Valvular Insufficiency

Valvular regurgitations / insufficiency in the neonate

When we talk about valvular regurgitation grading in the newborn period, things are a bit different than in older children or adults. Many “regurgitations” seen neonatally are physiologic/transient, and quantification is more limited. There is no universally‑accepted neonatal-specific grading scheme in the same way as for chronic disease in older patients. Here are some principles and a “practical” framework that neonatologists / pediatric cardiologists may use. In neonates, small amounts of regurgitation (especially TR or pulmonary regurgitation) are very common and often physiologic / “trivial.” The hemodynamics are shifting rapidly (pulmonary vascular resistance falling, ductal closure, changes in pressures) so what is seen early may resolve. Many quantitative parameters (e.g. EROA, regurgitant volume) are harder to apply because of small sizes, high heart rates, limited windows. Thus, most assessments are semi‑quantitative or qualitative, and the echo report will often use terms like “trivial,” “mild,” “moderate,” or “significant.” More detailed discussions of valvular insufficiency and stenosis, including their physiological and hemodynamic effects, are addressed in greater depth in the cardiac catheterization section.

• In newborns with hypoxic-ischemic encephalopathy (HIE), or during the early transitional period characterized by significant physiological stress, varying degrees of mitral insufficiency may be observed. Transient mitral insufficiency is therefore common in these settings and is most often functional rather than structural in nature. The papillary muscles are particularly vulnerable during hypoxic-ischemic states, as they lie within a myocardial “watershed” zone and are highly sensitive to impaired perfusion. When assessing the hemodynamic significance of mitral regurgitation, pulmonary venous Doppler provides important complementary information: preserved systolic forward flow velocity into the left atrium and the absence of a prolonged atrial reversal phase argue against elevated left atrial pressure. Additional insight can be obtained from pulsed-wave Doppler assessment of an inter-atrial shunt, if present, as elevated left atrial pressure due to significant mitral regurgitation is often associated with a restrictive left-to-right atrial shunt and a higher mean inter-atrial gradient (typically ≥ 5 mmHg). Because pulmonary venous systolic flow occurs during ventricular systole, its velocity is directly influenced by the severity of mitral regurgitation. When pulmonary venous Doppler, left atrial dimensions, left ventricular outflow tract pulsed-wave Doppler velocity–time integral (and estimated left ventricular output), and inter-atrial shunt Doppler findings are all reassuring, these collectively suggest that the mitral regurgitation is not hemodynamically significant. Qualitative assessment of the regurgitant jet also remains useful, as extension of the jet to the roof of the left atrium may indicate moderate significance, whereas more limited jets are typically mild. In most cases, this form of mitral insufficiency is self-limited and improves as myocardial function recovers. For asymptomatic infants, a focused follow-up echocardiographic assessment prior to discharge is usually sufficient and can be performed by pediatric cardiology or by targeted neonatal echocardiography in centers with appropriate expertise.

Acute mitral regurgitation leads to sudden volume overload of the LA during systole. The LA is non-compliant (has not had time to adapt), leading to markedly elevated LA pressures (especially v wave), pulmonary venous congestion → acute pulmonary edema, no significant LA dilation yet. 

• LA Pressure Waveform: 

  • a wave: May be blunted or masked 

  • v wave: Tall and early-peaking, due to regurgitant volume entering LA during systole (This “giant v wave” is a hallmark of acute severe MR) 

  • Giant v waves in the wedge pressure tracing (if using a PA catheter) suggest significant mitral regurgitation. 

Chronic Mitral Regurgitation: The LA gradually undergoes volume adaptation and dilation, becoming more compliant. Despite continued regurgitant flow, mean LA pressure may remain near-normal or only modestly elevated. Pulmonary venous congestion may be mild or absent at rest. But LA dilation predisposes to atrial arrhythmias (e.g., atrial fibrillation).

• LA Pressure Waveform: 

  • a wave: Often reduced or absent (especially if in atrial fibrillation) 

  • v wave: Still elevated but less dramatic than in acute MR due to increased compliance 

  • Chronic MR may present with preserved LV function but progressive LA and LV dilation, atrial arrhythmias, and symptoms of congestive heart failure. Pulmonary hypertension may develop secondarily if LA pressure chronically transmits backward into pulmonary veins.

Tricuspid Insufficiency / Regurgitation (TI/TR)

Tricuspid regurgitation refers to backward flow from the RV into the RA during systole. TR jet velocity is commonly used by echocardiography to estimate velocity/pressure gradients between RV-RA, as an estimation of RV systolic pressure (using a RA pressure of about 5 mmHg). 

