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OBJECTIVE—To examine the results of fetal cardiac scanning and audit the changes in performance resulting from the introduction of a training programme for obstetric ultrasonographers. METHODS—Using the database of the Northern Regional Congenital Abnormality Survey (NORCAS), fetuses with complex or significant congenital heart disease (CCHD) diagnosed prenatally in 1994 were identified. A simple programme of centralised and local training was instituted in 1995 by the department of paediatric cardiology to teach obstetric ultrasonographers in district general hospital maternity departments to identify congenital heart malformations. The results of the training programme were assessed by comparing the 1994 identification rate of CCHD with the rates for 1996 and 1997. RESULTS—Birth rate fell during the study from 35 026 in 1994 to 32 874 in 1997. Registration of CCHD also fell, from 115 in 1994 to 87 in 1997. Prenatal recognition of CCHD rose from 17% in 1994 to 30% in 1995 and 36% in 1996. In 1997 it fell slightly to 26.9%. The total number of scans did not change much year on year, but the number of parents choosing termination increased significantly (from 22.7% to 57%). CONCLUSIONS—A simple training programme for obstetric ultrasonographers increased their ability to detect serious congenital heart disease at a routine 18-20 week anomaly scan. With a termination rate of more than 50%, the incidence of CCHD in the population fell from 3.3/1000 to 2.6/1000 live births. This audit, conducted within a stable population using ascertainment by a well established fetal malformation registry, suggests that prenatal diagnosis may have a significant effect on the incidence of complex or serious congenital cardiac malformations. Keywords: congenital heart disease; fetal echocardiography

AIMS To correlate the size and position of isolated ventricular septal defects with closure rate in a cohort of children with mean follow up of more than six years. DESIGN A birth cohort was identified using the northern region cardiac database. The following were noted from case notes: defect size, position, means of closure, and age at closure. RESULTS 68 children were identified. 49 defects were small, 14 were moderate, and 5 were large. 13 cases required surgical closure, including 12 perimembranous defects. 35 defects closed spontaneously. Nine of the small muscular defects remained open and five of the small perimembranous defects remained open. The spontaneous closure rate for muscular defects was significantly greater than for perimembranous defects. Mean age of follow up for patients who still have defects is 76 months. CONCLUSIONS The position of a ventricular septal defect is extremely relevant to its natural history. Perimembranous defects accounted for most of the moderate and large defects that required surgical intervention. After more than six years almost a third of all perimembranous and just over two thirds of all muscular defects closed spontaneously.

AIMS—To examine the haemodynamic effects of brief alteration in arterial oxygenation in preterm infants with respiratory failure. METHODS—Eighteen preterm infants with respiratory failure, aged 9-76 hours, underwent detailed Doppler echocardiographic assessment at 86%, 96%, and 100% SaO2, achieved by altering the FIO2. Sixteen were receiving intermittent positive pressure ventilation, median FIO2 0.45 (0.20-0.65), median mean airway pressure 12 cm H2O (0-20). SaO2 was stable for 15 minutes at each stage. Four parameters of pulmonary arterial pressure were measured: peak velocity of tricuspid regurgitation and peak velocity of left to right ductal flow, TPV:RVET ratio and PEP:RVET ratio, measured at the pulmonary valve, along with flow velocity integrals at the aortic and pulmonary valves, and systemic arterial pressure. Ductal size was graded into closed, small, moderate, large with imaging, pulsed and continuous wave Doppler. RESULTS—Between 86% and 96% SaO2, there were no consistent changes, but in three of the 12 with a patent ductus arteriosus (PDA) there was ductal constriction, with complete closure in one. Between 96% and 100% SaO2, peak ductal flow velocity rose significantly in four of eight with a PDA. Ductal constriction occurred in four infants; in three this was associated with a significant fall in aortic flow integral and a rise in aortic pressure (4-6 mm Hg). Overall, 11 infants went from 86% to 100% SaO2 and pulmonary arterial pressure fell significantly in seven. CONCLUSION—A brief rise in SaO2 within the range maintained by most neonatal units can cause significant ductal constriction. The fall in pulmonary arterial pressure with 100% SaO2 seen in most infants was associated with a fall in pulmonary blood flow (or no change), rather than a rise, indicating that the dominant haemodynamic effect was ductal constriction rather than pulmonary vasodilation.

