Eduovisual
Cardiovascular
Mitral regurgitation: primary vs secondary etiology and management
— Primary MR: intrinsic valve pathology (myxomatous degeneration/MVP, rheumatic, endocarditis, flail leaflet, cleft, radiation, ergot/serotonin).
— Secondary (functional) MR: structurally normal leaflets; regurgitation results from LV/LA remodeling — ischemic cardiomyopathy with tethering, dilated cardiomyopathy, or atrial functional MR from chronic AF/HFpEF.
— New holosystolic apical murmur radiating to axilla in a previously asymptomatic outpatient on routine exam.
— Progressive dyspnea, orthopnea, or decreased exercise tolerance in a patient with known MVP, prior MI, or dilated CM.
— Acute pulmonary edema and hypotension days after inferior MI (papillary muscle rupture) or in IV drug user with fever (endocarditis with leaflet perforation).
— New AF in a middle-aged patient — often the first decompensation of chronic primary MR.
— Acute MR: normal-sized LA cannot accommodate volume → flash pulmonary edema, cardiogenic shock, often soft or absent murmur.
— Chronic MR: compensated by LA/LV dilation → patient asymptomatic for years; eventually decompensates with AF, PH, or HF.
Step 3 management: The single highest-yield outpatient decision is recognizing that asymptomatic severe primary MR with LVEF 30–60% or LVESD ≥40 mm is a Class I indication for surgery — do not wait for symptoms. For secondary MR, prioritize GDMT for HF first, then reassess MR severity before considering intervention.
— Often asymptomatic for years despite severe regurgitation — picked up by murmur on routine visit.
— Earliest symptom: exertional dyspnea or fatigue, often attributed to deconditioning.
— Palpitations from new atrial fibrillation are a frequent trigger for presentation and often herald hemodynamic decompensation.
— Late: orthopnea, PND, right-sided HF signs (edema, ascites) when pulmonary HTN develops.
— Sudden severe dyspnea, pink frothy sputum, hypotension.
— Classic stems: post-MI day 3–7 (papillary muscle rupture, usually posteromedial from RCA territory), IE with leaflet perforation, chordal rupture in MVP after exertion or trauma.
— Symptoms are those of the underlying cardiomyopathy: HFrEF symptoms (ischemic or non-ischemic) or HFpEF with AF (atrial functional MR).
— Patients often present with recurrent HF admissions despite GDMT.
— Prior rheumatic fever, strep infection in childhood, immigrant from endemic region → rheumatic MR (though MS more common).
— IV drug use, indwelling lines, recent dental/GU procedure → endocarditis.
— Mediastinal radiation (Hodgkin survivor) → radiation valvulopathy.
— Fen-phen, ergot, methysergide, cabergoline, MDMA → drug-induced valvulopathy (also tricuspid/pulmonic).
— Connective tissue disease (Marfan, Ehlers-Danlos, Loeys-Dietz) → MVP/flail leaflet.
— Prior MI, especially inferior or large anterior → ischemic functional MR.
Board pearl: A patient with severe chronic MR who develops new-onset AF or a drop in LVEF below 60% has crossed a surgical threshold even if "asymptomatic" — the heart is telling you it has decompensated. Document functional status carefully (DASI, 6MWT) because subjective denial of symptoms is common.
Key distinction: Acute MR → soft/short murmur + shock + clear lungs on CXR initially turning to flash edema; Chronic MR → loud holosystolic murmur + chronic LA/LV dilation on echo.
— Holosystolic, blowing murmur best heard at the apex, radiating to the left axilla (anterior leaflet pathology) or to the base/back (posterior leaflet pathology — can mimic AS).
— S3 gallop at apex reflects volume overload (not necessarily HF in MR — it's a marker of severe regurgitation).
— Soft S1, widely split S2 (early A2 from shortened LV ejection), P2 loud if pulmonary HTN.
— Apical impulse is displaced laterally and hyperdynamic in chronic severe MR.
— Mid-systolic click followed by late systolic murmur.
— Maneuvers: ↓ preload (standing, Valsalva strain) → click and murmur move earlier (closer to S1) and murmur lengthens. ↑ preload (squatting, passive leg raise) → click moves later, murmur shortens.
