A new method for measurement of right ventricular residual ratio using 121I-MAA

A new technique of precordial counting with 131I-MAA for measurement of right ventricular residual ratio (RVRR) was described. 131I-MAA was rapidly injected injected into the right ventricle at the time of right heart catheterization. The fraction of isotope discharged from this chamber per beat was determined with a crystal detector with tapered collimator which was pointed to the center of right ventricle. The radioisotope dilution curve was corrected by using the lung built up curve recorded by the other detector pointed to the lung field. Then, the right ventricular end-systolic volume (ESV) and the right ventricular end-diastolic volume (EDV) were calculated from the RVRR and stroke volume. In 6 patients with normal hemodynamics, the RVRR averaged 57.8 plus or minus 4.9%, the ESV 52.2 plus or minus 13.6 ml/M(2) and the EDV 89.4 plus or minus 15.1 ml/M(2). In 16 patients with heart diseases, the RVRR averaged 60.6 plus or minus 7.1%, the ESV 80.6 plus or minus 34.0 ml/M(2) and the EDV 127.2 plus or minus 43.6 ml/M(2). In 11 patients with chronic pulmonary diseases, the RVRR averaged 70.7 plus or minus 9.9%, the ESV 94.7 plus or minus 42.4 ml/M(2) and the EDV 133.0 plus or minus 46.5 ml/M(2). The RVRR in the last group increased significantly.     

Radionuclide analysis of right and left ventricular response to exercise in patients with atrial and ventricular septal defects

In patients with ventricular or atrial septal defect, the ventricle which is chronically volume overloaded might not appropriately respond to increased demand for an augmentation in output and thereby might limit total cardiac function. In this study we simultaneously measured right and left ventricular response to exercise in 10 normal individuals, 10 patients with ventricular septal defect (VSD), and 10 patients with atrial septal defect (ASD). The normal subjects increased both right and left ventricular ejection fraction, end-diastolic volume, and stroke volume to achieve a higher cardiac output during exercise. Patients with VSD failed to increase right ventricular ejection fraction, but increased right ventricular end-diastolic volume and stroke volume. Left ventricular end-diastolic volume did not increase in these patients but ejection fraction, stroke volume, and forward left ventricular output achieved during exercise were comparable to the response observed in healthy subjects. In the patients with ASD, no rest-to-exercise change occurred in either right ventricular ejection fraction, end-diastolic volume, or stroke volume. In addition, left ventricular end-diastolic volume failed to increase, and despite an increase in ejection fraction, left ventricular stroke volume remained unchanged from rest to exercise. Therefore, cardiac output was augmented only by the heart rate increase in these patients. Right ventricular function appeared to be the major determinant of total cardiac output during exercise in patients with cardiac septal defects and left-to-right shunt.     

Left atrial transport function in myocardial infarction. Importance of its booster pump function.

After myocardial infarction (MI), left ventricular (LV) end-diastolic pressure (EDP) is higher than mean pulmonary artery wedge pressure because of powerful atrial contraction. To evaluate the significane of atrial contraction to left ventricular function we studied 10 control (C) patients without cardiac disease and 17 patients from three to six weeks after acute myocardial infarction. Cardiac catheterization with simultaneous left ventricular diastolic pressure (DP) and left ventricular cineangiograms were obtained. Left ventricular volumes and pressure were (mean +/- SD): (SEE ARTICLE). Although left ventricular stroke volume was lower in the patients with myocardial infarction than in the control subjects (46 versus 56 ml/m2), atrial contraction contributed more to left ventricular filling during diastole (which is the same as left ventricular stroke volume) in the patients with myocardial infarction than in the controls (16 versus 10 ml/m2). The average atrial contribution to left ventricular end-diastolic volume was 11.9 per cent (C), 15.4 per cent (MI); to left ventricular end-diastolic pressure 20 per cent (C), 38.7 per cent (MI); and to left ventricular stroke volume 21.7 per cent (C), 35.1 per cent (MI). Atrial contribution to left ventricular stroke volume was 56 per cent in patients with a cardiac index less than or equal to 2.0 liters/min/m2 and 31 per cent in those with a cardiac index greater than 2 liters/min/m2 (p less than 0.01). Atrial contraction contributed 35 per cent to left ventricular stroke volume in patients with normal end-diastolic volume and in those with increased end-diastolic volume and 10 per cent to end-diastolic volume in patients with increased end-diastolic volume (p less than 0.001). In patients with myocardial infarction, atrial contraction made a large contribution to left ventricular filling and stroke volume irrespective of the type of left ventricular functional derangement that was present. The "booster pump" function of the atrium cannot be ignored in assessing left ventricular performance.     

