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At least 613 records · Page 34Linked to original sources
PubMed2000

Depressed low frequency power of heart rate variability as an independent predictor of sudden death in chronic heart failure.

AIMS: Identification of patients with chronic heart failure at risk for sudden death remains difficult. We sought to assess the prognostic value for all-cause and sudden death of time and frequency domain measures of heart rate variability in chronic heart failure. METHODS AND RESULTS: We prospectively enrolled 190 patients with chronic heart failure in sinus rhythm, mean age 61+/-12 years, 109 (57.4%) in NYHA class II and 81 (42.6%) in classes III or IV, mean cardiothoracic ratio 57.6+/-6.4% and mean left ventricular ejection fraction 28.2+/-8.8%, 85 (45%) with ischaemic and 105 (55%) with idiopathic dilated cardiomyopathy. Time and frequency domain measures of heart rate variability were obtained from 24 h Holter ECG recordings, spectral measures were averaged for calculation of daytime (1000h-1900h) and night-time (2300h-0600h) values. During follow-up (22+/-18 months), 55 patients died, 21 of them suddenly and two presented with a syncopal spontaneous sustained ventricular tachycardia. In multivariate analysis, independent predictors for all-cause mortality were: ischaemic heart disease, cardiothoracic ratio > or =60% and standard deviation of all normal RR intervals <67 ms (RR = 2.5, 95% CI 1.5-4.2). Independent predictors of sudden death were: ischaemic heart disease and daytime low frequency power <3.3 ln (ms(2)) (RR = 2.8, 95% CI 1.2-8.6). CONCLUSION: Depressed heart rate variability has independent prognostic value in patients with chronic heart failure; spectral analysis identifies an increased risk for sudden death in these patients.

Arrhythmias, Cardiac↗
PubMed2004

Intramyocardial lipid accumulation in the failing human heart resembles the lipotoxic rat heart.

In animal models of lipotoxicity, accumulation of triglycerides within cardiomyocytes is associated with contractile dysfunction. However, whether intramyocardial lipid deposition is a feature of human heart failure remains to be established. We hypothesized that intramyocardial lipid accumulation is a common feature of non-ischemic heart failure and is associated with changes in gene expression similar to those found in an animal model of lipotoxicity. Intramyocardial lipid staining with oil red O and gene expression analysis was performed on heart tissue from 27 patients (9 female) with non-ischemic heart failure. We determined intramyocardial lipid, gene expression, and contractile function in hearts from 6 Zucker diabetic fatty (ZDF) and 6 Zucker lean (ZL) rats. Intramyocardial lipid overload was present in 30% of non-ischemic failing hearts. The highest levels of lipid staining were observed in patients with diabetes and obesity (BMI>30). Intramyocardial lipid deposition was associated with an up-regulation of peroxisome proliferator-activated receptor alpha (PPARalpha) -regulated genes, myosin heavy chain beta (MHC-beta), and tumor necrosis factor alpha (TNF-alpha). Intramyocardial lipid overload in the hearts of ZDF rats was associated with contractile dysfunction and changes in gene expression similar to changes found in failing human hearts with lipid overload. Our findings identify a subgroup of patients with heart failure and severe metabolic dysregulation characterized by intramyocardial triglyceride overload and changes in gene expression that are associated with contractile dysfunction.

Adult↗
PubMed1990

Interactions between diabetes and family history of coronary heart disease and other risk factors for coronary heart disease among adults with diabetes in Utah.

