PubMed Health⌕ Search

Biomedical subjects

S D Colan

Publications and source records attributed to S D Colan.

At least 91 records · Page 5Linked to original sources

Response of the hypertrophied left ventricle to tachycardia: importance of maturation.

Pressure overload left ventricular (LV) hypertrophy (LVH) induces ventricular dysfunction during stress, which is commonly attributed to diminished myocardial capillary density and ischemia. Immature hearts with LVH have a normal coronary flow reserve and capillary density. The purpose of this study was to determine 1) whether young lambs with LVH had an abnormal response to chronotropic stress, 2) whether nonischemic mechanisms contributed to the abnormal response, and 3) whether the age at which LVH was induced affected the response. We assessed LV endomyocardial function, perfusion, and Ca(2+)-adenosinetriphosphatase (ATPase) mRNA levels in chronically instrumented lambs with and without LVH and adult sheep with and without LVH. Rapid pacing induced diastolic dysfunction, increased time constant of isovolumic relaxation using an iterative fit (tM), and elevated LV diastolic pressures in young lambs and adult sheep with LVH. During pacing, tM was greater in the adult sheep with LVH than in the young lambs with LVH. Ca(2+)-ATPase mRNA levels were 79% less in adult sheep with LVH than in those without. Ca(2+)-ATPase mRNA levels in lambs with and without LVH and adult sheep without LVH were similar. Diastolic dysfunction occurred in the absence of subendomyocardial hypoperfusion, suggesting a nonischemic mechanism. In adult sheep with LVH diastolic dysfunction was associated with a marked reduction in Ca(2+)-ATPase mRNA levels.

Aging↗

Growth of the aortic anastomosis, annulus, and root after the arterial switch procedure performed in infancy.

BACKGROUND: We investigated the size and growth potential of the neoaortic root and aortic anastomosis after the arterial switch operation (ASO) for D-transposition of the great arteries (D-TGA) performed in infants. Circumferential suture lines connecting the great arteries and extensive surgery on the arterial roots to transplant the coronary arteries are essential parts of the ASO. However, little is known about the growth of the aortic anastomosis, the neoaortic root, and the neoaortic annulus after the ASO performed in infancy. METHODS AND RESULTS: Serial echocardiograms on 50 patients with D-TGA who underwent ASO in infancy at our institution were reviewed, and the size of the aortic anastomosis, the neoaortic root, and the neoaortic annulus were compared with similar structures in a group of 312 control subjects. Before surgery, the native pulmonary root (future neoaortic root) was 1.59 SD larger (P < .001) and the native pulmonary annulus (future neoaortic annulus) was 1.4 SD larger (P < .001) in infants with D-TGA than the aortic root and annulus of control patients. At a mean of 22 months (12 months to 6 1/2 years) after surgery, the diameter of the aorta at the anastomosis was 0.45 SD smaller than the ascending aorta of control subjects (P < .001). The neoaortic root was 2.9 SD larger (P < .001) and the neoaortic annulus was 1.6 SD larger (P < .001) than the comparable structures in the control population. Most important, growth of the aortic anastomosis was commensurate with somatic growth, but the dilation of the neoaortic root appeared to be progressive over time. The neoaortic root was significantly more dilated in patients with a history of pulmonary artery banding (P < .001) and in patients with neoaortic regurgitation (P < .001). The presence of a ventricular septal defect was not significantly related to postoperative neoaortic root size. CONCLUSIONS: This study underlies the importance of continued acquisition and examination of the data regarding the long-term outcome of the arterial switch operation performed in infancy.

Anastomosis, Surgical↗

Diagnosis of intramural coronary artery in transposition of the great arteries using two-dimensional echocardiography.

