Time Of Cardiac Catheterization Research Articles

Functional and histopathologic correlation in patients with dilated cardiomyopathy: An integrated evaluation by multivariate analysis

To correlate left ventricular function and histologic features in patients with dilated cardiomyopathy, precise indexes of hemodynamics and semiquantitative histologic data were combined for multivariate analysis. Right endomyocardial biopsy was performed at the time of cardiac catheterization. Five hemodynamic indexes were used for functional assessment: ejection fraction, ratio of end-systolic stress to volume index, end-diastolic stress, time constant (T) of left ventricular pressure fall, and end-systolic stress. Six histologic findings (disarray of myofibers, hypertrophy of myofibers, scarcity of myofibrils, nuclear changes of myofibers, vacuolization of myofibers and proliferation of collagen fibers) were graded from (-) to (4+). Each finding was assigned to category (-) or (+) according to the absence or presence of significant abnormality. Ordinary statistical analysis revealed that, although ejection fraction was lower in category (+) for proliferation of collagen fibers, ratio of end-systolic to volume index was reduced for category (+) of hypertrophy of myofibers. A significant correlation was present between hypertrophy of myofibers and proliferation of collagen fibers by Spearman rank correlation. When principal component analysis was applied to the hemodynamic data, two principal components could be extracted. Fisher's discriminant analysis could clearly differentiate two categories (-) and (+) in the semiquantitative histologic finding of proliferation of collagen fibers. The analysis indicated that contractility was reduced with elevated afterload in that category (+). Thus, proliferation of collagen fibers may play a pivotal role in deteriorating contractility in patients with dilated cardiomyopathy.

A method of analyzing regional myocardial function: mean wall stress-area strain relationship.

We introduce a new method of defining regional work of the ventricle and evaluating regional myocardial function using the relationship between mean wall stress (sigma) and the natural logarithm of the reciprocal of wall thickness (ln (1/H)). The sigma-ln (1/H) relationship was studied during pressure loading, contractility change, volume loading and the development of ischemia in ten anesthetized dogs. The validity of our method is discussed. At the time of cardiac catheterization, our method was applied to three human subjects: one with a normal heart, one with anterior acute myocardial infarction, and one with inferior acute myocardial infarction. The functioning state of a region of the ventricular wall was evaluated quantitatively by the amount of regional work per stroke.

Allometric determination of the distance from the central venous pressure port to wedge position of balloon-tip catheters in pediatric patients.

Position of the CVP port on a flow-directed balloon-tip pulmonary arterial catheter affects the accuracy of both thermodilution cardiac output determinations and CVP measurements. Systemic allometry (the study of the growth of a part in relation to the total organism) has been used to determine an easily measured independent variable that would predict this position. Sixty-one pediatric patients (aged 0 to 165 months) were studied either at autopsy or at the time of cardiac catheterization. The distance from the central venous port to the wedge position was best predicted by nonlinear manipulation of age.

Factors affecting use of the Doppler-determined time from flow onset to maximal pulmonary artery velocity for measurement of pulmonary artery pressure in children

Measurement of the time from onset to maximal or peak velocity (TPV) of pulmonary artery (PA) flow has been proposed as a noninvasive means of determining PA pressure. The effects of age, heart rate, increased PA pressure and flow, pulmonary valve obstruction and altered PA vascular resistance on this measurement were evaluated. In 84 children, aged 1 day to 18 years, TPV was measured using continuous-wave Doppler echocardiography. The children were separated into 3 groups. Group I (n = 33) consisted of children with no cardiovascular abnormalities. Group II (n = 33) consisted of children with a variety of cardiovascular diseases producing varying PA pressures and flows. Group III (n = 18) consisted of children who had valvular pulmonic stenosis with PA to right ventricular gradients greater than 40 mm Hg. Doppler studies of group II and III patients were performed in conjunction with measurement of PA pressures and flows at the time of cardiac catheterization. In group I TPV showed a significant negative linear correlation with heart rate (r = −0.86, p < 0.001). The ratio of observed TPV to predicted TPV (TPVN) determined using the regression equation for TPV vs heart rate or TPV/TPVN was heart rate- and age-independent (p > 0.1) and ranged from 0.81 to 1.31 (mean 1.005). In group II TPV/TPVN was inversely related to the natural log of the PA pressures (systolic, r = −0.91; mean, r = −0.87; diastolic, r = −0.82; all p < 0.01), whether pressure elevation was due to increased flow, resistance or left atrial hypertension. It was not affected by increased flow in the absence of pressure elevation. In group III TPV/TPVN was prolonged beyond that expected for the PA pressures and beyond the group I range, but did not correlate with transvalvular pressure gradient. Changes in TPV/TPVN reflect changing PA input characteristics due to either decreasing vascular capacitance from pressure elevation or increased resistance from valvular obstruction.

