CONTENTS
- Aortic stenosis
- Aortic regurgitation
- Mitral stenosis
- Mitral regurgitation
- Tricuspid regurgitation
- Acute prosthetic valve dysfunction
- Complications of percutaneous valvular procedures
causes of aortic stenosis
general epidemiology
- Aortic stenosis is the most common valvular disorder.
- Severe AS is present in ~3% of patients >75 years old. (Gaggin 2021)
causes of AS
- Bicuspid valve (often presents ~50s-60s):
- A bicuspid aortic valve is a congenital lesion seen in 1-2% of the population.
- A bicuspid valve is associated with various aortic pathologies (aortic stenosis, aortic regurgitation, aortic dissection, aortic coarctation, aortic valve endocarditis, and aortic aneurysm).
- Age-related calcific AS (often presents 60s-80s):
- This is histologically and pathologically similar to atherosclerotic coronary artery disease, with similar risk factors (diabetes, smoking, hypertension, male gender, age).
- Rheumatic heart disease:
- Usually presents in the 30s-50s. (Sadhu 2023)
- It almost always also involves the mitral valve.
- Mediastinal radiation for lymphoma, breast, or esophageal cancer (risk increased if >30 Gray of radiation exposure; usually presents 15-20 years after exposure; can cause combined AS and AR). (Griffin 2022)
symptoms of aortic stenosis
typical progression of chronic aortic stenosis
- [0] Asymptomatic:
- ⚠️ Symptoms are usually absent until AS is severe.
- [1] Anginal chest pain:
- Angina may occur without coronary disease (due to left ventricular hypertrophy that out-strips the ability of coronary arteries to provide sufficient blood flow).
- (Of course, this needs to be differentiated from angina caused by progressive or unstable coronary artery disease.)
- Traditional prognosis without intervention: 5-year mean survival.
- [2] Exertional syncope:
- This usually reflects aortic stenosis causing a flow-limiting lesion, which prevents the patient from augmenting their cardiac output with exercise. However, it may also occur due to arrhythmia.
- Traditional prognosis without intervention: 3-year mean survival.
- [3] Heart failure (dyspnea, orthopnea, flash pulmonary edema).
- Traditional prognosis without intervention: Associated with a 2-year mean survival.
- [4] Atrial fibrillation:
- AF is poorly tolerated due to diastolic dysfunction.
- Traditional prognosis without intervention: 6-month mean survival.
other clinical aspects
- Heyde syndrome: gastrointestinal bleeding due to arteriovenous malformations (because the aortic valve chews up large multimers of von Willebrand factor, thereby impairing coagulation).
bedside evaluation of aortic stenosis
vital signs
- BP:
- Blood pressure is usually within normal limits.
- Systolic Bp >200 mm largely excludes severe AS.
- Pulse pressure is narrow.
- Tachypnea and hypoxemia may be seen.
auscultation
- AS causes a coarse systolic ejection murmur.
- Relationship to severity:
- More severe → murmur peaks later and obliterates S2.
- Low cardiac output → murmur gets quieter.
ECG
- LVH is seen in most patients with severe AS.
- LAA is common.
- LBBB is common. In advanced-stage disease, calcium from the valve may impinge on the conduction system and cause a complete heart block.
echocardiographic classification of aortic stenosis
[stage A] asymptomatic, mild AS
- Aortic Vmax 2-2.9 m/s.
- Mean pressure gradient <20 mm.
[stage B] asymptomatic, moderate AS
- Aortic Vmax 3-3.9 m/s.
- Mean pressure gradient 20-39 mm.
[stage C1] asymptomatic severe AS w/ preserved EF
- Severe AS: Aortic valve area <1 cm2 (or AVA index <0.6 cm2/m2).
- Aortic Vmax >4 m/s or mean pressure gradient >40 mm.
- LV ejection fraction is normal.
- (Very severe if Vmax >5 m/s, pressure gradient >60 mm.)
[stage C2] asymptomatic severe AS w/ reduced EF
- Severe AS: Aortic valve area <1 cm2 (or AVA index <0.6 cm2/m2).
- Aortic Vmax >4 m/s or mean pressure gradient >40 mm.
- LV ejection fraction is <50%.
[stage D1] symptomatic severe high-gradient AS
- Severe AS: Aortic valve area <1 cm2 (or AVA index <0.6 cm2/m2) but may be larger with mixed AS and AR.
- Aortic Vmax >4 m/s or mean pressure gradient >40 mm.
- (Symptoms may include dyspnea, angina, or exertional (pre)syncope.)
[stage D2] symptomatic severe low-flow, low-gradient AS with reduced LVEF
- Severe AS:
- Aortic valve area <1 cm2.
- AVA index <0.6 cm2/m2.
- Low flow:
- LV ejection fraction is <50%.
- SVi (stroke volume index) <35 ml/m2.
- Low gradient:
- Resting aortic Vmax <4 m/s.
- Mean pressure gradient <40 mm.
- Dobutamine stress echo: aortic valve area remains low (<1 cm2) even after the Vmax increases to >4 m/s. This excludes two possibilities:
- [i] Pseudo-severe AS (poor aortic valve opening secondary to low cardiac output; in this scenario, the valve area will increase to >1 cm2).
- [ii] Lack of contractile reserve: if dobutamine is unable to increase the Vmax >4 m/s, this indicates underlying myocardial failure; surgical valve replacement may not help. (Bagchi 2025)
- Clinical implication: augmentation of Vmax >4 m/s without an increase in valve area suggests benefit from valve replacement. (Bagchi 2025)
- (Symptoms may include dyspnea, angina, or exertional (pre)syncope.
[stage D3] symptomatic severe low-gradient AS with normal ejection fraction (paradoxical low-flow severe AS)
- Reflects profound diastolic failure due to LVH, with a small LV chamber size and low stroke volume.
- Severe AS: Aortic valve area <1 cm2 (or AVA index <0.6 cm2/m2).
- Low flow: SVi (stroke volume index) <35 ml/m2.