Congenital heart disease (prevalence 8 per 1000 live births) is the most common congenital abnormality. 12 It accounts for almost half of perinatal and infant deaths caused by congegenital malformation. 3-5 For some time it has been possible to diagnose severe congenital heart disease in the fetus at 18-20 weeks' gestation. This gives the options of counselling, planned delivery, intervention, or termination. The technique is well established but the expertise is available in fewer than 10 centres in the United Kingdom. Anomaly screening by ultrasound of all pregnancies at 18-20 weeks' gestation, including a cardiac assessment, has been advocated 6 and is being implemented This proposal is not universally accepted

OBJECTIVE--To identify coronary artery anomalies in patients with tetralogy of Fallot with an aortogram taken with steep caudal and left oblique angulation ("end-on" aortogram). DESIGN--Prospective evaluation of end-on aortogram in the preoperative angiographic assessment of consecutive patients with tetralogy of Fallot. SETTING--Regional paediatric cardiology centre. PATIENTS--34 patients, aged 3 months to 12 years (median age 9 months). METHODS--An aortogram was performed with steep caudal (38 degrees-45 degrees) and left oblique (0 degrees-30 degrees) angulation under general anaesthetic as part of routine preoperative angiographic assessment. RESULTS--The origins and courses of the coronary arteries were visualised in all patients and important coronary artery anomalies were identified in four patients: single left coronary artery; single right coronary artery (two patients); separate high origin of left anterior descending. These anomalous coronary vessels crossed the right ventricular outflow tract. CONCLUSIONS--It is important to identify preoperatively coronary arteries that may interfere with right ventricular outflow tract reconstruction. An aortogram with steep caudal and left oblique angulation is useful in identifying anomalous coronary arteries and more importantly it defines the relation of these vessels to the right ventricular outflow tract.

The first haemodynamic change during pregnancy seems to be a rise in heart rate. Starting between two and five weeks this continues well into the third trimester. Stroke volume increases slightly later than the heart rate and continues throughout the second trimester after an augmentation of venous return and a fall of systemic vascular resistance and afterload. Myocardial contractility is probably slightly increased. During the third trimester there is relatively little change in these cardiac indices. After delivery there is a very early and dramatic reduction in volume loading followed by a return towards normal cardiac output. Structural changes within the heart reflect the volume loading of pregnancy and include dilatation of the valve ring and increase in myocardial thickness. Post partum resolution of the ventricular hypertrophy seems to take longer than the rest of the post partum changes. The resemblance to the cardiovascular changes associated with training and exercise are fascinating and worthy of further study.

Systolic pulmonary arterial pressure was determined serially over the first 10 days of life in 33 babies with hyaline membrane disease by measuring the peak velocity of pansystolic tricuspid valve regurgitation, using Doppler ultrasound, and applying the Bernoulli equation. Results are presented in age groups 0-12, 13-36, 37-72, and 73-96 hours respectively. The incidence of tricuspid valve regurgitation was 92, 97, 80, and 64% (falling to 35% by day 10) compared with 53, 50, 31, and 0% in 17 healthy premature infants. In comparing healthy babies with those with hyaline membrane disease, no allowance was made for right atrial pressure. The derived 'right ventricle to right atrial (RV-RA) pressure difference', was expressed as a ratio of systemic arterial (systolic) pressure. Over the first three days, this ratio fell much faster in the healthy babies. Values were 0.78:1, 0.77:1, and 0.72:1 in babies with hyaline membrane disease and 0.87:1, 0.53:1, and 0.44:1 in healthy babies. Ductal patency was prolonged in babies with hyaline membrane disease (75% on day 4 compared with 6% in healthy babies). The incidence of bidirectional ductal flow, indicating balanced pulmonary and systemic arterial pressures, was 79, 53, 30, and 20%, and in healthy babies was 41% at 0-12 hours and zero thereafter. Pulmonary arterial pressure was then calculated by adding a right atrial pressure estimate of 5 mm Hg to the RV-RA difference when the babies were ventilated. Babies of lower gestation had lower values. The pulmonary: systemic arterial pressure ratio showed considerable temporal variability, but fell with age and was raised by high mean airway pressure and pneumothorax (through a reduction in systemic pressure), and less noticeably by carbon dioxide tension. It did not correlate significantly with other indices of disease severity. Hyaline membrane disease is associated with delayed postnatal circulatory adaptation characterized by pulmonary hypertension, systemic hypotension, and prolonged ductal patency.

