The Author's Contributions to Echocardiography Literature (Part I-1978-1990) †

Abstract

The author has undertaken multiple echocardiographic studies during his academic career; most of these were published in peer-reviewed journals. These studies include an evaluation of the role of echocardiography in the estimation of left-to-right shunt in isolated ventricular septal defects, an examination of the utility of contrast echocardiography in the diagnosis of anomalous connection of the right superior vena cava to the left atrium, a description of pitfalls in M-mode echocardiographic assessment of the aortic root in left ventricular hypoplasia syndromes, reviews of echocardiographic evaluation of left ventricular function, study of the role of contrast echocardiography in the evaluation of hypoxemia following open heart surgery, a quantification of left ventricular muscle mass by m-mode echocardiography in children, an examination of race and sex related differences in echocardiographic measurements in children, study of cardiac size and function in patients with sickle cell disease, an examination of afterload reduction in the management of primary myocardial disease, study of the utility of echo-Doppler studies in the evaluation of the results of balloon pulmonary valvuloplasty, study of the usefulness of Doppler in the prediction of pressure gradients in valvar pulmonary stenosis, a review of Doppler echocardiography in noninvasive diagnoses of heart disease, echo-Doppler studies of the evaluation of the results of balloon angioplasty of aortic coarctation, study of the value of Doppler in the prediction of pressure gradients across coarctation of the aorta, and a characterization of foramen ovale and transatrial Doppler velocity patterns in the normal fetus.

Keywords: Doppler echocardiography; afterload reduction; aortic coarctation; atrial septal defect; balloon angioplasty; balloon valvuloplasty; contrast echocardiography; left ventricular function; left ventricular hypoplasia syndromes; ventricular muscle mass; ventricular septal defect.

Figure 1

Scattergram demonstrating the relationship of left atrial internal dimension/m² (LAID/m²) with pulmonary-to-systemic flow ratio (Qp:Qs) in patients with isolated ventricular septal defects. The central line is regression line and the parallel lines demarcate the confidence intervals. The number of patients (N), regression equation and correlation coefficient (r) are shown in the insert at the top left. Reproduced from Rees AH, Rao P.S., et al. [1].

Figure 2

Scattergram demonstrating the relationship of the left atrium to aortic root ratio (LA:Ao) with pulmonary-to-systemic flow ratio (Qp:Qs) in patients with isolated ventricular septal defects. The central lines and insert are as in Figure 1. Reproduced from Rees AH, Rao P.S., et al. [1].

Figure 3

Scattergram demonstrating the relationship of left ventricular internal dimension/m² (LVIDd/m²) with pulmonary-to-systemic flow ratio (Qp:Qs) in patients with isolated ventricular septal defects. The central lines and insert are as in Figure 1. Reproduced from Rees AH, Rao P.S., et al. [1].

Figure 4

Selected M-mode recordings from the parasternal short axis view of the left atrium (LA), aorta (Ao), and right ventricular outflow tract (RVOT) while injecting agitated saline into veins of the right (R) hand (A) demonstrating the appearance of contrast echoes in the LA (arrow) first and then Ao (arrow). Similar tracings of the left ventricle (LV) and right ventricle (RV) (B) demonstrate appearance of contrast echoes in the LV (arrow) without contrast in the RV. Similar findings were seen while injecting agitated saline into veins of the left hand. These recordings indicate drainage of the superior vena cava into the left atrium. The start of agitated saline injection is marked with arrows at the bottom of each tracing. ECG, electrocardiogram. Reproduced (modified) from Truman T.A., Rao P.S., Kulungara R.J. [2].

Figure 5

Recordings similar to Figure 4 were made while injecting agitated saline into the veins of the feet and these reveal contrast in the RVOT (A) and RV (B) (arrows in A and B), suggesting that the inferior vena cava drains normally into the right atrium (not shown) and RV. The start of agitated saline injection is marked with arrows at the bottom of each tracing. ECG, electrocardiogram. Reproduced (modified) from Truman T.A., Rao P.S., Kulungara R.J. [2].

Figure 6

Angiographic frames from injections into the right innominate (A,B) and left innominate (LInV) (C) veins demonstrating direct opacification of the right superior vena cava (SVC), left atrium (LA), left ventricle (LV) and aorta (Ao) without opacification of the right heart structures. C, Catheter. Reproduced from Truman T.A., Rao P.S., Kulungara R.J. [2].