Right ventricular performance in mitral stenosis

Until recently, the dynamic geometry and pump function of the pressure-overloaded right ventricle in patients with mitral stenosis and pulmonary hypertension had not been well defined. With use of a recently developed method for calculating right ventricular volume in human beings, seven normal subjects and eight patients with mitral stenosis and pulmonary hypertension had right ventricular performance assessed from computer-analyzed biplane right ventriculograms. Patients with mitral stenosis had elevated values for systolic right ventricular pressure (mean ± standard error of the mean 25 ± 2 for normal subjects, 57 ± 6 mm Hg for patients with mitral stenosis), but normal values for right ventricular end-diastolic volume index (normal 95 ± 11, patients 81 ± 9 ml/m²) and ejection fraction (normal 0.49 ± 0.02, patients 0.58 ± 0.04). Comparison of right ventricular function using group performance curves of stroke work versus end-diastolic volume revealed the slope of the mitral stenosis line to be significantly greater than the normal line. A plot of right ventricular stroke volume versus end-diastolic volume, which removes pressure from the performance index, revealed that the two groups have similar performance. Left ventricular function measured by ejection fraction was reduced in mitral stenosis. These data suggest that the right ventricle performs normally in patients with mitral stenosis with moderate pulmonary hypertension and maintains normal size and ejection fraction.     

Ventricular function and coronary hemodynamics after intravenous nitroglycerin in coronary artery disease.

Left ventricular dynamics as well as systemic and coronary hemodynamics were determined in 14 patients with coronary artery disease (1) under control conditions, (2) under intravenous infusion of nitroglycerin, (3) under continued infusion of nitroglycerin with restored arterial and pulmonary artery pressures induced by the parallel infusion of dextran. Heart rate was kept constant by atrial pacing.Intravenous nitroglycerin infusion resulted in a significant reduction in left ventricular systolic (20 per cent) and end-diastolic pressure (43 per cent), peak $\text{dp}\text{dt}$ (13 per cent), cardiac index (16 per cent), stroke volume index (15 per cent), and stroke work index (30 per cent). Peak (dp/dt/total pressure) increased (15 per cent). Pulmonary vascular resistance markedly decreased (29 per cent), whereas total peripheral resistance did not change significantly (?3 per cent). Both coronary blood flow of the left ventricle (13 per cent) and myocardial oxygen consumption (15 per cent) decreased parallel to the reduction in preload and afterload. The action of nitroglycerin at restored left ventricular and pulmonary artery pressures was characterized by increase in peak $\text{dp}\text{dt}$ (12 per cent), peak ($\text{dp}\text{dt}$ total pressure) (18 per cent), cardiac index (13 per cent), stroke volume index (14 per cent), and stroke work index (10 per cent). Both coronary blood flow (28 per cent) and myocardial oxygen consumption (21 per cent) increased parallel to the enhancement of ventricular performance.The results demonstrate that intravenous nitroglycerin produces effective diastolic and systolic unloading of the heart associated with reduction in myocardial oxygen consumption and in coronary blood flow. There was marked vascular pooling which quantitatively averaged 437 ± 128 ml. This occurred concomitant with a 43 per cent decrease in left ventricular end-diastolic pressure or a 20 per cent decrease in peak systolic pressure. Significant coronary dilating properties of nitroglycerin could not be detected in these coronary patients. The increase in left ventricular contractility indices at restored pressure suggests a moderate but significant positive inotropic effect of nitroglycerin.     

