Severe Valvular Heart Disease in the Critically Ill

A valve lesion changes the route, timing, and pressure cost of blood movement. Its consequences depend on ventricular and atrial adaptation, rhythm, vascular load, and the speed with which the lesion developed. In critical illness, an apparently familiar stenosis or regurgitation can therefore produce a new circulatory state without an identical change in its underlying anatomy.

78.1 Describe the flow pathway before interpreting the circulation

A normal valve permits forward flow during one phase and limits backward flow during another. Stenosis restricts the available forward pathway. Regurgitation creates a backward pathway when closure should prevent it. The resulting circulation depends on how much useful blood crosses the whole system, rather than on the apparent vigor of one chamber.

Pressure and volume loading are related but different consequences. An obstructed outlet requires an additional pressure difference during ejection. An incompetent valve can require repeated handling of blood that has already passed through part of the circulation. Either lesion can ultimately produce low forward output, high upstream pressure, and organ congestion.

Location determines which structures first encounter the burden. Mitral obstruction raises the pressure required to move blood from left atrium to ventricle. Aortic obstruction increases the systolic pressure the left ventricle must generate. Mitral regurgitation sends systolic volume toward the atrium, while aortic regurgitation returns blood to the ventricle during diastole.

The right-sided valves follow the same conservation principles within a different pressure environment. Tricuspid regurgitation can enlarge the right ventricle and raise venous pressure while reducing useful pulmonary flow. A small left ventricular cavity may then reflect restricted delivery through the lungs rather than an isolated shortage of circulating volume.

Structural and functional lesions also differ. A damaged leaflet, disrupted chord, infected prosthesis, restricted calcified orifice, and geometrically distorted but intact apparatus can all produce valve dysfunction. Some flow abnormalities change substantially with chamber size or loading; others remain anatomically constrained despite altered pressures.

The relevant description therefore includes lesion, direction and phase of abnormal flow, acute or chronic development, chamber adaptation, rhythm, and current loading. Sepsis, ischemia, ventilation, fluid redistribution, and arrhythmia can expose limited reserve or modify regurgitation. A diagnostic label alone cannot explain why the patient deteriorated at this moment.

78.2 A pressure gradient depends on flow as well as the opening

Blood accelerates through a narrowed effective orifice. The resulting velocity and pressure difference depend on the flow passing through it, the opening available, and the unsteady conditions of the cardiac cycle. A fixed anatomical lesion therefore does not produce one fixed pressure gradient at every output.

For the simplified Doppler Bernoulli approximation, let v be the maximum jet velocity in m/s and ΔP the estimated local instantaneous pressure drop in mmHg. When upstream velocity is small and the approximation is otherwise appropriate:

In a constructed fixed-orifice comparison, velocity falls from 4 to 3 m/s because flow falls while effective area and the relevant flow pattern are held constant. The estimated drop falls from 64 to 36 mmHg. The lower gradient has not demonstrated that the obstruction improved. These values illustrate flow dependence rather than supply diagnostic severity thresholds.

Early Doppler work by Hatle related measured velocity to pressure differences in outflow obstruction. Its clinical value was the pressure–velocity link and localization through complementary Doppler methods. Modern interpretation must still consider measurement alignment, upstream velocity, serial obstructions, and downstream pressure recovery rather than adopting every historical simplifying claim. 1

The equation describes a local pressure conversion associated with the jet. It is not a direct measurement of irreversible energy loss or a constant vascular resistance. When upstream velocity is important, the simplified expression omits a relevant kinetic term. When obstruction changes during systole, one peak also omits the time course.

Low-flow states can consequently conceal a severe anatomical restriction behind a modest gradient. Conversely, high flow, regurgitant recirculation, or altered ejection can increase velocity without a matching reduction in valve area. Anatomy, forward flow, velocity profile, and loading must be reconciled before a gradient is interpreted as progression or relief.

78.3 Aortic stenosis loads both systole and diastolic reserve

The left ventricle ejecting through a stenotic aortic valve generates pressure above that in the aorta. Its load includes the valve and the arterial system beyond it. A radial pressure therefore does not describe the entire systolic pressure borne by the ventricular wall.