Figure 7

Artist’s portrayal of surgical correction of the superior vena cava (SVC) into the left atrium. (A) After incising the SVC, blood is seen going behind the atrial septum (AS) into the left atrium (solid arrow in A). The shadowed area was resected. (B) A pericardial patch was sewn in such a way as to divert the SVC flow into the right atrium (solid arrow in B). (C) A pericardia patch was placed to enlarge the SVC-right atrial junction. Ao, aorta; IVC, inferior vena cava; PV, pulmonary veins. Reproduced from Alpert B.S., Rao P.S., et al. [3].

Figure 8

Following surgical correction, recordings similar to Figure 4 were made while injecting agitated saline into the veins of the hand; these revealed contrast in the right ventricular outflow tract (RVOT) (A) and right ventricle (RV) (B), suggesting that the superior vena cava now drains normally into the right atrium (not shown) and RV. Ao, aorta; ECG, electrocardiogram; LA, left atrium; LV, left ventricle. Modified from Alpert B.S., Rao P.S., et al. [3].

Figure 9

First pass radionuclide angiographic study of the patient with anomalous connection of the right superior vena cava to the left atrium. (A) When radionuclide material (tecnetium-99m macro-aggregated albumin) was injected into a vein in the foot, the inferior vena cava (IVC), right ventricle (RV) and lungs were seen, indicating normal drainage of the IVC into the right atrium. (B) When the injection was made into a vein of the left hand, the left (L) arm vein, the superior vena cava (not marked), left atrium (not marked), left ventricle (LV) and aorta (AO) were seen, indicating anomalous entry of the superior vena cava into the LA. Reproduced from Rao P.S. [34].

Figure 10

(A) Selected M-mode recordings from the parasternal short axis view of the left atrium (LA), aorta (Ao), and pulmonary artery (PA), demonstrating near normal sized aorta in a baby with hypoplastic left heart syndrome. (B) Selected cine frame from aortic arch angiogram in postero-anterior projection of the same infant shown in A, demonstrating hypoplastic ascending aorta and seemingly normal aortic sinuses, explaining the finding of near normal sized aorta in A. AV, aortic valve; PV, pulmonary valve. Modified from Covitz W, Rao P.S., et al. [4].

Figure 11

Simultaneous recording of the electrocardiogram (ECG), phonocardiogram (PCG) and carotid pulse trace (CPT) to illustrate measurement of left ventricular ejection time (LVET) and Q wave of the ECG to S₂ (QS₂). The preejection period (PEP) is calculated by subtracting LVET from QS2. Reproduced from Rao P.S. [6].

Figure 12

(A) Selected M-mode recordings from the parasternal short axis view of the left atrium (LA), aorta (Ao), and right ventricular outflow tract (RVOT) illustrating measurements of preejection period (PEP) and ejection time (ET). (B) Selected M-mode recordings from the parasternal short axis view of the left ventricle (LV) and right ventricle (RV) showing mitral valve closure and Q-Mc (Q wave of the electrocardiogram (EKG) to mitral valve closure). Isovolumic contraction time (ICT) is calculated by subtracting Q-Mc from PEP, ensuring that both recordings are made from cardiac cycles of identical length. Modified from Rao P.S., Kulangara R.J. [5].

Figure 13

Selected M-mode recording from the parasternal short axis view of the left ventricle at the tips of the mitral valve illustrating measurements of left ventricular end-diastolic (LVEDD) and end-systolic (LVESD) dimensions to calculate shortening fraction (see Table 1). Reproduced from Rao P.S., Kulangara R.J. [5].

Figure 14

Selected video frames from apical four-chamber view of a two-dimensional (2-D) echocardiographic study demonstrating dense band of echoes between the right atrium (RA) and hypoplastic right ventricle (RV). Line drawings are shown beneath the 2D frames. Note that the mitral valve is closed in the left image while it is open in the right image. The atretic tricuspid valve echoes remain unchanged. LA, left atrium; LV, left ventricle. Reproduced from Covitz W., Rao P.S. [7].

Figure 15

Selected video frames from subcostal four-chamber view of a two-dimensional (2-D) echocardiographic study demonstrating atretic tricuspid valve (ATV) (thick arrow), represented by a dense band of echoes between the right atrium (RA) and hypoplastic right ventricle (RV). In (A), the mitral valve (MV) is closed, while in (B), it is open. Note the improvement from the pictures shown in Figure 14. LA, left atrium; LV, left ventricle. Reproduced from Rao P.S. [35].