Optimal right ventricular filling pressures and the role of pericardial constraint in right ventricular infarction in dogs.

BACKGROUND. Previous studies have reported an important role for right ventricular function in the pathophysiology of the low cardiac output state that can accompany right ventricular infarction. Some studies have suggested that right ventricular distensibility impairs right ventricular filling and stroke output; others have demonstrated that the pericardium can mediate depressed left ventricular filling and stroke output. METHODS AND RESULTS. To determine the role of pericardial constraint and optimal volume loading in an experimental model of right ventricular wall infarction, six mongrel dogs were studied before and after right ventricular wall infarction and after volume loading. The pericardium was then opened in two phases. In the first phase, the pericardium was opened partially to allow the atria to distend freely, and in the second phase, the pericardium was opened completely. The animals were preinstrumented with two sets of piezoelectric crystals attached to the right ventricular free wall, one in the infarct and the other in the noninfarct territory. Left ventricular size was estimated by left ventricular crystals on the anterior wall of the left ventricle. Right ventricular and left ventricular Millar catheters were used to assess intracavitary pressure, and a flat balloon was used to assess intrapericardial pressure. Right ventricular infarction reduced cardiac output by 23% and stroke volume by 30%. End-diastolic segment length and transmural pressure of the left ventricle decreased. Volume loading restored cardiac output to baseline values and was mediated by a significant increase in end-diastolic length in the noninfarct territory. This was achieved by increasing right ventricular end-diastolic pressure from 9 +/- 2 to 16 +/- 3 mm Hg (p less than 0.01). Partial opening of the pericardium mediated significant increases in both end-diastolic segment lengths of the left ventricle and the noninfarct territory. Left ventricular end-diastolic pressure decreased slightly by 3 mm Hg (p = NS). Complete opening of the pericardium increased cardiac output and stroke volume and mediated a significant decrease in right and left ventricular end-diastolic pressures. Left ventricular transmural pressure and end-diastolic segment lengths of the left ventricle and the noninfarct territory increased. Left ventricular diastolic pressure-segment length relations were shifted upward by right ventricular infarction. A partial opening of the pericardium shifted this relation downward in all animals, and complete opening of the pericardium shifted the relation rightward and further downward. CONCLUSIONS. Cardiac output is restored to baseline values by volume loading sufficient to increase the right ventricular diastolic pressure to 16 +/- 3 mm Hg. Evidence of pericardial constraint was observed and appears to be mediated by an atrioventricular interaction in addition to the direct ventricular interaction.     

Asynchronous volume changes of the two ventricles after Fontan operation in patients with a biventricular heart

Summary Coordinated contraction of the ventricle is an important determinant of pump function, which seems to be particularly important in Fontan circulation with one pumping ventricle. We analyzed the synchronism of contraction of the two ventricles in 11 patients with a biventricular heart who had undergone Fontan operation. Curves representing ventricular volume changes in a cardiac cycle measured on angiograms were smoothed and divided into 20 segments. We calculated the number of segments of the same directional volume changes (synchronous changes) between the two ventricles (synchronous ratio). We also calculated the total volume of the two ventricles (the two as one whole ventricle) by adding their volumes in each segment and calculated the ratio (stroke volume ratio) of theaortic stroke volume from the whole ventricle to the sum of stroke volumes of the morphological right and left ventricles. If the two ventricles ejected the blood in a completely synchronous manner, these ratios should be 1.0. In seven patients with synchronous ratios of 0.75 or greater and a stroke volume ratio of greater than 0.95, the cardiac index was 3.2 ± 0.31/min/m², the maximum total volume (corresponding to end-diastolic volume) was 106 ± 45% normal, and the ejection fraction was 0.44 ± 0.10. In four patients with ratios of less than 0.70 and 0.95, respectively, the parameters were 2.4 ± 0.5 (P < 0.05), 193 ± 92%, and 0.33 ± 0.08, respectively. The synchronous ratio was inversely correlated with cardiac output. In conclusion, synchronism of the cardiac cycle of the two ventricles affects Fontan circulation in patients with a biventricular heart.     