- Low gradient: Resting aortic Vmax <4 m/s or mean pressure gradient <40 mm.
- LV ejection fraction is preserved (>50%).
- (Symptoms may include dyspnea, angina, or exertional (pre)syncope.)
management of aortic stenosis
[1/3] management of precipitating factors
- Aortic stenosis is always chronic. Therefore, its acute presentation generally results from an acute precipitating factor. Identifying and reversing this factor may be essential to treatment.
- Potential precipitants may include:
- Arrhythmias (especially atrial fibrillation).
- Any cause of systemic vasodilation (e.g., sepsis, pregnancy, fever).
- Acute volume shifts (e.g., in the context of surgery).
- Hypertension.
- Myocardial ischemia (including caused by anemia).
- Pulmonary embolism.
- Medications (e.g., beta-blockers).
- Hypovolemia.
- Thyrotoxicosis.
- Renal failure. (35912478, 39663714)
[2/3] hemodynamic stabilization
- [1] Respiratory support for acute cardiogenic pulmonary edema:
- Noninvasive ventilation is indicated for acute cardiogenic pulmonary edema (BiPAP or CPAP).
- Intubation is often avoided if possible since it may cause acute hemodynamic deterioration.
- [#2a] Afterload reduction to target a MAP of ~65-70 mm (if MAP >> 70 mm):
- The UNLOAD trial evaluated 25 patients with EF <35%, severe AS, CI <2.2, and no inotropes/pressors. Treatment with nitroprusside to target a MAP of 65-70 was effective in improving cardiac function. (12724481 📄)
- Avoid hypotension, as this may impair coronary perfusion (often tenuous in patients with aortic stenosis). (38631792)
- [#2b] Vasopressor support (if MAP <60 mm)
- Traditional teaching was to use a pure alpha-agonist because the LV afterload was fixed (and due to the stenotic aortic valve). However, this isn't physiologically true. The LV afterload is a sum of the valve plus downstream vascular resistance.
- Vasopressor selection could probably be similar to other patients in cardiogenic shock (e.g., norepinephrine as a default agent).
- [#3] Maintain sinus rhythm if possible and avoid extremes of heart rate:
- Patients with severe AS have diastolic dysfunction, so they may tolerate AF poorly.
- Tachycardia may be poorly tolerated (inadequate diastolic filling time).
- Bradycardia may be poorly tolerated (stroke volume is relatively capped, so the cardiac output will fall). (Bagchi 2025)
- [#4] Diuresis for management of pulmonary edema:
- If the LVEDP is substantially elevated, diuresis won't cause hypotension.
- Patients with cardiogenic pulmonary edema should be diuresed. (15345490)
- However, the LV is preload-dependent, so aggressive diuresis may not be tolerated well.
- [#5] Inotropic support:
- This might be helpful for patients with reduced EF, especially if they fail to respond to interventions #1-4 and have no other treatment options.
- However, inotropic therapy isn't generally desirable in aortic stenosis. It carries risks, including aggravating myocardial ischemia and causing atrial or ventricular arrhythmias. (39735779)
- [#6] Mechanical circulatory support:
- [i] IABP can reduce afterload and improve coronary perfusion. (38631792) One small study demonstrated the ability of IABP to increase mean cardiac output from 1.77 L/min/m2 to 2.18 L/min/m2. (20962337)
- [ii] Impella is relatively contraindicated for aortic valve area <0.6 cm2 (it may not fit, or it may occlude the valve). For patients with severe LVH and a small ventricle cavity, it may be challenging to maintain a safe Impella position within the ventricle.
[3/3] valvular interventions
- BAV (balloon aortic valvuloplasty):
- This produces short-lived and modest clinical improvement.
- Indications for BAV may include:
- [1] Bridge to SAVR/TAVR in unstable patients with severe AS.
- [2] Palliative procedure.
- BAV is contraindicated in patients with combined aortic stenosis plus aortic regurgitation.
- Outcomes with BAV alone are poor.
- The ability to perform an urgent TAVR in many patients may make BAV obsolete. However, BAV could still be useful for selected patients as a bridge to TAVR (e.g., in the context of acute infection).
- SAVR/TAVR (surgical or transcatheter aortic valve replacement):
- Rough indications:
- Symptomatic severe AS.
- Asymptomatic severe AS and EF<50%.
- Asymptomatic, very severe AS (velocity >5 m/s) and low surgical risk.
- Asymptomatic, severe AS with decreased exercise tolerance or an exercise fall in Bp.
- Symptomatic, low-flow/low-gradient AS with reduced EF and a positive dobutamine stress study (stage D2 above).
- TAVR vs. SAVR:
- TAVR may be a superior option for patients at high risk of surgical complications. TAVR is rapidly becoming the default therapy for most patients.
- Due to longer valve longevity, SAVR might be a better option for younger patients.
- Sometimes, technical issues may prevent TAVR (e.g., extensive annular calcification may increase the risk of paravalvular leak, heart block, or aortic annular rupture). (Sadhu 2023)
- Timing:
- SAVR usually isn't done emergently.
- TAVR may be done more urgently. Registries show that TAVR outcomes for patients in active cardiogenic shock are relatively favorable.
- Rough indications:
pathophysiology
- Myocardial ischemia: LV hypertrophy leads to a tendency to develop myocardial ischemia (even with normal coronary arteries).
- Diastolic dysfunction: LVH leads to diastolic dysfunction. Subsequently, atrial fibrillation or reduced preload can impair diastolic filling.
causes of aortic regurgitation
causes of acute AR
- Endocarditis (leaflet perforation and/or flail).
- Prosthetic valve failure: This usually progresses gradually. However, dehiscence and paravalvular leaks can deteriorate rapidly.
- Iatrogenic:
- Status post balloon aortic valvuloplasty.
- Paravalvular leak after TAVR.
- A complication of left heart catheterization (rare).
- Blunt chest trauma.
- Aortic dissection via various mechanisms:
- Annular dilation.
- Direct extension of the dissection causes leaflet prolapse.
- Dissection flap interfering with leaflet closure.