We used a unique data base containing medical family history information from representative Utah families to investigate interactions between diabetes and family history of coronary heart disease and other risk factors for coronary heart disease. We compared nonrelated individuals reported to have had diabetes mellitus diagnosed over the age of 19 (948) with 2150 nondiabetic individuals. Among both men and women, diabetes and family history of early coronary heart disease magnified the risk for coronary heart disease, so that in diabetic individuals with a positive family history of coronary heart disease, about 74% of the coronary heart disease could be attributed to interaction. Relative to nondiabetics without a family history of early coronary heart disease, nondiabetics with family history had a relative risk of 4.5 (2.3-8.7), diabetics without a family history had a relative risk of 2.8 (1.6-4.9), and diabetics with a family history had a relative risk of 21.3 (9.1-50.0). Smoking also interacted with diabetes; among smoking diabetics, 47% of early heart disease may be attributable to interaction between smoking and diabetes. Smoking entailed the highest risk for diabetic women. Hypertension and diabetes appeared to act additively, with little interaction. Among women, family history of diabetes was a risk factor for coronary heart disease with a relative risk of 2.5 (1.0-6.4), whereas for men the relative risk was estimated to be 0.4 (0.2-1.1).

Adult↗
PubMed1999

Relation of Chlamydia pneumoniae serology to mortality and incidence of ischaemic heart disease over 13 years in the caerphilly prospective heart disease study.

OBJECTIVES: To investigate the effect of Chlamydia pneumoniae infection on future development of ischaemic heart disease and mortality. DESIGN: Prospective longitudinal study. SETTING: Caerphilly, South Wales. SUBJECTS: Plasma specimens were collected during 1979-83 from 1773 men aged 45-59 years. These were tested for IgG and IgA antibodies to C pneumoniae (TW183) by microimmunofluorescence. OUTCOME MEASURES: 13 year mortality and incident ischaemic heart disease events were ascertained from death certificates, hospital records, and electrocardiographic changes at follow up every 4 to 5 years. RESULTS: 642 men (36.2%) had IgG antibodies at a titre of >/=1 in 16, of whom 362 (20.4% of all men) also had detectable IgA antibodies. The prevalence of ischaemic heart disease (a history of past or current disease) at entry was similar at all IgG antibody titres but was positively related to IgA antibody titre. IgA antibody titre was positively correlated with plasma viscosity but not with other cardiovascular risk factors. Incidence of ischaemic heart disease was not associated with either IgG antibody titre or IgA antibody titre, but there were stronger and significant relations of IgA antibodies with all cause mortality and fatal ischaemic heart disease, which persisted after adjustment for conventional cardiovascular risk factors. The odds ratios associated with detectable IgA antibodies were 1.07 (95% confidence interval 0.75 to 1.53) for all incident ischaemic heart disease, 1. 83 (1.17 to 2.85) for fatal ischaemic heart disease, and 1.50 (1.10 to 2.04) for all cause mortality. CONCLUSION: This is the first prospective demonstration of an association between IgA antibodies to C pneumoniae, a putative marker of chronic infection, and subsequent risk of death from ischaemic heart disease. In contrast to earlier case-control studies, IgG antibodies were not associated with either prevalent or incident ischaemic heart disease.

Antibodies, Bacterial↗
PubMed1999

Effects of walking on coronary heart disease in elderly men: the Honolulu Heart Program.

BACKGROUND: Effects of walking on the risk of coronary heart disease morbidity and mortality have not been identified in the elderly. The purpose of this study was to determine whether walking is associated with a reduced risk of coronary heart disease in a sample of elderly men. METHODS AND RESULTS: For this study, distance walked (mile/d) was examined at a baseline examination that occurred from 1991 to 1993 in the Honolulu Heart Program. Incident coronary heart disease from all causes was observed over a 2- to 4-year follow-up period. Subjects followed up were 2678 physically capable elderly men aged 71 to 93 years. During the course of follow-up, 109 men developed coronary heart disease. Men who walked <0.25 mile/d had a 2-fold increased risk of coronary heart disease versus those who walked >1. 5 mile/d (5.1% versus 2.5%; P<0.01). Men who walked 0.25 to 1.5 mile/d were also at a significantly higher risk of coronary heart disease than men who walked longer distances (4.5% versus 2.5%; P<0. 05). Adjustment for age and other risk factors failed to alter these findings. CONCLUSIONS: Findings from the Honolulu Heart Program, which targeted physically capable elderly men, suggest that the risk of coronary heart disease is reduced with increases in distance walked. Combined with evidence that suggests that an active lifestyle reduces the risk of cardiovascular disease in younger and more diverse groups, this suggests that important health benefits could be derived by encouraging the elderly to walk.