As there is no other measurement of right ventricular preload, central venous pressure (CVP) measurement provides unique and important haemodynamic information. CVP is not measured routinely in neonatology and there is a shortage of data in the ventilated neonate. CVP was measured in 62 ventilated neonates. Thirteen had respiratory disorders (28-42 weeks' gestation, birth weight 860-4390 g) and 49 had congenital heart disease (birth weight 1600-4500 g, age 0.5-30 days). Data from other case reports are also presented. In the babies with respiratory distress, a value of zero was associated with clinical evidence of hypovolaemia and negative values, common in the unventilated neonate, did not occur in those who were ventilated. Values over 7 mm Hg were found in babies with evidence of myocardial dysfunction or persistent fetal circulation but were also found with transmitted high intrathoracic pressure, such as with pneumothorax. In the babies with congenital heart disease, values mostly lay between 4 and 8 mm Hg. Values outside this range, particularly above 8 mm Hg, were usually associated with profound metabolic acidosis, suggesting circulatory failure. While the main use of CVP measurement is in trend analysis, this report suggests that single measurements can be of value, though correct interpretation will depend on the context in which they are made.

Doppler echocardiograms were carried out on 51 healthy babies three times during the first 72 hours of life to estimate pulmonary arterial systolic pressure by measuring regurgitant tricuspid jet velocity and applying the Bernoulli equation. Tricuspid regurgitation was detected at some stage in all preterm babies and most of those born at full term. Pulmonary arterial pressure could be measured from peak regurgitant velocity in babies with pansystolic regurgitation. The incidence of pansystolic regurgitation among 34 term babies at 0-12, 13-36, and 32-72 hours of age was 22, 27, and 19%, and in 17 preterm babies (within the same age groups) was 53, 50, and 31%, respectively. Estimates of pulmonary artery pressure in the term babies were in accord with known catheter values. Pressure fell rapidly during the first day in all 51 babies. The ratio of pulmonary:systemic arterial pressure was comparable between the two groups throughout. Ductal flow patterns mirrored the fall in this ratio with age--bidirectional flow was associated with a ratio of between 0.88:1 and 1.22:1 and high velocity left to right flow with a ratio of between 0.49:1 and 0.66:1. Both these techniques are noninvasive ways of assessing neonatal pulmonary arterial pressure.

Doppler and direct measurements of right ventricle to right atrial pressure drop were made during cardiac catheterisation on 28 occasions in 26 infants with congenital heart disease. Age was 10 days to 12 months (median 4.5 months), and weight was 3.1 to 9.0 kg (median 4.7 kg). We measured peak velocity of tricuspid regurgitation by continuous wave Doppler, and the pressure drop was calculated using the modified Bernoulli equation (delta p = 4v2). There was a high correlation (r = 0.95) between direct and Doppler measurements. Doppler values tended to underestimate the right ventricle to right atrial pressure drop, but this was not of clinical significance (mean 2 mm Hg). The 95% confidence interval for the Doppler velocity was -0.41 to +0.26 m/sec, and was consistent across the range of pressures studied. Variability between observers was tested, by two observers performing sequential paired examinations on 16 newborn babies with tricuspid regurgitation. The coefficient of repeatability was 6.3 mm Hg (95% confidence interval 4.7 to 9.5 mm Hg) or 0.26 m/sec (0.18 to 0.50 m/sec). This method of right ventricular pressure estimation, validated previously only in older children and adults, is a reproducible and accurate technique in infants with tricuspid regurgitation.

Thirteen anaemic children on dialysis were assessed to determine the incidence of cardiac changes in end stage renal failure. Nine children had an increased cardiothoracic ratio on radiography. The electrocardiogram was abnormal in every case but no child had left ventricular hypertrophy as assessed by voltage criteria. However, left ventricular hypertrophy, often gross, was found on echocardiography in 12 children and affected the interventricular septum disproportionately. Cardiac index was increased in 10 patients as a result of an increased left ventricular stroke volume rather than heart rate. Left ventricular hypertrophy was significantly greater in those on treatment for hypertension and in those with the highest cardiac index. Abnormal diastolic ventricular function was found in 6/11 children. Children with end stage renal failure have significant cardiac abnormalities that are likely to contribute to the high cardiovascular mortality in this group. Anaemia and hypertension, or its treatment, probably contribute to these changes. Voltage criteria on electrocardiogram are of no value in detecting left ventricular hypertrophy. Echocardiography must be performed, with the results corrected for age and surface area, in order to detect and follow these abnormalities.

