mitral stenosis AHA guidlines 2014
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mitral stenosis AHA guidlines 2014 mitral stenosis AHA guidlines 2014 Presentation Transcript

  • D . B A S E M E L S A I D E N A N Y L E C T U R E R O F C A R D I O L O G Y A I N S H A M S U N I V E R S I T Y Mitral stenosis
  • Etiology 1-Rheumatic heart diseasegreat majority (inflammatory process due to cross-reactivity between streptococcal antigen and the valve tissue) 2-Infective endocarditis and mitral annular calcification accounted for 3.3 and 2.7 % of cases, respectively. 3-Other etiologies such as congenital malformation (rolled, thickened leaflet margins, hypoplasia of fusion of the papillary muscles, and short and thickened chordae tendineae), systemic lupus erythematosus, carcinoid heart disease, endomyocardial fibrosis, and rheumatoid arthritis were implicated in less than 1% of cases 4-Picture simulating mitral stenosis can result from obstruction of the mitral valveleft atrial myxoma or cor triatriatum, an uncommon congenital abnormality in which there is a membrane within the left atrium producing two left atrial chambers 5-Prosthetic valve dysfunction in this setting may result from acute or chronic thrombosis, pannus ingrowth on the atrial side of the valve, or leaflet calcification
  • PATHOPHYSIOLOGY --90% of individuals with rheumatic heart disease --Tiny nodules along the coapting portions of the valve leaflets leaflets thicken with eventual deposition of fibrin on the cusps and loss of normal valve morphology Fusion of the leaflet commissures, Thickening, fusion and shortening of the chordae tendineae symmetric, central oval-shaped orifice and a classic pattern of "doming" of the leaflets in diastole due to fusion of the leaflet tips at the commissures --Commisural fusion and chordal shortening are due to recurrent rheumatic fever with repetitive valve scarring, but leaflet thickening and calcification appear to be primarily due to the stress of chronic turbulent flow through a deformed valve {recurrent stenosis after mitral valvuloplasty, without intervening episodes of rheumatic fever, is due to leaflet thickening and calcification without recurrent commisural fusion}
  • AHA 2014
  • Cardiac hemodynamics --Pressure gradient between LA and LV in diastole reflected backward increase in pulmonary venous, capillary, and arterial pressures and resistance. -Mild to moderate MS only apparent with exercise or increase heart rate -Severe MS at rest --Increase LA pressure AF clinical decompensation via two mechanisms: the loss of atrial contraction; and the rapid ventricular response (reduction in the duration of diastole) --Pulmonary hypertension passive increase in pressure due to backward transmission of the elevated left atrial pressure; and reactive pulmonary vascular disease {Pulmonary arterial and arteriolar vasoconstriction; Hypertrophy of the pulmonary artery muscular layer}right-sided heart failure ** potentially completely reversible**
  • SYMPTOMS --Many patients with severe MS deny symptoms because slow progression of disease is "matched" by a gradual reduction in activity history of maximal physical activity --More rapid progression in areas of high prevalence may be due to the ineffective use of antibiotics and/or increased virulence of the Streptococcus organism
  • 1-Dyspnea: -Most common and often only symptomreduced compliance of the lungs and a decrease in vital capacity due to vascular congestion and interstitial edema -increase with: exertion, emotional stress, fever, pulmonary infection, sexual intercourse, AF, and pregnancy at rest orthopnea
  • 2-Hemoptysis: -Due to increased pulmonary pressures and vascular congestion -Sudden hemorrhage (pulmonary apoplexy) due to the rupture of thin walled and dilated bronchial veins when there is a sudden increase in left atrial pressure. This complication is rarely life-threatening, despite the large amount of bleeding. -Blood tinged sputum induced by severe coughing associated with paroxysmal nocturnal dyspnea or bronchitis. -Pink frothy sputum resulting from pulmonary edema