BACKGROUND: An intramural coronary is an uncommon but potentially significant risk factor for transfer of the coronary arteries as part of the arterial switch operation for transposition of the great arteries. Preoperative diagnosis is advantageous because it helps prevent accidental injury to the intramural coronary artery during transection of the aortic root and excision of the coronary artery ostium from the aorta. Therefore, we investigated the reliability of two-dimensional echocardiography for detecting an intramural coronary artery in infants with d-transposition of the great arteries. METHODS AND RESULTS: All infants with d-transposition of the great arteries who underwent echocardiography and primary surgical repair at this institution between January 1987 and June 1992 were identified by search of the cardiology data base. From this group, all patients diagnosed with an intramural coronary artery were identified by review of the echocardiographic, surgical, and autopsy reports. Among 435 infants with transposition, 29 infants were diagnosed as having an intramural coronary artery. In 27 cases, the diagnosis was confirmed at surgery or autopsy, and there were two false-positive echocardiographic diagnoses (specificity, 99.5%). Twenty of the 27 patients with an intramural coronary artery were correctly diagnosed prospectively by echocardiography (sensitivity, 75%), including 17 of 23 patients with an intramural left coronary artery or left anterior descending coronary artery and 3 of 4 patients with an intramural right coronary artery. Two primary diagnostic criteria were identified: a major coronary artery arising from the contralateral septal sinus, near the usually intercoronary commissure, and a course for this vessel within the posterior aortic wall between the great arteries, creating a "double-border" appearance. Retrospective review using these criteria identified 26 of the 27 intramural arteries with no false-positive diagnoses. CONCLUSIONS: We conclude that coronary echocardiography is a very promising technique for detecting an intramural coronary artery in transposition of the great arteries. Careful prospective application of the identified diagnostic criteria should greatly improve the diagnostic accuracy.

Coronary Vessel Anomalies↗

Transition from compensated hypertrophy to intrinsic myocardial dysfunction during development of left ventricular pressure-overload hypertrophy in conscious sheep. Systolic dysfunction precedes diastolic dysfunction.

BACKGROUND: Patients with aortic stenosis have a period of compensated left ventricular hypertrophy but may eventually develop congestive heart failure. Previous experimental studies showed either normal myocardial contractility in mild short-term pressure overload or myocardial dysfunction with severe pressure overload. Transition from compensated left ventricular hypertrophy to myocardial dysfunction has not been experimentally demonstrated in an adult large animal. Controversial issues in pressure-overload hypertrophy include whether the left ventricular dysfunction is due to insufficient hypertrophy (afterload mismatch) or to intrinsic myocardial dysfunction and whether diastolic dysfunction precedes systolic dysfunction. METHODS AND RESULTS: We induced left ventricular hypertrophy (41% increase in left ventricular to body weight ratio) by gradually tightening a hydraulic constrictor around the ascending aorta in 9 chronically instrumented conscious sheep. Afterload (end-systolic stress) elevation remained constant (approximately 33% greater than baseline) by adjustment of the aortic constrictor over 6 weeks, gradually increasing left ventricular pressure (from 117 +/- 6 to 163 +/- 5 mm Hg) as hypertrophy developed. Four sets (baseline, 2 weeks, 4 weeks, and 6 weeks) of serial hemodynamic studies were performed in each animal with beta-blockade, first with and then without aortic constriction to mechanically match loading conditions. Stepwise methoxamine infusion was performed to obtain load-independent assessment of myocardial contractility. Midwall shortening (P < .05) and shortening rate (P < .05) at mechanically matched loading conditions showed that myocardial dysfunction developed between the fourth and the sixth week. Shortening-preload-afterload (P < .05) and shortening rate-preload-afterload (P < .05) relations, load-independent contractility indices based on the systolic myocardial stiffness concept, also revealed depressed myocardial contractility at the sixth week. Time constant of left ventricular isovolumic relaxation and diastolic myocardial stiffness constant did not change over the 6 weeks. CONCLUSIONS: Transition from normal myocardial contractility to myocardial dysfunction was demonstrated. This transition occurred even when the elevation of afterload remained constant as hypertrophy incompletely adapted to increasing left ventricular pressure. Systolic dysfunction preceded diastolic dysfunction in this model.

Adaptation, Physiological↗

Right ventricular decompression and left ventricular function in pulmonary atresia with intact ventricular septum. The influence of less extensive coronary anomalies.