Echocardiography assessment of L-R ductal shunting has relied on indirect estimates of flow ie. left atrial, and left ventricular to aortic ratios (LA:Ao, LVEDD:Ao). Since left ventricular output (LVO) increases with L-R ductal shunting it could provide an alternative means of assessment. Measurement by echocardiography is innaccurate due to error in measurement of aortic root cross-sectional area (AoCSA). Doppler measurement of the aortic flow integral or ‘stroke distance’ (AoSD) is highly reproducible. LVO -AoCSA × AoSD × heart rate, therefore, AoSD & minute distance (MinDis=AoSD × heart rate) were evaluated as alternative methods, excluding AoCSA. Studies before and after ductal constriction or closure were compared in babies

In the presence of Tricuspid Regurgication (TR), Doppler ultrasound can accurately determine systolic pulmonary artery pressure (PAP) by application of the Bernoulli equation to the maximal TR jet velocity. 152 serial ultrasound scans were performed from birth to extubation on 20 neonates ventilated for HMD (27-39 weeks, 945-3020g). Maximal TR jet velocity was measured using continuous wave Doppler. Systemic blood pressure (BP) was measured directly by intraarterial catheter or by Doppler sphygmomanometry. PAP was expressed as a percentage of systemic BP (PAP/BP%). Results were compared with values obtained from 17 healthy preterm neonates examined serially from birth to 72 hours.

It is not always easy to distinguish between supraventricular tachycardia with aberration and ventricular tachycardia by electrocardiographic analysis alone. M mode echocardiography can often help by providing direct or indirect evidence of the relation between atrial and ventricular contraction. Sixteen consecutive patients with spontaneous sustained broad QRS complex tachycardia with heart rates of 120-225 beats/minute were examined. Echocardiographic evidence of 1:1 conduction was seen in three cases and 2:1 atrioventricular conduction in one (all four had supraventricular tachycardia, confirmed by intracardiac electrocardiography in three). Evidence of retrograde block was seen in 12 (all had ventricular tachycardia, with electrophysiological confirmation in 10). Satisfactory views of the mitral valve were obtained in all patients. Patients with ventricular tachycardia had a variable mitral valve opening time (range 42-110%) compared with those who had supraventricular tachycardia (9-15%). Aortic root and left atrial views gave direct evidence of atrial contraction in three cases, and subcostal right atrial wall views were diagnostic in four of five cases. Seven patients with ventricular tachycardia had been wrongly diagnosed elsewhere as having supraventricular tachycardia. This study confirms that echocardiography is a simple and rapid aid to accurate diagnosis in patients with broad QRS complex tachycardia.

We present details of 15 children, aged 3 months to 11 years, with discrete sub-aortic stenosis and ventricular septal defect. We emphasise a high index of clinical suspicion and echocardiography as the best means of diagnosing this dangerous combination. Physical signs were those of ventricular septal defect in all patients, with auscultatory evidence of additional sub-aortic stenosis in only one. Five patients had a short early diastolic murmur of mild aortic incompetence. The electrocardiograph showed isolated left ventricular hypertrophy in eight patients. Cardiac catheterisation and angiography identified the ventricular septal defect in all cases but detected the sub-aortic stenosis in only eight. Cross sectional echocardiography showed both lesions in all 11 patients to whom it was available.

Three patients with complex cyanotic congenital heart disease, who had previously undergone Blalock-Taussig shunt operations, developed severe stenoses at the pulmonary anastomosis of the shunts. All were successfully treated with balloon dilatation, which can thus be considered an effective alternative to reoperation.

The variability of Doppler echocardiographic estimation of cardiac output at the aortic orifice was investigated in eight healthy subjects. Cross sectional echocardiograms of the aortic orifice and aortic Doppler velocities were recorded and measured by four echocardiographers. Between subject variability was significantly larger than within subject variability for all variables. Variability owing to different echocardiographers and different measurement times was small compared with total variability. Coefficients of variation for aortic annular diameter, aortic velocity integral, and heart rate were 4.1%, 6.4%, and 5.0% respectively. The coefficient of variation for cardiac output was 8.8% and the 95% confidence interval for measurement of cardiac output by the Doppler method was 4.45 to 6.35 l/min. One echocardiographer reanalysed all the recordings and the results showed that recording the echocardiograms introduces a significantly larger source of error than measuring them. Thus serial measurements of cardiac output by the Doppler method can be performed with acceptable reproducibility; this indicates that the technique can be accurately applied in clinical practice.