Aged↗
PubMed2002

Validation of Heart Failure Events in the Antihypertensive and Lipid Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) Participants Assigned to Doxazosin and Chlorthalidone.

BACKGROUND: The Antihypertensive and Lipid Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) is a randomized, double-blind, active-controlled trial designed to compare the rate of coronary heart disease events in high-risk hypertensive participants initially randomized to a diuretic (chlorthalidone) versus each of three alternative antihypertensive drugs: alpha-adrenergic blocker (doxazosin), ACE-inhibitor (lisinopril), and calcium-channel blocker (amlodipine). Combined cardiovascular disease risk was significantly increased in the doxazosin arm compared to the chlorthalidone arm (RR 1.25; 95% CI, 1.17-1.33; P <.001), with a doubling of heart failure (fatal, hospitalized, or non-hospitalized but treated) (RR 2.04; 95% CI, 1.79-2.32; P <.001). Questions about heart failure diagnostic criteria led to steps to validate these events further. METHODS AND RESULTS: Baseline characteristics (age, race, sex, blood pressure) did not differ significantly between treatment groups (P <.05) for participants with heart failure events. Post-event pharmacologic management was similar in both groups and generally conformed to accepted heart failure therapy. Central review of a small sample of cases showed high adherence to ALLHAT heart failure criteria. Of 105 participants with quantitative ejection fraction measurements provided, (67% by echocardiogram, 31% by catheterization), 29/46 (63%) from the chlorthalidone group and 41/59 (70%) from the doxazosin group were at or below 40%. Two-year heart failure case-fatalities (22% and 19% in the doxazosin and chlorthalidone groups, respectively) were as expected and did not differ significantly (RR 0.96; 95% CI, 0.67-1.38; P = 0.83). CONCLUSION: Results of the validation process supported findings of increased heart failure in the ALLHAT doxazosin treatment arm compared to the chlorthalidone treatment arm.

Journal Article↗
PubMed2002

[Vascularization of the sinoatrial segment in the heart conduction system in bovine and canine hearts] ].

Vascularisation of the conductive heart musculature was investigated by means of the serial coronorography and injective-corrosive method in bovine and canine hearts. The S-A system of the bovine heart was in 50% of the investigated hearts was supplied by the anterior left by the anterior right sinus artery (Arteria nodus sinuatrialis anterior sinistra), and in 30% of the cases by the anterior right sinus artery (Arteria nodus sinuatrialis anterior dextra). Both anterior sinus arteries vascularize the S-A bovine heart system in 20% of the investigated cases. The S-A canine heart system, in 50% of the investigated cases, receive vascularization from the anterior left sinus artery, from the right anterior artery in 40% of the cases, and only in 10% of the investigated hearts is the S-A system supplied by the right and left posterior sinus arteries (Arteria nodus sinuatrialis posterior dextra et sinistra). The S-A system vascularisation of the conductive heart musculature is not conditional by the type of the arterial vascularisation of the heart.

Animals↗
PubMed1989

Formation of malonyl coenzyme A in rat heart. Identification and purification of an isozyme of A carboxylase from rat heart.