BACKGROUND: Right ventricular decompression (RVD) may cause myocardial ischemia in patients with pulmonary atresia with intact ventricular septum and associated coronary artery abnormalities. Although we have previously shown that mortality is very high when two or more coronary arteries are obstructed, the effects of lesser degrees of coronary abnormalities are unknown. We therefore evaluated the effect of RVD on left ventricular (LV) function in those with less extensive coronary artery abnormalities. METHODS AND RESULTS: Preoperative cineangiograms demonstrated fistulas with or without one coronary artery stenosis in 12 of 24 patients aged 2 days to 33 months at the time of RVD. Preoperative and postoperative two-dimensional echocardiograms were analyzed for global and regional LV function. One infant with fistulas involving two coronary arteries and stenosis of the right coronary artery died from severe global LV dysfunction after RVD. Despite this, mean LV end-diastolic volume (66 +/- 17 mL/m2) and mean LV ejection fraction (60 +/- 9%) were similar in patients with and without coronary artery abnormalities before and after RVD. Before RVD, regional LV dysfunction was seen in 8 of 132 (6%) regions in those with coronary artery abnormalities and in 3 of 132 (2%) in those without coronary artery abnormalities. After RVD, there were 16 of 132 (12%) abnormal regions in those with coronary artery abnormalities and 1 of 132 (< 1%) in those without coronary artery abnormalities. In regions with normal wall motion before RVD, the presence of coronary artery abnormalities was related to regional LV dysfunction after RVD (P < .001). CONCLUSIONS: Regional LV dysfunction was rare in patients without coronary artery abnormalities. In those with less extensive coronary artery abnormalities not involving obstruction to multiple coronary arteries, regional LV dysfunction was common before and increased after RVD, but severe global LV dysfunction was unusual.

Child, Preschool↗

Second natural history study of congenital heart defects. Aortic stenosis: echocardiography.

BACKGROUND: Recent advances in the field of echocardiography have made it possible to obtain a complete morphological and hemodynamic assessment of patients with aortic stenosis. Therefore, comprehensive two-dimensional and Doppler examinations were performed on patients with aortic stenosis returning for the Second Natural History Study of Congenital Heart Defects (NHS-2). METHODS AND RESULTS: Two hundred thirty-two patients with aortic stenosis underwent comprehensive two-dimensional and Doppler examinations. Of these, 96 were in the medically treated group, 49 had undergone aortic valve replacement, and 87 had had aortic valvotomy. The valve replacement group had a significantly smaller left ventricular diastolic cavity than did the medically treated group; both had smaller dimensions than the valvotomy group. There was no significant difference in left ventricular wall thickness or fractional shortening among the three groups. The valvotomy group had a significantly higher mean aortic valve gradient than did either the medically treated group or the valve replacement group. The degree of aortic regurgitation was more severe in the valvotomy group than in the other two groups. For all patients, there was a direct relation between the aortic valve gradient and the mean wall thickness and an inverse relation between the aortic valve mean gradient and fractional shortening. The only echocardiographic parameter that correlated with the presence or absence of symptomatology was the fractional shortening. CONCLUSIONS: These observations provide an objective measurement for assessing the status of the aortic valve and left ventricular response in patients with aortic stenosis returning for NHS-2. Limitations of echocardiography in this study are discussed.

Adolescent↗

Second natural history study of congenital heart defects. Pulmonary stenosis: echocardiography.

BACKGROUND: Two-dimensional and Doppler echocardiography can provide information about valve morphology, right ventricular size and function, and hemodynamics in patients with pulmonary stenosis. Therefore, two-dimensional and Doppler echocardiographic examinations were performed on patients with pulmonary stenosis returning for the Second Natural History Study of Congenital Heart Defects. METHODS AND RESULTS: Three hundred twenty-five patients with pulmonary stenosis underwent two-dimensional and Doppler echocardiographic examinations. Of these, 115 were in the medically treated group, and 210 had undergone a previous operation. Patients in the valvotomy group had a higher incidence of right ventricular dysfunction and a larger right ventricular diastolic dimension. The valvotomy group had a lower pulmonary valve mean gradient and a lower right ventricular systolic pressure than the medically treated group. For all patients, there was no significant correlation of the echocardiographic variables with the presence or absence of symptoms, reflecting the low incidence of patients with cardiac decompensation. CONCLUSIONS: These observations provide an objective measurement for assessing the status of the pulmonary valve and right ventricular response in patients with pulmonary stenosis. Limitations of echocardiography in this study are discussed.

Adolescent↗

Second natural history study of congenital heart defects. Ventricular septal defect: echocardiography.