- Uncommon:
- Spontaneous leaflet rupture.
- Acute rheumatic fever.
causes of chronic AR
- Dilation of the aortic valve annulus:
- Hypertensive aortic dilation.
- Marfan disease.
- Syphilis.
- Aortitis:
- Takayasu arteritis.
- Giant cell arteritis.
- Ankylosing spondylitis.
- Lupus.
- Aortic aneurysm of another etiology (e.g., familial).
- Bicuspid aortic valve (may cause combined AR and AS).
- Calcific degeneration.
- Rheumatic heart disease (may cause combined AR and AS, and mitral valve disease).
- Mediastinal radiation for lymphoma, breast, or esophageal cancer (risk increased if >30 Gray of radiation exposure; usually presents 15-20 years after exposure; can cause combined AS and AR). (Griffin 2022)
- Anorectic drugs (e.g., fenfluramine, phentermine).
symptoms of aortic regurgitation
symptoms/presentations of acute AR
- [1] Cardiogenic shock.
- [2] Pulmonary edema with severe dyspnea is often a dominant symptom.
- [3] Impella failure:
- Ongoing shock despite adequate device flow may suggest AR.
- With severe AR, Impella outflow may regurgitate into the LV, causing ineffective support. (37973348)
- (Edema and weight gain often aren't seen because there hasn't been sufficient time to retain sodium.) (Brown 2023)
symptoms of chronic AR
- Palpitations.
- Dyspnea on exertion.
- Reduced exercise capacity.
- Anginal chest pain (even in the absence of coronary disease). (Griffin 2022)
- Heart failure (e.g., peripheral edema, pulmonary edema).
bedside evaluation of aortic regurgitation
exam signs (primarily seen in chronic AR with left ventricular dilation, NOT acute mitral regurgitation)
- Wide pulse pressure. Palpation may reveal a bounding or water hammer pulse.
- Quincke sign: capillary pulsation in nail beds.
- De Musset sign (titubation): head nodding with each heartbeat.
- Muller sign: visible pulsations of the uvula.
- ⚠️ In acute AR, the pulse pressure may be increased, normal, or decreased (decreased because the forward stroke volume is decreased). (38631792) Reduced pulse pressure in a patient with severe AR may be a worrisome sign.
ECG
- Acute AR:
- ECG is likely to be normal.
- Conduction block may occur in endocarditis.
- Chronic AR:
- LVH and left atrial abnormality may develop.
- QRS prolongation may reflect diffuse myocardial disease (poor prognostic sign).
echocardiographic classification of aortic regurgitation
- (Regurgitant jet width)/(LV outflow tract):
- <25% is consistent with mild AR.
- 25-65% is consistent with moderate AR.
- >65% is consistent with severe AR.
- Vena contracta width:
- <0.3 cm is consistent with mild AR.
- 0.3-0.6 cm is consistent with moderate AR.
- >0.6 cm is consistent with severe AR.
- Pressure half-time:
- Traditionally, >500 ms was considered mild, 200-500 ms was considered moderate, and <200 ms was considered moderate.
- However, pressure half-time predominantly reflects how long AR has been present rather than its severity. (38631792)
- Regurgitant volume:
- <30 ml/beat is consistent with mild AR.
- 30-60 ml/beat is consistent with moderate AR.
- >60 ml/beat is consistent with severe AR.
- Regurgitant fraction:
- <30% is consistent with mild AR.
- 30-50% is consistent with moderate AR.
- >50% is consistent with severe AR.
- Regurgitant orifice area:
- <0.1 cm2 is consistent with mild AR.
- 0.1-0.3 cm2 is consistent with moderate AR.
- >0.3 cm2 is consistent with severe AR.
- Diastolic flow reversal in descending aorta:
- Brief, early diastolic reversal is consistent with mild AR.
- Holodiastolic flow reversal is consistent with severe AR. If flow reversal is pan-diastolic and >25 cm/s, severe AI is likely. (Griffin 2022) However, due to the rapid equalization of pressures between the LV and aorta in acute severe AR, flow reversal may not be holodiastolic. (38631792)
- Any degree of diastolic flow reversal in the abdominal aorta is consistent with severe AR. (38631792)
management of acute aortic regurgitation
medical therapies
- [#1] Chronotropic agents may reduce regurgitant filling time:
- The heart rate should increase as a compensatory mechanism in chronotropically competent patients. (38631792)
- Target a heart rate well over ~80 b/m.
- Bradycardia is not tolerated well because this increases regurgitation in diastole.
- Inotropic treatment may be helpful (e.g., dobutamine, isoproterenol). (35912478)
- Avoid sympatholytic agents (e.g., dexmedetomidine).
- [#2] Afterload reduction decreases the regurgitant fraction (if feasible based on MAP).
- The diastolic pressure gradient across the aortic valve drives regurgitation. Consequently, a reduction in the diastolic blood pressure will reduce the regurgitation. However, excessive reduction in diastolic blood pressure may provoke myocardial ischemia due to inadequate coronary artery blood flow. (20962337)
- Options may include:
- Sodium nitroprusside.
- Nitroglycerine (also provides venodilation, but venodilation may be beneficial, especially in patients with active pulmonary edema).
- Clevidipine > nicardipine.
- A target systolic BP of 100-120 mm may be appropriate. (39663714)
- [#3] Preload reduction for treatment of pulmonary edema. (38631792)
- Diuresis.
- Some vasodilators will additionally reduce preload (e.g., nitroprusside, nitroglycerine).
- [#4] Relatively low threshold for intubation:
- Patients will generally require intubation before surgery (see below), so attempting to avoid intubation is usually pointless.
- Intubation with sedation may improve oxygenation, eliminate the work of breathing, and promote perfusion of vital organs.
- ⚠️ Beta-blockers should generally be avoided. (Gaggin 2021)
- ⚠️ There are no real options for mechanical support devices:
- IABP is absolutely contraindicated in severe AR (it will increase regurgitation). (Griffin 2022)
- Impella use is contraindicated.
