Kembara Xtra - Medicine - Mitral Valve Prolapse One or both mitral valve leaflets protruding into the left atrium (LA) during ventricular systole is known as mitral valve prolapse (MVP). MVP can be divided into multiple categories depending on its etiology (primary or secondary; see "Etiology and Pathophysiology") or morphology (classic MVP and nonclassic MVP; see "Test Interpretation"). Although MVP frequently goes unnoticed and has a benign clinical course, it can occasionally be accompanied by symptoms like palpitations or consequences like mitral regurgitation (MR). Systolic click-murmur syndrome, myxomatous mitral valve, floppy valve syndrome, redundant cusp syndrome, and Barlow syndrome are among synonyms. Prevalence Prior to the current echocardiographic criteria, earlier studies estimated the prevalence at 5-15% and indicated a higher prevalence among women and with increasing age. The prevalence of MVP is now estimated at 2-3% of the general population and is equally distributed by gender and across the age spectrum. Pathophysiology and Etiology The mitral valve leaflets often experience myxomatous degeneration as part of MVP's pathogenesis. The valve spongiosa layer expands, collagen structure changes, and structurally aberrant chordae are all symptoms of myxomatous degeneration. MVP can also result from papillary muscle or chordae disturbance, malfunction, or rupture; this can happen independently of a process that causes myxomatous degeneration or as a byproduct of a process that causes myxomatous degeneration. ● The following factors are part of the multifactorial etiology of MVP: sporadic, family; primary MVP; secondary MVP "Syndromic" MVP: myxomatous degeneration linked to connective tissue illnesses, including Loeys-Dietz syndrome, pseudoxanthoma elasticum, Marfan syndrome, and Ehlers-Danlos syndrome. Atrial septal defect and Ebstein abnormality are linked to congenital heart disease. Disruption, malfunction, or rupture of the papillary/chordae (heart attack, endocarditis, rheumatic fever, injury, hypertrophic cardiomyopathy) Genetics: Research on the genetics of MVP is ongoing. Both autosomal dominant and X-linked family MVP have been identified in primary MVP. Variable penetrance for autosomal dominant. Numerous genetic loci have been found. MMVP1 is located on chromosome 16 (p11.2-p12.1), MMVP2 is located on chromosome 11, and MMVP3 is located on chromosome 13 (q31.3-q32.1). X-linked: The filamin A gene, located on chromosome Xq28, has been identified. Secondary MVP is linked to connective tissue problems, which frequently have genetic roots (see "Etiology and Pathophysiology" above). Risk Elements Both heritable and sporadic congenital defects as well as various disease processes are linked to the development of MVP. MVP seems to be more prevalent among those with leaner body mass. Accompanying Conditions Both heritable and sporadic congenital defects as well as various disease processes have been linked to the development of MVP. MVP is linked to the emergence of other medical diseases or consequences, including MR and stroke. Von Willebrand disease, primary hypomastia, thoracic skeletal anomalies, and prolapse of the tricuspid, pulmonic, or aortic valves are some related disorders that are less clearly either (i) a cause of MVP or (ii) caused by MVP. History When patients do experience symptoms, palpitations are most frequently the symptom that is related with MVP. Symptoms may be linked to MR as a result of MVP, to MVP itself, or to additional MVP problems including stroke, arrhythmia, etc. - Palpitations, unusual chest discomfort, weariness, exercise intolerance, orthostasis/syncope/presyncope, and neuropsychiatric symptoms like panic episodes are all associated with MVP. - Fatigue, dyspnea, exercise intolerance, orthopnea, and paroxysmal nocturnal dyspnea are symptoms linked to the progression of MR. clinical assessment Although not always audible, a midsystolic click is the main auscultatory finding. Additionally, a mid- to late-systolic murmur that is strongest at the apex may follow. Dynamic auscultation may be used to distinguish between systolic noises that sound similar. The click and murmur are moved toward S1 by actions that reduce end-diastolic volume: standing up, Valsalva. Squatting and raising your leg are two maneuvers that send the click and murmur nearer S2. Note: The Valsalva technique may be used to distinguish between hypertrophic obstructive cardiomyopathy (HOCM) and MVP since it intensifies the murmur in HOCM while lengthening the murmur in MVP. Exam results can also show that MVP caused MR to exist. - The optimal location to hear the MR holosystolic murmur is at the apex, with radiation to the left axilla. - The murmur's duration and MR severity are correlated. If an S3 is present, there may be significant regurgitation. Differential diagnosis: Tricuspid regurgitation, Papillary muscle dysfunction, Ejection clicks (do not vary time with systole), and Hypertrophic cardiomyopathy. Initial test results from the laboratory and imaging Following a suitable physical examination, a transthoracic echocardiography (TTE) is the diagnostic method of choice; an echocardiogram is necessary for a firm diagnosis. - Echocardiography is recommended for the diagnosis of MVP and evaluation of MR, leaflet morphology, and ventricular compensation in asymptomatic patients with physical symptoms of MVP (3)[C]. - In the absence of a constellation of clinical symptoms or physical findings suggestive of MVP, or a positive family history, echocardiography is not recommended to rule out MVP in asymptomatic patients with vague symptoms. Without any other indication, an electrocardiogram (ECG) is not necessary for the workup of MVP. - Palpitations are a typical symptom that causes an ECG. - Although the ECG in MVP is normally normal, it can occasionally show non-specific ST- to T-wave shifts, T-wave inversions, strong Q waves, and even prolonged QT. Tests in the Future & Special Considerations If an intervention is anticipated or the mitral valve is only partially visible on transesophageal echocardiogram (TTE), transesophageal echocardiography (TEE), particularly with 3D imaging, may be taken into consideration to further visualize anatomy. Patients with MVP and severe MR may need coronary angiography