previously reported due to the current use of a more stringent definition of MVP. (See 'Epidemiology' above.)
●Classification – MVP is classified as either primary (caused by degenerative disease in the absence of an identifiable connective tissue disease; may be sporadic or familial) or secondary (associated with an identifiable disorder such as Marfan syndrome or infective endocarditis) (table 1).
The morphology of primary MVP is classified as either classic (with markedly and diffusely thickened leaflets [≥5 mm] with bileaflet prolapse) or nonclassic (with limited or absent leaflet thickening [thickness <5 mm] and segmental prolapse) (figure 1). (See 'Diagnosis and evaluation' above and 'Pathophysiology' above.)
●Symptoms – MVP is widely heterogeneous in its presentation and outcome. Most patients with MVP have no associated symptoms. Most patients with MVP have mild, trace, or no mitral regurgitation (MR); severe MR occurs in approximately 4 percent and may or may not be associated with symptoms. (See 'Symptoms' above.)
Symptoms related to MVP are caused by complications such as dyspnea and fatigue caused by severe MR with associated heart failure, fever caused by infective endocarditis, and palpitations caused by atrial or ventricular arrhythmias. (See 'Complications' above.)
●When to suspect MVP – MVP should be suspected in patients with a nonejection click (single or multiple) with or without a late systolic or holosystolic murmur of MR (movie 4 and movie 5). Evaluation for MVP is also indicated for patients with a family history of MVP. (See 'General approach' above.)
●Diagnosis – MVP is diagnosed by transthoracic echocardiography. MVP is defined as systolic mitral leaflet displacement ≥2 mm above the annular plane in the parasternal or apical long-axis (three-chamber) views (image 1). (See 'Diagnosis and evaluation' above and 'Imaging definition of MVP' above.)
●Quantification of MR – Formal quantification of MR severity (including regurgitant volume and regurgitant orifice area) is indicated in all patients with MVP and more than mild MR, as this guides management and assessment of prognosis. (See 'Quantifying MR' above.)