Acetyl-CoA carboxylase is thought to be absent in the heart since the latter is highly catabolic and nonlipogenic. It has been suggested that the high level of malonyl-CoA that is found in the heart is derived from mitochondrial propionyl-CoA carboxylase, which also uses acetyl-CoA. In the present study, acetyl-CoA carboxylase was identified and purified from homogenates of rat heart. The isolated enzyme had little activity in the absence of citrate (specific activity, less than 0.1 units/mg); however, citrate stimulated its activity (specific activity, 1.8 units/mg in the presence of 10 mM citrate). Avidin inhibited greater than 95% of activity, and addition of biotin reversed this inhibition. Further, malonyl-CoA (1 mM) and palmitoyl-CoA (100 microM) inhibited greater than 90% of carboxylase activity. Similar to acetyl-CoA carboxylase of lipogenic tissues, the heart enzyme could be activated greater than 6-fold by preincubation with liver (acetyl-CoA carboxylase)-phosphatase 2. The activation was accompanied by a decrease in the K0.5 for citrate to 0.68 mM. These observations suggest that the activity in preparations from heart is due to authentic acetyl-CoA carboxylase. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis of the preparation from heart showed the presence of one major protein band (Mr 280,000) and a minor band (Mr 265,000) while that from liver gave a major protein band (Mr 265,000). A Western blot probed with avidin-peroxidase suggested that both the 280- and 265-kDa species contained biotin. Antibodies to liver acetyl-CoA carboxylase, which inhibited greater than 95% of liver carboxylase activity, inhibited only 35% of heart enzyme activity. In an immunoblot (using antibodies to liver enzyme) the 265-kDa species, and not the major 280-kDa species, in the heart preparation was specifically stained. These observations suggest the presence of two isoenzymes of acetyl-CoA carboxylase that are immunologically distinct, the 265-kDa species being predominant in the liver and the 280-kDa species being predominant in the heart.

Acetyl-CoA Carboxylase↗
PubMed1978

Partial artificial heart (ALVAD) use with subsequent cardiac and renal allografting in a patient with stone heart syndrome.

The abdominal left ventricular assist device (ALVAD) is an order of magnitude more effective than conventional intra-aortic balloon pumping (IABP) in unloading and providing circulatory support to the failing left ventricle. This is a report of a unique case which demonstrates that in the absence of pulmonary vascular obstruction or constriction, the ALVAD can substitute for both left and right heart function. A 21-year-old patient with a congenital bicuspid aortic valve developed acute valvular endocarditis which rapidly progressed to congestive heart failure. An operation was undertaken, the mitral and aortic valves were excised and replaced by porcine heterografts, and a fistula from the right sinus of Valsalva to the right ventricle was closed. When coronary circulation was restored, irreversible ischemic contracture of the left ventricle, or "stone heart" syndrome, developed and emergency ALVAD or partial artificial heart implantation was effected. This device functioned as a total artificial heart for nearly six days, while a donor heart was sought. The patient then underwent removal of the ALVAD and cardiac and renal allografting. The transplanted heart functioned well, but the patient expired fifteen days later from gram-negative sepsis.

Adult↗
PubMed1996

Neostigmine decreases heart rate in heart transplant patients.

PURPOSE: This study evaluated the effect of neostigmine on heart rate in cardiac transplant patients. METHODS: Neostigmine (2.5-50 micrograms.kg-1) was administered to ASA 1 or 2 patients with normally innervated hearts (controls), and to patients who had undergone recent (< six months before study) or remote (> six months before study) cardiac transplantation. RESULTS: Baseline heart rate was 66 +/- 3 beats.min-1 in controls (n = 10, mean +/- SEM), which was slower than that observed in recently (95 +/- 4 beats.min-1, n = 15, P < 0.001) and in remotely (88 +/- 3 beats.min-1, n = 16, P < 0.001) transplanted patients. Neostigmine produced a dose-dependent decrease in heart rate in all patients. Controls were the most sensitive to neostigmine, with a 10% decrease in heart rate produced by an estimated dose of 5.0 +/- 1.0 micrograms.kg-1. The recently transplanted group was the least sensitive, with the maximum dose producing only an 8.3 +/- 0.9% reduction. The response to neostigmine of the remotely transplanted patients was variable. The estimated dose to produce a 10% decrease in heart rate in this group was 24 +/- 6 micrograms.kg-1 which was greater than that for controls (P = 0.008). Administration of atropine (1.2 mg) reversed the neostigmine-induced bradycardia in all three groups. Reversal of the bradycardia consisted of a transient peak increase in heart rate in controls to 145 +/- 6% of baseline, a value which was greater than that observed in recent (103 +/- 1%, P < 0.001) and in remote (109 +/- 3%, P < 0.001) transplants. CONCLUSIONS: Neostigmine produces a dose-dependent bradycardia in heart transplant patients. Some remotely transplanted patients may be particularly sensitive to the bradycardic effects of neostigmine.

