Right-heart intracardiac phonocardiography in 80 subjects without organic heart disease. A study of the origin of innocent heart murmurs.
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OBJECTIVES: The goal of this study was to assess the safety and efficacy of pulmonary vein antrum isolation in patients with moderate valvular heart disease or open-heart surgery and atrial fibrillation (AF). BACKGROUND: Valvular heart disease and open-heart surgery are commonly associated with AF and increase the risk of adverse events in AF patients. METHODS: A total of 391 consecutive patients who had pulmonary vein antrum isolation performed between December 2000 and December 2002 were screened. A total of 142 of these patients had clinically significant valvular disease or prior cardiac surgery. End points included AF recurrence and pulmonary vein antrum isolation complication rates. RESULTS: Patients with valvular heart disease or prior open-heart surgery were older, had larger left atria and a more advanced New York Heart Association class. They did not differ significantly with respect to gender, but had a longer history of AF. Procedure times were similar between patients with and without valvular heart disease or prior open-heart surgery. After 18 +/- 7 months in the lone AF patients, 11 +/- 5 months in patients with valvular heart disease, and 10 +/- 5 months in patients with prior open heart surgery, there was a trend toward lower recurrence of AF in patients with lone AF who enjoyed a 98% overall cure rate after up to 2 pulmonary vein antrum isolations versus 93% among patients with valvular heart disease (P = .04) and prior open heart surgery (P = .07). Complication rates were comparable between groups. CONCLUSIONS: Pulmonary vein antrum isolation is safe and effective in patients with moderate valvular heart disease and the patients who developed AF after open-heart surgery. These results have implications for our understanding of the pathophysiology of AF in patients with moderate valvular heart disease or past cardiac surgery and should be considered when discussing treatment options in these patients.
Major untoward events, such as life-threatening arrhythmias and acute coronary events, have been suggested to be triggered by the activation of the autonomic nervous system in patients with coronary artery disease. Analysis of heart rate variability by conventional time and frequency domain methods, as well as by newer methods derived from nonlinear system theory, has offered a novel approach for studying the abnormalities in cardiovascular neural regulation in ischemic heart disease. Heart rate variability has been shown to be altered among patients with ischemic heart disease as compared to their age-matched controls without the evidence of ischemic heart disease. There are also obvious differences in various measures of heart rate variability between patients with uncomplicated coronary artery disease and those with coronary artery disease with complicated myocardial infarction. Impaired high-frequency oscillations of heart rate is the most prominent feature in patients with uncomplicated coronary artery disease, suggesting mainly an impairment in vagal autonomic regulation. Patients with prior myocardial infarction have a reduced overall heart rate variability, and a specific spectral pattern with a reduced low-frequency spectral component has been observed in patients with prior myocardial infarction and impaired left ventricular function. Recent studies have shown that the new nonlinear measures, particularly fractal analysis methods of heart rate dynamics, can detect subtle changes in heart rate behavior that are not easily detected by traditional analysis methods from ambulatory recordings. Patients with prior myocardial infarction have steeper power-law slope analyzed from the ultra and very low-frequency spectral bands, and they also have more random short-term heart rate dynamics analyzed by the detrended fluctuation method. A large body of data indicate that reduced overall heart rate variability is associated with an increased risk of mortality and nonfatal cardiac events in patient with ischemic heart disease. Of particular note, recent studies indicate that fractal analysis methods perform even better than the traditional analysis methods of heart rate variability as predictors of death and the onset of life-threatening arrhythmic events in post-infarction populations. These findings support the notion that heart rate variability analysis methods, such as fractal and complexity measures as well as conventional techniques, give valuable clinical information among patients with ischemic heart disease.