- VA ECMO would cause over-distension of the left ventricle.
- LAVA-ECMO may be an option at selected centers.
surgery vs TAVR
- Acute AR is an interventional emergency.
- Medical therapies listed above are merely temporizing and will not work in isolation. The goal is to stabilize the patient and bridge them to an intervention.
- TAVR is an increasing option, especially for patients who aren't candidates for SAVR. TAVR has been described as a salvage treatment for severe AR, even in the context of endocarditis. (37973348)
management of chronic aortic regurgitation
Patients are often stable for several years. However, after systolic dysfunction develops, symptoms will likely follow within three years – with an associated risk of mortality as high as 10%/year. (Griffin 2022)
pharmacologic therapy
- Medical management generally has a limited role.
- Vasodilators:
- Indications may include:
- (1) AR in the context of hypertension.
- (2) The patient should ideally have surgery but isn't a surgical candidate.
- First-line agents are dihydropyridine calcium channel blockers (e.g., amlodipine, nifedipine XR, felodipine).
- ACEi/ARB are frequently used also. (Griffin 2022)
- Indications may include:
- Beta-blockers may be cautiously considered for patients with aortic root dilation (>4.5 cm) to reduce aortic wall stress. However, bradycardia is poorly tolerated in AR, so beta-blockers may cause hemodynamic deterioration. (Griffin 2022)
indications for surgical AVR
- Severe AR plus any one of the following:
- Symptoms (irrespective of LV function).
- EF <50-55%.
- Severe LV dilation (LV end-systolic diameter >5-6.5 cm, depending on surgical risk).
- Progressive aortic enlargement.
- Undergoing other cardiac surgery.
pathophysiology of AR
acute AR
- A sudden volume load is imposed upon an unprepared left ventricle (or, even worse, a patient with pre-existing diastolic heart failure with a steeper end-diastolic pressure-volume curve). (37973348)
- LVEDP and PCWP increase markedly, causing cardiogenic pulmonary edema.
- Stroke volume increases, but the effective forward stroke volume is reduced (because much of this blood flow is going backward). Consequently, systemic hypotension and shock may occur.
- Markedly elevated LVEDP may cause premature mitral valve closure. This can sometimes be followed by subsequent diastolic mitral regurgitation (i.e., complete blood flow reversal across the mitral valve in diastole). (35912478)
- Reduced diastolic pressures may decrease coronary perfusion. (38631792)
causes of mitral stenosis
- Rheumatic heart disease.
- Senile calcific disease (prominent calcifications extend inward from the mitral annulus).
- MAC (mitral annular calcification) may progress inwards to involve the leaflets. (Sadhu 2023)
- Prosthetic valve dysfunction (e.g., degeneration, thrombosis, or endocarditis).
- Systemic inflammatory disorders (e.g., lupus, rheumatoid arthritis).
- Radiation valvulitis (usually presents >10-20 years after mediastinal radiotherapy).
- Endocarditis with large vegetations that obstruct the valve orifice.
- Congenital mitral stenosis.
- Carcinoid syndrome (in the context of right-to-left shunting or pulmonary involvement). (Sadhu 2023)
symptoms of mitral stenosis
general symptoms
- Dyspnea, orthopnea, paroxysmal nocturnal dyspnea.
- Exercise intolerance.
- Chest discomfort.
- Hemoptysis.
- High rate of atrial fibrillation, which may cause:
- Symptomatic palpitations.
- Systemic embolization (e.g., stroke).
- Atrial fibrillation onset may cause acute hemodynamic deterioration.
- Ortner syndrome (hoarseness due to vocal cord paralysis due to impingement of the left atrium on the left recurrent laryngeal nerve). (Gaggin 2021)
causes of acute deterioration include:
- Atrial fibrillation (especially with rapid ventricular rate).
- Any cause of increased cardiac output, e.g.:
- Infection/sepsis.
- Fever.
- Pregnancy.
- Hyperthyroidism.
diagnosis of mitral stenosis
findings on bedside examination
- Cardiogenic pulmonary edema may be present.
- Reduced cardiac output may occur.
- Pulmonary hypertension develops in advanced mitral stenosis, with consequent signs (e.g., systemic congestion).
ECG features of mitral stenosis
- Left atrial enlargement (“P-mitrale”) is the classic ECG manifestation. However, atrial fibrillation may occur (obscuring this).
- Features of pulmonary hypertension (e.g., right axis deviation).
right heart catheterization findings
- Giant a-waves on the wedge tracing.
radiographic features
- Dilation of the left atrium.
- Features of pulmonary hypertension.
- Cardiogenic pulmonary edema.
- Mitral valve calcification on CT scan correlates with mitral valve sclerosis or stenosis. 📖 (30737548)


echocardiographic classification of mitral stenosis
- Planimetered mitral valve area:
- 4-5 cm2 is normal.
- <2.5 cm2 often correlates with exertional symptoms.
- <1.5 cm2 often correlates with symptoms at rest and is considered severe.
- <1 cm2 is considered critical. (Sadhu 2023)
- Diastolic pressure half-time:
- <150 ms is consistent with mild MS.
- >150 ms is consistent with severe MS.
- Left atrial dilation:
- Mild-moderate enlargement is consistent with mild MS.
- Severe enlargement is consistent with severe MS.
- PA pressure: Elevated PASP >50 mm is consistent with severe MS.
- Mean pressure gradient:
- A mean gradient >10 mm is consistent with severe MS.
- Gradients depend on heart rate and blood flow, so this may be inaccurate for critically ill patients. (38631792)
management of mitral stenosis
treat any precipitating event
- Similar to aortic stenosis, mitral stenosis is a chronic process. Consequently, acute presentations may be triggered by precipitating disorders (similar to those listed above for aortic stenosis ⚡️).
- Any underlying acute pathology should be aggressively treated.
medical therapy: mitral stenosis
- Respiratory support:
- Noninvasive ventilation (BIPAP or CPAP) may be helpful in acute cardiogenic pulmonary edema.