Cholinesterase Inhibitors↗
PubMed1998

Clinical and haemodynamic correlates of heart rate variability in children with congenital heart disease.

UNLABELLED: Heart rate variability (HRV) represents a noninvasive parameter for studying the autonomic control of the heart. Cardiac patients have a complex autonomic disturbance. The relation of HRV to this abnormality in children with congenital heart disease (CHD) has not yet been examined. The present study examined HRV indices from 24 h Holter recordings in 258 children with an operated or non-operated CHD, to determine their differences as an indicator of the severity of heart disease. The latter was defined clinically as New York Heart Association (NYHA) functional classes I to IV and haemodynamically by invasive parameters. Five time-domain measures (SDNN, SDNNi, SDANNi, rMSSD and pNN50) and three frequency-domain measures (LF, HF and balance LF/HF) were compared with normal ranges. HRV was reduced in children with CHD, except in patients of NYHA class I. The level of reduction depended on the NYHA functional class. None of the measures was significantly related to haemodynamic data. CONCLUSION: Heart rate variability is reduced in children with Congenital heart disease depending on the functional limitation but not on haemodynamic disturbances. Heart rate variability indices are sensitive markers of the clinical state.

Adolescent↗
PubMed1992

Patterns of beat-to-beat heart rate variability in advanced heart failure.

Diminished heart rate variability is associated with high sympathetic tone and an increased mortality rate in heart failure cases. We constructed Poincaré plots of each sinus R-R interval plotted against the subsequent R-R interval from 24-hour Holter recordings of 24 healthy subjects (control group) and 24 patients with heart failure. Every subject in the control group had a comet-shaped Poincaré plot resulting from an increase in beat-to-beat dispersion as heart rate slowed. No patient with heart failure had this comet-shaped pattern. Instead, three distinctive patterns were identified: (1) a torpedo-shaped pattern resulting from low R-R interval dispersion over the entire range of heart rates, (2) a fanshaped pattern resulting from restriction of overall R-R interval ranges with enhanced dispersion, and (3) complex patterns with clusters of points characteristic of stepwise changes in R-R intervals. Poincaré pattern could not be predicted from standard deviations of R-R intervals. This first use of Poincaré plots in heart rate variability analysis reveals a complexity not readily perceived from standard deviation information. Further study is warranted to determine if this method will allow refined assessment of cardiac-autonomic integrity in heart failure, which could help identify patients at highest risk for sudden death.

Death, Sudden↗
PubMed1991

Heterotopic heart transplantation and native heart ventricular arrhythmias.

Heterotopic heart transplantation has been said to be contraindicated in patients with serious native heart arrhythmias that produce hemodynamic instability. Placement of heterotopic allografts, however, can theoretically act as a biological biventricular assist device to provide hemodynamic support during these unstable rhythms. Further, this operation might beneficially alter the hemodynamic milieu of heart failure such that the arrhythmias are ameliorated. Described is our experience with 4 patients with heart failure receiving heterotopic cardiac allografts, documenting changes in native heart arrhythmia that occurred. These cases demonstrate that heterotopic grafts can adequately sustain hemodynamics during malignant native heart dysrhythmia. We believe native heart ventricular arrhythmias are not a contraindication to heterotopic heart transplantation.

