On inotropic support, the LV function has improved, although there is still some brightness of the papillary muscle from possible ischemia/inflammation.
The images show parasternal long-axis M-mode tracings of the left ventricle in a neonate, demonstrating reduced systolic function. On the left, quantitative measurements reveal a left ventricular internal diameter in diastole (LVIDd) of 1.99 cm and in systole (LVIDs) of 1.63 cm, corresponding to a fractional shortening of 18%. There is some paradoxical motion of the interventricular septum. Normal FS of 28% in a term newborn (at least).
The right-sided M-mode image confirms similarly reduced contractile excursion throughout the cardiac cycle, with poor systolic thickening. Overall, these findings are consistent with moderate left ventricular systolic dysfunction.
Mitral insufficiency by colour in PLAX. The Papillary Muscles are bright.
PLAX. There is improvement of the function compared to the first evaluation, on epinephrine. The papillary muscles are observed to be echogenic.
In neonatal myocarditis, the papillary muscles (especially of the mitral valve) may appear increased in echogenicity (brighter) on 2D echocardiography. This reflects myocardial edema, inflammatory cell infiltration, and early necrosis within the ventricular wall and subendocardial regions — the same pathological processes that involve the rest of the myocardium. However, because the papillary muscles are compact muscular structures with a high density of small vessels and a marginal perfusion reserve, they are particularly vulnerable to ischemic and inflammatory injury. As a result, they tend to show echogenic changes earlier and more prominently than the surrounding myocardium.
Mechanisms of Increased Echogenicity
Interstitial and intracellular edema: Inflammation leads to accumulation of fluid and cellular infiltration, which increases acoustic impedance mismatches and therefore echogenicity.
Myocyte necrosis and fibrosis (subacute/chronic stage): When the inflammatory process leads to tissue disorganization and collagen deposition, the echogenic signal further increases.
Microvascular compromise: Myocardial perfusion is often impaired due to endothelial swelling and microthrombi; papillary muscles, being endocardial, are among the first to exhibit ischemic changes (watershed area of the heart).
Perivascular lymphocytic infiltration: Common in viral myocarditis (especially enterovirus, parechovirus), producing heterogeneous echotexture with patchy brightness.
Apical RV view. No hypertrophy. Function normal. FAC 35%.
RV with Zoom in Apical view.
TAPSE is within normal for a newborn (about 1 cm).
Simpson’s biplane showing moderately reduced systolic function. The end-diastolic volume (LVEDV) is 8.8 mL and the end-systolic volume (LVESV) is 5.4 mL, corresponding to a stroke volume of 3.4 mL and an ejection fraction of 38.8% in the A4C (and 45.6% by biplane). The contour tracing shows limited inward endocardial motion and decreased apical shortening, consistent with moderate global left ventricular systolic dysfunction. These findings align with the overall picture of myocardial injury or inflammation, such as seen in neonatal myocarditis or diffuse cardiomyopathy. However, this is improved compared to initial assessments. Normal EF when 55% or more in a newborn.
There is mitral insufficiency. No LVOT obstruction.
Mitral insufficiency.
Tricuspid Insufficiency.
TDI values for s' septum within normal limit. See normative values.
S' normal at lateral LV. E' reduced at lateral TDI outlining possibly some LV diastolic concerns. See normative values.
RV TDI with normal values.
RVSP estimated at 35 mmHg. Infra-systemic. There is always a risk of post-capillary pulmonary hypertension in the context of LV dysfunction.
Each panel shows 2D gray-scale apical four-chamber views with corresponding longitudinal strain curves and bull’s-eye or segmental maps. The global longitudinal strain (GLS or GS) values range from about –9 % to –12 %, and the corresponding ejection fractions are 34–45 %, indicating moderate to severe LV systolic dysfunction.