  • 3-Thromboembolism: -Over 80 percent of patients with MS who have an embolism are in AF -Transient AF and infective endocarditis -Early percutaneous balloon mitral commissurotomy prevents systemic embolism in patients with and without AF -Predictors in absence of AF: Left atrial thrombus The degree of reduction in mitral valve area Significant aortic regurgitation -LA(most) most common=cerebral circulation,spleen, kidneys, and the coronary circulation -RA PE
  • 4-Chest pain: Most commonly the result of pulmonary hypertension and right ventricular hypertrophy May be due to underlying coronary artery disease or a coronary artery embolism 5-Infective endocarditis: -Uncommon once the valve becomes calcified and very rigid -Antibiotic prophylaxis against endocarditis is NOT recommended in patients with native valve mitral stenosis in the absence of prosthetic replacement
  • 6-Right-sided heart failure: -Increased jugular venous pressure -Edema of both legs, which may progress to involve the upper thighs, sacral area, and abdominal wall; ascites and pleural effusions can also occur. -Hepatomegaly in which the liver may be pulsatile if tricuspid regurgitation is present 7-Hoarseness: LAcompression of the recurrent laryngeal nerve leading to hoarseness (Ortner's syndrome or cardiovocal syndrome) 8-Fatigue due to the reduction in cardiac output
  • PHYSICAL EXAMINATION -The arterial pulses are reduced in volume due to the decreased stroke volume, AF. -When MS is severe vasoconstriction, resulting in pinkish-purple patches on the cheeks (mitral facies). -Pulmonary hypertension and right ventricular hypertrophy prominent "a" wave (atrial contraction). The "a" wave is absent in patients with AF and only a prominent "v" wave (atrial filling during ventricular systole when the tricuspid valve is closed) is seen. If present, tricuspid regurgitation can lead to a prominent "c-v" wave (reflecting regurgitation of blood into the right atrium) and the neck veins are very pulsatile. -Palpation and percussion of the chest wall reveals an apical impulse that is generally normal. However, if pulmonary hypertension is present, there may be a right ventricular heave (substernal lift) and a palpable S2. -Advanced disease may be associated with the signs of right-sided heart failure
  • Cardiac auscultation 1-Heart sounds: As a result of the elevated left atrial pressure, the stenotic (but noncalcified) mitral leaflets are still widely separated at the onset of ventricular contraction. Thus, the first heart sound (S1) is loud, reflecting the increased excursion of the leaflets. As the leaflets become more rigid and calcified, their motion is limited and S1 becomes soft. The second heart sound is initially normal but, with the development of pulmonary hypertension, P2 becomes increased in intensity and may be widely transmitted. As pressure increases further, splitting of S2 is reduced and ultimately S2 becomes a single sound. A third heart sound of left ventricular origin is never heard in pure MS because of the obstruction to flow across the mitral valve. However, it may be present if there is coexisting aortic or mitral regurgitation or may be generated from the right ventricle. A fourth heart sound may be heard, most often originating from the right ventricle when it is hypertrophied and dilated and the patient is still in sinus rhythm
  • 2-Opening snap: An opening snap (OS) of the mitral valve is heard at the apex when the leaflets are still mobile. The OS is due to the abrupt halt in leaflet motion in early diastole, after rapid initial rapid opening, due to fusion at the leaflet tips. It is best heard at the apex and lower left sternal border. The OS following S2 may be mistaken for a split S2. As the MS progresses and left atrial pressure is higher, the OS occurs earlier after S2 or A2. Thus, the shorter the A2- OS interval, the more severe the mitral stenosis.