- Intubation may cause hemodynamic instability and is ideally avoided if possible. (39663714)
- Atrial fibrillation management:
- AF is generally poorly tolerated due to:
- [i] Loss of atrial kick.
- [ii] Tachycardia.
- Aggressive management may be required, including emergent cardioversion.
- If achievable, a rhythm control strategy is ideal.
- AF is generally poorly tolerated due to:
- Heart rate control in general:
- A slow heart rate may improve mitral stenosis (due to improved diastolic filling time).
- ⚠️ If there is concomitant RV failure, negative inotropy may exacerbate RV failure.
- Diuresis to manage pulmonary congestion.
- This is similar to aortic stenosis: Some diuresis is often required, but overzealous diuresis may drop the preload too much. (39663714)
- Right heart failure with systemic congestion could be an argument for more aggressive diuresis.
- Anticoagulation indicated for:
- MS plus AF.
- MS plus prior embolic event.
- MS plus left atrial thrombus.
- (Note: this is considered valvular AF, so the CHADS2VASC score doesn't apply, and warfarin is the preferred oral anticoagulant.)
medical therapy: RV failure
- DON'T FORGET ABOUT THE RIGHT VENTRICLE.
- Mitral stenosis usually causes pulmonary hypertension and right ventricular failure.
- If these are present, they may require additional management (discussed here: 📖).
MCS
- There aren't great MCS options since mitral stenosis is pre-ventricular.
- IABP is too distal to decompress the left atrium.
- Impella placement won't help the underfilled LV.
- Advanced ECMO modalities (LAVA-ECMO) may be an option.
percutaneous mitral balloon valvotomy
- Indicated for patients with all of the following:
- (1) Severe MS.
- (2) Favorable valve morphology.
- (3) Absence of left atrial thrombus or moderate-to-severe MR.
- (4) One of the following:
- Severe, symptomatic MS.
- Asymptomatic MS that is very severe (mitral valve area <1 cm2).
- New onset AF.
- Suboptimal valve anatomy, yet not a candidate for surgery.
- Results can be reasonably durable, with event-free survival of ~85% after 3-7 years. (Sadhu 2023)
- Potential complications include:
- Death (1%).
- Stroke.
- Cardiac perforation.
- Severe mitral regurgitation requiring cardiothoracic surgery (7%). (20962337)
- Residual atrial septal defect that may require closure. (Sadhu 2023)
surgery
- Indicated for severe, symptomatic mitral stenosis who aren't at high risk for surgery.
- For rheumatic mitral stenosis, percutaneous valvotomy may be preferable (if technically possible).
interventional management for calcific (senile) mitral stenosis
- Severity classification is based on gradient criteria (rather than other echocardiographic parameters, such as pressure half-time):
- <5 mm mean gradient is mild MS.
- 5-10 mm mean gradient is moderate MS.
- >10 mm mean gradient is severe MS.
- Guidelines refer only to medical therapy. There are no recommendations regarding percutaneous intervention or surgery. (Gaggin 2021)
prognosis
- Once severe pulmonary hypertension evolves, mean survival is ~3 years. (Sadhu 2023)
causes of mitral regurgitation
primary MR
- Endocarditis.*
- Leaflet perforation.
- Chordal disruption; flail valve.
- Related to myocardial ischemia*
- [1] Posterior papillary muscle rupture following RCA infarction (usually ~2-7 days afterward).
- [2] Papillary muscle dysfunction is common.
- [3] Secondary MR (see below; mitral valve dilates due to left ventricular dilation).
- Myxomatous degeneration (abnormal elasticity of the mitral valvular apparatus, including the annulus, chordae tendineae, and leaflets). (Griffin 2022)
- Primary mitral valve prolapse.
- Associated with connective tissue diseases:
- Marfan syndrome.
- Ehlers-Danlos syndrome.
- Osteogenesis imperfecta.
- Chordal rupture* in the context of a myxomatous valve may cause acute-on-chronic deterioration.
- Trauma.*
- Rheumatic heart disease may cause MR or combined MR/MS. (Sadhu 2023)
- Radiation heart disease.
- Less common etiologies:
- Infiltrative diseases (e.g., amyloid).
- Lupus (Libman-Sacks lesion).
- Drug toxicity (e.g., fenfluramine/phentermine). (Sadhu 2023)
- * Indicates: may cause acute mitral regurgitation.
secondary MR (aka functional MR)
- The mitral valve is structurally normal.
- MR is due to dilated cardiomyopathy:
- Papillary muscle displacement.
- Annular dilation.
symptoms of mitral regurgitation
acute MR
- The primary manifestation is usually acute cardiogenic pulmonary edema.
- Mitral regurgitation may cause asymmetric pulmonary edema, primarily involving the right upper lung. 📖
- Less often, reduced forward flow causes cardiogenic shock. (Griffin 2022)
chronic MR
- Over time, the left atrium expands, accommodating regurgitant blood flow and reducing pulmonary edema. However, dyspnea and orthopnea may also occur.
- Inadequate cardiac output eventually becomes more prominent (e.g., fatigue, lethargy).
- Complications of chronic, untreated MR:
- Pulmonary hypertension and cor pulmonale may lead to systemic congestion.
- Atrial fibrillation.
clues to the diagnosis of MR in the ICU
- Shock with normal or hyperdynamic LVEF.
- Rapid escalation in vasopressor requirements without clinical improvement, often with the development of poor perfusion (these patients will respond poorly to afterload).
- Pulmonary edema (especially suggestive if it is unilateral).
- Failure to wean from mechanical ventilation. Spontaneous breathing trials increase preload and afterload, which may worsen MR severity (especially in patients with LV systolic dysfunction who are subject to LV dilation). (37530859)
diagnosis of MR
physical examination
- MR usually causes a pansystolic murmur, loudest at the apex.
- Severe MR may lead to rapid equalization of pressures between the left ventricle and the atrium, causing a soft and brief murmur.
chest radiograph
- Mitral regurgitation may cause asymmetric pulmonary edema, primarily involving the right upper lung. 📖
- Chronic mitral regurgitation:
- The left atrium dilates first. This may produce a widened carina and a double density overlying the heart.