Chronic pressure loading often produces wall thickening that helps contain systolic stress. Grossman and colleagues related pressure and volume overload to different hypertrophic patterns in human catheterization studies. This supports the connection between geometry and load without making hypertrophy proof of preserved reserve or defining an individual patient’s wall stress from arterial pressure alone. 2

The thicker chamber can have impaired relaxation, reduced compliance, increased oxygen requirements, and restricted coronary reserve. Filling pressure may rise sharply with a modest volume addition. Conversely, a reduction in useful filling can lower stroke volume when the ventricle cannot compensate through ejection or rate.

Tachycardia can shorten filling and diastolic coronary-perfusion time while increasing demand. Loss of coordinated atrial contribution can further alter filling, although its importance varies with the chamber and rhythm. Hypotension can reduce coronary support, particularly when ventricular diastolic pressure is high.

These mechanisms explain sensitivity to abrupt loading changes without implying that output is completely fixed or that every vasodilator response is identical. Khot and colleagues studied nitroprusside in selected critically ill patients with severe aortic stenosis, low systolic function, and low output, excluding patients with hypotension or a need for inotropic/pressor support. Forward performance improved during monitored treatment. The small uncontrolled study demonstrates a contribution from arterial loading in that population; it is not a prescription for an unstable hypotensive patient or proof of a universal survival benefit. 3

The physiological task is to distinguish the fixed valve burden from superimposed arterial load, filling limitation, ischemia, and rhythm. A change in one component can help or harm the net circulation while the valve remains narrowed.

78.4 Dynamic obstruction is not the same as a fixed valve stenosis

A small, forcefully contracting ventricle can develop an obstruction that changes during systole. Septal geometry, mitral apparatus motion, reduced filling, and increased contractile activation can narrow the outflow pathway. Midventricular cavity narrowing can create another dynamic gradient.

Systolic anterior motion of the mitral apparatus can contribute to outflow obstruction and mitral regurgitation simultaneously. The resulting murmur, high velocity, hypotension, and vigorous contraction can be misleading if they are interpreted simply as a failing weak pump or a fixed aortic valve lesion.

Loading changes matter because they alter cavity geometry and forces during ejection. Reduced filling or reduced arterial load can permit more cavity narrowing under some conditions, while greater contractile stimulation can intensify the dynamic obstruction. The net response depends on the substrate and accompanying circulation.

Chauvet and colleagues observed dynamic intraventricular obstruction in a septic-shock cohort, frequently with small hypercontractile ventricles and measured flow responses after filling interventions. The study supports recognizing a load-sensitive phenotype. Its selected observations do not prove that all such patients are simply volume depleted, that every gradient has the same anatomical origin, or that fluid administration improves survival. 4

The waveform and anatomical sampling help locate the obstruction. A late-peaking velocity pattern can support a dynamic mechanism, but signal origin must be confirmed. Mitral regurgitant flow, fixed valve obstruction, and serial narrowing can contaminate or complicate the interpretation.

This distinction changes how a physiological response is understood. Stronger contraction is not automatically useful if it intensifies an obstruction. Raising filling pressure may alter geometry while also increasing pulmonary congestion. A favorable gradient change matters when it accompanies improved forward flow and tolerable upstream pressure.

The diagnosis therefore requires the valve, ventricular cavity, mitral apparatus, flow location, and contemporaneous loading to tell the same story. It should not be inferred from a high ejection fraction or one Doppler contour alone.

78.5 Mitral stenosis couples filling time to pulmonary pressure

Mitral stenosis restricts movement from the left atrium to the left ventricle during diastole. Sustaining a given filling flow requires a pressure difference across the valve. The upstream consequence can be increased left atrial and pulmonary venous pressure even while the ventricle receives inadequate volume.

Heart rate changes the time available. Faster rate commonly shortens diastole disproportionately, so the same minute flow must cross the valve within less total filling time. Higher flow during the remaining interval can increase the required gradient. Fever, pregnancy, anemia, and other high-demand states can therefore expose a previously compensated restriction through different combinations of flow and rate.

Atrial fibrillation adds irregular filling intervals and removes coordinated atrial contraction. Its effects depend on ventricular compliance, valve restriction, rate, and prior adaptation. It should not be reduced to one fixed percentage of cardiac output lost with the atrial contribution.