  • 3-Diastolic murmur : -Low-pitched diastolic rumble that is most prominent at the apex, patient lying on the left side in held expiration and by using the bell of the stethoscope, after exercise (very light pressure also may help. (Strong pressure will instead completely eliminate the low frequencies of MS). -Although the intensity of the diastolic murmur does not correlate with the severity of the stenosis, the duration of the murmur is helpful since it reflects the transvalvular gradient. -This early diastolic murmur is decrescendo, becoming softer as the left atrial pressure falls and the transvalvular gradient decreases. If the patient is still in sinus rhythm, the increase in atrial pressure after atrial contraction, results in an increase in the loudness of the murmur, termed "presystolic accentuation" -The diastolic murmur may be inaudible or absent when MS is very severe, due to the very slow flow across the mitral valve. -The diastolic murmur and OS are diminished with inspiration, but augmented with expiration (in contrast to tricuspid stenosis). With inspiration, the A2-OS interval widens and a distinct P2 may be heard. -Increasing venous return, eg, by lying the patient down and lifting the legs, augments the gradient; as a result, the diastolic murmur lengthens while the A2-OS intervals shortens. Similar changes are seen in response to exercise. In contrast, reducing venous return with amyl nitrate, the Valsalva maneuver, or squatting shortens the murmur and lengthens the A2-OS interval.
  • 4-Additional sounds, murmurs: -A pulmonary ejection sound, which diminishes with inspiration when the pulmonary arteries dilate. -With the development of tricuspid regurgitation, there is a holosystolic murmur best heard along the right sternal border which increases with inspiration. -A faint and brief murmur of pulmonic regurgitation (Graham Steell murmur) may be heard at the base. -Murmurs of mitral or aortic regurgitation may also be present if these valve lesions coexist with MS
  • Electrocardiogram --The QRS amplitude and morphology are normal unless there is mitral regurgitation or coexistent aortic valve disease. --Left atrial hypertrophy and enlargement results in a P wave that becomes broader (duration in lead II>0.12 sec), is of increased amplitude, and is notched (due to the delay in left atrial activation). This is termed "P-mitrale." The left atrial changes also produce a prominent negative terminal portion of the P wave in lead V1. --The P waves changes are not seen in patients with atrial fibrillation. The fibrillatory waves are coarse, generally >0.1 mV in amplitude, reflecting left atrial hypertrophy. --Pulmonary hypertension and right ventricular hypertrophy frontal axis shifts to the right (S>R in lead I and aVL) and a tall R wave develops in V1 and V2 (R>S or R/S ratio >1).
  • Chest x-ray -Left atrial enlargement may produce a "double density," the left heart border becomes straightened, the left bronchus is elevated, and, on the lateral projection, the left atrium is displaced posteriorly, impinging on the esophagus. -Calcification of the annulus may be observed -Enlargement of the main pulmonary artery due to pulmonary hypertension, while the aorta and left ventricle are often small. -Pulmonary vascular congestion with redistribution or "cephalization" of pulmonary blood flow to the upper lobes, dilated pulmonary vessels, Kerley B lines at the bases, and interlobar effusions (Kerley C lines). In more severe cases, Kerley A lines (straight dense lines running toward the hilum) may be seen
  • Pulmonary arteriogram in pulmonary hypertension secondary to mitral stenosis
  • Echocardiography 1-Transthoracic: --(2-D) echocardiography: -Mitral leaflets are thickened, have reduced motion during diastole, and show doming, which is indicative of commissural fusion -The mitral valve area can be accurately measured by planimetry in short axis views. -Estimates of leaflet motion, the degree of calcification and fibrosis of the leaflets, and assessment of the subvalvular apparatus can help establish the role for surgical or balloon valvotomy. Also, commisural calcification -Left atrial size, and left and right ventricular size and systolic function can be assessed. --Doppler: -Mean transvalvular gradient and the pressure half-time valve area can be accurately calculated from the diastolic velocity curve. (severe=MVA<1, mean PG>10mmHg) -Pulsed, continuous wave, and color Doppler are used to evaluate coexisting mitral regurgitation. -Pulmonary pressures are calculated from the velocity of the tricuspid regurgitation jet and right atrial pressure, which is estimated from the size and respiratory variation in the inferior vena cava