BACKGROUND: Two-dimensional and Doppler echocardiography can provide structural and hemodynamic information for patients with ventricular septal defects (VSDs). Therefore, two-dimensional and Doppler echocardiographic examinations were performed on patients with VSDs returning for the Second Natural History Study of Congenital Heart Defects. METHODS AND RESULTS: Five hundred fifty-six patients with VSDs underwent two-dimensional and Doppler echocardiographic examinations. Three hundred twenty-four patients were in the medically treated group, and 232 had undergone a previous operation. The location of the VSD was classified in 235 patients. Several Doppler measurements were used to calculate pulmonary artery pressures: tricuspid regurgitation peak systolic velocity, peak systolic velocity of VSD jet, pulmonary regurgitation end-diastolic velocity, and pulmonary artery acceleration time. The two methods that were found to be reliable consisted of the tricuspid regurgitation peak systolic velocity and the pulmonary regurgitation end-diastolic velocity. These measurements were obtained in only 26% of patients at all centers. At one center in which adult and pediatric echocardiography was performed in a single laboratory, these values were obtained in 60% of patients. CONCLUSIONS: Two-dimensional and Doppler echocardiography has the ability to provide a noninvasive method of assessing morphology and hemodynamics in patients with VSDs. However, the reliability and accuracy of hemodynamic measurements are dependent on operator experience.

Blood Pressure↗

Cardiac structure and function in children with human immunodeficiency virus infection treated with zidovudine.

BACKGROUND: Abnormalities of cardiac structure and function are common in children infected with the human immunodeficiency virus (HIV). It is unclear, however, whether these abnormalities are attributable to the disease itself, associated infections, or possible cardiotoxic effects of the most commonly used treatment, zidovudine. METHODS: We performed echocardiography in 24 children with symptomatic HIV infection immediately before they started zidovudine therapy and a mean of 1.32 years after therapy began. Sixteen of these children were also studied a mean of 1.26 years before starting zidovudine treatment. Comparison groups included 27 age-matched children with symptomatic HIV infection who had not received zidovudine and 191 normal children. RESULTS: As compared with the normal children, the children treated with zidovudine had progressive left ventricular dilatation and an increase in ventricular-wall stress at end-systole (a measure of ventricular afterload); dilatation and stress were significantly elevated both before and during zidovudine treatment. The ratio of ventricular thickness to internal dimension was below normal before zidovudine treatment began (P < 0.001). After treatment with zidovudine, however, overall left ventricular mass was increased (P = 0.02), as was peak wall stress (a stimulus to ventricular hypertrophy) (P = 0.01). Ventricular contractility remained normal, but fractional shortening of the left ventricle was decreased (P = 0.004). No statistically significant differences were detected at follow-up in any of these measurements between HIV-infected children treated with zidovudine and those not so treated. CONCLUSIONS: Progressive left ventricular dilatation occurred in children with symptomatic HIV infection. Compensatory hypertrophy also occurred but was inadequate to maintain peak systolic wall stress within the normal range. The progressive elevation of ventricular afterload due to dilatation resulted in depressed ventricular performance, but intrinsic ventricular contractility remained normal. Zidovudine did not appear to worsen or ameliorate these cardiac changes.

Acquired Immunodeficiency Syndrome↗

Developmental modulation of myocardial mechanics: age- and growth-related alterations in afterload and contractility.

Somatic growth is associated with alterations in myocardial mechanics in children with heart disease and in most animal models of congenital heart disease. However, the effect of age and body size on myocardial contractility and loading conditions in normal infants and children is not known. Therefore, 256 normal children aged 7 days to 19 years (34% less than 3 years old) were evaluated with noninvasive indexes of left ventricular contractility and loading conditions. Two-dimensional and M-mode echocardiographic recordings of the left ventricle were obtained with a phonocardiogram, indirect pulse tracing and blood pressure recordings. Left ventricular dimensions, wall thickness and pressure measurements obtained from these data were used to calculate peak and end-systolic circumferential and meridional wall stress and mean and integrated meridional wall stress. Velocity of shortening adjusted for heart rate was compared with end-systolic stress to assess contractility independently of loading status. The subjects were stratified for gender and each of the derived variables was related to age and body surface area. Ventricular shape, assessed as the major/minor axis ratio, and the circumferential/meridional stress ratio were found to be invariant with growth. The ratio of posterior wall thickness to minor axis dimension did not change with age, despite the normal age-related increase in blood pressure. The increase in pressure despite unvarying ventricular shape and wall thickness/dimension ratio resulted in a substantial increase in wall stress that was most dramatic during the first few years of life. In association with the increase in afterload, systolic function decreased with age. However, the age-related decrease in the velocity of shortening was greater than that expected from the increase in afterload alone, indicating a higher level of contractility in infants and children during the first years of life than in older subjects. The process of normal growth and development, similar to that in children with heart disease, is associated with a rapid decrease in the trophic response to hemodynamic loads, resulting in an age-associated increase in wall stress. There is a similar but somewhat more rapid decrease in contractility, with the highest values seen in the youngest patients.

