Kembara Xtra - Medicine - Mitral Regurgitation A primary, secondary (functional), or mixed mitral valve (MV) closure disorder that causes a backflow of the left ventricular (LV) stroke volume into the left atrium (LA). If left untreated, this condition can result in enlargement of the LV and LA, increased pulmonary pressures, atrial fibrillation (AF), heart failure (HF), and sudden cardiac death. Different forms of mitral regurgitation (MR) - Primary versus secondary (functional) - Acute versus chronic - Primary versus mixed Secondary: no valvular abnormalities are discovered. Primary: abnormalities at any level of the MV structures (annulus, leaflets, chordae tendineae, and papillary muscles). The papillary muscle is displaced by the aberrant and dilated LV, which produces leaflet tethering and annular dilatation that hinders coaptation. Mixed: anomalies that are a combination of primary and secondary categories. heart and pulmonary systems are impacted. Epidemiology According to data from 2000, 2.5 million Americans have moderate to severe MR. By 2030, the prevalence of this most prevalent valvular condition is predicted to quadruple (1). Prevalence According to echocardiogram severity: - Mild MR: 19% (or up to 40% with minor jets). 1.9% for Moderate MR - Extreme MR 0.2% Degenerative (myxomatous disease, annular calcification): group (1), 60–70% - 20% Ischemic - 2-5% endocarditis - Arthritic: 2-5% Pathophysiology and Etiology Acute MR-Leaflet Perforation: Trauma, Infectious Endocarditis - Trauma, spontaneous rupture, infective endocarditis, or rheumatic fever can cause a rupture of the chordae tendineae. - Trauma, severe myocardial ischemia, or acute myocardial infarction (MI) can cause papillary muscle dysfunction or rupture. Primary Chronic MR Degenerative conditions include mitral annulus calcification and mitral valve prolapse (MVP), while inflammatory conditions include lupus and eosinophilic endocarditis. Anorectic medicines and toxicity-induced valvulopathy Congenital (functional cleft leaflet) - Secondary Ischemic conditions include CAD/MI Nonischemic conditions include dyssynchrony from right ventricular pacing, annular dilatation from prolonged AF, and cardiomyopathy from any cause. Acute MR: Sudden LA and LV volume overload results from acute MV injury. Without LV remodeling, a sudden increase in LV volume load causes reduced forward cardiac output and the potential for cardiogenic shock. Chronic MR: Increased regurgitant volume is offset by LV eccentric hypertrophy, maintaining forward cardiac output and reducing pulmonary congestion. But LV dysfunction can arise from LV remodeling. Patients are more likely to develop AF as a result of the LA's compensatory dilatation for the increased regurgitant volume. Ischemia during acute MI, papillary muscle rupture, inadequate coaptation of leaflets, and restricted valve movement from chronic ischemia are all examples of ischemic MR. Age, hypertension, RHD, endocarditis, and anorectic medications are risk factors. General Prevention: Risk factor reduction for heart disease; antibiotic prophylaxis for poststreptococcal RHD; and the discontinuation of endocarditis prophylaxis. MVP and MR are frequent conditions in Marfan syndrome. RHD, previous MI, connective tissue disorder, acute MR characterized by sudden onset of orthopnea and paroxysmal nocturnal dyspnea, and chronic MR by exertional dyspnea and fatigue - Palpitations: persistent/paroxysmal AF Clinical examination: acute magnetic resonance imaging; rapid and thready pulses; indications of inadequate tissue perfusion and peripheral vasoconstriction. S3 and S4 (if in sinus rhythm) and hyperdynamic precordium without an apical shift - Systolic murmur at the base and border of the left sternum Early, middle, or holosystolic murmur; rales; a mild, low-pitched decrescendo murmur; a leftward displacement of the LV apical impulse; and a systolic thrill at the apex (which signals severe MR). - Loud P2 (if pulmonary hypertension) and a soft S1 and widely split S2, S3 gallop. - Ankle edema, jugular venous distension, and ascites if right-sided HF develops. - Holosystolic murmur at apex radiating to axilla or to left parasternal border. Multiple Diagnoses Aortic stenosis (AS) is often midsystolic but can be lengthy; it is difficult to distinguish from holosystolic and radiates to the carotid