Arrhythmias, Cardiac↗
PubMed1989

Does fetal heart rate predict subsequent heart rate in childhood?

An investigation to determine whether there is any relationship between extremes of fetal heart rate during labour and subsequent heart rate at the age of 10 was carried out using data from the 1970 cohort of British Births. In 11,000 nationally representative children it was found that low fetal heart rate (below 120 beats/min) was associated with a heart rate at age 10 which was significantly lower than in those children whose fetal heart rate had remained between 120 and 160 beats/min (P less than 0.01). This relationship could not be explained by fetal asphyxiation, maternal antenatal hypotension or the method of pain relief during labour. There was no equivalent relationship with high fetal heart rate during labour. This could imply that some fetuses with low heart rates are not exhibiting fetal distress but have an inherent tendency to relatively slow heart rates.

Child↗
PubMed1995

Continuous positive airway pressure increases heart rate variability in congestive heart failure.

OBJECTIVES: Our objective was to determine whether continuous positive airway pressure augments the low heart rate variability of congestive heart failure, a marker of poor prognosis. BACKGROUND: Nasal continuous positive airway pressure improves ventricular function in selected patients with heart failure. METHODS: In 21 sessions in 16 men (mean [+/- SE] age 56 +/- 2 years) with New York Heart Association functional class II to IV heart failure, we assessed the effects of 45 min with (n = 14) and without (as a time control, n = 7) nasal continuous positive airway pressure (10 cm of water) on heart rate variability and end-expiratory lung volume. Coarse-graining spectral analysis was used to derive total spectral power (PT), its nonharmonic component (fractal power [PF]) and the low (0.0 to 0.15 Hz [PL]) and high (0.15 to 0.50 Hz [PH]) frequency components of harmonic power. Standard deviation of the RR interval, high frequency power and the PH/PT ratio were used to estimate parasympathetic activity in the time and frequency domains, and the PL/PH ratio was used to estimate cardiac sympathetic activity in the frequency domain. RESULTS: Use of continuous positive airway pressure increased end-expiratory lung volume by 445 +/- 82 ml (p < 0.01) and both time (p < 0.006) and frequency domain indexes of heart rate variability: Total spectral power (p < 0.01), nonharmonic power (p < 0.023) and low (p < 0.04) and high (p < 0.05) frequency components of harmonic power all increased. Time alone had no effect on these variables. By comparison, the PH/PT ratio increased during nasal continuous positive airway pressure (p < 0.004), whereas the PL/PH ratio was unchanged. Breathing rate remained constant in both groups. CONCLUSIONS: Short-term application of nasal continuous positive airway pressure increases heart rate variability and time and frequency domain indexes of parasympathetic activity without influencing cardiac sympathetic activity. This increase may occur reflexively, through stimulation of pulmonary mechanoreceptor afferents.

Adult↗
PubMed1994

Complex heart rate variability and serum norepinephrine levels in patients with advanced heart failure.

OBJECTIVES: This study was designed to examine the relation of the Poincaré plot heart rate variability pattern to sympathetic nervous system activity as assessed by serum norepinephrine. BACKGROUND: Poincaré plots demonstrate a complexity of beat to beat behavior not readily detected by other heart rate variability measures. Previous studies have described two abnormal Poincaré patterns in patients with heart failure: a torpedo pattern with reduced beat to beat variability and a complex pattern with clustering of points. METHODS: To assess the relation of these plots to sympathetic activity, plasma norepinephrine at rest and a standard deviation measure of heart rate variability were analyzed in 21 patients with heart failure (mean left ventricular ejection fraction [+/- SD] 0.22 +/- 0.05). RESULTS: Eleven subjects had a torpedo-shaped and 10 subjects had a complex Poincaré plot pattern. These two groups did not differ significantly in age, functional class, disease etiology, left ventricular ejection fraction, heart rate, ventricular ectopic activity or in a standard deviation measure of heart rate variability. However, patients with a complex Poincaré plot pattern had higher norepinephrine levels (722 +/- 373 pg/ml) than patients with torpedo-shaped plots (309 +/- 134 pg/ml) (p = 0.003). Patients with a complex pattern also had more severe hemodynamic decompensation, as evidenced by their higher levels of pulmonary capillary wedge and mean pulmonary artery pressures and lower values for cardiac index than those of patients with a torpedo-shaped plot. CONCLUSIONS: Complex Poincaré plots are associated with marked sympathetic activation and may provide additional prognostic information and insight into autonomic alterations and sudden cardiac death in patients with heart failure.