BACKGROUND: The present investigation was designed to obtain an absolute measurement of myocardial blood flow and of its transmural distribution in ischemic heart disease and idiopathic dilated cardiomyopathy and to provide a reference standard for cardiac imaging in nuclear cardiology. METHODS AND RESULTS: Regional myocardial blood flow and its transmural distribution were estimated by the reference microsphere method in eight patients with idiopathic dilated cardiomyopathy (n = 4) or ischemic heart disease (n = 4) during heart transplant procedure. Before aortic clamping, 99mTc-labeled human albumin microspheres were injected into the left atrium while arterial blood was sampled from the aorta at a constant rate. No complications were observed during or after the procedure. From the excised heart, myocardial slices for gamma camera imaging and well counting analysis were obtained. Myocardial blood flow was assessed by a well counter, correlated with the extent of fibrosis expressed as collagen per total tissue proteins obtained from 4-hydroxyproline and glycine as determined by high-performance liquid chromatography. Microsphere distribution, as seen by gamma camera images in a different slice, was correlated with the extent of fibrosis assessed by histological analysis of the same myocardial specimen. Mean transmural myocardial blood flow was 0.49 +/- 0.17 and 0.38 +/- 0.15 mL.min-1 x g-1 in idiopathic dilated cardiomyopathy and ischemic heart disease, respectively (P < .01). Endocardial-to-epicardial flow ratio was lower in ischemic heart disease than in idiopathic dilated cardiomyopathy patients (0.99 +/- 0.33 versus 1.16 +/- 0.30, P < .05). Mean myocardial fibrosis was 9 +/- 6% in idiopathic dilated cardiomyopathy and 25 +/- 28% in ischemic heart disease. In both groups, no correlation was found between myocardial blood flow values and the extent of fibrosis. In ischemic heart disease, regional myocardial blood flow was not significantly affected by the severity of coronary stenosis (< or = 70% or > 70%) either in the endocardium (0.44 +/- 0.24 versus 0.36 +/- 0.16 mL.min-1 x g-1, P = NS) or in the epicardium (0.50 +/- 0.33 versus 0.38 +/- 0.33 mL.min-1 x g-1, P = NS). By gamma camera imaging, transmural microsphere distribution appeared more homogeneous in idiopathic dilated cardiomyopathy than in ischemic heart disease (mean coefficient variation, 18% and 27%, respectively; P < .02); the severity of perfusion impairment did not correlate with the extent of fibrosis evaluated by histological criteria. CONCLUSIONS: Heart transplant surgery offers a valuable model to assess absolute myocardial perfusion in human heart failure. Myocardial blood flow is markedly depressed in failing hearts of both ischemic heart disease and idiopathic dilated cardiomyopathy patients; a different transmural myocardial blood flow distribution is observed in ischemic heart disease than in idiopathic dilated cardiomyopathy, with prevalent endocardial perfusion in the latter but not the former condition. In patients with end-stage heart failure, myocardial blood flow appears to be similarly impaired in fibrotic and viable regions. Mechanisms other than myocardial fibrosis and coronary lesions appear to operate in determining myocardial blood flow impairment in heart failure.
Frequency analysis of heart sounds has been gaining recognition as a possible indicator of several heart and valve diseases, although a comprehensive study of normal heart sounds has not been published. Relating the frequency content of normal heart sounds to certain physical characteristics surrounding the generation of these sounds could lead to a valuable diagnostic tool and give a better understanding of the mechanism of heart sounds production. In this study, the first and second heart sounds from seventy-four normal, and seven hypertensive volunteers were recorded, digitized and analysed using a Fast Fourier Transform algorithm. Statistical analysis was used to relate physical characteristics (sex, blood pressure, and body surface area) of the subjects to the frequency content of normal heart sounds and to compare normal and hypertensive heart sounds. Statistical analysis showed that the major concentration of energy, for both first heart sound (S1) and second heart sound (S2), is below 150 Hertz (Hz) which may indicate that both sounds are caused by vibrations within the same structure, possibly the entire heart. However S2 spectra have greater amplitude than S1 spectra above 150 Hz, which may be due to vibrations within the aorta and pulmonary artery. Relationships observed between body surface area, sex, blood pressure, and the frequency content of heart sounds indicate that as heart size increases, the amplitude of the frequency coefficients above 150 Hz decreases. These observations were more identifiable in the S1 spectra than in the S2 spectra, possibly because the S2 higher frequency components may mask subtle changes in the S2 spectra caused by heart size changes. However, when the changes in heart size are significant, as in hypertension or increased body surface area, trends in the S2 spectra can be observed.