arteries (unlike MR). In contrast to MR, tricuspid regurgitation is holosystolic but localized to the left lower sternal border, does not spread to the axilla, and may become more intense with inspiration. A strong holosystolic murmur at the lower left sternal border that extends to the right sternal border (not the axilla) is a sign of a ventricular septal defect (VSD). Initial test results from the laboratory and imaging Chest x-ray (CXR): Acute MR: Normal heart size, pulmonary edema - Chronic MR: expansion of the LA and LV ECG for acute MR differs according to the underlying causes (such AMI). Chronic LA enlargement, MR mitrale, and AF LV hypertrophy with previous MI-related Q waves Cardiac enzymes, brain natriuretic peptide, if necessary, and a transthoracic echocardiography (TTE). Delineation of the mechanism of MR Monitoring of asymptomatic moderate to severe LV dysfunction (ejection fraction [EF] and end-systolic dimension [ESD]) Evaluation of MV apparatus and LV size and function after a change in sign/symptom in MR patient. Baseline evaluation of LV size and function, right ventricular function and LA size, pulmonary artery pressure, and severity of MR. Reassess following MV repair or replacement. - Acute MR findings: vegetations or flail leaflets as etiological evidence Standard LA and LV sizes Findings from chronic MR include: Enlarged LA and LV; Evidence of degenerative, rheumatic, ischemia, and other causes; Tests in the Future & Special Considerations Time intervals for subsequent TTE Heart magnetic resonance imaging (CMR): - TTE data are unreliable in determining LV and RV volumes, function, or MR severity (2)[B]. Transesophageal echocardiography (TEE) is performed during surgery to identify the underlying anatomic causes of MR and to direct correction. - Nondiagnostic data from noninvasive imaging on the severity, MR mechanism, and/or state of LV function Exercise hemodynamics using cardiac catheterization or Doppler echocardiography. - In symptomatic patients with chronic primary MR, a discrepancy exists between symptoms and the severity of MR as determined by resting TTE. Testing on an exercise treadmill (2)[C] - To determine the symptom status and exercise tolerance in asymptomatic primary MR patients. Noninvasive imaging techniques can be used to determine the cause of chronic secondary MR and/or to determine the viability of the myocardium. These techniques include cardiac CT angiography, stress nuclear/positron emission tomography, and CMR. Other diagnostic techniques involving cardiac catheterizationLeft ventriculography and hemodynamic assessment - Noninvasive testing cannot determine the extent of MR, the function of the LV, or the necessity of surgery. Prior to MV surgery in patients at risk for CAD, coronary angiography Interpretation of Tests The following structural factors must be integrated for the purpose of quantifying severe MR: LA size is dilated unless it is acute. If not acute, dilated LV size Doppler criteria include a broad central jet (>50% of LA), pulmonary vein systolic flow reversal, and flail leaflet in the MV morphology. Quantitative parameter: 50% regurgitation fraction, effective regurgitant orifice area of 0.40 cm2, regurgitation volume of 60 mL. Acute, severe MR is managed with medical therapy, which primarily serves to preoperatively stabilize hemodynamics. Vasodilators (nitroprusside, nicardipine) are used to increase hemodynamic compensation, however their effectiveness is frequently hindered by systemic hypotension. Primary Chronic MR Diabetics, -blockers, angiotensin-converting enzyme inhibitors (ACE-I) or angiotensin receptor blockers (ARBs), and perhaps aldosterone antagonists, as suggested in standard HF therapy, are used to treat symptoms in people who are asymptomatic and do not require long-term medical treatment. LV dysfunction or symptoms (stages B to D) are secondary. Aldosterone antagonists, -blockers, ACE-I or ARBs, as prescribed by conventional therapy Procedures Patients with mild to moderate MR are not candidates for isolated MV surgery. Acute MI followed by acute, severe MR - Papillary muscle displacement following acute papillary muscle rupture requiring urgent MV repair or replacement Medical stabilization that is aggressive and an intra-aortic balloon pump In most cases, revascularization is also necessary in addition