Hemodynamics in endomyocardial fibrosis

Nine patients with endomyocardial fibrosis have been studied. The clinical diagnosis was confirmed by right ventricular angiography in all of them. They were submitted to right and left ventricular catheterization and had the cardiac pressures, the pulmonary arteriolar resistance, and the cardiac index measured. The ratio between the end-diastolic and systolic ventricular pressures has been taken as an index of the degree of impairment to ventricular filling, and, based on this, patients were classified into two groups: I, predominant or isolated right ventricular disease (seven patients); and II, predominant left ventricular disease (two patients).Group I patients were characterized by a right ventricular $\text{D}{}_2\text{S}$ ratio above 60 per cent, severe tricuspid regurgitation, a diastolic pulmonary artery pressure slightly lower than the right ventricular plateau and end-diastolic pressures, and a reversal of the gradient between the left ventricular end-diastolic pressure and the right atrial mean pressure; these two latter findings strongly suggesting a diastolic blood flow between the right atrium and the left ventricle.The two patients in Group II did not show evidences suggestive of tricuspid regurgitation or of an early opening of the pulmonic valve. Even presenting high values for the left ventricular $\text{D}{}_2\text{S}$ ratio, the pulmonary arteriolar resistance was normal in one patient and mildly elevated in the other patient.     

Relation of size of secondary ventricles to exercise performance in children after fontan operation

The effects of the nondominant or secondary ventricle on the Fontan circulation are not known. The present study used cardiac magnetic resonance imaging to investigate the relations between secondary ventricular size and global cardiac performance. The Fontan cross-sectional study collected data from 7 centers participating in the Pediatric Heart Network. Subjects with complete cardiac magnetic resonance imaging data and an identifiable secondary ventricle were included in the analysis. Relationships between body surface area-adjusted parameters of the secondary ventricle (mass, end-diastolic volume, mass/volume ratio, and stroke volume) and the following measures were assessed. These measures included the percentage of predicted peak oxygen consumption and oxygen consumption at the ventilatory anaerobic threshold, ejection fraction of the main ventricular chamber, echocardiographic diastolic function grade, serum B-type natriuretic peptide, primary ventricular end-diastolic pressure, and parent-reported physical functioning summary score on the Child Health Questionnaire. Of the 546 enrolled subjects, 123 (age 12.1 ± 3.3 years, 56% male) had undergone cardiac magnetic resonance imaging, and 38 had achieved maximal aerobic capacity. A larger secondary ventricular end-diastolic volume, lower mass/volume ratio, and greater secondary/total ventricular stroke volume ratio were associated with a greater exercise capacity. No significant relationships were found between the measures of the secondary ventricle and the other outcomes. In conclusion, in children after the Fontan operation, a larger and less hypertrophied secondary ventricle with a greater contribution to stroke volume was associated with a better exercise capacity.     

Dimensional changes of the left ventricle during acute pulmonary arterial hypertension in dogs

Left ventricular dimensions and volumes were measured by an endocardial marker technique in eight closed chest dogs during progressive increases of 10 mm Hg in mean pulmonary arterial pressure. Right ventricular volumes were measured by biplane cineanglography.

Increasing mean pulmonary arterial pressure caused a progressive increase in right ventricular volume; at a mean pulmonary arterial pressure of 60 mm Hg, right ventricular end-diastolic volume increased by 48 percent and end-systolic volume by 50 percent. Left ventricular volumes began to decrease significantly at a mean pulmonary arterial pressure of 30 mm Hg, and when a mean pulmonary arterial pressure of 60 mm Hg was reached, left ventricular end-diastolic volume had decreased by 30 percent and left ventricular end-systolic volume by 19 percent. Changes in ventricular filling pressure dlrectionally followed the volume changes of the respective ventricle. Left ventricular stroke volume decreased 45 percent at a mean pulmonary arterial pressure of 60 mm Hg but increasing heart rate prevented a decrease in cardiac output.