— Murmur may be soft, short, or absent because LA and LV pressures rapidly equalize.
— Tachycardia, hypotension, pulmonary rales, cool extremities — cardiogenic shock physiology.
— MR vs TR: TR increases with inspiration (Carvallo sign), MR does not.
— MR vs VSD: VSD murmur loudest at left lower sternal border with thrill; harsher quality.
— MR vs AS: AS radiates to carotids, has slow-rising pulse; MR radiates to axilla with sharp upstroke.
— MR vs HOCM: HOCM ↑ with Valsalva/standing (opposite of most murmurs); MR unchanged or softer.
— Brisk carotid upstroke (vs delayed in AS).
— Prominent v wave in JVP if severe TR coexists; large v wave on PCWP tracing in acute MR.
Board pearl: A patient with flash pulmonary edema and a barely audible apical murmur post-MI has acute papillary muscle rupture until proven otherwise — get bedside TTE/TEE immediately and call CT surgery. Do not wait for full diuresis.
— Chronic MR: left atrial enlargement (P mitrale — broad, notched P in lead II; biphasic P in V1 with deep negative terminal component), LVH with volume-overload pattern, and atrial fibrillation in up to 30–50% of severe chronic cases.
— Acute ischemic MR: ECG findings of recent MI (typically inferior).
— Chronic: cardiomegaly with LA enlargement (double density at right heart border, splaying of carina >70°, posterior LA bulge on lateral), pulmonary venous congestion late.
— Acute: normal heart size with florid pulmonary edema — a critical Step 3 clue.
— BNP/NT-proBNP: elevated levels in asymptomatic severe MR predict adverse outcomes and may push toward earlier surgical referral.
— Basic metabolic panel, CBC, troponin (if ischemic etiology suspected).
— Blood cultures × 3 if endocarditis on differential — before antibiotics if hemodynamically stable.
— TSH (high-output states, AF workup), HbA1c, lipid panel for cardiac risk profile.
— Confirms diagnosis, defines mechanism (primary vs secondary), quantifies severity, assesses LV size/function, LA size, pulmonary pressures.
— Severity parameters: vena contracta width ≥0.7 cm, effective regurgitant orifice area (EROA) ≥0.4 cm², regurgitant volume ≥60 mL, regurgitant fraction ≥50% = severe primary MR.
— Secondary MR uses lower thresholds (EROA ≥0.4 cm² OR ≥0.2 cm² per some guidelines) given different geometry.
Step 3 management: Every patient with a new MR murmur or unexplained dyspnea gets a TTE as the next step — not stress test, not CT, not cath. Repeat TTE intervals depend on severity: mild every 3–5 yr, moderate every 1–2 yr, severe asymptomatic every 6–12 months.
Key distinction: Acute MR with normal-sized heart on CXR but pulmonary edema is a giveaway — the LA hasn't had time to dilate.
— Indicated when TTE images are inadequate, mechanism is unclear, or pre-procedurally to plan repair vs replacement vs TEER (transcatheter edge-to-edge repair).
— Mandatory for suspected endocarditis with negative or equivocal TTE.
— Identifies flail leaflet, ruptured chordae, leaflet perforation, vegetations, prolapse segment (A1-A3, P1-P3) — essential for surgical planning.
— For patients with severe MR but no symptoms — assess exertional changes in MR severity, pulmonary artery systolic pressure, and LV contractile reserve.
— Exercise PASP >60 mmHg during stress in asymptomatic severe primary MR is a Class IIa indication for surgery.
— Also used to unmask symptoms in patients who claim to be asymptomatic.
— Gold standard for regurgitant volume and fraction quantification when echo is discordant or technically limited.
— Assesses myocardial fibrosis (LGE) — predicts outcomes, especially in secondary MR and post-MI patients.
— Confirms pulmonary HTN, measures PCWP, identifies large v waves (>2× mean PCWP suggests severe MR).
— Used when noninvasive data are discordant or before high-risk intervention.
— Required pre-operatively in patients >40 years, with CAD risk factors, or with suspected ischemic etiology to plan concomitant CABG.
— Ventriculography can grade MR (1–4+) but is now rarely needed.