Davies and colleagues related beat-to-beat end-diastolic gradients to cycle length in selected patients with mitral stenosis and atrial fibrillation. Their work demonstrates why pressure observations depend on the interval being sampled. Its derived nomogram is not a universal critical-care valve-area or heart-rate rule. 5

Human pacing experiments by Heidenreich and colleagues also demonstrated a useful contribution from appropriately timed atrial contraction in selected aortic- and mitral-stenosis patients. The small physiological preparation does not quantify a universal dependence or establish a rhythm-intervention outcome benefit in every critically ill patient. 6

Persistent pulmonary venous hypertension can add pulmonary vascular remodeling and right ventricular load. Acute hypoxemia, acidemia, lung injury, or ventilatory pressure may further burden that circulation. Additional volume can then raise atrial pressure more than useful systemic flow.

Interpret the gradient with rate, rhythm, flow, chamber pressures, and the measurement method. A higher gradient during tachycardia need not prove worsening anatomy, while a low gradient during low output cannot independently exclude an important restriction.

78.6 Mitral regurgitation divides total ejection between two routes

During mitral regurgitation, left ventricular systolic emptying divides between the aorta and left atrium. The total stroke volume inferred from cavity volumes includes both routes. A relatively preserved ejection fraction can therefore coexist with inadequate systemic forward flow.

Define total chamber stroke volume as SVtotal, forward aortic volume as SVforward, and mitral regurgitant volume as SVreg, all in mL/beat. Forward cardiac output (CO) is expressed in L/min, with heart rate in beats/min. In a simple model without another important shunt or competing regurgitant pathway:

For constructed end-diastolic volume 160 mL and end-systolic volume 64 mL, total stroke volume is 96 mL and ejection fraction 60%. If 56 mL returns to the atrium, forward stroke volume is 40 mL. At 100 beats/min, forward output is 4.0 L/min. Total chamber emptying of 9.6 L/min is not systemic delivery.

The division depends on more than two fixed resistances. Effective regurgitant opening, leaflet coaptation, ventricular geometry, pressure differences, and the duration and pattern of systole all matter. Functional regurgitation can change as ventricular or annular dimensions change, even when no leaflet has torn.

Rosario and colleagues studied patients during treatment of severe heart failure and found reduced regurgitation associated with a smaller effective regurgitant orifice rather than a corresponding change in its driving gradient. This demonstrates a geometrical contribution in a selected cohort; the combined treatment and observational design do not isolate one drug or prove the same response in structural leaflet rupture. 7

Pulmonary consequences depend on atrial compliance and pressure as well as regurgitant amount. Ventricular consequences depend on the repeated volume load and the effective systolic load. A falling ejection fraction during a loading change can consequently coexist with better forward flow, while an apparently vigorous chamber can continue sending substantial volume backward.

78.7 Aortic regurgitation returns part of systolic flow during diastole

An incompetent aortic valve permits blood to return from the aorta to the left ventricle during diastole. The ventricle must subsequently handle pulmonary venous inflow plus the returning volume. Gross systolic aortic ejection therefore exceeds the net systemic volume when important regurgitation is present.

For constructed systolic forward volume 90 mL and diastolic return 50 mL, net systemic volume is 40 mL per cycle. At 90 beats/min, gross systolic flow is 8.1 L/min but net delivery is 3.6 L/min. These assumed quantities describe conservation; they are not estimated from pulse pressure alone or interchangeable with the mitral-regurgitation calculation when lesions coexist.

Regurgitant volume depends on the effective opening, the changing aorta-to-ventricle pressure difference, and the time available. Slower rate lengthens the diastolic interval per beat, potentially permitting more return. Faster rate can shorten that interval while increasing demand and reducing coronary-perfusion and filling time. The net minute response cannot be predicted from diastolic duration alone.

The coronary environment can become unfavorable through two simultaneous changes: lower aortic diastolic pressure and higher ventricular diastolic pressure. The resulting pressure difference is only an approximation to actual myocardial perfusion, but it helps explain why a large gross stroke volume does not guarantee adequate coronary support.

Chronic volume loading can produce chamber enlargement and compensatory remodeling. Initially, substantial volume may be accommodated without a proportionate pressure rise. Progressive dysfunction, altered relaxation, ischemia, or an acute additional insult can remove that reserve.

Arterial waveforms also evolve. A wide pulse pressure can accompany chronic regurgitation, but its magnitude depends on arterial properties, rate, output, and measurement location. Acute severe regurgitation with rapid pressure equilibration can lack the familiar peripheral appearance. Neither the pulse contour nor the loudness of a murmur independently measures the effective regurgitant volume.

The useful interpretation follows gross ejection, diastolic return, net flow, chamber pressure, and coronary conditions together, with explicit attention to acute versus chronic adaptation.