Figure 16

Apical four-chamber view pictures of another infant with tricuspid atresia (large arrows in A,B) with ostium primum atrial septal defect (slanted arrow in B). Note small right ventricle (RV) and a ventricular septal defect (small arrows in A and B). LA, left atrium; LV, left ventricle; RA, right atrium. Reproduced from Covitz W., Rao P.S. [36].

Figure 17

Selected video frames from apical four-chamber, 2-dimensional echocardiographic views of a neonate with tricuspid atresia showing an enlarged left ventricle (LV), a small right ventricle (RV) and a dense band of echoes at the site where the tricuspid valve echo should be (ATV) (thick arrow) with closed (A) and open (B) mitral valve. A moderate sized ventricular septal defect (VSD) (thin arrows) is shown. LA, Left atrium; RA, Right atrium. Reproduced from Rao P.S. [39].

Figure 18

Classification based on morphology of the tricuspid valve is shown diagrammatically. (A) classic muscular type is shown with a thick band of tissue at the location where the tricuspid valve should be. (B) Membranous type, (C) Valvular type with fused valve leaflets, (D) Ebstein’s type with fused valve cusps along with Ebstein type of downward displacement of the tricuspid valve, (E) Atrioventricular (AV) canal (septal defect) type with common AV leaflet sealing off the right ventricle (RV) from the right atrium (RA), and (F) Unguarded muscular shelf type where the RV is divided into inlet and outlet portions by a muscular shelf. LA, left atrium; LV, left ventricle. Reproduced from Rao P.S. [40].

Figure 19

Selected video frame from subcostal view of a neonate with tricuspid atresia demonstrating right-to-left (R to L) shunt (arrow) across the interatrial communication. LA, Left atrium; RA, Right atrium. Reproduced from Rao P.S. [39].

Figure 20

Selected video frames from precordial long axis views of a neonate with tricuspid atresia with normally related great arteries demonstrating enlarged left atrium (LA) and left ventricle (LV), a small right ventricle (RV) and a moderate sized ventricular septal defect (VSD) (thick arrow) on 2D (A) and color flow (B) imaging. Turbulent flow (B) with a Doppler flow velocity of 2.91 m/s by continuous wave Doppler (C) suggests some restriction of the VSD. Ao, Aorta; PA, pulmonary artery. Reproduced from Rao P.S. [39].

Figure 21

(A) Selected video frame from precordial long axis views of a neonate with tricuspid atresia and transposition of the great arteries demonstrating the left atrium (LA), left ventricle (LV), a very small right ventricle (RV) and a moderate sized ventricular septal defect (not marked). The vessel coming off of the LV is traced in (B) and shown to bifurcate into left (LPA) and right (RPA) pulmonary arteries, confirming that this is the main pulmonary artery (MPA). Ao, Aorta. Reproduced from Rao P.S. [39].

Figure 22

Selected video frame from precordial long axis view with color flow mapping of another neonate with tricuspid atresia and transposition of the great arteries illustrates the left atrium (LA), left ventricle (LV), a small right ventricle (RV) and a moderate sized ventricular septal defect (VSD). The vessel coming off of the LV bifurcates into left (LPA) and right (RPA) pulmonary arteries. Reproduced from Rao P.S. [39].

Figure 23

Two-dimensional echocardiographic video frames demonstrating (a) atretic tricuspid valve (ATV) between the right atrium (RA) and right ventricle (RV), (b) a large subtruncal ventricular septal defect (VSD), (c) thickened and somewhat domed truncal valve (TV) leaflets, and (d) origin of the pulmonary artery (PA) from the posterior aspect of the truncus arteriosus (TA). LA, Left atrium; LV, left ventricle. Reproduced from Rao P.S., et al. [22].

Figure 24

Video frame from a two-dimensional echocardiographic and color Doppler study demonstrating (A) atretic tricuspid valve (ATV) between the right atrium (RA) and right ventricle (RV) and blood flow from the left atrium (LA) into the left ventricle (LV) across the mitral valve. The RV (arrow) is very small and hypoplastic. (B) LV and RV with a large ventricular septal defect (VSD) below the truncus arteriosus (TA). Turbulent flow across the truncal valve suggests truncal valve stenosis. (C) origin of the pulmonary artery (PA) from the TA by color flow (arrow), and (D) division of right (RPA) and left (LPA) pulmonary arteries from the PA (labeled in d) in a short-axis view. TV, truncal valve leaflets. Reproduced from Rao P.S., et al. [22].