The decrease in left ventricular volume as pulmonary arterial pressure was Increased was associated with a disproportionate reduction in the left ventricular septal-lateral axis. At end-diastole, this dimension decreased by 22 percent at a mean pulmonary arterial pressure of 60 mm Hg, the anterior-posterior axis decreased by 8 percent and the base-apex axis by 4 percent. A similar disproportionate decrease of the septal-lateral axis occurred at end-systole. Even at the modest increase in mean pulmonary arterial pressure to 20 mm Hg, only the septal-lateral dimension was significantly shortened, and the right ventricular end-diastolic volume had increased by 17 percent but left ventricular end-diastolic volume was not significantly changed. Thus, during acute pulmonary hypertension, the right ventricle progressively dilates resulting in a distinctive change in the shape of the left ventricle that suggests septal buiging and that may impair left ventricular function.     

Characterization of the human right ventricular pressure-volume relation: effect of dobutamine and right coronary artery stenosis

Right ventricular function was assessed in 15 patients using right ventricular pressure-volume loops. Right ventricular pressure using a micromanometer-tipped catheter, thermodilution cardiac output and gated blood pool scintigrams were simultaneously obtained. To help isolate the right ventricle, a slant hole collimator was used. The measurements were repeated during dobutamine infusion, which was titrated so there was minimal change in systemic pressure and heart rate. The right ventricular pressure-volume loop resembles the usual left ventricular loop except that the isovolumic contraction phase is often not as distinct, and right-sided ejection may continue well beyond right ventricular peak systolic pressure. Systolic but not diastolic function improved with dobutamine administration. There was no significant difference in right ventricular systolic function (ejection fraction, stroke work index, stroke volume index and cardiac index) or in end-diastolic volume index between patients without (Group I) and with (Group II) significant right coronary artery stenosis. However, there was a small but significant difference in right ventricular end-diastolic pressure (5.3 +/- 2.5 and 8.1 +/- 1.8 mm Hg [p less than 0.05]) for Group I and II, respectively. Thus, the right ventricular pressure-volume loop can be used to graphically display right ventricular function and improvement in contractility with dobutamine. The right ventricular isovolumic contraction phase and ejection phase differ from those in the usual left ventricular loop. Although there was a small difference in right ventricular end-diastolic pressure in patients with and without right coronary artery stenosis, the right ventricular pressure-volume loop did not provide additional discriminatory information between these two groups of patients.     

Evaluation of right ventricular volumes measured by magnetic resonance imaging

Right ventricular volumes were determined in 12 patients with different levels of right and left ventricular function by magnetic resonance imaging (MRI) using an ECG gated multisection technique in planes perpendicular to the diastolic position of the interventricular septum. Right ventricular stroke volume was calculated as the difference between end-diastolic and end-systolic volume and compared to left ventricular stroke volume and to stroke volume determined simultaneously by a classical indicator dilution technique. There was good agreement between right ventricular stroke volume determined by MRI and by the indicator dilution method and between right and left ventricular stroke volume determined by MRI. Thus, MRI gives reliable values not only for left ventricular volumes, but also for right ventricular volumes. By MRI it is possible to obtain volumes from both ventricles simultaneously in a noninvasive way and without exposing the patient to radiation.     

Regional changes in hemodynamics and cardiac myocyte size in rats with aortocaval fistulas. 2. Long-term effects