— Pre-procedural planning for transcatheter mitral interventions (TEER, transcatheter mitral valve replacement).
Board pearl: When TTE shows "moderate" MR but the patient has severe symptoms or progressive LV dilation, the next step is TEE or cardiac MRI — discordance between symptoms and severity grading should prompt advanced imaging, not reassurance. Avoid premature closure.
— Stage A: at risk (MVP without MR, mild rheumatic changes).
— Stage B: progressive MR (mild–moderate, asymptomatic, normal LV).
— Stage C: asymptomatic severe MR. C1 = normal LV (EF >60%, LVESD <40 mm); C2 = LV decompensation (EF ≤60% OR LVESD ≥40 mm).
— Stage D: symptomatic severe MR.
— Symptomatic severe primary MR (Stage D) regardless of LV function.
— Asymptomatic severe primary MR with LVEF 30–60% or LVESD ≥40 mm (Stage C2).
— Asymptomatic severe primary MR undergoing other cardiac surgery (e.g., CABG, AVR).
— Asymptomatic severe MR with preserved LV if likelihood of successful repair >95% at a Comprehensive Valve Center and expected mortality <1%.
— Progressive LV dilation, new AF, or exercise PASP >60 mmHg.
— GDMT for HF is first-line: ARNI/ACEI/ARB, beta-blocker, MRA, SGLT2 inhibitor, diuretics. CRT if eligible (LVEF ≤35%, LBBB, QRS ≥150 ms).
— Only after maximally tolerated GDMT for ≥3 months should valve intervention be considered.
— TEER (MitraClip) is Class IIa for persistently symptomatic severe secondary MR with LVEF 20–50%, LVESD ≤70 mm, PASP ≤70 mmHg (COAPT trial criteria).
— Surgery for secondary MR has shown no mortality benefit and is reserved for select cases.
Step 3 management: The most testable trap is treating secondary MR like primary MR — sending an ischemic cardiomyopathy patient to mitral surgery before optimizing GDMT. Always ask: is the valve broken, or is the ventricle broken? Fix the ventricle first when it's secondary.
Key distinction: Surgery in primary MR is life-extending; in secondary MR, the underlying myopathy drives prognosis, and TEER only helps a carefully selected subset.
— No proven benefit from vasodilators, ACEI/ARB, or beta-blockers in asymptomatic patients with normal LV function and preserved BP. This is a frequent Step 3 distractor.
— Treat comorbid HTN aggressively per standard targets — uncontrolled HTN worsens MR.
— Endocarditis prophylaxis is not routinely indicated for native MR alone (only for prior IE, prosthetic valves, certain congenital lesions, or cardiac transplant valvulopathy).
— Diuretics (loop diuretics) for congestion.
— ACEI/ARB for afterload reduction if symptomatic with HTN or reduced LVEF.
— Beta-blockers and ivabradine can be helpful in MVP with sympathetic overactivity.
— ARNI (sacubitril/valsartan) preferred over ACEI/ARB.
— Beta-blocker: carvedilol, metoprolol succinate, or bisoprolol — titrate to maximum tolerated dose.
— MRA: spironolactone or eplerenone if K <5.0 and eGFR >30.
— SGLT2 inhibitor: dapagliflozin or empagliflozin — benefit independent of diabetes.
— Loop diuretic for volume management; titrate to euvolemia.
— Hydralazine + isosorbide dinitrate in Black patients with persistent symptoms or as ACEI/ARB alternative.
— Anticoagulation per CHA₂DS₂-VASc; valvular AF (rheumatic MS or mechanical valve) requires warfarin, but MR alone is "non-valvular" — DOACs are acceptable.
— Rate vs rhythm control individualized; rhythm control increasingly favored in HF.
— IV nitroprusside or nitroglycerin for afterload reduction (if BP allows).
— IV diuretics, inotropes (dobutamine) if cardiogenic shock.
— Intra-aortic balloon pump as bridge to surgery in acute ischemic MR.
Board pearl: Vasodilator therapy is not first-line for asymptomatic primary MR — this is a classic wrong answer. The right answer is serial echo surveillance and timely surgical referral when thresholds are met.
— Repair > replacement for primary MR — preserves subvalvular apparatus, lower operative mortality, no anticoagulation, better long-term LV function.