Comparison of high pulse repetition frequency and continuous wave doppler echocardiography for velocity measurement and gradient prediction in children with valvular and congenital heart disease

To compare the ability of high pulse repetition frequency and continuous wave Doppler echocardiography to detect the peak velocity of a jet flow disturbance and to predict pressure gradients accurately, two groups of children with valvular or congenital heart disease were examined using both Doppler techniques. The use study group included 84 children or adolescents (aged 1 day to 19 years) who underwent examination in the echocardiography laboratory with both Doppler techniques in a randomized sequence. The peak velocity recorded with high pulse repetition frequency Doppler echocardiography was compared with the peak velocity recorded with the continuous wave technique. The accuracy study group included 41 children or adolescents (aged 1 day to 16 years) who underwent examination with both Doppler techniques at the time of cardiac catheterization. Doppler pressure gradients were calculated from the peak velocity using the simplified Bernoulli equation and were compared with peak instantaneous gradients and peak to peak gradients measured at catheterization. In the use study, a high correlation was found between peak velocities detected by high pulse repetition frequency and continuous wave Doppler echocardiography (r = 0.94, SEE = 0.28 m/s). In the accuracy study, close correlations were found between measured peak to peak pressure gradients and pressure gradients calculated from continuous wave (r = 0.95, SEE = 7.9 mm Hg) and high pulse repetition frequency Doppler echocardiography (r = 0.94, SEE = 8.7 mm Hg).(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of a new cardiotonic agent, MDL-17,043, on myocardial contractility and left ventricular performance in congestive heart failure

MDL-17,043, a newly synthesized imidazole derivative, has been shown to manifest both inotropic and peripheral vasodilating properties in experimental animals and to be effective when administered orally. Although MDL-17,043 has been demonstrated to inhibit cyclic adenosine monophosphate (AMP) phosphodiesterase activity in vitro, whether its inotropic activity derives from increased myocellular levels of cyclic AMP is not yet known. After intravenous administration of MDL-17,043 to seven patients with severe congestive heart failure (CHF) at the time of cardiac catheterization, the rate of left ventricular (LV) pressure rise increased almost immediately from a control of 878 ± 161 to a peak of 1010 ± 217 mm Hg/sec ( p < 0.01), while cardiac index tended to increase but not significantly. Subsequently, as mean aortic pressure decreased from 86.4 ± 15.9 at control to 75.6 ± 16.4 mm Hg ( p < 0.01), cardiac index rose from 1.87 ± 0.35 at control to 2.30 ± 0.27 L/min/m 2 at peak effect ( p < 0.01), while pulmonary capillary wedge pressure fell from 23.7 ± 5.1 to 13.1 ± 4.6 mm Hg ( p < 0.01). Concomitantly, the rate of LV pressure rise returned to control value. Thus, intravenous administration of MDL-17,043 improves myocardial contractility and LV performance in patients with severe CHF. This manifest improvement in LV performance most probably results from both the positive inotropic and direct vasodilating effects of MDL-17,043.

Acute electrophysiologic, hemodynamic and left ventricular effects of nifedipine and beta-blocker interactions Maintenance of global and regional left ventricular wall motion