78.8 Acute lesions encounter chambers that have not adapted

The same regurgitant volume can produce different pressures depending on the receiving chamber’s compliance and prior size. Acute mitral regurgitation introduces systolic volume into an atrium that may not have enlarged or adapted. A sharp pressure rise and pulmonary edema can develop without the large atrium or ventricle familiar from chronic disease.

Acute aortic regurgitation can similarly load a relatively unadapted ventricle during diastole. Rapid ventricular pressure elevation can reduce the gradient for mitral inflow and bring ventricular pressure above atrial pressure before systole. Early mitral closure or diastolic mitral regurgitation can follow under those conditions.

Downes and colleagues described these Doppler findings in a small comparison of acute and chronic severe aortic regurgitation. The study supports the pressure–timing mechanism in selected patients; neither the presence nor absence of one sign supplies a universal diagnostic rule for every acute lesion. 8

The initiating anatomy matters. Chordal or papillary disruption, leaflet perforation, aortic-root disease, prosthetic dysfunction, and infection create different problems even when the immediate consequence is pulmonary edema and shock. A new regurgitant finding must be connected to its cause and the possibility of multiple lesions.

Chronic adaptation changes the presentation without making the lesion harmless. Greater atrial or ventricular accommodation may conceal substantial abnormal flow behind less dramatic pressure changes. Over time, remodeling, arrhythmia, pulmonary vascular changes, and myocardial dysfunction can reduce reserve.

An acute deterioration on chronic disease can therefore contain both an old volume burden and a new pressure or contractile disturbance. The current ejection fraction, chamber size, murmur, and prior study must be interpreted on that timeline.

This distinction prevents two errors: waiting for chronic anatomical enlargement before recognizing acute severe dysfunction, and attributing every new episode to irreversible progression of the valve when loading, rhythm, ischemia, or another illness has changed. The pressure and forward-flow consequences remain the immediate physiological questions.

78.9 Right-sided valve disease connects regurgitation with congestion

Tricuspid regurgitation returns part of right ventricular systolic ejection to the atrium rather than through the pulmonary circulation. Increasing regurgitant volume can therefore enlarge the chamber and venous pressure signal without providing equivalent left-heart inflow. Longitudinal annular motion or visual contraction cannot independently quantify that useful forward volume.

The lesion can arise from leaflet damage, device interaction, annular enlargement, atrial disease, or ventricular remodeling. Pulmonary vascular load and left-sided valve disease can initiate or amplify the cycle. Right ventricular enlargement can worsen coaptation, while worsening regurgitation adds further volume and venous congestion.

Systemic venous pressure then affects hepatic, renal, and intestinal drainage. Respiratory transmission and hydrostatic reference still matter, but an externally influenced intravascular pressure is not physiologically irrelevant. Neither central venous pressure (CVP) alone nor a venous waveform measures total body volume or proves that additional filling would improve output.

Pulmonary pressure estimation requires the same care. Tricuspid jet velocity describes the systolic pressure difference between the right ventricle and atrium. Deriving pulmonary artery pressure requires an appropriate atrial-pressure estimate and absence of important intervening outflow obstruction. Severe regurgitation, incomplete signals, and altered pressure contours can complicate the calculation.

Kim and colleagues compared echocardiography with simultaneous catheterization in severe tricuspid regurgitation. Estimates could agree reasonably well when the pressure components were assessed carefully, while individual uncertainty remained. The study argues against both blind confidence and a blanket claim that every estimate in severe tricuspid regurgitation is unusable; its proposed atrial-pressure refinements are not universal corrections for critically ill patients. 9

Tricuspid stenosis creates a different inflow limitation, while pulmonary valve obstruction or regurgitation changes right ventricular outflow or diastolic volume. These less common configurations follow the same requirement to identify the actual pathway. Their circulatory consequence depends on ventricular reserve, pulmonary load, and the ability to deliver useful flow through the lungs.

78.10 Match Doppler, pressure waves, and volumes to the same question

Doppler peak gradients and catheter peak-to-peak gradients are different quantities. Doppler estimates an instantaneous drop from a velocity at a particular location. Peak-to-peak subtraction uses ventricular and arterial maxima that may occur at different times. A mean gradient additionally depends on the sampled ejection or filling interval.