— Posterior leaflet prolapse repair has >95% success rate at Comprehensive Valve Centers.
— Techniques: triangular/quadrangular resection, neochord placement, annuloplasty ring.
— Reserved for valves not amenable to repair (extensive rheumatic disease, severe calcification, complex bileaflet pathology).
— Mechanical valve: durable but requires lifelong warfarin (INR 2.5–3.5 for mitral mechanical valves) — DOACs contraindicated.
— Bioprosthetic valve: preferred age >65–70, women planning pregnancy, contraindications to anticoagulation; 10–15 year durability.
— Primary MR: Class IIa for symptomatic severe MR with prohibitive surgical risk and favorable anatomy.
— Secondary MR: Class IIa per COAPT trial criteria — symptomatic despite maximal GDMT, LVEF 20–50%, LVESD ≤70 mm, PASP ≤70 mmHg.
— Lower efficacy than surgery but lower morbidity; performed via femoral vein/transseptal approach.
— Emerging option; currently FDA-approved for valve-in-valve in failed bioprostheses and valve-in-ring procedures.
— Papillary muscle rupture, acute IE with hemodynamic instability, traumatic chordal rupture → emergent surgical repair/replacement.
— IABP, inotropes, afterload reduction as bridge.
— Maze/PVI ablation for AF at time of mitral surgery.
— LAA exclusion reduces stroke risk.
— Concomitant CABG if significant CAD.
CCS pearl: In simulated cases of acute papillary muscle rupture post-MI, the winning sequence is: stabilize (intubate, IABP, pressors/inotropes) → emergent TEE → cardiothoracic surgery consult → OR within hours. Delaying for "medical optimization" loses points and patients.
— Higher prevalence of degenerative MR and mitral annular calcification (MAC), often with mixed MR/MS physiology.
— Frailty assessment is critical: gait speed, grip strength, comprehensive geriatric assessment influence surgical vs transcatheter decisions.
— STS risk score >8% or high frailty score → favor TEER over surgery in selected anatomies.
— Bioprosthetic valves preferred to avoid anticoagulation-related bleeding.
— Cognitive screening (Mini-Cog, MoCA) before complex valve decisions — informs surrogate decision-making and shared decision-making process.
— CKD is an independent predictor of mortality after both surgery and TEER.
— Contrast-induced nephropathy risk: minimize contrast during pre-procedural CT/angiography; consider CO₂ angiography or low-volume protocols.
— Anticoagulation: warfarin remains required for mechanical valves regardless of CKD; for AF with bioprosthetic or native valve MR, apixaban is preferred in CKD (including dialysis per current ACC guidance).
— Dose-adjust diuretics; monitor for over-diuresis worsening renal function.
— Hyperkalemia from MRA + ACEI/ARB + ARNI common — monitor weekly during titration in eGFR <45.
— Cirrhosis with portal HTN may have high-output state masquerading as functional MR.
— Cardiac cirrhosis from right HF (from severe pulmonary HTN due to MR) — distinguishes etiology, alters prognosis.
— Coagulopathy and thrombocytopenia complicate anticoagulation decisions; consult hepatology before mechanical valve.
— Warfarin metabolism unpredictable in cirrhosis — TEER may be safer than surgery in Child-Pugh B/C.
— Beta-blockers and diuretics may precipitate falls in frail elderly — review at every visit.
Step 3 management: For the frail 82-year-old with severe symptomatic primary MR and STS >8%, the right answer is referral to a multidisciplinary Heart Valve Team for TEER evaluation, not surgery and not "continue medical therapy." Shared decision-making documentation is essential.
— Physiologic ↑ in plasma volume and ↓ in SVR is generally well tolerated in mild–moderate MR; severe MR carries higher risk.
— mWHO classification: mild MR = class I; severe MR with symptoms or LV dysfunction = class III–IV.
— Preconception counseling: optimize MR before pregnancy; severe symptomatic MR should undergo repair before conception when feasible.
— Avoid ACEI/ARB/ARNI/MRA/SGLT2i in pregnancy (teratogenic/fetal harm).
— Safe options: hydralazine, methyldopa, labetalol, loop diuretics (cautiously), digoxin.
