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Case of biventricular hypertrophy and biventricular failure. Hypertrophy often indicates some degree of diastolic dysfunction with altered filling properties and compliance of the ventricles. As such, these patients are susceptible to increased heart rate, during which the filling time is impaired.
NH-TNE Teaching on Cardiac Hypertrophy
NH-TNE Teaching on Cardiac Hypertrophy
May 6, 2025
Neonatal Hypertension: Estimated blood pressure values in well infants > 2 weeks from 26 - 44 weeks postconceptional age
Neonatal Hypertension: Estimated blood pressure values in well infants > 2 weeks from 26 - 44 weeks postconceptional age
Some preterm infants—particularly those with bronchopulmonary dysplasia (BPD)—may develop significant systemic hypertension, defined as blood pressure exceeding the 95th percentile for postmenstrual age (as per established references - Dionne et al.). This condition may result from a combination of elevated systemic vascular resistance (SVR), prior acute kidney injury, increased vascular stiffness, or exposure to corticosteroids. Systemic hypertension can contribute to left ventricular (LV) remodeling, increased LV stiffness, ongoing adaptation with LV hypertrophy and elevated left ventricular end-diastolic pressure (LVEDP), which may subsequently raise left atrial (LA) pressure and impair pulmonary venous drainage—thereby exacerbating pulmonary vascular disease. Indeed, Laplace's law, in the context of the heart, explains how the heart compensates for increased workload through hypertrophy. When the heart faces increased afterload (like from high blood pressure / high systemic vascular resistances) or volume overload, it responds by thickening its walls (hypertrophy). This thickening, according to Laplace's law, helps to normalize the stress on the heart muscle caused by the increased pressure or volume. However, this adaptation has limits, and excessive hypertrophy can lead to heart failure
When evaluating the right ventricular (RV)/pulmonary arterial compartment in relation to the LV/aortic compartment, whether through septal morphology or shunt directionality (e.g., across post-tricuspid defects), it is essential to interpret findings within the broader context of systemic hemodynamics. Elevated systemic blood pressure may lead to underestimation or mischaracterization of pulmonary hypertension (PH). For example, an infant may have elevated RV and pulmonary artery pressures, but the LV may appear round at peak systole—suggestive not of low RV afterload, but of concurrent systemic hypertension. Similarly, a VSD or PDA may shunt left to right because of high systemic vascular resistance relative to pulmonary vascular resistances (even if the PVR and/or PA pressures are elevated). As such, a right to left post-tricuspid shunt may not be present, despite elevated PVR and/or RV/PA pressures in the setting of high SVR and/or LV/PA pressures.
Similarly, the right ventricle (RV) may be exposed to elevated afterload with associated remodeling and reduced compliance. Concurrently, the LV may exhibit hypertrophy and diastolic dysfunction secondary to systemic hypertension, resulting in even greater impairment in LV compliance. In this setting, a left-to-right shunt at the atrial level may persist or become more prominent, despite elevated right ventricular end-diastolic pressure (RVEDP), due to the relatively higher left atrial pressures driven by impaired LV filling. As such, the expected bidirectional or right ot left shunting at the atrial level may not be present. This paradox underscores the importance of comprehensive assessment of biventricular relaxing/filling properties, shunt physiology, and systemic hemodynamics when interpreting TnECHO findings in infants with complex cardiopulmonary interactions.
In patients with suspected or confirmed systemic hypertension, early involvement of nephrology is advised. Evaluation should include abdominal ultrasound with renal Doppler to assess for renovascular pathology, and serial monitoring of renal biomarkers and electrolytes (plasma and urine creatinine, urine and serum electrolytes). Antihypertensive therapy should be tailored to the clinical context, with agents such as angiotensin-converting enzyme (ACE) inhibitors (e.g., enalapril) and diuretics (e.g., hydrochlorothiazide, spironolactone) considered based on renal function, volume status, and hemodynamic profile.
Anti-Hypertensive Medications can be found in the Cardiovascular Agents section.
References
Dionne JM, Abitbol CL, Flynn JT. Hypertension in infancy: diagnosis, management and outcome. Pediatr Nephrol. 2012 Jan;27(1):17-32. doi: 10.1007/s00467-010-1755-z. Epub 2011 Jan 22. Erratum in: Pediatr Nephrol. 2012 Jan;27(1):159-60. PMID: 21258818.