  • Hatle formula
  • 2-Three-dimensional: This technique can provide an en-face cross sectional view of the mitral orifice, to which planimetry can be applied to determine the valve area. 3-Stress echocardiography: -Is helpful when symptoms seem to be more severe than expected based on resting hemodynamics (such as resting valve area); these patients often have exertional pulmonary hypertension. -Mechanical relief of MS is recommended in patients with elevated pulmonary pressures (>60 mmHg systolic) with exertion. 4-TEE: -To assess the presence of absence of left atrial thrombus and to further evaluate the severity of mitral regurgitation in patients being considered for percutaneous mitral balloon valvotomy -To assess mitral valve morphology and hemodynamics if transthoracic echocardiography provides suboptimal data AHA 2014: I-TEE should be performed in patients considered for percutaneous mitral balloon commissurotomy to assess the presence or absence of left atrial thrombus and to further evaluate the severity of mitral regurgitation (MR) . (Level of Evidence: B)
  • AHA 2014
  • Cardiac catheterization and angiography --To assess the severity of MS if noninvasive tests are not conclusive or there is a discrepancy between the results of noninvasive tests and clinical findings related to the severity of MS. --When there is a discrepancy between mitral valve area and the Doppler-derived mean gradient; catheterization should include left ventriculography to evaluate the severity of mitral regurgitation --To assess the cause of severe pulmonary arterial hypertension if it is out of proportion to the severity of MS determined by noninvasive testing.
  • AHA2014: Class IIa 1. Exercise testing is reasonable in selected patients with asymptomatic severe VHD to 1) confirm the absence of symptoms, or 2) assess the hemodynamic response to exercise, or 3) determine Prognosis . (Level of Evidence: B)
  • EVALUATION AND FOLLOW-UP --Too early unnecessary risk for a complication of the procedure with little or no short-term benefit, since the MS may remain asymptomatic and stable for many years. --Delaying intervention  irreversible pulmonary hypertension and/or right heart failure --ACC/AHA repeat echocardiography to assess pulmonary artery pressure in asymptomatic stable patients every year in those with severe MS, every one to two years with moderate MS, every three to five years with mild MS, and any time there is a change in clinical status
  • PHYSICAL ACTIVITY AND EXERCISE --Exercise should be symptom-limited. This will prevent extreme elevations in the transmitral gradient that may lead to pulmonary edema --Patients in sinus rhythm with mild MS with peak pulmonary artery systolic pressures less than 50 mmHg can participate in all competitive sports. --Patients with moderate MS who are in sinus rhythm or atrial fibrillation (AF) and have peak pulmonary artery systolic pressures less than 50 mmHg can participate in low and moderate static and dynamic competitive sports. --Patients with severe MS who are in sinus rhythm or atrial fibrillation and patients with peak pulmonary artery systolic pressures greater than 50 mmHg should not participate in any competitive sports. --Patients with MS of any severity who are in or have a history of AF and are treated with anticoagulation should not participate in any competitive sports associated with a risk of bodily contact or possible trauma
  • Diuretics --Usually with a loop diuretic+ dietary salt restriction are appropriate when there are manifestations of pulmonary vascular congestion --Right-sided heart failure
  • Digoxin --Symptomatic left and/or right ventricular systolic dysfunction. --Controlling a rapid ventricular rate during AF, although it should not be considered a first-line drug for this indication
  • Beta blockers --Decrease heart rate and cardiac output at rest, causing a decrease in the transmitral gradient, pulmonary capillary wedge pressure, and mean pulmonary pressure. --Blunt the heart rate and cardiac output responses to exercise --Exercise capacity may not be increased by beta blockers but it is not reduced --In NYHA IV {exclude HF} AHA 2014: Class IIa 1. Heart rate control can be beneficial in patients with MS and AF and fast ventricular response. (Level of Evidence: C) Class IIb 1. Heart rate control may be considered for patients with MS in normal sinus rhythm and symptoms associated with exercise . (Level of Evidence: B)
  • Secondary prevention of rheumatic fever -Preventing repeated attacks of rheumatic fever may play a role in delaying the progression of MS {progressionresponse to turbulent blood flow through the rheumatically deformed valve}