Regional changes in hemodynamics and cardiac myocyte size were examined in adult rats 5 months after creating a large aortocaval fistula. At that time, cardiac output, left and right ventricular pressures, and left and right ventricular dP/dtmax were measured. Subsequently, isolated cardiac myocytes were collected from the left ventricle, right ventricle, and septum for cell size measurements. Compared with sham-operated controls, percent dry weight was reduced in the liver and kidney but was unchanged in the lung. Heart rate, left ventricular systolic pressure, left ventricular dP/dtmax, and systolic aortic pressure were not changed in rats with fistulas. However, cardiac output, stroke volume, left ventricular end-diastolic pressure, and all measured parameters in the right ventricle were significantly increased. Mean cell volume and the ratio of heart weight to body weight were both elevated 92%. Cell volume, cell length, and cross-sectional area increased significantly in each heart region examined. Hypertrophy was more pronounced in cells from the right ventricle and the endomyocardium of the left ventricle. The percentage of cells with mononucleation or binucleation was not changed in any heart region of rats with fistulas. In summary, despite evidence of renal and hepatic congestion, most indexes of cardiac function were normal or elevated 5 months after creation of a large volume-overload-induced hypertrophy. Data from isolated cardiac myocytes suggested that cellular hypertrophy, rather than hyperplasia, was responsible for the increased cardiac mass.     

Venous delay, a major source of error in isotopic cardiac output determination.

The high correlation reported for cardiac output determinations by ^99mTc-HSA has not held for other unselected series. To investigate possible causes, cardiac output was determined simultaneously by two indicators: ^99mTc-HSA and indocyanine green both injected by rapid flush technique, the ^99mTc via antecubital vein and the dye (DD) via superior vena cava. Precordial counting rates were obtained by scintillation camera and dilution curves were derived by computer program from selected areas in right (RV) and left ventricles (LV). Thirty consecutive studies showed significant (p < 0.001) correlation (r = 0.81) between ^99mTc and DD output but a determination index of only 66 per cent. Varying degrees of persistence of counting rate were noted in the subclavian region in the absence of demonstrable venous obstruction. In seven studies (Group I) there was no isotope hang-up in the subclavian region; in 17 (Group II), counts in the subclavian region persisted only through RV visualization, and in six studies (Group III) counts persisted even when radioactivity was at its peak concentration over LV. Correlation coefficients (^99mTc output with DD output) varied inversely with delay; r was 0.90 for Group I and Group II, and 0.64 for Group III (determination indices 81 per cent, 81 per cent, and 41 per cent, respectively).Results suggest that unexpected delay in arrival of radioactive bolus into the heart results in erratic distortion of cardiac output values. Unless monitored, delay often remains unsuspected; in a consecutive series of 63 ^99mTc studies severe delay occurred in 16 per cent.The reason for the delay is not clear. It did not seem related to the speed of circulation, to the presence of venous obstruction, or to anatomical variations. It could not be related to the speed of injection or to the physical characteristics of the injectate.     

Predominant right ventricular dysfunction after right ventricular destruction in the dog

Right and left ventricular function was assessed by observing the response to rapid blood volume expansion before and after extensive cauterization of the right ventricle in open chest dogs. In the control period, left ventricular end-diastolic pressure surpassed right ventricular end-diastolic pressure by an average of 11.5 mm Hg after volume expansion whereas, after destruction of the right ventricle, pressure in this chamber surpassed pressure in the left ventricle by an average of 4 mm Hg. In contrast, after left ventricular damage, left ventricular end-diastolic pressure averaged 25 mm Hg more than right ventricular end-diastolic pressure. Despite extensive damage to the right ventricular free wall, the right ventricle continued to generate a near normal pressure and aortic flow could be increased above control levels by volume expansion. We conclude that, in contrast to previous evidence, damage to the right ventricle produces a syndrome of predominant right ventricular dysfunction. However, cauterization of the entire free wall of the right ventricle does not reproduce the more profound right ventricular dysfunction noted in infarction of the right ventricle in man.     