Adolescent↗

Bulboventricular foramen size in infants with double-inlet left ventricle or tricuspid atresia with transposed great arteries: influence on initial palliative operation and rate of growth.

Bulboventricular foramen obstruction may complicate the management of patients with single left ventricle. Bulboventricular foramen size was measured in 28 neonates and infants greater than 5 months old and followed up for 2 to 5 years in those patients whose only systemic outflow was through the foramen. The bulboventricular foramen was measured in two planes by two-dimensional echocardiography, its area calculated and indexed to body surface area. One patient died before surgical treatment. The mean initial bulboventricular foramen area index was 0.94 cm2/m2 in 12 patients (Group A) in whom the foramen was bypassed as the first procedure in early infancy. The remaining 15 patients underwent other palliative operations but the bulboventricular foramen continued to serve as the systemic outflow tract. There was one surgical death. Six (Group B) of the 14 survivors developed bulboventricular foramen obstruction during follow-up (mean initial bulboventricular foramen area index 1.75 cm2/m2). The remaining eight patients (Group C) did not develop obstruction during follow-up and had an initial bulboventricular foramen larger than that in the other two groups (mean initial bulboventricular foramen area index 3.95 cm2/m2). All patients with an initial bulboventricular foramen area index less than 2 cm2/m2 who did not undergo early bulboventricular foramen bypass developed late obstruction.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗

Diagnosis of anomalous left coronary artery by Doppler color flow mapping: distinction from other causes of dilated cardiomyopathy.

BACKGROUND: Anomalous origin of the left coronary artery from the pulmonary trunk is difficult to diagnose reliably by two-dimensional echocardiography. Therefore, Doppler color flow mapping was tested in 29 patients with dilated cardiomyopathy or anomalous left coronary artery, or both. METHODS AND RESULTS: All patients with anomalous left coronary artery (10 patients) or dilated cardiomyopathy (27 patients) (excluding those with other known causes for cardiomyopathy) examined between January 1988 and May 1991 were identified. The direction of flow in the three main segments of the left coronary system was determined by Doppler color flow mapping. In all 10 patients with anomalous left coronary artery, flow mapping demonstrated an abnormal jet from the left coronary artery into the pulmonary trunk and retrograde flow in at least two segments of the left coronary system. The diagnosis was confirmed in all 10 patients at operation. Doppler color flow mapping, performed in 19 of the 27 patients with dilated cardiomyopathy, demonstrated anterograde flow in at least one segment of the left coronary system in 16 of the 19 patients; flow direction was not determined in the other 3 patients. Coronary artery anatomy was confirmed by aortic root or left ventricular angiography in 14 patients and at autopsy in 1 patient and was not directly confirmed in 4 patients. Left ventricular function spontaneously improved to normal in three of the latter four patients, a clinical course not consistent with anomalous left coronary artery. The left coronary artery appeared to arise from the aortic root by two-dimensional echocardiographic imaging alone in all patients with dilated cardiomyopathy and in 5 of 10 patients with anomalous left coronary artery (50% false negative diagnoses). CONCLUSIONS: Detection of an abnormal jet into the pulmonary trunk and retrograde flow in the left coronary system by Doppler color flow mapping is reliable for diagnosing anomalous left coronary artery whereas two-dimensional echocardiographic imaging alone is often inconclusive or misleading. Determining flow direction in the left coronary system in patients with dilated cardiomyopathy is useful for excluding anomalous left coronary artery but is technically more difficult to document in this condition than in anomalous left coronary artery.

Adolescent↗

Myocardial function in immature and mature sheep with pressure-overload hypertrophy.