— Anticoagulation in pregnancy with mechanical mitral valve is complex: warfarin (especially >5 mg/day) → fetal embryopathy first trimester; LMWH with anti-Xa monitoring is often preferred in first trimester, then warfarin in second/third, switch to LMWH or UFH near delivery.
— Delivery: vaginal delivery with epidural and assisted second stage preferred; C-section for obstetric indications.
— Causes: cleft mitral valve (often with AV canal defect, Down syndrome), isolated MVP, rheumatic disease in endemic regions, endocarditis, Kawasaki-associated.
— Repair strongly preferred — preserves growth potential and avoids prosthesis size mismatch.
— Benign in most; risks include progression to severe MR, AF, IE (low risk without prior IE), and rarely sudden cardiac death (associated with bileaflet MVP, female sex, complex ventricular arrhythmias).
— No exercise restriction unless severe MR or arrhythmia.
— Severe MR with LV dilation → restrict to low-intensity competitive sports per AHA/ACC eligibility guidelines.
Board pearl: A pregnant patient on an ACEI for HF or HTN in the setting of MR must be switched immediately — usually to hydralazine + nitrates or labetalol. Counsel about contraception in any reproductive-age woman started on ACEI/ARB/ARNI/SGLT2i.
— Occurs in 30–50% of severe chronic MR; often the first sign of decompensation.
— Triggers further LA dilation, worsens MR, increases stroke risk.
— Anticoagulation per CHA₂DS₂-VASc; rhythm control increasingly favored.
— Group 2 PH from chronic LA pressure elevation.
— PASP >50 mmHg at rest or >60 mmHg with exercise is a surgical trigger in asymptomatic severe MR.
— Persistent PH after valve correction predicts worse outcomes — argues for earlier intervention.
— LV dilation → eccentric hypertrophy → eventual systolic dysfunction.
— Once LVEF <60% in severe primary MR, irreversible LV damage may already be occurring (the EF appears "preserved" because of the low-impedance LA pathway — true LV function is worse than EF suggests).
— MVP with MR has elevated baseline risk; antibiotic prophylaxis only for prior IE, prosthetic valves, repaired congenital lesions with residual defects, or post-transplant valvulopathy.
— Rare but documented in arrhythmic MVP — bileaflet prolapse, mitral annular disjunction, papillary muscle fibrosis (LGE on MRI), complex VEs.
— From AF or LA thrombus in severely dilated LA even without AF.
— AV block requiring pacemaker (5–10%), stroke (1–2%), atrial fibrillation (30–40%), reoperation for failed repair, systolic anterior motion (SAM) after repair causing LVOT obstruction.
— Residual MR, single leaflet device attachment, mitral stenosis from over-clipping, device embolization.
Key distinction: "Preserved" LVEF in severe primary MR is misleading — the LV ejects partly into the low-pressure LA. An EF of 55% in severe MR is borderline-low, and waiting until EF <50% means you're operating on a damaged ventricle. Operate at the 60% threshold.
— Acute severe MR with pulmonary edema or cardiogenic shock — papillary muscle rupture, IE with leaflet destruction, chordal rupture.
— Hemodynamic instability requiring vasopressors, inotropes, IABP, or mechanical circulatory support.
— Acute MR complicating MI — needs emergent cath, IABP, and CT surgery.
— New diagnosis of severe MR with symptoms (NYHA III–IV).
— Newly decompensated chronic MR with HF symptoms or new AF.
— Suspected endocarditis with valve involvement (also ID consult and CT surgery if hemodynamically significant).
— Stage C2 (asymptomatic with LV decompensation) primary MR — valve team referral.
— All Stage D and C2 primary MR.
— Secondary MR persistent despite optimized GDMT for ≥3 months.
— Complex anatomy (bileaflet prolapse, prior cardiac surgery, MAC, prohibitive surgical risk).
— Pregnant patient with severe MR.
— Symptomatic severe primary MR.
— Asymptomatic severe primary MR meeting Class I or IIa criteria.
— Concomitant CAD requiring CABG.
— Acute severe MR — emergent.
— Stage A (at-risk) and Stage B (progressive) MR.
— Stable Stage C1 (asymptomatic severe with preserved LV) with reliable follow-up.