To assess potential cardiac effects of nifedipine and β-blocker interactions, 10 men receiving chronic β-blocker therapy for angina underwent hemodynamic, electrophysiologic and left ventricular (LV) functional analyses at the time of cardiac catheterization before and after buccal administration of 10 mg of nifedipine. Although this combination is usually well tolerated, there have been occasional reports suggesting that the combination of nifedipine and β-blocking agents may increase the likelihood of congestive heart failure, severe hypotension or exacerbation of angina. All patients had class II or III stable angina pectoris and were receiving at least 160 to 240 mg/day of propranolol or equivalent doses of β-blocker therapy. Nifedipine produced no acute electrophysiologic changes, including heart rate, PR interval, AH interval, HV interval, sinus node recovery time or heart rate at which atrioventricular nodal block occurred. Hemodynamic effects included no significant change in mean right atrial pressure (7 ± 1 vs 5 ± 1 mm Hg), while mean pulmonary artery pressure decreased significantly (20 ± 2 vs 17 ± 1 mm Hg, p ≤0.05). In addition, LV end-diastolic pressure decreased significantly from 16 ± 2 to 10 ± 1 mm Hg (p ≤50.05), with a nonsignificant decrease in mean aortic pressure from 93 ± 5 to 86 ± 4 mm Hg. Likewise, no significant change occurred in cardiac index (3.2 ± 0.4 vs 3.0 ± 0.4 liters/min/m2) or systemic vascular resistance (1,157 ± 247 vs 1,170 ± 236 dynes/s/cm 5). Left ventricular ejection fraction (EF) was the same before and after nifedipine (73 ± 2 % vs 74 ± 2%). Segmental EF (5-segment area method) showed no differences in function when jeopardized segments (supplied by a coronary artery with ≥50% stenosis) were compared with nonjeopardized (normal blood supply) segments. Jeopardized segmental EF was 53 ± 3 % before and 56 ± 3 % after nifedipine, while nonjeopardized segments revealed a 58 ± 3 % EF before nifedipine and a 58 ± 3 % EF after the drug. Conversely, analysis by segmental function revealed significant improvement in depressed segments (EF ≤ 45 % ) after nifedipine from 38 ± 2 % to 47 ± 3 % (p ≤50.05) compared with normal segments (EF >45 %) from 60 ± 2 % to 59 ± 1 % (difference not significant). It is concluded that nifedipine and β-blocker interactions produced no significant adverse effects on electrophysiologic, hemodynamic or LV functional parameters in patients with normal LV function at rest. Furthermore, depressed segments appeared to normalize after the addition of nifedipine.

Intracoronary platelet activation in ischemic heart disease: Effects of ticlopidine

Plasma levels of platelet factor 4 have been measured in the aortic and coronary sinus blood of 35 patients: group I (n = 12) with normal coronary arteriograms; group II (n = 15) with angiographically proven coronary artery disease; and group III (n = 8) composed of patients with ischemic heart disease who were being treated with the antiaggregant agent ticlopidine at the time of cardiac catheterization. The mean increase in platelet factor 4 levels through the coronary circulation was 27.4 ± 21.9 ng/ml (mean ± standard deviation) in group II, compared with −1 ± 4.5 ng/ml in group I ( p < 0.01). In group III plasma levels of platelet factor 4 in aortic and coronary sinus samples were all within the normal range. Thus, we conclude that platelet activation constantly occurs in the coronary circulation of patients with stable coronary artery disease, and can be prevented with ticlopidine.

The pacing stress test reexamined: Correlation of pacing-induced hemodynamic changes with the amount of myocardium at risk

To assess the relation between extent of ischemia and the magnitude of hemodynamic changes, 25 patients (5 with normal coronary arteries and 20 with significant coronary obstructive disease) were studied with rapid atrial pacing and thallium scintigraphy at the time of cardiac catheterization. Hemodynamic variables were measured before, during and after maximal pacing. Thallium was injected intravenously during maximal pacing and scans in three standard views were obtained immediately in the catheterization laboratory, with delayed scans obtained 4 hours after the cessation of pacing. The three thallium scans were each subdivided into five segments, and a thallium score was obtained on the basis of the total number of segments that were hypoperfused. Each patient was assigned a total thallium score corresponding to thallium defects at maximal pacing, as well as a redistributed thallium score corresponding to the difference between thallium score at maximal pacing and that 4 hours later. With pacing, patients with normal coronary arteries demonstrated no significant change in baseline hemodynamic variables, whereas patients with coronary artery disease exhibited a decrease in cardiac index, an increase in systemic vascular resistance, a widening of arteriovenous oxygen difference, an increase in pulmonary capillary wedge pressure and mean pulmonary artery pressure during maximal pacing and an increase in left ventricular end-diastolic pressure immediately after pacing. There was a significant correlation (Spearman rank r = 0.64, p less than 0.01) between redistributed thallium score and an increase in left ventricular end-diastolic pressure in the postpacing period. Moreover, there was an even higher correlation (Spearman rank r = 0.90, p less than 0.001) between total thallium score and the postpacing increase in end-diastolic pressure. It is concluded that in patients with coronary artery disease the magnitude of pacing-induced hemodynamic changes reflects both the amount of myocardial tissue at ischemic jeopardy and the total mass of hypoperfused myocardium during maximal pacing stress.