  • Prevention of endocarditis The 2007 American Heart Association guidelines on the prevention of bacterial endocarditis recommended that only patients with the highest risk of the development of endocarditis receive antimicrobial prophylaxis—not MS--
  • Prevention of thromboembolism --The 2014 ACC/AHA valvular disease guidelines and 2008 Eighth ACCP consensus conference recommended long-term oral anticoagulation (target INR 2.5, range 2.0 to 3.0) in patients with MS who have a prior embolic event, left atrial thrombus, or paroxysmal, persistent, or permanent AF, since all forms of AF carry a similar risk for thromboembolism --The ACCP consensus conference suggested the addition of low-dose aspirin (50 to 100 mg/day) in patients who have an embolic event or have left atrial thrombus despite oral anticoagulation at a therapeutic INR. An alternative strategy is to adjust the oral anticoagulant dose to achieve a higher target INR (target INR 3.0, range 2.5 to 3.5) --The ACC/AHA guidelines suggested that oral anticoagulation may be considered in patients with severe MS, an enlarged left atrium>55mm, and spontaneous echo contrast, although the evidence was less well established {??bleeding}
  • Statin therapy The rates of decrease in mitral valve area and increase in mean transmitral gradient were lower in the statin group compared with the untreated group  Further study in randomized controlled trials is required
  • AF --Hemodynamically unstable immediate electrical cardioversion is indicated. --Hemodynamically stable patients controlling the ventricular rate (with a beta blocker without intrinsic sympathomimetic activity, calcium channel blocker [verapamil or diltiazem], or, less preferably, digoxin) and anticoagulation {2-3} --Cardioversion is not indicated before intervention unless unstable --Rate control strategy is generally preferred, with a rhythm control strategy, long-term anticoagulation is still required in most patients ----Substitution of vitamin K antagonists by new agents is not recommended, because specific trials in patients with VHD are not available
  • RFA --The 2006 ACC/AHA/ESC guidelines on AF concluded that catheter ablation is a reasonable alternative to pharmacologic therapy for the prevention recurrent AF in symptomatic patients with little or no left atrial enlargement. The presence of left atrial enlargement would exclude many patients with MS ----Surgical ablation should be considered in patients with symptomatic AF and may be considered in patients with asymptomatic AF, if feasible with minimal risk
  • Pregnancy --COP= 30-50% increase --During active labor, additional increases in cardiac output and stroke volume occur with each uterine contraction (additional 50 percent) --Following delivery, there is an abrupt increase in preload, resulting from the autotransfusion of uterine blood into the systemic circulation and to aortal caval decompression in the absence of a gravid uterus up to six weeks postpartum --To minimize medical treatment failures during pregnancy, women with MS should be evaluated before pregnancy: Symptomatic mitral stenosis (NYHA class II to IV) or severe pulmonary hypertension (pulmonary artery pressure >75 percent of systemic pressure) intervention pre
  • --Management: -Diuretic therapy for pulmonary congestion(safe) avoid hypovolemia (placental hypoperfusion). -If symptoms progress despite diuretic therapy, a beta blocker should be tried, beginning with very low doses. A cardioselective drug may be preferred. -fail  PMBV at experienced centers or surgical closed commissurotomy -Severe mitral stenosis at labor invasive hemodynamic monitoring with a right heart catheter is appropriate  goal pulmonary capillary wedge pressure of approximately 14 mmHg. Invasive hemodynamic monitoring should be continued in the immediate postpartum period because of large intravascular volume shifts {Cesarean section should be performed only for obstetric indications, better in patient on warfarin  for foetus} --Routine endocarditis prophylaxis is not necessary for either cesarean or vaginal delivery
  • + AF: --Hemodynamically unstable  electrical cardioversion is both safe and effective. If an antiarrhythmic drug is needed to maintain sinus rhythm  quinidine and procainamide are the drugs of choice. --Beta blockers are preferred for control of the ventricular rate. CCB (verapamil or diltiazem) are more likely to cause maternal hypotension, especially when given intravenously --Anticoagulation should be continued during pregnancy. Warfarin is typically avoided in the first trimester because of its known teratogenic effects, particularly between the sixth and ninth weeks.