- The left ventricle dilates later on.

ECG findings may include:
- Left atrial abnormality.
- Left ventricular hypertrophy.
- Right atrial abnormality and right ventricular hypertrophy due to pulmonary hypertension.
- Atrial fibrillation.
- Evidence of prior MI (for patients with post-MI mitral regurgitation). (Sadhu 2023)
right heart catheterization
- Tall v-waves may be seen in the wedge tracing.
- Pulmonary hypertension may be seen.
- Wedge pressure is generally elevated.
echocardiography in MR
[1] echocardiography for the diagnosis of MR
- ⚠️ Flail mitral leaflet can be missed if there is a narrow and eccentric regurgitant jet. Transthoracic echocardiography has a sensitivity of only ~80% for flail mitral valve so transesophageal echocardiography may be needed. (30987913)
[2] traditional echocardiographic classification of severity
- Effective regurgitant orifice measured by the PISA method (proximal iso-velocity surface area):
- Regurgitant volume:
- <60 ml is consistent with non-severe MR.
- >60 ml is consistent with severe MR.
- Regurgitant volume is calculated as the effective regurgitant orifice area (EROA) multiplied by the mitral regurgitant velocity time interval (VTI). Consequently, it may have the same limitations as the EROA discussed immediately above. (37530859)
- Regurgitant fraction:
- <50% is consistent with non-severe MR.
- >50% is consistent with severe MR.
- Vena contracta:
- <0.7 cm is consistent with mild MR.
- >0.7 cm is consistent with severe MR.
- Vena contracta is best used for a central MR jet. It isn't reliable if there are eccentric jets that hug the wall (Coanda effect).
- Peak velocity <5 m/s is consistent with severe MR. (35912478)
[3] additional aspects often important in ICU
- Systolic pulmonary vein flow reversal
- This is usually seen on TTE in severe acute MR. It may be helpful in patients with eccentric/complex jets. (39663714)
- This is performed by placing a pulsed-wave Doppler within one of the right pulmonary veins in the fir field on the apical 4-chamber view. Normally, there may be a short period of minimal flow reversal during atrial systole. (37530859)
- Ejection fraction:
- MR will afterload the LV, so the EF should generally be hyperdynamic.
- If the EF is <60%, this may be abnormal and suggestive of systolic decompensation. (37530859; Sadhu 2023)
- Left atrial volume or area: may help differentiate acute vs. chronic mitral regurgitation.
- LA dilation is nonspecific, so this doesn't necessarily prove chronic MR.
- An absence of LA dilation excludes chronic, severe MR. (37530859)
- Patients may also have acute-on-chronic MR, so the distinction isn't absolute.
management of acute mitral regurgitation
cardiovascular optimization
- [1] A relatively fast heart rate may be helpful (reduce the duration of regurgitation).
- Dobutamine may be helpful (especially among patients with systolic heart failure).
- [2] Afterload reduction may promote forward blood flow and reduce regurgitation.
- Options:
- Nitroprusside.
- High-dose nitroglycerine (may be helpful following MI or in acute pulmonary edema).
- (Clevedipine > nicardipine.)
- Unfortunately, in patients with profound hypotension, norepinephrine may be required to maintain a minimal blood pressure consistent with life.
- ⚠️ Excessive use of vasoconstrictors (e.g., norepinephrine) may increase afterload, aggravate LV dilation, and worsen mitral regurgitation.
- Options:
- [3] Diuresis: MR tends to cause volume overload of the left ventricle.
- [4] Respiratory therapy:
- BiPAP/CPAP: Positive airway pressure will reduce preload and afterload.
- Relatively low threshold for intubation:
- Patients will generally require intubation before surgery (see below), so avoiding intubation may be pointless in some situations.
- Intubation with sedation may improve oxygenation, eliminate the work of breathing, and promote perfusion of vital organs.
- PEEP escalation may be helpful to reduce preload and afterload further.
- [5] Device therapy:
- IABP: This may reduce the regurgitant fraction and substantially improve cardiac output. (20962337)
- Impella
- This is relatively contraindicated in papillary muscle rupture. Depending on the mitral valve lesion, care must be taken to position the Impella adequately.
- It may be challenging to position a patient with a normal LV size. (35912478)
- 🛑 Surgical repair is the definitive therapy, as surgery will generally cause rapid improvement in cardiac function. Consequently, device therapy shouldn't delay surgery.
surgery (vs. mitraclip)
- Emergent surgery is generally required for acute, severe MR.
- For patients status post-MI or patients with potential coronary artery disease, surgery should be a combined CABG plus mitral valve repair/replacement.
- Mitraclip may be an option for some patients.
management of chronic MR
- Surgical repair should ideally be performed before significant LV dysfunction develops.
- After severe left ventricular dysfunction has developed (e.g., EF <30%), it may be too late to perform surgery. (Griffin 2022)
- There is increasing evidence supporting percutaneous, transcatheter mitral valve intervention.
physiology and anatomy
- Chronic MR:
- Initially, gradual dilation of the LA and LV is compensatory.
- Eventually, dilation becomes maladaptive (causing increasing annular dilation and worsening mitral regurgitation). This causes patients to fall off the Starling curve. (37530859)
causes
- Acute TR:
- Endocarditis (may cause papillary muscle rupture).
- RV myocardial infarction (causing papillary muscle dysfunction).
- Blunt chest trauma.
- Iatrogenic:
- Endomyocardial biopsy.
- Pacemaker/ICD lead.
- Chronic TR (overall more common):
- Secondary (functional) TR due to RV dilation is the most common etiology:
- Chronic pulmonary hypertension of any etiology (e.g., left-sided valvular disease, chronic pulmonary disease).
- Right ventricular dilation due to intrinsic myocardial disease (e.g., idiopathic dilated cardiomyopathy).
- Right atrial enlargement in the context of permanent AF. (Sadhu 2023)
- Myxomatous valve degeneration
- It may be associated with mitral valve prolapse.