DIAGNOSIS OF PULMONARY HYPERTENSION IN CHILDREN WITH ENDOCARDIAL CUSHION DEFECTS BY M-MODE ECHOCARDIOGRAPHY

Selective Echo parameters have been used in separating children with VSD with and without pulmonary artery hypertension (PAH). This study was performed to assess specific Echo parameters in pts with endocardial cushion defects (ECD) with and without PAH. 22 pts (2 months - 11 years, 17 females/5 males) were compared with 27 normal controls (C). 5 pts had ASD I°, 3 pts had VSD of the ECD variety and 14 pts had complete A-V canal. Pts were divided into Group I (GI) 4 pts with pulmonary artery systolic pressure (PASP) 50 mm Hg were recognized with no false positive. Thus, these two parameters (early tricuspid closure and increased right isovolumic contraction index) are useful in detecting PAH in children with ECD and could be used to optimize the time of cardiac catheterization.

Spontaneous closure of secundum atrial septal defect in infants and young children

The records of 264 pediatric patients with uncomplicated ostium secundum atrial septal defect (ASD) were reviewed. Eighty-seven patients were younger than age 4 years at the time of cardiac catheterization. Subnormal weight gain, frequent pneumonia, cyanosis or tachypnea were present in 26 patients (30%). Of the 36 infants at catheterization, 17 (48%) had the previously described symptoms, including 12 (33%) who had congestive heart failure. Eight of the 36 infants were found to have closed their defect at a subsequent catheterization. Six of 18 patients who underwent cardiac catheterization between 1 and 2 years of age also had spontaneously closed their ASD at subsequent study. Statistical analysis of hemodynamic data revealed no difference (except a smaller shunt size) between ASDs that closed and those that did not in patients who were <4 years at initial catheterization. Analysis of hemodynamic data revealed no statistical differences between groups of patients with an ASD who were younger than and those older than 4 years at time of diagnostic study. Patients with ASDs that closed were significantly different from patients with atrial level shunting thought to be secondary to a valve-incompetent foramen ovale with respect to age at initial study (11 versus 2 months, p <0.001), mean left atrial pressure (7.7 versus 12.3 mm Hg, p <0.02) and difference between mean right and left atrial pressures (1.0 versus 4.2 mm Hg, p <0.01). Because of this high incidence of spontaneous closure of ASD, even in symptomatic patients, intensive medical management rather than surgical correction is recommended for patients with ASD who are younger than age 2 years. Elective surgical repair of ASD diagnosed after age 4 years is recommended because spontaneous closure after that age is probably unlikely.

Intracoronary nifedipine in human beings: Magnitude and time course of changes in left ventricular contraction/relaxation and coronary sinus blood flow

Eight patients, all men, having at least 75% stenosis of the proximal, middle or both segments of the left anterior descending coronary artery, underwent intracoronary drug studies at the time of cardiac catheterization after saphenous vein bypass grafting. Nifedipine, 0.1 mg dissolved in saline solution, was infused into a left anterior descending graft that was the primary blood supply to each patient's anterior left ventricular wall and septum. High fidelity left ventricular pressure and its first derivative, dP/dt, and aortic pressure were sampled synchronously with coronary sinus blood flow by the thermodilution technique. The time constant of isovolumic pressure decay (T) was derived. In five patients, percent systolic shortening and mean shortening velocity were determined from myocardial markers implanted into the midwall of the myocardium at the time of cardiac surgery. In response to nifedipine, left ventricular systolic pressure decreased and end-diastolic pressure increased up to 60 seconds. Both positive and negative dP/dt also decreased up to 60 seconds, whereas coronary sinus blood flow increased up to 5 minutes. T was increased at 1 minute but returned to baseline by 3 minutes. Percent systolic shortening and mean shortening velocity were decreased at 1 minute but returned to control level by 3 minutes. Thus, although both left ventricular systolic and diastolic function were depressed by intracoronary administration of nifedipine, coronary sinus blood flow was augmented and remained increased long after changes in left ventricular contraction and relaxation had subsided. These temporal differences are consistent with animal studies showing a differential depressant effect of nifedipine on calcium uptake in smooth muscle and cardiac muscle.