• Tricuspid Regurgitation (TR): Trivial / mild TR is very common in neonates. You look at the jet into the right atrium, measure the width of the vena contracta (if feasible), see whether there is systolic flow reversal in hepatic veins. If you see hepatic vein flow reversal, that is more concerning (i.e. moderate/severe). 

• In newborns with hypoxic-ischemic encephalopathy (HIE) or during the early transitional period marked by significant physiological stress, varying degrees of tricuspid regurgitation may be observed. As with mitral insufficiency, tricuspid regurgitation in this context is most often functional rather than structural, reflecting transient right ventricular dilation/dysfunction, altered loading conditions, and the heightened sensitivity of the right ventricle to changes in afterload and myocardial perfusion. The tricuspid valve apparatus, including the papillary muscles, is vulnerable during hypoxic-ischemic states, particularly in the setting of elevated pulmonary vascular resistance or impaired right ventricular contractility and/or secondary right ventricular dilation (which stretches the tricuspid annulus and can also lead to some degree of TR). 

• Assessment of the hemodynamic significance of tricuspid regurgitation should incorporate systemic venous Doppler evaluation (IVC and SVC), as the pattern of flow within the hepatic veins and inferior vena cava provides important insight into right atrial pressure. Preserved forward systolic flow velocities with minimal or absent atrial flow reversal duration argues against significantly elevated right atrial pressure, whereas dampened systolic velocities, jet to the roof of the right atrium (RA), RA dilation ,and coronary sinus dilation suggests more significant regurgitation or right-sided pressure overload. Right atrial dimensions can provide valuable contextual information, as acute functional mild tricuspid regurgitation is often associated with normal or only mildly enlarged right atrial size, while progressive dilation raises concern for sustained volume or pressure loading. Evaluation of right ventricular output using pulsed-wave Doppler at the right ventricular outflow tract, together with assessment of right ventricular size and systolic performance, helps determine whether regurgitation is compromising effective forward flow. When systemic venous Doppler findings, right atrial dimensions, and estimated right ventricular output are reassuring, tricuspid regurgitation is unlikely to be hemodynamically significant. In most cases, this form of tricuspid regurgitation is transient and improves as pulmonary vascular resistance falls and right ventricular function recovers. For asymptomatic infants, a focused follow-up echocardiographic assessment prior to discharge is generally sufficient and may be performed by pediatric cardiology or by targeted neonatal echocardiography in centers with appropriate expertise.

• By echocardiography, TR jet peak velocity obtained using the CW-Doppler best aligned with the jet is often used to estimate the RV-RA gradient using the modified Bernouilli equation. The peak velocity must be estimate at the tip of the full enveloppe of the spectral Doppler curve (measure at the "chin" and not at the "beard" level). This gradient is then used to estimate RV systolic pressure. The TRJ enveloppe can also be used to calculate the dP/dT of the right ventricle. It can also be used to estimate the systolic/diastolic duration time ratio. More in the Pulmonary Hypertension and Right Ventricular Function section.

  • When referring to the tricuspid regurgitation jet (TRJ), the expression “measure at the chin and not at the beard level” is an analogy used to emphasize where along the Doppler envelope the velocity should be measured. In practical echocardiographic terms, this means that the TRJ peak velocity should be measured at the densest, most well-defined portion of the continuous-wave Doppler envelope, where the signal truly represents the maximal pressure gradient between the right ventricle and the right atrium. The “chin” refers to the smooth, bright outer contour of the jet, whereas the “beard” represents the fuzzy, low-intensity spectral dispersion that can occur due to turbulence, gain oversaturation, or suboptimal alignment. Measuring within this lower-density, noisy portion of the signal can lead to underestimation or overestimation of the true peak velocity. In neonates, this distinction is particularly important because tricuspid regurgitation jets are often short, dynamic, and load-dependent. Accurate measurement requires careful optimization of Doppler alignment, gain, and scale, with calipers placed on the outer edge of the clearly defined envelope rather than within the scattered spectral noise. This ensures that the derived right ventricular systolic pressure estimate is physiologically meaningful and not artifactually distorted by signal broadening or poor signal quality.

• Acute TR:

  • Sudden rise in RA pressure with large systolic regurgitant wave (‘cv wave’).

  • Prominent hepatic vein systolic reversal on Doppler.
    
    

• Chronic TR:

• More commonly functional (due to annular dilation from RV pressure or volume overload).

• RA enlargement, elevated mean RA pressure.