- Marfan syndrome.
- Rheumatic heart disease.
- Carcinoid syndrome (also associated with tricuspid stenosis).
- Secondary (functional) TR due to RV dilation is the most common etiology:
symptoms of TR
- The symptoms primarily reflect RV failure. It may be challenging to distinguish symptoms attributable to tricuspid valve disease from symptoms of the underlying disease (e.g., endocarditis with septic pulmonary emboli).
- Symptoms may include:
- Dyspnea.
- Systemic edema.
- Ascites, abdominal bloating, anorexia.
bedside evaluation for TR
- Clinical manifestations resemble RV failure.
- Jugular vein distension with a prominent V-wave may be seen.
- A holosystolic murmur may be appreciated over the left sternal border that increases with inspiration. (Brown 2023)
investigation of TR
- Blood cultures if endocarditis is possible.
- ECG:
- ? Signs of inferior MI.
- ? Signs of chronic pulmonary hypertension.
- ? Signs of right atrial abnormality.
- Echocardiography features may include:.
- Systolic flow reversal in the hepatic veins.
- Dilated IVC.
- Right heart catheterization:
- Elevated right atrial pressure.
- Steep y-descent.
- In extreme cases, ventricularization of right atrial pressures. (38631792)
- PE evaluation if clinically indicated.
echocardiographic grading of TR
- Anatomic features that may be worrisome:
- Flail or grossly distorted leaflets.
- Severe annular dilation (>40 mm or 21 mm/m2) is generally seen in severe tricuspid regurgitation (unless the TR is acute). (Sadhu 2023)
- Marked leaflet tethering.
- Hemodynamic features of severe TR:
- Central jet area >10 cm2.
- Vena contract width >7 mm.
- PISA (proximal isovelocity surface area) radius >0.9 cm.
- EROA (effective regurgitant orifice area) >0.4 cm2
- Regurgitant volume >45 ml
- CW jet density and contour: dense, triangular, and early peak.
- Hepatic vein and/or IVC shows systolic flow reversal.
- Associated features of RV failure:
- Dilation of RA, RV, and IVC (with reduced IVC respirophasic variation).
- Diastolic septal flattening (reflective of RV volume overload). Alternatively, a flattened septum throughout systole and diastole may be consistent with chronic pulmonary hypertension causing TR (with both volume and pressure overload).
- RV systolic failure may occur in the late phase. (Gaggin 2021)
pathophysiology of TR
- Acute severe TR in isolation is typically well tolerated. (37973348) Therefore, hemodynamic deterioration may reflect a combination of TR and another disease process (e.g., RV failure).
- The vicious spiral of TR:
- [1] TR usually begins due to RV dilation (functional/secondary TR).
- [2] TR leads to further volume overload of the right ventricle, which promotes further RV dilation.
- [3] Worsening RV dilation causes increased TR, which generates a vicious spiral.
management of TR
- The management of acute TR is generally medical. However, surgical treatment may be necessary in rare cases if the patient is refractory to medical therapy. Recently, percutaneous tricuspid valve insertion has also become an option.
- Underlying etiologies may require therapy, for example:
- Endocarditis requires antibiotics.
- RVMI may require coronary revascularization.
- Left-sided heart failure.
- Medical management of TR resembles the therapy for RV failure, for example:
- Diuresis.
- Inotropic therapy.
- Pulmonary vasodilation.
- Maintaining an adequate heart rate (a faster heart rate may improve forward flow).
causes include
- Endocarditis.
- Prosthetic valve thrombosis.
- Valve degeneration (e.g., leaflet calcification, tear).
- Paravalvular leak.
symptoms
- Thromboembolism may result from endocarditis or thrombosis.
- Hemolysis may occur (e.g., due to a paravalvular leak).
- Heart failure (symptoms will vary depending on the valve's location, acuity of dysfunction, and type of dysfunction).
evaluation
- Blood cultures if endocarditis is possible.
- Hemolysis evaluation (e.g., LDH >600 shouldn't be seen with a normally functioning prosthesis). (Brown 2023)
- ECG (new AV conduction delay may suggest aortic ring abscess).
- Echocardiography (TTE +/- TEE).
- Cardiac CT may be used for some valves.
management
- Management depends on the specifics.
- Endocarditis therapy is discussed further here [REF].
- Post-TAVR complications are discussed further here [REF].
- Prosthetic valve thrombosis is discussed further below.
prosthetic valve thrombosis
presentation
- Thrombosis may cause valve stenosis and/or regurgitation. The presentation varies depending on the valve location and the tempo of the thrombosis. Patients may present indolently or acutely with shock.
- Left-sided valve thrombosis may result in systolic thromboembolic events.
- Acute valve thrombosis is especially common within the first 3-12 months after insertion. (20962337)
management overview
- [1] Ensure adequate anticoagulation (in the acute phase, this often involves a heparin infusion).
- [2] Consult CT surgery if the patient is potentially a surgical candidate.
- [3] Consider fibrinolytic therapy vs intensification of anticoagulation.
- [3a] For shocked or acutely unstable patients, anticoagulation intensification won't work rapidly enough.
- [3b] For stable patients, anticoagulation intensification could be an option.
surgery
- Potential indications may include:
- Left-sided thrombosis that is large or mobile (>0.8 cm2).
- Advantages of surgery:
- Reduced risk of thromboembolism (most relevant in left-sided thrombosis).
- Reduced risk of recurrent prosthetic valve thrombosis.
- Disadvantages of surgery: this is a very high-risk procedure. Operating for prosthetic valve thrombosis involves one of the following scenarios, both of which are high-risk:
- [1] Redo surgery on a patient who previously received a surgical valve.
- [2] Surgery on a patient with a percutaneous valve (e.g., TAVR). The rationale for percutaneous valve implantation in the first place was probably that the patient was a poor surgical candidate.
fibrinolytic therapy
- Fibrinolytic therapy is often required for unstable patients who aren't good candidates for cardiothoracic surgery. Since fibrinolysis is very high-risk, pursuing it should be a team decision. Unfortunately, fibrinolysis remains the best option for many patients.