Quantification of pressure gradients across stenotic valves by Doppler ultrasound

Two-dimensional echocardiography has proven very useful in assessing valvular heart disease, but the technique is limited in certain groups of patients and is unable to quantify a transvalvular pressure gradient. Advances in the Doppler ultrasound techniques have made it possible to noninvasively measure velocity of flow across a stenotic heart valve and to calculate the pressure gradient. A commercially available, continuous and pulse wave Doppler instrument was utilized to assess the transvalvular pressure gradient in patients with mitral and aortic stenosis and the transmitral pressure half-time to calculate mitra valve area. Thirty-five consecutive adult patients with suspected aortic stenosis and 30 adult patients with suspected mitral stenosis underwent Doppler ultrasound examination within 24 hours of cardiac catheterization. An adequate Doppler examination was obtained in 81% of the patients with aortic stenosis, with a correlation between the Doppler-derived transaortic gradient and the catheterization-derived gradient of 0.94. The Doppler-measured gradient accurately separated those patients with significant aortic stenosis (gradients of greater than 50 mm Hg) from those patients with noncritical aortic stenosis. Similarly, an adequate Doppler examination was obtained in 90% of the adult patients with mitral stenosis. There was also close correlation between the mitral valve area and mean pressure gradient measured by the Doppler technique and that obtained at the time of cardiac catheterization (r = 0.87 and 0.85, respectively). The Doppler technique proved to be useful in those patients who had also undergone prior mitral commissurotomy. This study confirms that the combined continuous pulse wave Doppler technique will serve as a valuable addition to the diagnostic capabilities offered by echocardiography.

Aortic stenosis and rupture of mitral chordae tendineae

Ten patients with aortic stenosis and ruptured mitral chordae tendineae constituted 8% of 125 consecutive surgical cases of chordal rupture. Their ages ranged from 54 to 87 years (mean 68). Six patients presented with acute onset of congestive heart failure, and eight were in New York Heart Association functional class III or IV at the time of cardiac catheterization. Extensive mitral anulus calcification was observed by fluoroscopy in seven patients. The mean aortic valve area index was 0.4 cm2/m2 and nine patients had moderate to severe mitral regurgitation by angiography. Calcific aortic stenosis affected a tricuspid valve in nine cases and a bicuspid valve in one case. One patient had a rheumatic mitral valve and one a redundant myxomatous mitral valve; the remaining eight had no abnormality of the mitral apparatus commonly regarded as predisposing to chordal rupture. Mitral anulus calcification and ventricular anatomic and hemodynamic alterations in aortic stenosis may contribute to rupture of the mitral chordae tendineae.

Programmed electrical stimulation of the heart in coronary artery disease

The induction of ventricular arrhythmia in patients with a history of malignant ventricular arrhythmia by programmed electrical stimulation (PES) is associated with a poor prognosis. However, the incidence and significance of inducible arrhythmia in patients with stable coronary artery disease (CAD) who do not have a history of serious arrhythmia are unknown. We studied 32 such patients (31 men, mean age 55 years) with PES at the time of cardiac catheterization. Fourteen patients (Group I) manifested greater than or equal to 3 extraventricular responses when challenged with 1 to 3 propagated right ventricular extrastimuli during ventricular pacing. Twelve (86%) of these 14 had evidence of left ventricular dysfunction (LVD), defined by a global ejection fraction of less than 50% or regional wall motion abnormalities. The remaining 18 patients (Group II) manifested less than or equal to 2 responses to extrastimulation. Only 4 (22%) of these 18 had LVD. Proximal 3-vessel CAD was more frequent in Group I patients (10 of 14, 71%) than in Group II (7 of 18, 39%). Only 5 patients (4 from Group I and 1 from Group II) demonstrated complex arrhythmia during exercise testing or ambulatory monitoring. The induction of extraventricular responses during PES may serve as an independent marker of electrical instability in the coronary population and is a much more common finding in those with LVD.