OBJECTIVES: To assess the prognostic value of heart rate response to exercise in adult congenital heart disease (ACHD) patients. BACKGROUND: An abnormal heart rate response to exercise is related to autonomic dysfunction and may have prognostic implications in ACHD. METHODS: We identified 727 consecutive ACHD patients (mean age [+/- SD] 33 +/- 13 years) with varying diagnoses and without pacemakers. Peak oxygen consumption (peak VO2), resting heart rate, and the increase in heart rate from resting level to peak exercise ("heart rate reserve") were measured. We also quantified the decrease in heart rate ("heart rate recovery") after cessation of exercise. RESULTS: During a median follow-up of 28 months, 38 patients died. Lower values of heart rate reserve, peak heart rate, heart rate recovery, and peak VO2 (p < 0.01 for each) were associated with increased mortality in univariate analysis. Furthermore, heart rate reserve predicted mortality independently of antiarrhythmic therapy, functional class, and peak VO2. Stratifying patients by diagnostic groups revealed that a lower heart rate reserve was also associated with a greater risk of death in patients with complex anatomy, Fontan circulation, and tetralogy of Fallot (p < 0.05 for each). CONCLUSIONS: An abnormal heart rate response to exercise identifies ACHD patients with a higher risk of mortality in the midterm, even after accounting for antiarrhythmic medication and exercise capacity. Heart rate reserve is a simple and inexpensive way to identify ACHD patients at higher mortality risk.
STUDY OBJECTIVE: The aim was to assess the changes in sympatho-vagal balance which occur with exercise. DESIGN: The power spectrum of RR interval fluctuations (low frequency [LF] and high frequency components [HF]) was determined before, during, and after graded work load exercise on a cycle ergometer. The power spectrum of the respiratory signal, oxygen consumption, and respiratory volumes were also evaluated. In all subjects HF was considered to be an index of respiratory sinus arrhythmia. In normal subjects HF and LF were considered to be indices of relative vagal and sympathetic activity, respectively, whereas in heart transplant subjects HF was considered as a respiratory modulation of the intrinsic heart rate, and not dependent on autonomic tone. Heart rate variability was evaluated as RR interval variance. SUBJECTS: 15 normal subjects (six trained cyclists and nine healthy sedentary subjects) and six orthotopic heart transplant recipients took part in the study. MEASUREMENTS AND MAIN RESULTS: During the first part of exercise, heart rate increased, RR interval variance decreased, HF decreased, and the relative amount of LF increased both in sedentary and athletic subjects, suggesting a relative increase in sympathetic tone. However, when approaching peak exercise, while heart rate further increased and the variance slightly decreased, the relative proportion of LF decreased and HF proportionally increased. At peak exercise HF accounted for 99.9% of heart rate variability in athletic subjects and for 88.9% in sedentary subjects (p less than 0.001 v baseline and v LF in both groups). In heart transplant subjects both the variance and the HF increased from the beginning of exercise (p less than 0.05), and showed a direct correlation with ventilatory variables and an inverse correlation with heart rate (r = 0.794, p less than 0.001, multiple regression analysis). No measurable LF components could be obtained in these subjects. During recovery, while the heart rate decreased and the RR interval variance increased, there was a relative increase in LF and a relative decrease in HF in normal subjects (either sedentary or athletic). Similarly, in heart transplant subjects, there was a decrease in HF during recovery. Thus the increase in HF at peak exercise in normal subjects contrasts with all the other data which suggest a prevalence in sympathetic tone during the entire exercise and the early recovery period, but appears similar to the increase in HF observed in heart transplant subjects due to the effect of increased ventilation during exercise. CONCLUSIONS: These findings suggest that at peak exercise a non-autonomic mechanism, possibly intrinsic to the heart muscle, may determine heart rate fluctuations in synchrony with ventilation in the intact as well as in the denervated human heart.
ABSTRACT The heart is the first organ to form and function during development. In the pregastrula chick embryo, cells contributing to the heart are found in the postero-lateral epiblast. During the pregastrula stages, interaction between the posterior epiblast and hypoblast is required for the anterior lateral plate mesoderm (ALM) to form, from which the heart will later develop. This tissue interaction is replaced by an Activin-like signal in culture. During gastrulation, the ALM is committed to the heart lineage by endoderm-secreted BMP and subsequently differentiates into cardiomyocyte. The right and left precardiac mesoderms migrate toward the ventral midline to form the beating primitive heart tube. Then, the heart tube generates a right-side bend, and the d-loop and presumptive heart segments begin to appear segmentally: outflow tract (OT), right ventricle, left ventricle, atrioventricular (AV) canal, atrium and sinus venosus. T-box transcription factors are involved in the formation of the heart segments: Tbx5 identifies the left ventricle and Tbx20 the right ventricle. After the formation of the heart segments, endothelial cells in the OT and AV regions transform into mesenchyme and generate valvuloseptal endocardial cushion tissue. This phenomenon is called endocardial EMT (epithelial-mesenchymal transformation) and is regulated mainly by BMP and TGFbeta. Finally, heart septa that have developed in the OT, ventricle, AV canal and atrium come into alignment and fuse, resulting in the completion of the four-chambered heart. Altered development seen in the cardiogenetic process is involved in the pathogenesis of congenital heart defects. Therefore, understanding the molecular nature regulating the 'nodal point' during heart development is important in order to understand the etiology of congenital heart defects, as well as normal heart development.