- Risks of fibrinolytic therapy include:
- [1] Systemic bleeding (5%; always a risk with any fibrinolytic treatment).
- [2] Thromboembolism of the clot:
- ~12% risk with left-sided prosthetic valve thrombosis. Clot detachment may cause stroke or other systemic arterial embolization). (20962337)
- Larger thrombus size is associated with increased complication risk (<0.8 cm2 is associated with 6% risk; 0.8-1.6 cm2 is associated with ~29% risk; >1.6 cm2 is associated with 47% risk). (37225366)
- [3] Intracranial hemorrhage (patients with left-sided mechanical valves often have subacute strokes and abnormal cerebral vasculature, so they are at relatively high risk of intracranial hemorrhage when treated with thrombolysis).
- Best candidates for fibrinolysis:
- Recent onset of symptoms (<14 days; clot is less organized and more likely to dissolve).
- D-dimer elevation supports the presence of an acute thrombus that may be susceptible to thrombolysis. Alternatively, a normal D-dimer level might suggest a chronic/organized clot that is less likely to respond to thrombolysis.
- Smaller thrombus with less risk of embolization (<0.8 cm2).
- Low systemic bleeding risk (see contraindications to systemic thrombolysis 📖).
- Not a surgical candidate.
- Protocol for fibrinolysis:
- Before starting, review all anticoagulant medications and relevant coagulation studies (e.g., INR, fibrinogen, oral anticoagulants, and antiplatelet agents).
- For patients on oral anticoagulation (e.g., warfarin or DOAC), allowing the medication to wear off or reversing it may be desirable. To prevent thrombosis, a heparin infusion may be used in place of chronic oral anticoagulation.
- The TROIA protocol for thrombolysis seems to be reasonable. This involves an infusion of 25 mg alteplase over six hours. Heparin infusion should be held during alteplase infusion. (23489534) A repeat dose may be required if there isn't an adequate response to the first dose. Fibrinogen levels should be followed with avoidance of substantial hypofibrinogenemia. 🌊
- The subsequent PROMETEE protocol used 25 mg of alteplase infused slowly over 25 hours. This was associated with a 90% success rate with a very low rate of complications. (26299240)
TAVR complications
- Discussed here: 📖
transcatheter edge-to-edge mitral valve repair
- [1] Mitral stenosis: Increased trans-mitral gradients (>5 mm) may occur.
- [2] Failure to resolve mitral regurgitation: Single leaflet detachment can occur (either intraprocedurally or within 1-2 days).
- [3] Worsening mitral regurgitation can result from damage to the valve leaflets or apparatus.
- [4] Device embolization is rare (but this could cause systemic arterial embolization).
TMVR (transcatheter mitral valve replacement)
- [1] LVOT obstruction.
- Hemodynamic stabilization is similar to the treatment of dynamic LV outflow tract obstruction.
- [2] Perivalvular leak.
- Severe leaks may cause cardiogenic shock or heart failure.
- Less severe leaks may cause hemolysis.
- [3] Device migration or embolization.
- [4] Ventricular perforation leading to tamponade.
transcatheter tricuspid valve repair and replacements
- Complications of tricuspid valve repair are similar to transcatheter mitral valve repair.
- After tricuspid valve replacement, RV failure may result from increased RV afterload. (37973348)
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References
- Gaggin, H. K., & Januzzi, J. L., Jr. (2021). MGH Cardiology Board Review. Springer Science & Business Media.
- Griffin, B.P., Kapadia, S.R., Menon V. (2022). The Cleveland Clinic Cardiology Board Review. Wolters Kluwer.
- Brown, D. L., & Warriner, D. (2023). Manual of Cardiac Intensive Care. Elsevier Health Sciences.
- Sadhu, J., Husaini, M., & Williams, D. (2023). The Washington Manual Cardiology Subspecialty Consult. Lippincott Williams & Wilkins.
- 35912478 Bernard S, Deferm S, Bertrand PB. Acute valvular emergencies. Eur Heart J Acute Cardiovasc Care. 2022 Aug 9;11(8):653-665. doi: 10.1093/ehjacc/zuac086 [PubMed]
- 37530859 Duncan CF, Bowcock E, Pathan F, Orde SR. Mitral regurgitation in the critically ill: the devil is in the detail. Ann Intensive Care. 2023 Aug 2;13(1):67. doi: 10.1186/s13613-023-01163-4 [PubMed]
- 37973348 Zern EK, Frank RC, Yucel E. Valvular Heart Disease in the Cardiac Intensive Care Unit. Crit Care Clin. 2024 Jan;40(1):105-120. doi: 10.1016/j.ccc.2023.05.002 [PubMed]
- 38631792 Keane RR, Menon V, Cremer PC. Acute Heart Valve Emergencies. Cardiol Clin. 2024 May;42(2):237-252. doi: 10.1016/j.ccl.2024.02.009 [PubMed]
- 39663714 Lüsebrink E, Lanz H, Kellnar A, Karam N, Kapadia S, Makkar R, Abraham WT, Latib A, Leon M, Sannino A, Shuvy M, Guerrero M, Fam N, Butler J, Adamo M, Rudolph V, Tang GHL, Stocker TJ, Rommel KP, Lurz P, Thiele H, Massberg S, Praz F, Prendergast B, Hausleiter J. Management of acute decompensated valvular heart disease. Eur J Heart Fail. 2024 Dec 11. doi: 10.1002/ejhf.3549 [PubMed]
- 39735779 Miller PE, Senman BC, Gage A, Carnicelli AP, Jacobs M, Rali AS, Senussi MH, Bhatt AS, Hollenberg SM, Kini A, Menon V, Grubb KJ, Morrow DA; American College of Cardiology Critical Care Cardiology Section. Acute Decompensated Valvular Disease in the Intensive Care Unit. JACC Adv. 2024 Dec 26;3(12):101402. doi: 10.1016/j.jacadv.2024.101402 [PubMed]