Pacemaker-Induced Pseudotricuspid Regurgitation

A patient with aortic stenosis and ventricular pacemaker had clinical findings suggesting tricuspid regurgitation. Her presentation was actually caused by regular and constant cannon waves resulting from ventriculoatrial conduction of paced beats. The correct diagnosis was confirmed by abolition of hepatic pulsations during atrial pacing at the time of cardiac catheterization. Therapy consisted of restoring antegrade atrioventricular conduction.

Two-dimensional echocardiographic identification of pulmonary artery branch stenosis

Pulmonary artery branch stenosis is a not uncommon congenital lesion, noted in approximately 4% of children at the time of cardiac catheterization. Real-time 2-dimensional echocardiography was used to examine 10 patients with angiographically documented pulmonary branch stenosis. Five cases of pulmonary artery branch narrowing were identified by echocardiography without prior knowledge of angiographic findings. In 5 other patients whose angiographic results were known, the narrowings were identified in 4 of 5 cases. These results demonstrate the feasibility of evaluating pulmonary branch stenosis with the nonionizing, noninvasive method of 2-dimensional echocardiography.

Oxygen consumption in adult patients during cardiac catheterization.

The determination of cardiac output by the Fick principle requires the quantitation of the arteriovenous oxygen (O2) content difference across the pulmonary bed and the O2 consumption. Since a correct measurement of O2 consumption may be difficult, an assumed value is sometimes substituted into this equation. Despite this practice, there is no appropriate reference standard for O2 consumption applicable to the adult catheterization laboratory. Therefore, we determined O2 consumption in 108 patients (69 men and 39 women, mean age, 49 years) at the time of catheterization by multiplying the arteriovenous content difference by the indicator dilution cardiac output, thereby eliminating errors related to the collection and analysis of the timed collection of expired air. O2 consumption index (O2 consumption/m2 of body surface area) averaged 126 +/- 26 ml/min/m2 (mean +/- SD), but there was wide variability(65-250 ml/Min/m2). O2 consumption was not affected by patient age or sex but was lower in those who were mildly sedated before catheterization (sedated, 121 +/- 22 ml/Min/m2; nonsedated, 132 +/- 28 ml/min/m2; p = 0.023). Thus, O2 consumption varies greatly among adults at the time of cardiac catheterization, so that any attempt at estimating this variable is fraught with major potential error.

Noninvasive pulsed Doppler determination of cardiac output in neonates and children

Mean blood flow velocity (VAo) in the ascending aorta was measured noninvasively in 33 children, ages 3 days to 17 years, by pulsed Doppler technique at the time of cardiac catheterization. Measurements were made from a suprasternal approach with a portable, range-gated device. The ascending aortic diameter was determined echocardiographically and aortic cross sectional area calculated (A = pi d2/4 cm2). Aortic flow (QAo) was computed from Doppler recordings: QAo (ml/minute) = VAo (cm/second) X A (cm2) X 60 (second/minute). Values were compared with cardiac outputs determined according to the Fick principle, using measured oxygen consumption calculated oxygen capacity, and oxygen saturation. Subjects with aortic valve abnormalities or left ventricular outflow tract obstruction were excluded from study. Agreement between the two methods was excellent (linear regression r = 0.98, slope = 1.07, y-intercept = -4.5 ml, range 403 to 5.540 ml/minute). The Doppler technique is a quick, noninvasive, and accurate method of determining ascending aortic blood flow in neonates and children.

New prognostic criteria for children with cyanotic congenital heart disease.

Available oxygen and oxygen unloading capacity were determined at the time of cardiac catheterisation, from blood gas analysis, p 50 in vivo, and haemoglobin, in 79 children with cyanotic congenital heart disease, their age ranging from 2 weeks to 14 years. The patients were followed up for six months to find out how many of those without surgical intervention survived. Actuarial analysis showed that the six month survival rate among the patients with low available oxygen or oxygen unloading capacity was significantly lower (24% and 49%, respectively) compared with those with normal indices (90% and 96%, respectively). Both available oxygen and oxygen unloading capacity were superior to arterial oxygen saturation and arterial oxygen content as prognostic criteria. Haemoglobin and haematocrit were of little value in prognosis. Available oxygen appeared to be the best prognostic criterion for survival at six months. It is concluded that available oxygen and oxygen unloading capacity are useful prognostic criteria in children with cyanotic congenital heart disease. These new criteria, when used in conjunction with the conventional methods of assessing the cardiac lesion, may be of considerable help to the physician in evaluating the prognosis of the patient.