Sehgal, A., Elsayed, K., Nugent, M. et al. Sequelae associated with systemic hypertension in infants with severe bronchopulmonary dysplasia. J Perinatol 42, 775–780 (2022). https://doi.org/10.1038/s41372-022-01372-y
Reyes-Hernandez ME, Bischoff AR, Giesinger RE, Rios DR, Stanford AH, McNamara PJ. Echocardiography Assessment of Left Ventricular Function in Extremely Preterm Infants, Born at Less Than 28 Weeks' Gestation, With Bronchopulmonary Dysplasia and Systemic Hypertension. J Am Soc Echocardiogr. 2024 Feb;37(2):237-247. doi: 10.1016/j.echo.2023.08.013. Epub 2023 Aug 22. PMID: 37619910.
Sehgal A, Krishnamurthy MB, Clark M, Menahem S. ACE inhibition for severe bronchopulmonary dysplasia - an approach based on physiology. Physiol Rep. 2018 Sep;6(17):e13821. doi: 10.14814/phy2.13821. PMID: 30187692; PMCID: PMC6125606.
Stanford AH, Reyes M, Rios DR, Giesinger RE, Jetton JG, Bischoff AR, McNamara PJ. Safety, Feasibility, and Impact of Enalapril on Cardiorespiratory Physiology and Health in Preterm Infants with Systemic Hypertension and Left Ventricular Diastolic Dysfunction. J Clin Med. 2021 Sep 29;10(19):4519. doi: 10.3390/jcm10194519. PMID: 34640535; PMCID: PMC8509219.
Case of a newborn with biventricular hypertrophy and biventricular dysfunction (systolic)
Case of a newborn with biventricular hypertrophy and biventricular dysfunction (systolic)
Sweep in parasternal long axis outlining that the aortic and pulmonary valve are opening and closing (no atresia - anatomical or functional)
Parasternal short axis outlining the biventricular hypertrophy. The RV seems to be "rocking" and with poor systolic contraction. The septum is dyskinetic with paradoxical movements. The LV free wall also appears to have areas of regional dysfunction.
Case of LV hypertrophy
Case of LV hypertrophy
In this patient, there is systolic anterior motion of the mitral valve - an indicator of LV hypertrophy. There is intra-cavitary acceleration of flow by colour. There is mitral regurgitation. The estimated peak LV pressure in systole is up to 84 mmHg by CW-Doppler.
LV hypertrophy in parasternal long axis with septal hypertrophy
Some degree of systolic anterior motion of the mitral valve. Septal hypertrophy.
Some dynamic obstruction secondary to the septal hypertrophy
Intra-cavitary acceleration with mitral insufficiency.
CW-Doppler estimating the peak systolic LV pressure by mitral insufficiency and capturing some of the intra-cavitary acceleration.
Mitral insufficiency - possibly secondary to the distortion of the mitral apparatus due to the LV hypertrophy. One may also appreciate some degree of RV hypertrophy.
Still frames in the context of significant hypertrophy
Still frames in the context of significant hypertrophy
LV inflow CW-Doppler with some Dagger-Shape negative signal obtained from the ejection phase towards the LVOT, outlining intra-cavitary acceleration and dynamic obstruction.
Biventricular hypertrophy appreciated in diastole.
E/A (two measurements) outlining impaired relaxation from the hypertrophy where A is much higher than the E velocity.
Hypertrophy at mid-papillary muscle level in PSAX. We can appreciate that the pillar are hypertrophied, as well as there is circumferential hypertrophy. We can appreciate in diastole and systole.
Below - still frames of the flow into the LV cavity showcasing the acceleration from inflow to outflow tract. However, we can appreciate that there is flow from below the LVOT feeding post-aortic valve the ascending aorta.
M-Mode showcasing hypertrophy in the PLAX. We can also appreciate some SAM in systole.
PLAX zoom in the LVOT - flow accelerated just below the aortic valve but passing through the LVOT. This is because of dynamic obstruction within the cavity during contraction.
Case of a newborn on high dose steroids who developed biventricular hypertrophy
Case of a newborn on high dose steroids who developed biventricular hypertrophy
Short axis with significant circumferential hypertrophy of the LV, as well as some hypertrophy of the papillary muscles
Parasternal long axis outlining LV hypertrophy and septal hypertrophy.
3D volumes showing circumferential hypertrophy
Acceleration in the LV outflow tract (dynamic sub-aortic acceleration from the septal hypertrophy). There is pseudo (incomplete) systolic anterior motion of the mitral valve. There is also some degree of RV hypertrophy.
Tilted 4 chamber view to evaluate the LVOT with a posterior sweep showing that the papillary muscles are hypertrophied.
Nyquist (velocity filter) at 148 cm/s. Less aliasing but still some subjective acceleration at the LVOT. The LVOT is narrowed from the dynamic contraction of the septum and some degree of pseudo-SAM (systolic anterior motion of mitral valve).
Focus and zoom on the LVOT
LVOT view. Filling seems preserved in diastole.
Intracavitary acceleration at a Nyquist of 92.4 cm/s.