Ischemic heart failure: Sustained inotropic response to small doses of L-epinephrine without toxicity

As a prelude to a study of severe ischemic heart failure, the therapeutic response of the ischemic ventricle to epinephrine and acetylstrophanthidin in nontoxic doses was determined in 24 intact anesthetized dogs undergoing a first episode of acute regional ischemia. A thrombotic obstruction was produced in the left anterior descending coronary artery, effecting moderate left ventricular dysfunction. The elevation of end-diastolic pressure and reduced stroke volume in control dogs were not significantly altered by administration of strophanthidin. Epinephrine (0.05 μg/kg per min) elicited a significant reduction in end-diastolic pressure and increase in stroke volume. The latter was not attended by an increased incidence of ventricular fibrillation, whereas fibrillation occurred in half of the group given strophanthidin. Thus, the catecholamine was selected to study pump failure.Severe ischemic heart failure was assessed in two groups with scar from previous infarction for up to 4 hours. By 60 minutes of ischemia, the increase in end-diastolic pressure and volume and decrease in stroke volume and ejection fraction were comparable in both groups. Thereafter, alternate animals received small doses of epinephrine (0.05 to 0.15 μg/kg per min) with graded increments at 60 minute intervals to counter tachyphylaxis and findings were compared with those in control dogs. Over the subsequent 3 hours, there was progressive deterioration of left ventricular function in the untreated group with an increase in end-diastolic pressure from 10 ± 1 to 33 ± 2.4 mm Hg. End-diastolic volume increased by 63 percent; stroke volume and ejection fraction decreased by 48 and 66 percent, respectively. The infusion of epinephrine was attended by a significantly lower end-diastolic pressure of 20 ± 2.5 mm Hg, whereas end-diastolic volume, stroke volume and ejection fraction were restored to control levels after 4 hours of ischemia. Mortality in the untreated group was 62 percent by 4 hours; all seven animals in the treated group survived.     

Levels of brain natriuretic peptide in children with right ventricular overload due to congenital cardiac disease

OBJECTIVE: To evaluate the role of the concentration of brain natriuretic peptide in the plasma, and its correlation with haemodynamic right ventricular parameters, in children with overload of the right ventricle due to congenital cardiac disease. METHODS: We studied 31 children, with a mean age of 4.8 years, with volume or pressure overload of the right ventricle caused by congenital cardiac disease. Of the patients, 19 had undergone surgical biventricular correction of tetralogy of Fallot, 11 with pulmonary stenosis and 8 with pulmonary atresia, and 12 patients were studied prior to operations, 7 with atrial septal defects and 5 with anomalous pulmonary venous connections. We measured brain natriuretic peptide using Triage(R), from Biosite, United States of America. We determined end-diastolic pressures of the right ventricle, and the peak ratio of right to left ventricular pressures, by cardiac catheterization and correlated them with concentrations of brain natriuretic peptide in the plasma. RESULTS: The mean concentrations of brain natriuretic peptide were 87.7, with a range from 5 to 316, picograms per millilitre. Mean end-diastolic pressure in the right ventricle was 5.6, with a range from 2 to 10, millimetres of mercury, and the mean ratio of right to left ventricular pressure was 0.56, with a range from 0.24 to 1.03. There was a positive correlation between the concentrations of brain natriuretic peptide and the ratio of right to left ventricular pressure (r equal to 0.7844, p less than 0.0001) in all patients. These positive correlations remained when the children with tetralogy of Fallot, and those with atrial septal defects or anomalous pulmonary venous connection, were analysed as separate groups. We also found a weak correlation was shown between end-diastolic right ventricular pressure and concentrations of brain natriuretic peptide in the plasma (r equal to 0.5947, p equal to 0.0004). CONCLUSION: There is a significant correlation between right ventricular haemodynamic parameters and concentrations of brain natriuretic peptide in the plasma of children with right ventricular overload due to different types of congenital cardiac disease. The monitoring of brain natriuretic peptide may provide a non-invasive and safe quantitative follow up of the right ventricular pressure and volume overload in these patients.     