Fifteen patients aged 1-19 years (mean 10.9) with previously unoperated aortic coarctation underwent percutaneous balloon angioplasty between January 1985 and February 1986. Nine (60%) were hypertensive at presentation. Under general anaesthetic the systolic coarctation gradient was 24-50 mm Hg (mean 29) and the coarctation diameter was 4-9 mm (mean 5.5). Meditech balloon catheters 8-18 mm in diameter were inflated 1-4 times at 410-760 kPa. After dilatation the systolic coarctation gradient decreased to 0-20 mm Hg (mean 6) and the coarctation diameter increased to 7-20 mm (mean 12). One patient developed a fusiform aneurysm of the aorta at the coarctation site immediately after the procedure. At reinvestigation 6-16 months (mean 12.5) after dilatation 14 of the 15 patients were normotensive. In 13 patients the residual coarctation gradient was 0-10 mm Hg (mean 3). Two patients had recoarctation with residual gradients of 20 and 24 mm Hg and underwent successful repeat dilatation. One patient had developed a small discrete aneurysm at the coarctation site. Balloon angioplasty is thus a safe and effective method of relieving unoperated aortic coarctation. The frequency of aortic aneurysm and recoarctation is small and probably related to balloon size. This early experience is encouraging, but long term results and further experience are required before this approach is used to treat coarctation generally.

Summary Serial haemodynamic investigations were performed in 20 women who had epidural anaesthesia before elective Caesarean section. Cardiac output was measured by Doppler and cross-sectional echocardiography at the aortic valve. Measurements were performed after preloading the circulation with Ringer lactate solution (mean volume 805 ml) and then 10, 20, 30 and 40 minutes after administration of 0.5% bupivacaine. Preloading increased mean stroke volume from 84 to 94 ml and mean cardiac output from 7.01 to 7.70 litres/minute. Relative to basal values, mean arterial pressure decreased in all subjects after administration of bupivacaine (mean –14%, range –1 to –33%). Five subjects were given ephedrine because of hypotension. In three of these subjects hypotension was associated with a marked decrease in cardiac output. No significant changes in arterial blood pressure or cardiac output were demonstrated relative to basal values in the remaining 15 subjects. Ephedrine induced consistent increases in blood pressure and cardiac output.

Seventeen cases are described in which both atria connect directly to a chamber with right ventricular characteristics. The atria connected through separate atrioventricular valves in six hearts and a common valve in 11. All hearts had a posterior rudimentary chamber. The septum which separated it from the main chamber was directed to the crux of the heart. Ten hearts were from patients with atrial situs solitus and seven from patients with atrial situs ambigous. Arterial connections were concordant in three cases, had a double outlet from the main ventricular chamber in nine and single outlet of the heart in five. The patent artery always arose from the main chamber, with pulmonary atresia in three and aortic atresia in two. This and other studies indicate that double inlet atrioventricular connection does not predict the morphology of the main chamber. Although usually associated with a main chamber of left ventricular type, it may also be associated with a main chamber having right ventricular characteristics. Both types should be considered as univentricular hearts; the posterior chamber in hearts of right ventricular type are analogous to the anterior chamber in univentricular hearts of left ventricular type and are a rudimentary chamber rather than a hypoplastic ventricle. In the right ventricular form of univentricular heart, the trabecular zone of the rudimentary chamber is of left ventricular type.

To evaluate the ability of two dimensional echocardiography to identify and classify ventricular septal defects, 280 infants and children with clinically significant ventricular septal defects were studied. Multiple precordial and subcostal echocardiographic planes were scanned in each patient in an attempt to identify the defects. Defects visualised were classified on the basis of the structures which formed their margins. Subsequent correlation of this information with angiographic (280 patients), surgical (130 patients), and pathological (31 patients) data confirmed that defects in the following sites produced a specific two dimensional echocardiographic pattern. (a) Perimembranous inlet, (b) perimembranous outlet, (c) muscular inlet, (d) single trabecular, (e) muscular outlet, and (f) doubly committed subarterial. A defect was identified and correctly classified in 252 patients. Individual defects were identified with varying degrees of accuracy. All subarterial (24 patients) defects were correctly identified and classified, as were muscular defects of the inlet (18 patients) and outlet (six patients) septa. Of the 185 perimembranous defects, 182 were identified. Only 23 of the 43 single trabecular defects were identified. Small multiple ("Swiss cheese") defects (four patients) were not identified. We conclude that two dimensional echocardiography provides a reliable non-invasive method of identifying and classifying the following ventricular septal defects: (a) perimembranous defects, (b) doubly committed subarterial defects, and (c) muscular defects of the inlet and outlet septa. In our experience it fails consistently to visualise defects in the trabecular septum.