— Patient education, BP control, AF anticoagulation, surveillance echo.
— Acute pulmonary edema with hemodynamic instability → ICU, intubate if needed, IV nitroprusside or IV NTG + IV furosemide, urgent TTE/TEE.
— Stable symptomatic worsening → telemetry floor for diuresis, GDMT optimization, planned echo.
CCS pearl: Always order cardiology consult and echo in the first action block for any new severe MR or acute MR presentation. Delay in advancing the clock without these orders loses critical points. Document goals of care for elderly or frail patients early.
— Systolic murmur, but crescendo-decrescendo, RUSB, radiating to carotids, with delayed/diminished carotid upstroke (pulsus parvus et tardus).
— Symptoms: angina, syncope, dyspnea.
— Echo: high transvalvular gradient, calcified aortic valve.
— Holosystolic murmur at LLSB, increases with inspiration (Carvallo).
— JVP with large v wave, pulsatile liver, peripheral edema.
— Often secondary to RV dilation from pulmonary HTN (which itself may be from MR).
— Harsh holosystolic murmur at LLSB with thrill.
— Post-MI VSD (also days 3–7, anterior MI from LAD) can mimic acute papillary muscle rupture clinically — TEE differentiates.
— Systolic murmur at LLSB that increases with Valsalva and standing, decreases with squatting (opposite of MR).
— Often has associated MR from systolic anterior motion (SAM) of mitral valve.
— Diastolic murmur, not systolic — but coexists with MR in rheumatic disease ("mixed mitral valve disease").
— Opening snap + low-pitched diastolic rumble.
— Mid-systolic click ± late systolic murmur; benign in most.
— MR (papillary muscle rupture): new apical murmur, pulmonary edema, V wave on PCWP.
— VSD: new harsh LLSB murmur with thrill, oxygen step-up RA → RV on right heart cath.
— Free wall rupture: tamponade physiology, PEA arrest — usually fatal.
Board pearl: When a post-MI patient develops a new murmur and shock, the bedside swan or oxygen step-up can distinguish acute MR (giant v wave) from VSD (step-up at RV) — but in practice, TEE is the diagnostic test of choice and is faster, safer, and definitive.
— May present with dyspnea and pulmonary edema mimicking acute MR; functional MR often coexists.
— TTE clarifies relative contributions of LV dysfunction vs valvular regurgitation.
— Can cause acute ischemic MR (papillary muscle dysfunction without rupture) and flash pulmonary edema.
— Always check ECG and troponin in new dyspnea + murmur.
— Dyspnea, hypoxia, tachycardia — but clear lungs, RV strain on echo, no apical murmur.
— Dyspnea + bilateral infiltrates — but fever, leukocytosis, no LA enlargement on CXR.
— Wedge pressure normal vs elevated in MR.
— Right HF signs with preserved LV function — Kussmaul sign, pericardial knock, calcified pericardium on imaging.
— Mimics HFpEF with elevated filling pressures; often has secondary MR from atrial dysfunction.
— Clues: low voltage on ECG + thick walls on echo (amyloid), LGE patterns on cardiac MRI, monoclonal gammopathy workup (SPEP, free light chains, urine immunofixation).
— Severe anemia, thyrotoxicosis, AV fistula, beriberi — can produce systolic flow murmurs that mimic MR but resolve when underlying state corrected.
— Common in young patients, pregnancy, fever — soft, early-mid systolic, no radiation, normal exam otherwise.
— Dyspnea and palpitations without cardiac pathology — but cardiac exam, ECG, echo are essential before this diagnosis.
Key distinction: Distinguishing functional MR from primary MR with HF changes management entirely — functional MR responds to GDMT; primary MR with HF needs valve intervention. Always identify the mechanism on TEE before committing to a treatment pathway.
— Aspirin 81 mg daily + 3 months of warfarin (INR 2–3) or DOAC post-repair per institutional protocol (warfarin still preferred by many centers).
— Lifelong aspirin if no other anticoagulation indication.
— Continue beta-blocker if on it; ACEI if LV dysfunction persists.
— Warfarin (INR 2–3) for 3–6 months, then transition to aspirin 81 mg daily lifelong.