Figure 25

Selected video frame of continuous wave Doppler across the ventricular septal defect of the same baby shown in Figure 22. Low velocity flow across the ventricular septal defect suggests that the defect is nonobstructive. Reproduced from Rao P.S. [39].

Figure 26

Selected video frames from suprasternal notch views of the aortic (Ao) arch in 2D (A) and color flow (B) images of a neonate with tricuspid atresia and transposition of the great arteries demonstrating coarctation of the aorta (CoA) and hypoplastic transverse aortic arch (TAA). The association of CoA with tricuspid atresia plus transposition of the great arteries is well known. DAo, descending aorta. Reproduced from Rao P.S. [39].

Figure 27

Selected M-mode recording from the parasternal short axis view of the left atrium (LA), aorta (Ao), and right ventricular outflow tract (RVO) while injecting agitated saline into the right atrial line, demonstrating the appearance of contrast echoes almost simultaneously in the Ao and RVO without opacification of the LA, and suggesting that there is no interatrial shunt, and that the shunt is distal to the atria. The time of injection is marked by an arrow at the left top of the figure. ECG, electrocardiogram. Reproduced from Rao P.S., et al. [8].

Figure 28

Selected M-mode recording from the parasternal short axis view of the left ventricle (LV) and right ventricle (RV) demonstrate the almost simultaneous appearance of contrast echoes in the LV and the RV, indicating that that the right-to-left shunt is at the ventricular level. The time of injection is marked by an arrow at the left top of the figure. ECG, electrocardiogram. Reproduced from Rao P.S., et al. [8].

Figure 29

Left ventricular muscle mass in diastole expressed as g/M² is illustrated for white (filled circles) and black (filled triangles) children and sickle cell disease patients (filled squares). Means and standard deviations are shown. Note higher muscle mass in black than in white children by cubed-function (p < 0.05) and Teichholz (p < 0.01) methods; this difference is not significant (p > 0.10 by Ratshin’s method. The diastolic left ventricular muscle mass in sickle cell disease is increased (p < 0.001) when compared with normal subjects by all three methods. Reproduced from Rao P.S., et al. [9].

Figure 30

Left ventricular muscle mass in systole expressed as g/M² is illustrated for white (filled circles) and black (filled triangles) children and sickle cell disease patients (filled squares). Means and standard deviations are shown. Note similar muscle mass in black and in white children by cubed-function (p > 0.1) and Teichholz (p > 0.1) methods and it is higher (p < 0.01) by Ratshin’s method. The systolic left ventricular muscle mass in sickle cell disease is increased (p < 0.001) when compared with normal subjects by all three methods. Reproduced from Rao P.S., et al. [9].

Figure 31

Left ventricular muscle mass in diastole calculated by Teichholz method is plotted against hemoglobin. Note significant (R = 0.74; p < 0.001) correlation between these parameters. Similar correlations were noted between the diastolic and systolic left ventricular muscle mass calculated by all three methods on the one hand, and hemoglobin values on the other. Reproduced from Rao P.S., et al. [9].

Figure 32

Gender-related differences in the measurements of aortic root and left atrium are illustrated for male black (filled circles) and female black (unfilled circles) children. Means and standard deviations (SD) are shown. Note larger (p < 0.001) aortic root size in males than females for all age groups. The left atrial size was larger (p < 0.05 to 0.001) in males than females in most age groups. Reproduced from Rao P.S., Thapar M.K. [10].

Figure 33

Gender-related differences in the measurements of aortic root and left atrium are illustrated for male white (filled circles) and female white (unfilled circles) children. Means and standard deviations (SD) are shown. Note that there is no consistent difference for all age groups in the aortic root and left atrial sizes between male and female white children. Reproduced from Rao P.S., Thapar M.K. [10].

Figure 34

Race-related differences in the measurements of left atrium (LA) and LA to aortic root (Ao) ratio are illustrated for black (filled circles) and white (unfilled circles) children. Means and standard deviations (SD) are shown. Note the larger (p < 0.05 to < 0.001) LA and LA/Ao ratio in black than white children for all age groups. Reproduced from Rao P.S., Thapar M.K. [10].