Balloon dilatation of the aortic valve was attempted in 34 consecutive children aged 16 months to 17 years (median 7 years), weight range 9-60 (median 22) kg. Previous surgical valvotomy had been performed in two patients (twice in one of them). The valve was not crossed in one patient. In the remaining 33 patients the pressure difference between the left ventricle and the ascending aorta during systole was reduced from 71 (30) to 28 (19) mm Hg. In 24 patients recatheterisation 2-19 (mean 9) months later showed gradients that were similar to those immediately after balloon dilatation (35 (20) v 31 (20) mm Hg). The two patients with the highest residual gradients immediately after balloon dilatation showed a spontaneous reduction in gradient at repeat catheterisation, whereas the patient who had twice had previous surgical valvotomy showed an increase in gradient from 37 to 99 mm Hg over nine months and required aortic root replacement. Balloon dilatation was repeated in two patients and this caused a further reduction in gradient. New aortic regurgitation occurred in nine (27%) patients (grade I, 8; grade II, 1) and aortic regurgitation was exacerbated (grade I to II) in two of the nine with pre-existing aortic regurgitation. External iliac artery avulsion occurred in one (3%) patient and two (6%) required intravenous streptokinase because the femoral artery became occluded. There were no other complications. Open valvotomy was performed in the child in whom the valve was not crossed, but no other child required aortic valve operation. Balloon dilatation of the aortic valve gave reasonable short term palliation and was well tolerated. It is an alternative to surgical valvotomy for initial palliation of congenital aortic stenosis in many children.

Twenty-three patients with total anomalous pulmonary venous connection were studied by two-dimensional echocardiography. In all cases the diagnosis was made before invasive procedures, with surgical or angiocardiographic confirmation. Eleven patients had supracardiac drainage (three to the coronary sinus, two to the right atrium,) and seven had infracardiac drainage. In the majority of cases the precise pattern of drainage could be identified by combining suprasternal, praecordial, and subcostal views. In 12 cases where the suprasternal cut was used a pulmonary venous confluence could be identified, having a cross-like structure in nine, with three others appearing as a dilated channel behind and separate from the left atrium. Thus, two-dimensional echocardiography reliably makes the diagnosis of total anomalous pulmonary venous connection and in the majority the precise pattern of drainage can be determined.

The possibility was considered that the presence and magnitude of asymmetry of left ventricular (LV) contraction in patients with previous myocardial infarction (MI) could be determined from volume and dimensional characteristics of contraction derived independently from the frontal (AP) and lateral (LAT) views of biplane cineangiograms. Accordingly, regression analyses were determined from biplane cineangiograms in 18 patients without MI to compute end-diastolic (EDV) and end-systolic (ESV) volumes in the AP and LAT views (V biplane = 1.03V calc AP-7.7 ml, r = 0.989, SEE = 8.7 ml; V biplane = 0.85V calc LAT+5.9 ml, r = 0.99, SEE = 8.2 ml). Comparative measurements of EDV, stroke volume (SV), and ejection fraction (EF) in these patients were identical in AP and LAT films, with a small random error (EDV AP = 136.7 ± 13.0 ml; EDV LAT = 136.7 ± 13.4 ml; SEE for SV = ± 13.0 ml ( ± 16%), SEE for EF= ± 0.03 ( ± 5%). In 20 patients with MI EDVs calculated from AP and LAT films were also identical (189.9 ± 18.1 ml and 184.2 ± 17.1 ml, respectively). However, SV exhibited substantial variation between the two views (SV AP = 76.7 ± 5.5 ml and SV LAT = 51.5 ± 4.7 ml, P < 0.001), as did EF (EF AP = 0.45 ± 0.03 and EF LAT = 0.31 ± 0.03, P < 0.001). In addition, directly measured extent of LV minor circumferential shortening was comparable in AP and LAT films in patients without MI (5.15 ± 0.50 cm and 5.25 ± 0.47 cm, respectively), while in patients with MI these measurements differed significantly (4.74 ± 0.41 cm and 2.73 ± 0.31 cm, respectively; P < 0.001). It is concluded that a systematic error will result when estimates of SV and EF, as well as mean circumferential fiber shortening rate, are derived from single plane cineangiograms in patients with MI.