• Progressive RV dilation and dysfunction over time.
  
  

RA Pressure Waveform:

• v wave: Prominent and early, merging with ‘c’ wave (forming a large ‘cv’ wave). This is because the v wave is during ventricular contraction, with backflow into the RA by the TR.

• y descent: Rapid (RA quickly empties into RV).
  
  

RV Tracing:

• May show elevated systolic pressure if coexisting pulmonary hypertension.

• May show elevated end-diastolic pressure with RV dysfunction.
  
  

Systemic Effects:

• Potentially cyanosis if there is a right to left inter-atrial shunt that is of significant volume, leading to deoxygenation of the left atrial content. 

• Hepatic congestion, pulsatile liver.

• Peripheral edema, ascites.

• Increased jugular venous pressure with prominent systolic pulsations.

Aortic insufficiency (AI) — also called aortic regurgitation 

AI/AR profoundly affects left ventricular (LV) dynamics, loading conditions, and pressures, both acutely and chronically. In aortic insufficiency, the aortic valve fails to close completely during diastole, allowing retrograde flow of blood from the aorta into the LV. If aortic insufficiency is mild, and there's good-quality CW Doppler across the aortic valve, the diastolic pressure gradient between the aorta and LV can help estimate LVEDP: LVEDP ≈ Aortic diastolic pressure − AR end-diastolic gradient. Important conditions for this to be valid: 

• No mitral stenosis or obstruction: Otherwise, LA and LV diastolic pressures are not equal. 

• Minimal aortic insufficiency: Severe AI distorts the diastolic waveform and may overestimate the gradient. 

• Good Doppler alignment: Poor angle of insonation can underestimate velocities, skewing gradient calculations. 

• Steady rhythm: In arrhythmias like AFib, beat-to-beat variations may make this unreliable. 

• Normal aortic compliance: Very stiff aortas (e.g., in older children or adults) can have altered pressure decay.

• Aortic Regurgitation (AR): AR is rare in newborns in structurally normal hearts. If present, assess the diastolic CW / continuous‑wave signal, measure deceleration slope / pressure half‑time (PHT; if possible), and see if there is diastolic flow reversal in the descending aorta / branch vessels. A steep deceleration and dense jet → more severe. 

  • PHT > 500 ms → mild; PHT < 200 ms → severe

Immediate (Acute) Effects on LV:

• Volume Overload During Diastole: The LV receives blood from both the left atrium and the aorta, dramatically increasing end-diastolic volume. This acutely increases LV end-diastolic pressure (LVEDP). The non-compliant LV cannot accommodate this sudden increase → steep rise in diastolic pressure, leading to: elevated left atrial pressure → Pulmonary venous congestion → pulmonary edema. 

• Low forward stroke volume and hypotension: Widened pulse pressure (↓ diastolic BP due to the steal effect, ↑ systolic BP due to increased stroke volume) 

• Pressure Tracings (LV and Aorta): LV diastolic pressure rises abnormally high. Aortic diastolic pressure falls due to regurgitation. Widened pulse pressure: hallmark of AI. Aortic pressure waveform may show a steep downstroke in diastole ("water-hammer" pulse) 

Chronic AI:

• Eccentric Hypertrophy and Remodeling: Chronic volume overload leads to LV dilation (eccentric hypertrophy) to maintain stroke volume via Frank-Starling mechanism. LV becomes more compliant, so LVEDP may remain normal for years despite volume overload. 

• LVEDV (end-diastolic volume) is incrased

• LVEDP: Normal or mildly elevated early, rises over time 

• Stroke volume: Increased (due to augmented preload), but forward stroke volume is reduced due to regurgitation 

• Ejection fraction: May be preserved early but declines with LV systolic dysfunction in late stages 

• Aortic diastolic pressure remains low (runoff into LV). LV pressure curve shows a gradual rise during diastole, no isovolumic relaxation phase (since aortic valve is incompetent). Bounding peripheral pulses (Corrigan’s pulse), head bobbing (de Musset’s sign), capillary pulsations (Quincke’s sign). Chronic AI can lead to progressive LV dilation, Heart failure symptoms (dyspnea, fatigue), Subendocardial ischemia from reduced coronary perfusion (↓ diastolic aortic pressure) and increased LVEDP.

Angiography can provide a qualitative assessment of valve regurgitation:

• Contrast injected into the aorta will show reflux into the left ventricle.

  • Grade 1 (Minimal): Barely visible opacification of the left ventricle.

  • Grade 2 (Mild): Opacification of the left ventricle, but less dense than the aorta.