Electrocardiography, Ambulatory↗
PubMed1992

Adenine nucleotide catabolism in human myocardium during heart and heart-lung transplantation.

The influence of ischemia and reperfusion on nucleotide concentration in human myocardium was investigated during heart and heart-lung transplantation. Myocardial preservation during heart transplantation was achieved by infusion of cold St. Thomas' Hospital cardioplegic solution followed by storage in Ringer's solution at 4 degrees C during transport. In contrast, the hearts of heart and lung donors were preserved by core cooling using cardiopulmonary bypass and infusion of cold blood cardioplegia containing 26 mM potassium. The heart-lung block was transported in cold donor blood. Nucleotides and their catabolite concentrations were measured in donor tissue specimens taken before organ collection, before commencement of implantation and 30 min after aortic clamp removal. During reperfusion, samples of coronary sinus and arterial blood were collected and analysed for nucleotide catabolite concentration. Myocardial ATP and total nucleotide pool remained almost unchanged during the ischemic transport of the donor organs with only very small increases in myocardial inosine and hypoxanthine concentrations. However, a significant decrease of total adenine nucleotide pool by 10%-20% was demonstrated between the start of implantation and 30 min post-reperfusion. A release of inosine + hypoxanthine was greatest in the 1st minute (15-25 microM), but was still substantial after 10 min of reperfusion (5-15 microM). Metabolic changes tended to be more pronounced during heart-lung transplantation than during heart transplantation.

Adenine Nucleotides↗
PubMed1996

Reduction in lymphocyte beta-adrenergic receptor density in infants and children with heart failure secondary to congenital heart disease.

To identify changes in catecholamine levels and beta-adrenergic receptor density in children with varying degrees of congestive heart failure, we measured plasma norepinephrine (NE), epinephrine, and beta-adrenergic receptor levels in 91 noncyanotic patients using high-performance liquid chromatography and a radioligand binding assay. Plasma NE levels in 41 patients with heart failure (694 +/- 236 pg/ml) were significantly higher than those in 50 patients without it (274 +/- 68 pg/ml, p < 0.001). In addition, beta-adrenergic receptor density was significantly lower in patients with heart failure (0.81 +/- 0.48 fmol/10(6) cells) than in those without it (2.43 +/- 1.09 fmol/10(6) cells, p < 0.001), but epinephrine levels were not significantly different between the 2 groups. The receptor reduction in heart failure correlated well with elevated plasma NE levels (r = -0.60, p < 0.001). The degree of left to right shunt flow and pulmonary systolic pressure correlated directly with plasma NE levels and inversely with beta-adrenergic receptor density. From the best compromise between sensitivity and specificity, the optimal cutoff point for heart failure was > 390 ng/ml for NE and < 1.30 fmol/10(6) cells for beta-adrenergic receptor density, respectively. A follow-up study in 15 of 30 patients with heart failure after surgery showed a significant decrease in plasma NE and an increase in beta-adrenergic receptor density. Changes in plasma NE levels and beta-adrenergic receptor density occur concurrently with clinical symptoms of heart failure and may be used as indexes for assessing the presence and severity of heart failure in infants and children.

Adolescent↗