Figure 35

Race-related differences in the measurements of left ventricular (LV) posterior wall thickness and LV mass are illustrated for black (filled circles) and white (unfilled circles) children. Means and standard deviations (SD) are shown. Note the larger (p < 0.05 to < 0.001) LV posterior wall thickness and LV mass in black than white in all but 11-19 year-old females. Reproduced from Rao P.S., Thapar M.K. [10].

Figure 36

Bar graph showing comparison of hemoglobin, gm% in black (filled bars) and white (open bars) white children. Means and standard deviations (SD) are shown. Note the significantly lower (p < 0.05 to < 0.01) hemoglobin values in black than white children for all age-gender subgroups. Reproduced from Rao P.S., Thapar M.K. [10].

Figure 37

Left ventricular (LV) function indices, namely shortening fraction in percent (%) (left panel), velocity of circumferential fiber shortening (Vcf) in circumferences/sec (center panel) and pre-ejection period (PEP)/LV ejection time (LVET) ratio (right panel) prior to (Before) and following (After) hydralazine therapy are illustrated. Means and standard deviations are shown. Note the significant (p < 0.01 to 0.001) improvement in all LV function indices. Circ: circumferences.

Figure 38

Left ventricular end-diastolic dimension (LVEDD)/m² in mm (closed circles) and velocity of circumferential fiber shortening (Vcf) in circumferences/sec (open circles) are shown from prior to start of hydralazine therapy (0) and at 1, 3, 6, 9, 12, 18, 24, 30, 36 and 42 months following initiation of hydralazine therapy. Means and standard deviations (SD) are shown. The number of subjects at 30, 36 and 42 months is small, and therefore, only mean values are shown. Note the gradual improvement in LVEDD and Vcf. Statistically significant (p < 0.05 to < 0.01) change becomes apparent from 12 months follow-up onwards. Reproduced from Rao P.S., Andaya W.G. [12].

Figure 39

Pre-ejection period (PEP)/left ventricular ejection time (LVET) ratio (open circles) and shortening fraction in percent (%) (closed circles) are shown from prior to start of hydralazine therapy (0) and at 1, 3, 6, 9, 12, 18, 24, 30, 36 and 42 months following initiation of hydralazine therapy. Means and standard deviations (SD) are shown. The number of subjects at 30, 36 and 42 months is small and therefore, only mean values are shown. Note the gradual improvement in PEP/LVET and shortening fraction. Statistically significant (p < 0.05 to < 0.001) change becomes apparent from 12 months follow-up onwards. Reproduced from Rao P.S., Andaya W.G. [12].

Figure 40

Selected M-mode recording from the parasternal short axis view of the left ventricle (LV) prior to (A) and following (B) hydrazine therapy. Note the significant improvement in the LV size and function.

Figure 41

Selected M-mode recording from the parasternal short axis view of the left ventricle (LV) prior to (A) and following (B) hydrazine therapy from a different infant. Also, note the significant improvement in the LV size and function.

Figure 42

Antero-posterior view of chest x-rays prior to (A) and following (B) hydralazine therapy. Moderate cardiomegaly and pulmonary venous congestion were seen prior to therapy (A) which improved remarkably after therapy (B).

Figure 43

Antero-posterior view of chest x-rays prior to (A) and following (B) hydralazine therapy from a different infant. Moderate cardiomegaly with pulmonary venous congestion was seen prior to therapy (A) which improved remarkably after therapy (B), similar to that seen in Figure 42.

Figure 44

Bar graph showing right (RV) and left (LV) ventricular end-diastolic dimensions prior to (Before), immediately after (Immed. After) balloon pulmonary valvuloplasty and at a median follow-up of 14 months (Follow-up). Means and standard deviations (SD) are shown. Note that there is small but not statistically significant (p > 0.05) decrease in RV dimension immediately after balloon pulmonary valvuloplasty, but at follow-up, there was a significant (p < 0.01) decrease in RV dimension. There was no change (p > 0.05) in LV dimension either immediately after balloon pulmonary valvuloplasty or at follow-up. Reproduced from Rao P.S. [13].