Pressure can partly recover downstream from a high-velocity jet as kinetic energy is reconverted. Baumgartner and colleagues demonstrated clinically important Doppler–catheter differences related to this process in aortic stenosis. The location of pressure sampling consequently matters; disagreement is not automatically proof that one instrument malfunctioned or that a fixed correction applies. 10

Conservation provides another measurement route. If the same forward systolic volume crosses an upstream outflow tract and the stenotic valve, each area multiplied by its corresponding velocity–time integral represents that volume. Estimated valve area is therefore upstream area times upstream integral divided by valve-jet integral, under the model’s assumptions.

Diameter error affects a circular area through its square. Sampling position, alignment, irregular rhythm, beat selection, changing flow, and serial lesions can further distort the result. A precise-looking area should be reconciled with anatomy and the other observations rather than promoted to an independent truth.

Regurgitant assessment likewise requires integration. Color-jet appearance depends on driving pressure, settings, receiving chamber, and jet direction. Eccentric flow, multiple jets, and changing orifice geometry can challenge simplified flow-convergence assumptions. Measurements from different beats or loading states may not conserve the same volume.

Pressure waves add complementary information. Fuchs and colleagues found that large wedge V waves were neither sensitive nor specific for severe mitral regurgitation. Atrial compliance and other filling abnormalities affect the contour, so a large wave does not measure regurgitant volume or exclude another cause of high atrial pressure. 11

Prosthetic and mixed lesions add further pathways and flow dependence. Unexpected gradients require context about flow, size, motion, and prior measurements rather than automatic attribution to thrombosis. A coherent account matches location, timing, pressure reference, and volume boundaries across all measurements.

78.11 Support and valve correction change several loads at once

Circulatory support changes the operating state without necessarily changing the lesion. Added filling can support useful flow while raising atrial, pulmonary, or venous pressure. Vasoconstriction can preserve coronary pressure while increasing systolic load or changing regurgitant division. Vasodilation can improve forward ejection while reducing perfusion pressure in a circulation with limited reserve.

Rate and rhythm interventions also have competing effects. More filling time, better atrial timing, altered regurgitant duration, and changed myocardial demand can pull in different directions. The appropriate physiological interpretation depends on the actual lesion and response rather than a universal rate for all stenotic or regurgitant disease.

Positive-pressure support can reduce left ventricular transmural load and respiratory work while altering venous return and pulmonary vascular loading. Its net benefit cannot be inferred from improved oxygenation alone, especially with right ventricular dysfunction or fixed inflow restriction. Chapter 79 develops additional device-specific pathways and constraints.

Correcting regurgitation changes the load itself. Reducing the backward outlet may improve net delivery while exposing limited ventricular systolic reserve. Hashimoto and colleagues associated post-repair changes in estimated ventricular–arterial mechanics with an acute ejection-fraction decline in a selected retrospective cohort. Those model-dependent observations do not prove that every decline represents new myocardial injury or that one response predicts every patient’s outcome. 12

Clinical procedural evidence must retain its comparison. Simard and colleagues associated successful transcatheter mitral-regurgitation reduction with better outcomes in a shock registry; success versus failure was not randomized. Goel and colleagues described aortic-valve replacement outcomes among selected shock patients undergoing the procedure, comparing them with other treated patients rather than an untreated shock group. These studies provide feasibility and prognosis information without isolating a causal survival effect or establishing a universal procedure recommendation. 13 14

The assessment therefore asks what improved, what new burden appeared, and whether forward flow and organ function benefited at a tolerable pressure cost. Mechanistic plausibility and procedural success remain distinct from demonstrated patient benefit in a relevant population.

78.12 Integrate forward flow, chamber performance, and pressure consequences

Return to the constructed mitral-regurgitation example: end-diastolic volume 160 mL and end-systolic volume 64 mL give total stroke volume 96 mL and ejection fraction 60%. Regurgitant volume 56 mL leaves forward stroke volume 40 mL. At 100 beats/min, forward output is 4.0 L/min.

Suppose a later measured state has end-diastolic volume 150 mL, end-systolic volume 70 mL, and regurgitant volume 30 mL. Total stroke volume is 80 mL and ejection fraction approximately 53.3%, while forward stroke volume is 50 mL. At 90 beats/min, forward output is 4.5 L/min.

Ejection fraction has fallen while useful output has risen. With arterial oxygen content held at 18 mL O₂/dL for this example, systemic delivery increases from 4.0 × 10 × 18 = 720 to 4.5 × 10 × 18 = 810 mL O₂/min. These are constructed observations, not predicted effects of one drug, rhythm change, or procedure.