The effect of pressure-overload left ventricular hypertrophy (LVH) on myocardial function is controversial. A major factor in the controversy may be the age at which the pressure overload was induced. The goal of this study was to determine whether the age at which the LVH was induced affected systolic myocardial function. We studied lambs (n = 8) and sheep (n = 7) with LVH induced by constricting the ascending aorta and their sham-operated controls (n = 7 and n = 7). This new, unsedated, ovine model of LVH was large enough to accommodate chronic surgical implantation of instrumentation and the induction of pressure-overload hypertrophy in both young and adult age groups. Solid-state intraventricular pressure transducers and sonomicrometer crystal were used to assess instantaneous left ventricular pressure and dimensions. Myocardial contractility was assessed with midwall shortening at common preload and afterload. Load alterations were induced by graded infusion of methoxamine. There was depressed myocardial function in adult sheep with LVH compared with adult controls. Lambs with and without LVH had normal left ventricular myocardial function, similar to adult controls. Similar results were obtained in studies after beta-adrenergic receptor blockade. We conclude that maturation decreases the ability of the myocardium to maintain normal contractility in the presence of pressure-overload hypertrophy.

Adrenergic beta-Antagonists↗

Different responses of extent and velocity of contraction to dobutamine in conscious sheep.

The shortening- and shortening rate-preload-afterload relations, based on the concept of the myocardial end-systolic stress-strain relation (ESSSR), are a newly developed load- and size-independent assessment of myocardial contractility. The purpose of this study was to apply this assessment to compare extent and velocity of myocardial contraction during graded infusions of dobutamine. Seven chronically instrumented unsedated sheep were studied at rest and during graded infusions of dobutamine (2.5-20 micrograms.kg-1.min-1). The ESSSR were linear over a wide range of load alterations, whereas the end-systolic pressure-diameter relations (ESPDR) were generally nonlinear. Midwall shortening rate (SRm) at common preload and afterload representing contraction extent increased with each dose of dobutamine through 20 micrograms.kg-1.min-1. In contrast, midwall shortening (Sm) increased through dobutamine 5 micrograms.kg-1.min-1 but not at higher dobutamine infusion rates. Conventional endocardial shortening and the slope of the ESPDR, fitted to a linear model, exhibited responses similar to Sm. The velocity of circumferential endocardial fiber shortening (Vcf,c), Vcf,c-afterload relation, and maximum first derivative of left ventricular pressure exhibited responses similar to SRm. Thus both the extent and velocity of contraction increased at low doses of dobutamine, whereas only the velocity increased at high doses. Potential mechanisms for the saturated response of the extent of contraction include 1) shorter systolic time for contraction due to earlier onset of relaxation and 2) the utilization of myocardial contractile energy for left ventricular wall deformation at small cavity volumes at high doses of dobutamine.

Animals↗

Natural history and patterns of recovery of contractile function in single left ventricle after Fontan operation.

BACKGROUND: Before the era of the Fontan procedure, the typical course of patients with single left ventricle (LV) consisted of heart failure and death during the second or third decade of life. Despite the advent of effective palliative therapy, ventricular dysfunction remains a significant clinical problem for these patients. METHODS AND RESULTS: To investigate the causes of ventricular dysfunction in these patients and to determine whether Fontan-type repair reverses deterioration of LV function, the ventricular dimensions, volume, shape, wall stress, and systolic function were determined by echocardiography in 84 patients 0.2-35 years old with double-inlet single LV or tricuspid atresia. Measurements were obtained in 67 patients after palliation (arterial shunt or pulmonary artery band) and in 47 patients a median of 4.4 years after a Glenn (n = 9) or a Fontan operation (n = 38). Before a Fontan procedure, ventricular volumes were 2 to 3 times normal. Ventricular afterload, assessed as circumferential and meridional end-systolic wall stress, became abnormal after 2 years of age. With age, LV shape changed progressively from ellipsoidal to spherical, as indicated by the decrease in long axis:short axis ratio from normal (1.9) toward unity. Concomitantly, the ratio of circumferential to meridional end-systolic wall stress fell from 1.3 to unity, the ratio of a sphere at equilibrium. This age-related change in shape and load occurred in concert with progressive deterioration of LV systolic function and contractility. Aortic oxygen saturation, an indicator of pulmonary blood flow and therefore volume work in single-ventricle physiology, was inversely and independently correlated with contractility. In the group of patients in whom a Glenn or a Fontan operation was performed at < 10 years of age, ventricular dimensions, volumes, and wall stress diminished and LV function and contractility improved after surgery (p < 0.001). In patients undergoing surgery after 10 years of age, few had improvement of LV function after surgery. Postoperative ventricular function and contractility were inversely related to age at surgery and to aortic oxygen saturation measured before surgery. CONCLUSIONS: Although Fontan-type repair of single ventricle early in life is associated with reversal of the abnormal contractile mechanics associated with age and volume load, this capacity for recovery diminishes with age at surgery.