Figure 45

Bar graph showing Doppler flow velocity (left panel) in m/sec, calculated Doppler gradient (center panel) in mmHg and catheterization (CATH) measured peak-to-peak gradient (right panel) in mmHg before (B), immediately after (I.A.) and at a median follow up of 14 months (F-U) after balloon pulmonary valvuloplasty. Means and standard deviations (SD) are shown. Note that there is significant (p < 0.01) decrease in Doppler flow velocity, calculated Doppler gradient and catheterization measured gradient both immediately after balloon pulmonary valvuloplasty and at follow-up. Reproduced from Rao P.S. [13].

Figure 46

Scattergram demonstrating the relationship of Doppler-derived (by modified Bernoulli equation) peak instantaneous and catheterization-measured peak to peak pulmonary valve systolic pressure gradients. Note that the linear regression analysis indicated a correlation coefficient (R) of 0.61. Reproduced from Rao P.S. [14].

Figure 47

Scattergram demonstrating the relationship of Doppler-derived (by modified Bernoulli equation) peak instantaneous and catheterization-measured peak to peak pulmonary valve systolic pressure gradients; this is similar to Figure 33, but after removal of data sets form five patients with severe stenosis and one patient with severe infundibular stenosis. Note that the linear regression analysis indicated improvement in correlation coefficient (R) to 0.91. Reproduced from Rao P.S. [14].

Figure 48

Selected right ventricular (RV) cineangiographic frames from lateral projection demonstrating severe infundibular constriction immediately following balloon pulmonary valvuloplasty (A) which has resolved (B) during a study six months later. PA, pulmonary artery. Reproduced from Rao P.S. [14].

Figure 49

Doppler flow velocity recordings from the main pulmonary artery prior to (A), immediately after (B) balloon pulmonary valvuloplasty and at 10-month follow-up (C). Note the high Doppler flow velocity prior to balloon pulmonary valvuloplasty indicating severe gradient in A; the Doppler velocity immediately after balloon pulmonary valvuloplasty has a triangular pattern, indicating the infundibular gradient in B and corresponding to A in Figure 50. At follow-up 10 months later, the Doppler velocity had fallen (C) and corresponded to B in Figure 50, suggesting resolution of infundibular obstruction. Reproduced from Rao P.S. [14].

Figure 50

Selected two-dimensional, subcostal, four-chamber echocardiographic frames with an open (a) and closed (b) atrioventricular valve. Line drawings on the right of a and b are made for greater clarity and for labeling. A large ostium primum atrial septal defect (1⁰ ASD) is shown in a. When the large atrioventricular valve leaflet is open (a), it completely closes the right ventricle (RV) from the right atrium (RA) and ventricular septal defect (VSD) and allows emptying of blood from both atria into the left ventricle (LV). When atrioventricular valve leaflet is closed (b), it continues to occlude the RV from the RA while allowing the VSD to freely communicate between RV and LV. Ap, Apex; AtTV, atretic tricuspid valve; Ba, base; L, left; LA, left atrium; R, right. Reproduced from Rao P.S. [15].

Figure 51

Selected right atrial (RA) angiographic frame in postero-anterior view demonstrating that the floor of the right atrium is formed by one of the leaflets of the atrioventricular valve; this is marked by a large arrow. The contrast material exited the RA via an ostium primum atrial septal defect shown by small arrows with subsequent opacification of the left ventricle (LV). C, catheter; LA, left atrium. Reproduced from Rao P.S. [15].

Figure 52

Line drawings demonstrating two dimensional echocardiographic appearances in subcostal four-chamber view of the muscular (a), membranous (b), and atrioventricular canal (c) variants of tricuspid atresia. (a) The atretic tricuspid valve is represented by a thick band of echoes between the right atrium (RA) and the small right ventricle (RV) in the muscular type. (b) The tricuspid valve is represented by a thin line in the membranous type. Note that crux of the heart (arrows in a and b) is well seen in both these types (a and b). The attachment of the anterior leaflet of the detectable atrioventricular valve to the left side of the interatrial septum is evident. (c) In the atrioventricular canal type of tricuspid atresia, the anterior leaflet of the detectable atrioventricular canal is attached to the anterior wall of the heart, occluding the right ventricle from the right atrium and allowing blood exit of both atria into the left ventricle (LV). Crux cordis and the atrioventricular portion of the interventricular septum are not seen. Reproduced from Rao P.S. [15,40].