The interpretation still requires pressures and context. Lower pulmonary venous pressure with improved breathing would add evidence of reduced upstream burden, but pressure references and ventilatory conditions must match. Persistently high pressure could reflect residual regurgitation, poor compliance, another valve lesion, or additional myocardial disease.

Measurement uncertainty also matters. The calculated difference between total and forward volumes can amplify errors if independently acquired inputs are unsuitable. Actual regurgitant quantification must use compatible beats and account for other lesions or shunts rather than treating the example as a bedside algorithm.

The same discipline applies to stenosis. A gradient falling as output deteriorates is different from a gradient falling after a true reduction in obstruction. Atrial or ventricular enlargement can represent adaptation, consequence, or loss of reserve rather than one stage defined by size alone.

Severe valve physiology becomes coherent when every pressure and volume is linked to its phase and pathway. Forward transport, upstream consequences, coronary conditions, rhythm, and chamber reserve then explain why the patient can improve despite a less impressive fraction, or deteriorate despite a familiar pressure or vigorous contraction.

References

1. Hatle L. Noninvasive assessment and differentiation of left ventricular outflow obstruction with Doppler ultrasound. Circulation. 1981;64:381–387. Original Doppler study.

2. Grossman W, Jones D, McLaurin LP. Wall stress and patterns of hypertrophy in the human left ventricle. J Clin Invest. 1975;56:56–64. Original physiological study.

3. Khot UN, Novaro GM, Popović ZB, et al. Nitroprusside in critically ill patients with left ventricular dysfunction and aortic stenosis. N Engl J Med. 2003;348:1756–1763. Original selected-patient study.

4. Chauvet JL, El-Dash S, Delastre O, et al. Early dynamic left intraventricular obstruction is associated with hypovolemia and high mortality in septic shock patients. Crit Care. 2015;19:262. Original cohort.

5. Davies SW, Gardener JE, Bowker TJ, et al. A new method of haemodynamic assessment of mitral stenosis in atrial fibrillation: construction of a nomogram. Br Heart J. 1990;64:395–399. Original physiological study.

6. Heidenreich FP, Shaver JA, Thompson ME, Leonard JJ. Left atrial booster function in valvular heart disease. J Clin Invest. 1970;49:1605–1618. Original human pacing experiment.

7. Rosario LB, Stevenson LW, Solomon SD, et al. The mechanism of decrease in dynamic mitral regurgitation during heart failure treatment: importance of reduction in the regurgitant orifice size. J Am Coll Cardiol. 1998;32:1819–1824. Original physiological study.

8. Downes TR, Nomeir AM, Hackshaw BT, et al. Diastolic mitral regurgitation in acute but not chronic aortic regurgitation: implications regarding the mechanism of mitral closure. Am Heart J. 1989;117:1106–1112. Original Doppler study.

9. Kim O, Kim J, Choi KH, et al. New echocardiographic algorithm for estimating right atrial pressure in severe tricuspid regurgitation: insights from simultaneous cardiac catheterization. J Am Heart Assoc. 2025;14:e041981. Original simultaneous-measurement study.

10. Baumgartner H, Stefenelli T, Niederberger J, et al. “Overestimation” of catheter gradients by Doppler ultrasound in patients with aortic stenosis: a predictable manifestation of pressure recovery. J Am Coll Cardiol. 1999;33:1655–1661. Original pressure-recovery study.

11. Fuchs RM, Heuser RR, Yin FC, Brinker JA. Limitations of pulmonary wedge V waves in diagnosing mitral regurgitation. Am J Cardiol. 1982;49:849–854. Original catheterization study.

12. Hashimoto K, Nagai T, Kamioka N, et al. Increased afterload in patients with acute reduction in left ventricular ejection fraction following mitral valve transcatheter edge-to-edge repair. Echocardiography. 2025;42:e70095. Original retrospective study.

13. Simard T, Vemulapalli S, Jung RG, et al. Transcatheter edge-to-edge mitral valve repair in patients with severe mitral regurgitation and cardiogenic shock. J Am Coll Cardiol. 2022;80:2072–2084. Original registry study.

14. Goel K, Shah P, Jones BM, et al. Outcomes of transcatheter aortic valve replacement in patients with cardiogenic shock. Eur Heart J. 2023;44:3181–3195. Original registry study.