to valve surgery. MV surgery for chronic severe MR and severe primary MR Symptomatic patients (stage D) may be taken into consideration if there is no significant LV dysfunction (EF > 30%) but there is severe LV dysfunction (EF 30%).MV restoration is appropriate for asymptomatic patients (stage C1) with preserved LV function (EF >60% and ESD 40 mm): Asymptomatic patients Mild/moderate LV dysfunction (EF 30-60% and/or ESD 40 mm, stage C2) At a heart valve center of excellence, the probability of a successful and long-lasting repair without residual MR is >95%, and the predicted mortality is 1%. Progressive LV enlargement or a decline in EF on successive imaging studies The likelihood of a successful and long-lasting repair is high in nonrheumatic MR with new start of AF or resting pulmonary hypertension (pulmonary artery systolic pressure >50 mm Hg). Patients with are advised to get MV repair rather than MV replacement. When a successful and long-lasting repair is possible, MR may involve the anterior leaflet as well as the posterior leaflet. Transcatheter MV repair: Can be taken into account for patients with significant symptoms (NYHA classes III/IV) despite adequate GDMT for heart failure who have favorable anatomy for the repair, a fair life expectancy, but a high surgical risk due to severe comorbidities.- secondary MR with severe MV operations Aortic valve replacement, coronary artery bypass graft surgery, and more (2)[C] Despite receiving the best GDMT for HF, patients with significant symptoms (NYHA grades III and IV) may still be evaluated.In ischemic MR patients, chordal-sparing MVR is favored to reduced annuloplasty repair. Patients who meet the criteria for device therapy and are symptomatic (stages B to D) are advised to undergo cardiac resynchronization therapy. Transcatheter MV repair: LVEF 20-50%, LV end-systolic diameter 7.0 cm, moderately severe or severe secondary MR, and maximally tolerated GDMT as determined by a multidisciplinary team with experience in the evaluation and treatment of HF and MV disease. Aspects of Geriatrics With preexisting CAD or the necessity for MV replacement, medical therapy alone is preferred for patients with MR who are over 75 years old due to greater surgical mortality and lower survival (relative to those with AS). Repairing MVs is preferable to replacing them. Admission ABCs (airway, breathing, and circulation) stabilization for acute MR. start the IV, oxygen, and monitoring. In addition to nitroprusside, dobutamine and/or aortic balloon counterpulsation may be used in hypotensive patients. Take care of underlying reasons, such as MI. Furosemide and morphine are used to treat acute pulmonary edema. Consult a surgeon immediately. Chronic MR Follow-Up: Asymptomatic Consider serial CXRs and ECGs as well as stress testing if exercise capacity is questioned. Mild MR with normal LV size and function and no pulmonary hypertension: annual clinical evaluation and TTE every 3 to 5 years or more frequently depending on course. Moderate MR: annual clinical evaluation and TTE every 1 to 2 years. Severe MR: clinical evaluation and TTE every 6 to 12 months. Patient Education Exercise following MV repair: Avoid contact or trauma-prone sports. Sports with a modest level of competition are permitted. Competitive athletes with MR who are asymptomatic, have sinus rhythm, normal pulmonary artery pressures, and LV size and function are not subject to any restrictions. Activities with low to moderate dynamic and static cardiac demand are permitted for those with mild symptoms and LV dilatation. Contact sports are not permitted for people with AF and anticoagulation. Acute, severe MR prognosis: The probability of death from surgery is 50%; the chance of death from medicinal care alone is 75% in the first 24 hours and 95% at two weeks. Chronic MR: 10% yearly rate of progression to symptoms and subnormal resting LVEF. Asymptomatic severe MR with normal LVEF. Severe MR with symptoms: 33% of patients survive 8 years without surgery; 5% of patients die each year. Pregnancy Considerations MR at high risk for maternal and/or fetal danger with NYHA functional classifications III and IV. Acute pulmonary edema, CHF, AF, bleeding risk with anticoagulation, endocarditis, and sudden cardiac death are among the complications.
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