Cardiac Surgical Procedures↗

Course in the intensive care unit after 'preparatory' pulmonary artery banding and aortopulmonary shunt placement for transposition of the great arteries with low left ventricular pressure.

BACKGROUND: In patients with transposition of the great arteries with low left ventricular pressure, pulmonary artery banding with aortopulmonary shunt placement has been advocated to "prepare" the left ventricle for systemic work before an arterial switch operation. METHODS AND RESULTS: In 28 patients, this preparatory procedure was performed with one death. A successful arterial switch operation was performed at a median of 7 days later in 24 of 27 survivors; one child had a Senning performed, and two others died. During this interval period, the left ventricular-to-right ventricular pressure ratio increased from 48 +/- 8% to 98 +/- 19%, and left ventricular mass (indexed for body surface area) increased from 46 +/- 17 to 72 +/- 23 g/m2. After the preparatory procedure, the initial postoperative period was frequently characterized by a low-output syndrome of variable length and severity. Prolonged mechanical ventilation, extended inotropic support, and/or a significant metabolic acidosis was present in 21 of 28 patients in the immediate postoperative period. CONCLUSIONS: The low-output syndrome is most likely due to a combination of acute (fixed) right ventricular volume overload from the shunt and acute (transient) left ventricular dysfunction from the pulmonary artery band. This low-output syndrome should be anticipated following the preparatory procedure.

Blood Vessel Prosthesis↗

Mechanics of left ventricular systolic and diastolic function in physiologic hypertrophy of the athlete heart.

Due to a number of factors, there is tremendous diversity in the pattern of cardiac mechanics encountered in athletes. Nevertheless, there are several trends that can be identified and several conclusions are possible. Hypertrophy of a mild-to-moderate degree and out of proportion to body size is a common finding. Some athletes experience ventricular dilation with appropriate hypertrophy and preservation of the ventricular mass-to-volume ratio, whereas others manifest concentric hypertrophy with an increased mass-to-volume ratio. The functional changes that are encountered appear to be secondary to the structural alterations, and there is no evidence of altered myocardial systolic or diastolic properties. Some athletes with hypertrophy have reduced wall stress when they are evaluated at rest, and the velocity of shortening is augmented due to the reduced afterload. Due to adaptation to a high output state, some athletes appear preload reduced when evaluated at rest. Although velocity of shortening is not affected by preload status, fractional shortening is inversely related to preload. The magnitude of systolic shortening is therefore the net result of altered preload and afterload and cannot be understood without assessing both of these parameters. When the various determinants of systolic shortening are included, contractility appears to be normal. There have been several reports of depressed contractility immediately following extreme exertion, but the significance of this remains to be determined.

Adaptation, Physiological↗

Pulmonary valve-moderator band distance and association with development of double-chambered right ventricle.

Double-chambered right ventricle (DCRV), a form of right ventricular outflow obstruction that sometimes accompanies a ventricular septal defect (VSD), is associated with superior and rightward displacement of the septal insertion of the moderator band. It was hypothesized that this superior displacement is present and identifiable by echocardiography in patients with a VSD even before right ventricular outflow tract obstruction develops. Eight patients who had a previous echocardiographic study showing a VSD alone were echocardiographically diagnosed as having DCRV. Their initial echocardiographic studies were reviewed, and superior displacement of the moderator band was quantified by measuring the distance between the pulmonary valve and moderator band, normalized to tricuspid anulus diameter. These measurements were compared with those from the initial studies of the following 3 other groups: (1) an age-matched group of 10 patients with no structural heart disease; (2) an age-matched group of 10 patients with a VSD who did not develop DCRV; and (3) a group (not age-matched) of 10 patients with VSD and DCRV in whom subpulmonary obstruction was present on the initial study. The 8 patients who eventually developed subpulmonary obstruction had significant superior displacement of the moderator band at the time of their initial echocardiogram compared with that of the 2 age-matched control groups (p less than 0.01). In contrast, there was no significant difference in moderator band displacement between these patients and the 10 with DCRV who already had right ventricular outflow obstruction at their initial study (p = not significant).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