— DOACs can be used after 3 months in stable patients per recent guidelines, but warfarin preferred initially.
— Lifelong warfarin (INR 2.5–3.5) — DOACs are contraindicated.
— Add aspirin 81 mg if low bleeding risk and high thromboembolic risk.
— Patient must understand the implications: bleeding precautions, INR monitoring, food/drug interactions, contraception, pregnancy planning.
— DAPT (aspirin + clopidogrel) for 1–6 months, then aspirin alone.
— Continue full GDMT for secondary MR — TEER does not replace medical therapy.
— Strict BP control (<130/80 if tolerated).
— Lipid management per ASCVD risk; statin if indicated.
— Smoking cessation, weight management, diabetes control.
— Annual influenza, pneumococcal series, COVID-19 boosters (especially post-surgery).
— Antibiotic prophylaxis for dental procedures involving gingival manipulation in patients with prosthetic valves, prior IE, repaired congenital heart disease with residual defects, or transplant valvulopathy.
— Excellent oral hygiene is more important than prophylactic antibiotics.
— Native MR alone does NOT warrant prophylaxis — a frequent wrong answer.
— Use CHA₂DS₂-VASc; DOACs preferred (this is "non-valvular AF").
Step 3 management: A patient discharged after MVR with a mechanical valve must leave with warfarin started, bridging plan (LMWH/UFH) until INR therapeutic, INR clinic follow-up scheduled within 1 week, and patient education documented. Missing any element is a transition-of-care failure.
— Mild MR (Stage B): every 3–5 years.
— Moderate MR (Stage B): every 1–2 years.
— Severe MR (Stage C1): every 6–12 months, with clinical assessment at each visit.
— Any change in symptoms or exam → immediate echo, regardless of last interval.
— TTE at 30 days, 6 months, and 12 months post-repair/replacement, then annually.
— TEER: TTE at 30 days, 6 months, annually thereafter.
— Symptoms: NYHA class, exercise tolerance, weight changes, orthopnea.
— Vital signs, BP control, heart rate (especially if AF).
— Anticoagulation: INR every 4 weeks once stable (mechanical valves), more often if unstable.
— Lab monitoring: BMP, BNP, hemoglobin (warfarin can mask GI bleed).
— Phase II cardiac rehab post-surgery or post-TEER — improves functional capacity, QoL, and adherence.
— Aerobic exercise tailored to functional status; resistance training after wound healing.
— Recognize HF symptoms: weight gain >3 lb in 3 days, increasing dyspnea, edema.
— Daily weights and sodium <2 g/day in HF.
— Dental hygiene; alert dentist to valve disease/prosthesis.
— Pregnancy planning for women of reproductive age — preconception cardiology consult.
— Contraception counseling if on teratogenic meds (ACEI/ARB/ARNI/SGLT2i/warfarin).
— Post-sternotomy: no driving for 4–6 weeks, no heavy lifting (>10 lb) for 6–8 weeks.
— Post-TEER: typically resume normal activity in 1–2 weeks.
Board pearl: A patient with severe asymptomatic MR who refuses surveillance echo is at risk for silent LV decompensation. Document shared decision-making; consider stress testing or BNP as adjuncts. Loss to follow-up is the single most common preventable cause of late surgical failure.
— Must include: surgical mortality estimate (STS score), risk of stroke, pacemaker, reoperation, infection, transfusion, bleeding, and the specific trade-off between repair durability and TEER's lower upfront morbidity but lower efficacy.
— For mechanical valves, explicit discussion of lifelong warfarin, INR monitoring burden, pregnancy implications, and bleeding risk — failure to document this is a malpractice landmine.
— Use validated tools (frailty index, STS score) and discuss in the context of goals of care.
— Avoid the "ageism" trap: chronological age alone should not exclude evaluation — but futile interventions in advanced frailty/dementia should be honestly discussed.
— Involve palliative care early for symptomatic severe MR in patients ineligible for intervention.
— Confirm decisional capacity at each major decision point; engage healthcare proxy if impaired.
— Document advance directives, POLST, and code status before high-risk surgery.
— Post-discharge anticoagulation errors after mechanical MVR are a leading cause of readmission and death — anticoagulation reconciliation, bridging plan, INR clinic appointment within 1 week, and written patient instructions must be in place.