  • NB. Warfarin+ pregnancy --Teratogenic effects: -Potentially teratogenic (low MW, cross placenta) Embryopathy , spontaneous abortion and stillbirth. -The teratogenic effect appears to be dose related, with doses less than 5 mg/day providing the highest margin of safety {regardless of INR} -most common bone and cartilage nasal and limb hypoplasia --CNS abnormalities (including optic atrophy, microcephaly, mental retardation, spasticity, and hypotonia) -Immaturity of fetal enzyme systems and the relatively low concentration of vitamin K-dependent clotting factors render the fetus more sensitive than the mother to the anticoagulant effects of warfarin  risk of hemorrhagic fetal death during vaginal delivery warfarin should be discontinued after 34 to 36 weeks of gestation -Preterm cesarean delivery may prevent hemorrhagic fetal death, and fresh frozen plasma should be administered to the neonate, mother -safe in lactation
  • --UFH (c): -Relative difficulty of maintaining a stable therapeutic response, the inconvenience of parenteral administration, and the complications of heparin-induced thrombocytopenia and bone demineralization in patients treated for more than seven weeks -Guided by APTT --LMW heparin (B): -Sustained, stable therapeutic response -Reduce the inconvenience of parenteral administration -Laboratory monitoring of the anticoagulant effect of LMW heparin is generally not performed in nonpregnant patients, but some authors recommend measuring anti- factor Xa levels four hours after injection in pregnant patients -Less likely to precipitate heparin-associated thrombocytopenia, unclear whether bone loss may be significantly reduced -American College of Obstetricians and Gynecologists has stated that LMW heparin can be considered in women who are candidates for prophylactic or therapeutic anticoagulation during pregnancy - Patients should be switched to subcutaneous unfractionated heparin about two weeks prior to the expected delivery; this will permit regional anesthesia for labor {epidural haematoma}
  • Mechanical prosthetic heart valves: --FDA  LMWH is not recommended for thromboprophylaxis in pregnant women with prosthetic heart valves. --However, other expert panels disagree, and the American College of Chest Physicians recommended that LMWH remain a therapeutic option in this setting
  • 2008 ACCP Guidelines One of three approaches for anticoagulation during pregnancy: --Aggressive adjusted-dose unfractionated heparin throughout the pregnancy; heparin is administered subcutaneously every 12 hours in doses adjusted to keep the mid-interval aPTT at least twice control or to attain an anti-Xa level of 0.35 to 0.70 U/mL. After a stable dose is achieved, the aPTT should be measured at least weekly. --Adjusted-dose subcutaneous LMW heparin therapy throughout the pregnancy in doses adjusted according to weight to achieve the manufacturer's recommended anti-Xa level four hours after subcutaneous injection. --Unfractionated or LMW heparin therapy (as above) until the thirteenth week, a change to warfarin until the middle of the third trimester, and then restarting unfractionated or low molecular weight heparin until delivery Heparin can be restarted 12 hours post-cesarean delivery and 6 hours post- vaginal birth, if no significant bleeding has occurred replaced with warfarin (stopping the heparin when the INR is therapeutic)
  • Other indications for AC in pregnancy Venous thromboembolism Atrial fibrillation associated with significant underlying heart disease Antiphospholipid antibody syndrome Heart failure, particularly in the presence of a ventricular thrombus Eisenmenger syndrome Paroxysmal nocturnal hemoglobinuria
  • AHA 2014 The patient and family should be sufficiently educated by the Heart Valve Team about all alternatives for treatment so that their expectations can be met as fully as possible using a shared decision- making approach.