Figure 53

Continuous wave Doppler flow velocity recordings from suprasternal notch view directing the Doppler signal towards the descending aorta prior to (top) and twelve hours following (bottom) balloon angioplasty of aortic coarctation. Note the reduction of peak Doppler flow velocity from 3.47 m/s to 2.35 m/s after balloon angioplasty. Also note that the pandiastolic flow seen prior to angioplasty is no longer seen after angioplasty. Reproduced from Rao P.S. [17].

Figure 54

(A,B) Two-dimensional (2D) echo images prior to (A) and following (B) balloon angioplasty of aortic coarctation show improvement in (B). (C–E) Continuous wave Doppler flow velocity recordings from suprasternal notch directing the Doppler signal towards the descending aorta prior to (C) and immediately following (D) balloon angioplasty of aortic coarctation and at six months after angioplasty (E) are shown. Note the reduction of peak Doppler flow velocity from (C) to (D) with further fall in (E). Also note that the diastolic flow is seen throughout the entire diastole (pandiastolic) prior to angioplasty (C), and is seen only is early diastole immediately after angioplasty (D) and at six-month follow-up (E), there was no diastolic flow at all. Reproduced from Rao P.S. [17].

Figure 55

Line drawing of the Doppler flow velocity curve sampled from the descending aorta distal to coarctation site from a suprasternal notch view demonstrating measurement of duration-related parameters. AFT: antegrade flow time; AT: acceleration time; ECG: electrocardiogram; DFV: Doppler flow velocity curve; RRI: R-R interval of the ECG. Reproduced from Rao P.S., Carey P. [18].

Figure 56

Linear regression analysis of catheterization-measured peak-to-peak and Doppler-derived (modified Bernoulli equation) peak instantaneous gradients across aortic coarctation are shown in (A,B). Note the similar correlation coefficients irrespective of the inclusion of proximal Doppler velocities. Similar regression analysis of catheterization-measured peak-to-peak gradients and antegrade flow time (milli seconds) (C) and antegrade flow time fraction (%) (D) show minimal increase in correlation coefficient (r = 0.82) when antegrade flow time is used. Filled triangles: Native coarctations; Filled squares: coarctations immediately after balloon angioplasty (IABA); Filled circles: coarctations at follow-up (FU). Reproduced from Rao P.S., Carey P. [18].

Figure 57

Linear regression analysis of catheterization-measured peak-to-peak gradients across aortic coarctation and predicted gradient calculated by the formula shown in the text indicated a better correlation (r = 0.92). Filled triangles: Native coarctations; Filled squares: coarctations immediately after balloon angioplasty (IABA); Filled circles: coarctations at follow-up (FU). Reproduced from Rao P.S., Carey P. [18].

Figure 58

Catheterization-measured peak-to-peak gradients across aortic coarctation is expressed as a function of descending aortic pandiastolic flow (PDF) distal to the coarctation site. All patients with PDF (filled circles) had gradients of 25 mmHg or more. All but five patients without PDF (filled triangles) had gradients less the 25 mmHg. Three (marked with asterisk) of these five patients had long segment coarctations. Reproduced from Rao P.S., Carey P. [18].

Figure 59

Drawing of the fetal heart demonstrating how the measurements are secured. Diameter (d) of the patent foramen ovale, as measured is shown. The angle (θ) is measured at the origin of the flap of foramen ovale with the atrial septum. The angle varied between 30 and 50 degrees; it was at least 30 degrees in all fetuses. LA: left atrium; LV: left ventricle; RA: right atrium; RV: right ventricle. Reproduced from Wilson AD, Rao P.S., Aeschlimann S. [19].

Figure 60

Plot of the diameter of the foramen ovale against diameter of the aorta. The numbers indicate the number of subjects with that particular measurement. Note excellent correlation with an r value of 0.84, y intercept of 0.605 and slope of 0.817. Reproduced from Wilson A.D., Rao P.S, Aeschlimann S. [19].

Figure 61

Pulse Doppler recording with the sample volume placed on the left atrial side of the foramen ovale (insert at the top) demonstrating transatrial flow. The majority of the flow is from the right atrium (RA) to the left atrium (LA) (bottom of the baseline). Left-to-right atrial shunt (above the baseline) is also seen, as marked by single arrows in the first three beats. Double arrows on the fourth beat shows Doppler recording of the ascending aortic flow, which serves to reference the timing of ventricle systole. Reproduced from Wilson AD, Rao P.S., Aeschlimann S. [19].