  • Grade 3 (Moderate): Equivalent opacification of the left ventricle and aorta.

  • Grade 4 (Severe/Massive): Greater opacification of the left ventricle than the aorta. This angiographic grading system (1-4) is historical and similar to echocardiographic quantification, though echo is often preferred today.

Pulmonary Insufficiency / Regurgitation (PI/PR)

Pulmonary insufficiency is characterized by retrograde flow from the pulmonary artery into the right ventricle during diastole, due to an incompetent pulmonary valve. If there is trivial PR, one may use echocardiography to estimate PA-RV velocities in order to estimate mean PA pressure (using an estimated RV-EDP of 5 mmHg - about the RA pressure).

• Pulmonary Regurgitation (PR): Mild PR can be seen (especially soon after birth when pulmonary pressures are high). One watches for jet width relative to the pulmonary annulus, the density of diastolic signal, and whether there is diastolic flow reversal in pulmonary artery branches.

  1. Jet width / pulmonary annulus ≥ 0.7 for severe PR. PHT of the PR jet < 100 ms as a criterion for severe. Diastolic flow reversal in main or branch PAs

• Acute PR:

  1. RV Volume Overload: Sudden increase in diastolic filling from both the RA and regurgitant pulmonary flow.

  2. RV is non-compliant → Elevated diastolic pressures → RA pressure elevation.

  3. Pulmonary artery diastolic pressure falls (steep slope in diastole on waveform).
     
     

• Chronic PR:

• 1. RV adapts via hypertrophy.

  2. Gradual dilation of RV, often with preserved systolic function early.

  3. Over time → RV systolic dysfunction, elevated RA pressure, tricuspid annular dilation, and functional TR.
     
     

Pressure Tracings:

• PA: Wide pulse pressure (↑ systolic, ↓ diastolic), rapid diastolic decline.

• RV: Elevated end-diastolic pressure over time; loss of isovolumic relaxation phase due to MPA to RV flow at closure of pulmonary valve.

• RA: Gradual elevation in mean pressure, large ‘v’ wave if TR coexists (During ventricular contraction, there is reflux into the right atrium which increases the RA pressure).

Reference: Adapted from Skinner, J., Alverson, D., & Hunter, S. (Eds.). (2000). Echocardiography for the neonatologist (1st ed.). London: Churchill Livingstone.

Examples by Neonatal Echocardiography

Tricuspid regurgitation

Pulmonary insufficiency

Mitral insufficiency

Aortic insufficiency

Aortic regurgitation pressure half-time

In above examples, the PHT are 200 msec and 161 msec. The first peak diastolic velocity gradient is 26 mmHg. If the diastolic BP in the Aorta is around 35, it informs you that the diastolic LV pressure is around: LV early diastolic pressure = 35-26 mmHg = 9 mmHg at the beginning of diastole, and LV end-diastolic 35-13=22 mmHg at end of diastole (peak of filling). This is again a very imprecise estimate as it depends on having a full arterial pressure curve and being able to accurately measure diastolic blood pressure in the aorta (such as with an umbilical arterial catheter), and ideally time the diastolic arterial measurement with early and end diastole. 

In aortic regurgitation (AR), pressure half-time (PHT) is an echocardiographic Doppler parameter that provides an indirect estimate of the severity of regurgitation.

• Pressure Half-Time (PHT): the time (in milliseconds) it takes for the pressure gradient between the aorta and the left ventricle to decrease by half during diastole. It is measured using continuous wave Doppler of the AR jet in the apical 5-chamber or long-axis view (values obtained from the adult literature).

  1. >500 ms: Mild AR

  2. 200–500 ms: Moderate AR

  3. <200 ms: Severe AR (suggests rapid pressure equalization)

• In severe AR, blood rapidly flows back into the LV → the aortic and LV pressures equalize quickly → shorter PHT. The IVRT of the LV is also shorter or inexistant, since there is filling of the LV by the AR during the very early diastole. 

• In milder AR, the flow is slower and pressure equalizes more gradually, resulting in a longer PHT.

• PHT is load-dependent and affected by:

  1. LV diastolic compliance (i.e. high LV filling pressures)

  2. Aortic pressure 

  3. Heart rate

• PHT is not reliable in:

  • Acute AR (pressures equalize rapidly due to noncompliant LV)

  • Aortic stenosis or high afterload states

• PHT should always be interpreted in context with other parameters (vena contracta, jet width, flow reversal in descending aorta, regurgitant volume/fraction, etc.)