Intra-cavitary acceleration with some degree of mild miltral insufficiency.
The RV hypertrophy is appreciated in this tilted 4 chamber view with some RV focus.
Parasternal long axis. One with a zoom on the LVOT / Aortic valve. The other one with colour showing some mitral regurgitation.
Parasternal long axis. One with a zoom on the LVOT / Aortic valve. The other one with colour showing some mitral regurgitation. One may also appreciate some degree of RVOT free wall hypertrophy.
Some images below (frozen) showing some pseudo-systolic anterior motion of the mitral valve, associated with mitral regurgitation and some acceleration in the left ventricular outflow tract.
Case of severe hypertrophic cardiomyopathy
Case of severe hypertrophic cardiomyopathy
Significant hypertrophy appreciated from the parasternal long axis view. The hypertrophy is septal and at the level of the LV free wall. The LV cavity is almost completely obliterated.
Colour clips indicating acceleration of flow in the out flow tract.
Seep in the parasternal long axis with colour. The RV may be seen with some degree of hypertrophy and filling by colour.
Parasternal short axis view outlining the significant hypertrophy.
Another sweep in the parasternal short axis view. The Aortic valve may be seen. It seems to open and close and be tri-leaflet.
Significant hypertrophy observed in the apical 4 chamber view. There is "kissing" ventricular walls.
There is mitral insufficiency by colour flow.
Acceleration of flow at the level of the LV outflow tract. There is filling of the aorta with flow that seems to originate from below the valve (not retrograde from the ductus)
There is some degree of RV hypertrophy with some tricuspid insufficiency and intra-cavitary acceleration by colour (although the Nyquist is at 61 cm/s)
This view outlines well the biventricular hypertrophy with the significant septal hypertrophy.
Subcostal view.
Subcostal short axis view. Outlining the RVOT with flow through the pulmonary valve.
Flow may be seen in the descending aorta.
Inflow PW-Doppler.
M-Mode in the parasternal long axis view outlining the significant hypertrophy of the septum and the posterior wall.
LV Intra-cavitary peak gradient of at least 81 mmHg estimated by CW-Doppler
RV Intra-cavitary peak gradient of at least 33 mmHg estimated by CW-Doppler. The “Dagger-Shaped” Doppler Signal.
The “Dagger-Shaped” Doppler Signal: A Marker of Dynamic Muscular Obstruction
The “Dagger-Shaped” Doppler Signal: A Marker of Dynamic Muscular Obstruction
On spectral Doppler echocardiography, a distinctive dagger-shaped waveform is a hallmark of dynamic muscular obstruction, typically seen in the ventricular outflow tracts.
This curved, late-peaking Doppler envelope reflects a progressive acceleration of blood flow due to dynamic narrowing during systole, most commonly observed in:
Left ventricular outflow tract (LVOT) obstruction in hypertrophic cardiomyopathy (HCM), where systolic anterior motion of the mitral valve and septal hypertrophy produce a characteristic dagger-shaped spectral profile.
Right ventricular outflow tract (RVOT) obstruction, particularly in infants with unrepaired Tetralogy of Fallot (TOF). Here, continuous-wave Doppler may reveal:
A curved dagger-like contour, indicating dynamic muscular obstruction.
A triangular contour, typically reflecting fixed obstruction at the pulmonary valve level.
Recognizing this spectral morphology is essential, as it helps differentiate dynamic intramyocardial obstruction from fixed anatomical stenosis and can guide clinical interpretation in both congenital and acquired cardiac conditions.
TR of 37 by CW-Doppler
Measurement of the septum by 2D (B-mode) Echocardiography
Case of septal hypertrophy in the context of infant of diabetic mother
Case of septal hypertrophy in the context of infant of diabetic mother
Parasternal long axis outlining the biventricular hypertrophy, with some septal hypertrophy.
Parasternal short axis outlining the biventricular hypertrophy, with some septal hypertrophy. There is flattening of the interventricular septum at the peak of systole.
Apical 4 chamber view. There is subjective paradoxical movement of the septum, although this view is not the most optimal to appreciate that.
Colour box outlines the tricuspid regurgitant jet. There is also flow going through the LVOT to the aorta.
5 chamber view (tilted)
The patent ductus arteriosus is bidirectional, right to left in systole.
Inter-atrial communications that are mainly left to right.
Subcostal view. one may appreciate that the blood flow is going through the aortic valve to the ascending aorta, at the level of the LVOT.
Presentation of DrsJuliana Quintero Salazar & Pasinee Kanaprach on management of IDM-related hypertrophy
Presentation of DrsJuliana Quintero Salazar & Pasinee Kanaprach on management of IDM-related hypertrophy
HOCM 2.pdf
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