and TEE if cardiac surgical referral is intended. Angiography is rarely utilized for diagnostic purposes but may be suggested for hemodynamic assessment when noninvasive techniques are equivocal. If the patient experiences palpitations, ambulatory ECG monitoring or an event monitor may be considered, albeit they are not necessary for MVP alone. The parasternal long-axis annular plane of the valve on an echocardiography is where MVP is defined as anterior, posterior, or bileaflet prolapse of at least 2-mm superior displacement into the LA during systole, with or without accompanying leaflet thickening. - Classification morphological: Classic MVP (also known as Barlow syndrome): prolapse with >5 mm of thickness in the leaflets Nonclassical MVP (fibroelastic deficiency): prolapse with less than 5 mm of thickening of the leaflets When a section or segments of a leaflet protrude into the LA during systole, this is referred to as "flail" mitral prolapse. Usually, this is accompanied by torn chordae or ruptured papillary muscle. Management Patients with milder prolapse and modest symptom burden should be reassured; a normal lifestyle and consistent exercise are also recommended. Patients may be advised to give up alcohol, cigarettes, and caffeine if MVP is accompanied with palpitations, weariness, or anxiety. It is possible to treat MVP with orthostatic symptoms by consuming more liquids and salt. Support stockings could be useful as well. Medication For MVP with "high-risk" echocardiographic characteristics (thickening >5 mm or valve redundancy), aspirin (75 to 325 mg daily) may be recommended. MVP and transient ischemic attacks (TIAs) patients should take aspirin (75 to 325 mg daily). Patients with MVP and transient ischemic attacks who continue to have TIAs while taking aspirin may want to think about taking warfarin. Patients with MVP with a history of stroke who don't have high-risk echocardiographic characteristics such thickness >5 mm or valve redundancy, MR, atrial fibrillation, or left atrial thrombus may be considered aspirin (75 to 325 mg daily). Patients with MVP with a history of stroke who also have MR, atrial fibrillation, a left atrial thrombus, or high-risk echocardiographic characteristics (thickening >5 mm or valve redundancy) may be candidates for warfarin. Patients who have MVP and palpitations may benefit from -blocker therapy. Note: MVP alone is no longer regarded as sufficient to warrant antibiotic treatment for infected endocarditis (IE). Referral MVP with considerable symptoms, high-risk characteristics, or concurrent cardiac conditions should be referred to a cardiologist. Patients who have a surgical repair indication should be referred for cardiothoracic surgery. When a heritable illness is detected, patients may choose to consider genetic counseling. Surgical Techniques The most frequent cause of chronic primary MR necessitating surgery in high-income nations is MVP and myxomatous valve degeneration. Indications for referral for mitral valve repair include the following: Asymptomatic patients with atrial fibrillation or pulmonary hypertension may also be considered for surgical intervention. - In symptomatic patients with severe primary MR. - In asymptomatic MR patients with left ventricular (LV) systolic dysfunction (left ventricular ejection fraction [LVEF] 60%, left ventricular end-systolic diameter [LVESD] 40 mm). Minimally invasive surgery and surgery for asymptomatic patients without LV systolic dysfunction are areas of ongoing research. If surgery is indicated for MR, mitral valve repair is generally preferred over replacement when possible due to lower rates of operative mortality and long-term complications. Follow-up: Every 3 to 5 years, asymptomatic MVP patients with no detectable MR can be clinically monitored. In asymptomatic individuals with established valvular heart disease, periodic TTE monitoring is advised at intervals based on the severity, size, and location of the valve lesion. Patients who exhibit high-risk characteristics on their initial echocardiography, such as moderate to severe MR, or who have symptoms may require serial echocardiograms. They should also be monitored clinically at least once a year. Diet Limiting caffeine, alcohol, and smoking should be advised for patients with MVP and palpitations. Patient Education Patients should be informed that the diagnosis of MVP alone does not constitute a contraindication to pregnancy and that MVP is frequently a benign condition. Patients should be advised to report any change in symptom status as soon as possible, since this may necessitate repeat echocardiogram. Patients should be informed about sporadic familial MVP incidence. If a patient has MVP with any one of the following characteristics, it is advised that they refrain from participating in high-intensity competitive sports: - Prior resuscitation from cardiac arrest - Prior moderate LV enlargement or LV dysfunction - Uncontrolled tachyarrhythmias - Prolonged QT interval - Unexplained syncope - Aortic root enlargement For asymptomatic patients without problems, the prognosis is excellent; MVP is frequently benign and has a typical life expectancy. Overall, the development and progression of MR as well as the occurrence of additional severe complications have a significant impact on the prognosis of MVP. Complications The most frequent cause of chronic primary MR in high income nations is MR—MVP with myxomatous valve degeneration. Severe MR may lead to a wide range of other problems, including: - Heart failure brought on by acute or progressive MR - Left atrial dilatation with accompanying paroxysmal supraventricular tachycardias (including atrial fibrillation) and pulmonary hypertension with related RV dysfunction Arrhythmias, such as ventricular premature beats, supraventricular tachycardias, and premature atrial complexes While still uncommon, sudden cardiac death (SCD) happens more frequently in patients with MVP than in the general population (0.14 SCD incidents per 100 patient-years). Bileaflet prolapse, ventricular fibrosis, complicated ventricular ectopy, and ST-T wave abnormalities are potential risk factors for SCD in MVP. strokes and transient ischemic attacks (TIAs) Endocarditis that is infectious
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