Left ventricular function in systole and diastole in constrictive pericarditis

Left ventricular function was studied in systole and diastole in 30 patients with constrictive pericarditis. Left ventricular end-diastolic volume was used to divide the patients into three arbitrary groups: severe constriction (EDV < 25 ml./M.²), moderate constriction (EDV 25 to 50 ml./M.²), and mild constriction (EDV > 50 ml./M.²).The patients had high ventricular diastolic and venous filling pressures (mean LVEDP = 23 ± 7 mm. Hg, mean RVEDP = 20 ± 7 mm. Hg). Measurements related to absolute fiber shortening (stroke index, stroke work index, and left ventricular ejection rate) were reduced and linearly related to the degree of constriction as assessed by the end-diastolic volume.Measurements of relative fiber shortening or lengthening (ejection and filling fraction and circumferential fiber shortening) were normal despite great reduction in ventricular volumes.Velocity measurements, peak LV $\text{dp}\text{dt}$ and mean velocity of circumferential fiber shortening were normal or slightly reduced.These changes were reflected in the systolic time interval measurements pre-ejection phase, left ventricular ejection time, and the ratio $\text{PEP}\text{LVET}$.Diastolic function of the ventricle was abnormal; the distensibility index of the ventriculo-pericardial system ($\text{ΔV}\text{ΔP}$) was low and the passive elastic modulus in-increased. The change in compliance correlated with the degree of constriction and there was a linear relationship between compliance and EDV.The ventricle was underloaded despite the high filling pressure and stroke work index was reduced; extrinsic compression raised the diastolic pressure and reduced left ventricular volumes.     

Maturational changes in myocardial pump performance in newborn lambs

We examined the left ventricular stroke volume response to fluid loading in 24 acutely instrumented newborn lambs and the right ventricular response in 12 lambs. Newborn lambs (group 1, ages 2 to 4 days) demonstrated a limited response to acute volume loading for both left and right ventricles. With maturation, the left ventricle exhibited a progressively greater ability to respond to acute volume loading, with greater peak stroke volumes achieved at higher end-diastolic pressures. The response of the right ventricle remained limited at all ages examined, with peak stroke volume achieved at lower end-diastolic pressures. We conclude that postnatal maturation of the left ventricle results in a progressively greater stroke volume response in older lambs, while the response of the right ventricle remains limited.     

Left ventricular function during spontaneous angina pectoris: effect of sublingual nitroglycerin

Global and regional left ventricular function was assessed at rest, during spontaneous angina pectoris and after nitroglycerin therapy in 14 patients with ischemic heart disease. Cardiac output, left ventricular pressure and left ventricular volume were measured when patients experienced spontaneous angina pectoris during cardiac catheterization. In every patient control measurements had already been made; further measurements were made after nitroglycerin had relieved pain. Subsequent coronary angiography showed significant two or three vessel disease in all 14 patients. The S-T segment was depressed in every patient during pain (average 0.26 + 0.04 mV; mean + standard error of the mean [SEM]). During spontaneous angina, there was a significant increase in left ventricular end-diastolic pressure (17 ± 2 to 35 ± 2 mm Hg, p < 0.001), left ventricular end-diastolic volume (77 ± 6 to 88 ± 8 ml/m², p < 0.005) and left ventricular end-systolic volume (35 ± 4 to 52 ± 7 ml/m², p < 0.001). Concomitantly stroke index decreased from 42 ± 2 to 36 ± 3 ml/beat per m² (p < 0.01) and ejection fraction from 56 ± 4 to 44 ± 4 percent (p < 0.001).Assessment of regional left ventricular performance during spontaneous angina revealed either development of new areas or extension of already existing areas of abnormal wall motion in all patients. Nitroglycerin restored global and regional left ventricular function to a normal state. In six individual patients there was an excellent correlation between the S-T depression (V₅) and left ventricular end-diastolic pressure during spontaneous angina (correlation coefficient [r] = 0.88 to 0.96) and after nitroglycerin therapy (r = 0.76 to 0.84). For the group, there was a good correlation between change in S-T depression and changes in left ventricular end-diastolic pressure (r = 0.87) and left ventricular end-diastolic volume (r = 0.78). Thus, these data indicate marked systolic and diastolic dysfunction of the left ventricle during spontaneous angina pectoris, characterized by decreases in stroke index and ejection fraction and increases in left ventricular end-systolic and end-diastolic volumes and left ventricular filling pressure.