— Medication reconciliation: stopped beta-blockers, restarted ACEI/ARB, diuretic dosing — verify at discharge and at first follow-up (within 7–14 days).
— Communication to PCP within 48–72 hours of discharge.
— Avoid premature closure: a "moderate MR" label can mask progressive disease — repeat imaging when clinical picture changes.
— Time-out and pre-procedural verification for TEER, including correct anatomy and device size.
— Failure to counsel a prosthetic valve patient about IE prophylaxis is a documented malpractice issue.
— Counsel about syncope risk if applicable; report to DMV per state law if recurrent syncope.
— Suspected IV drug use causing endocarditis triggers public health considerations; coordinate with addiction medicine — do not discharge without an MOUD plan if opioid use disorder is identified.
Step 3 management: The classic Step 3 vignette — patient discharged on warfarin post-mechanical MVR without INR clinic follow-up readmits with valve thrombosis — is preventable. The correct answer to "next best step at discharge" is always arrange anticoagulation monitoring + scheduled follow-up + documented patient education.
— Marfan, Ehlers-Danlos, Loeys-Dietz, osteogenesis imperfecta, ADPKD, pectus excavatum, scoliosis, straight back syndrome.
— Vena contracta ≥0.7 cm.
— EROA ≥0.4 cm².
— Regurgitant volume ≥60 mL.
— Regurgitant fraction ≥50%.
— Systolic flow reversal in pulmonary veins.
Board pearl: When a vignette mentions MVP + sudden cardiac death in a young woman + complex ventricular ectopy, think arrhythmic mitral valve prolapse with mitral annular disjunction — emerging entity requiring MRI for fibrosis assessment and possible ICD in select cases.
"60yo M with chronic MVP, denies symptoms; echo shows severe MR, LVEF 58%, LVESD 42 mm. Next step?"
→ Mitral valve repair (Class I) — the LV is already decompensating.
"Day 5 post-inferior MI, new apical holosystolic murmur, BP 80/50, pulmonary edema on CXR."
→ Bedside TEE + IABP + emergent surgery (papillary muscle rupture).
"55yo with ischemic CM, EF 30%, severe functional MR, NYHA III on max GDMT for 4 months."
→ TEER (MitraClip) per COAPT criteria.
"62yo with severe MR finds new-onset AF on routine ECG, denies symptoms."
→ Refer for mitral valve repair (Class IIa) — new AF is a surgical trigger.
"Murmur becomes earlier and longer with Valsalva."
→ MVP (decreased preload → click moves earlier).
"Pregnant woman with MR on lisinopril."
→ Discontinue ACEI immediately, switch to hydralazine/labetalol.
"Asymptomatic moderate MR with preserved LV — best therapy?"
→ Serial echo every 1–2 years, BP control — NOT ACEI prophylactically.
"Mitral mechanical valve, recent stroke despite INR 2.1."
→ INR target is 2.5–3.5 for mitral mechanical; uptitrate warfarin and add low-dose aspirin.
"Patient with MVP and trivial MR before dental cleaning — antibiotics?"
→ No prophylaxis (native MR alone doesn't qualify).
"Asymptomatic severe MR, normal LV — next echo when?"
→ 6–12 months.
Key distinction: Step 3 emphasizes management decisions over diagnosis. Most stems already give the echo data; the question is what to do next — surveillance, surgery, GDMT, TEER, or anticoagulation. Anchor on stage (A–D), mechanism (primary vs secondary), and symptom status.
The single core teaching: in primary MR, the valve is broken and earlier mitral valve repair at well-defined LV thresholds (EF ≤60% or LVESD ≥40 mm) saves lives, while in secondary MR, the ventricle is broken and optimized GDMT comes first with TEER reserved for COAPT-eligible patients who remain symptomatic.
Board pearl: Three numbers win most MR questions on Step 3: EF 60%, LVESD 40 mm, and surveillance every 6–12 months for severe asymptomatic MR. If you can recite those, plus distinguish primary from secondary mechanism, you can answer the majority of board stems on this topic with confidence and avoid the classic trap of treating functional MR as if it were degenerative.