  • Heart Valve Centers of Excellence 1) are composed of experienced healthcare providers with expertise from multiple disciplines; 2) offer all available options for diagnosis and management, including complex valve repair, aortic surgery, and transcatheter therapies; 3) participate in regional or national outcome registries; 4) demonstrate adherence to national guidelines; 5) participate in continued evaluation and quality improvement processes to enhance patient outcomes; and 6) publicly report their available mortality and success rates.
  • TECHNIQUE -- Transseptal puncture is used to gain access to the mitral valve from the left atrium. A single deflated balloon or a double-balloon is advanced from the venous circulation to the right atrium, across the interatrial septum to the left atrium, and across the stenotic mitral valve. Inflation and rapid deflation of the balloon opens the stenotic valve via separation of the fused commissures --TEE can guide the procedure  general anesthesia --Intracardiac echocardiography can delineate the extent of valvular deformity and may also be useful in visualizing several key steps cost, inability to accurately measure mitral valve area or adequately assess mitral regurgitation
  • --OUTCOMES: -Short-term: Excellent from 1.0 cm2 to approximately 2.0 cm2 Decrease in left atrial pressure and the transmitral pressure gradient, a reduction in pulmonary artery pressure, and an increase in cardiac output. An additional benefit is a reduction in left atrial stiffnessincrease in left atrial pump function in patients in sinus rhythm and an increase in left atrial reservoir function in those with atrial fibrillation -Long-term: Pulmonary vascular resistance declines and normalizes in many patients.
  • Predictors of adverse events (death, mitral valve surgery, and repeat PMBV): -Echocardiographic score >8, which was associated with lower success rates and smaller increases in mitral valve area -Increasing age (palliative in elderly with CI to surgery) -Prior surgical commissurotomy -NYHA functional class IV -Higher postprocedural pulmonary artery pressure -Preprocedural mitral regurgitation ≥2+ -Postprocedural mitral regurgitation ≥3+
  • --PMBV versus surgical commissurotomy: The outcome after PMBV was as good or better than after surgery in patients who are candidates for valvotomy. --Mitral valve replacement combined with TV repair may produce better outcomes in patients with severe MS and severe TR than PMBV
  • AHA 2014 IIb Percutaneous mitral balloon commissurotomy may be considered for symptomatic patients with mitral valve area greater than 1.5 cm2 if there is evidence of hemodynamically significant MS based on pulmonary artery wedge pressure greater than 25 mm Hg or mean mitral valve gradient greater than 15 mm Hg during exercise. (Level of Evidence: C) Mitral valve surgery and excision of the left atrial appendage may be considered for patients with severe MS (mitral valve area ≤1.5 cm2, stages C and D) who have had recurrent embolic events while receiving adequate anticoagulation. (Level of Evidence: C)
  • Noncardiac surgery --In symptomatic patients or in patients with systolic pulmonary artery pressure >50 mmHg, correction of MS— by means of PMC whenever possible—should be attempted before non-cardiac surgery if it is high risk. If valve replacement is needed, the decision to proceed before non- cardiac surgery should be taken with caution and individualized. --Asymptomatic patients with significant MS and a systolic pulmonary artery pressure <50 mmHg, non-cardiac surgery can be performed safely ----Control heart rate (particularly in MS), to avoid fluid overload as well as volume depletion and hypotension (particularly in AS)
  • Other valvular lesions --When either stenosis or regurgitation is predominant, management follows the recommendations concerning the predominant VHD --Interaction between the different valve lesions ex. associated MR may lead to underestimation of the severity of AS --Indications for intervention are based on global assessment of the consequences of the different valve lesions, i.e. symptoms or presence of LV dilatation or dysfunction --The decision to intervene on multiple valves should take into account the extra surgical risk --The choice of surgical technique should take into account the presence of the other VHD.
  • Thank you