OBJECTIVE: Neurohormonal activation has major impact on the pathophysiology of congestive heart failure. The Munich Mild Heart Failure Trial was designed to test the hypothesis that interference with the renin-angiotensin system by angiotensin converting enzyme inhibition favourably influences the natural history of heart failure. DESIGN AND PATIENTS: 170 patients, median New York Heart Association (NYHA) class II, were randomised to double blind treatment with 25 mg captopril twice a day or placebo in addition to standard treatment for a median observation period of 2.7 years. MAIN OUTCOME MEASURES: Progression of heart failure to NYHA class IV on an optimally adjusted standard treatment, death due to progressive heart failure, and sudden death. RESULTS: Heart failure progressed to class IV in nine patients (10.8%) treated with captopril and in 23 patients (26.4%) treated with placebo (p = 0.01). The mean survival time until this end point was 223 days longer in the captopril group (Kaplan-Meier life table analysis; p = 0.02). Also, progressive deterioration to severe heart failure was a powerful predictor of total mortality and death from heart failure; 80% of deaths due to progressive heart failure occurred after this end point. There were fewer deaths caused by progressive heart failure in the captopril group than in the placebo group (4 v 11; p = 0.10) but similar numbers of sudden deaths (11 v 10). Progressive heart failure was the cause of death in 18.2% of all deaths in the captopril group and 50% in the placebo group. Total heart failure events (the end point on which power calculation was based) were also more common in the placebo group (19 v 32 events) but not significantly so. Total mortality was similar to both groups (22 of 83 v 22 of 87). CONCLUSIONS: Angiotensin converting enzyme inhibition in conjunction with standard therapy early in the course of congestive heart failure slowed the progress of heart failure and thus favourably altered the natural history of the disease.
In 18 horses, the pulmonary artery wedge pressure and the heart rate were measured during pharmacological stress load. 12 horses were healthy (4 trained, 8 untrained) and 6 horses had a heart disease (3 trained, 3 untrained). Pharmacological stress induction was carried out with the sympathomimetic drug dobutamine at a dosage rate of 7.5 microg/kg/min over 10 minutes of infusion. At the fourth minute, the parasympatholytic drug atropine was administered (5 microg/kg bw), and the heart rate and the pulmonary artery wedge pressure were continuously measured over 26 minutes. During sole dobutamine infusion, a significant decrease in heart rate and a significant increase in pulmonary artery wedge pressure were observed. After the application of atropine in the fourth minute, a significant increase in heart rate (from 35.7 +/- 6 up to 106 +/- 38/ min) and in pulmonary artery wedge pressure (from 15.7 +/- 3 up to 24 +/- 8.6 mmHg) were visible in the group of healthy horses. The horses with heart diseases had a significantly higher increase in both parameters (heart rate and pulmonary artery wedge pressure) with a significantly positive correlation (r = 0.7). The heart rate increased in the horses with heart diseases from 35.2 +/- 2,8 beats/min up to 132 +/- 45.7 beats/min and the pulmonary artery wedge pressure increased from 17.3 +/- 3,2 mmHg up to 32.7 +/- 13 mmHg. The cardiac status (healthy or heart disease) as well as the training level of the horses (untrained or trained) had a significant influence on the heart rate and the pulmonary artery wedge pressure. The untrained horses (healthy and heart disease) showed significantly higher values over a longer period of time than did the trained horses with the same cardiac status. Additionally the influence of pharmacological stress induction on echocardiographic parameters was investigated. The left atrial size (p = 0.015) and left ventricular diameter were significanly different in the systole (p = 0.008) and in the diastole (p = 0.001) between healthy horses and horses with heart diseases. All horses showed a positive correlation between the pulmonary artery wedge pressure and the left atrial size (r = 0.8), as well as between the left ventricular systolic (r = 0.6) and the diastolic diameter (r = 0.6). The correlation between the pulmonary artery wedge pressure and the left atrial size was nearly the same in the healthy horses (r = 0.74) and in the horses with heart diseases (r = 0.76). Regarding the training level, all untrained horses had a significantly higher correlation between the pulmonary artery wedge pressure and the left atrial size (r = 0.87) in comparison to the trained horses (r = 0.74). Particularly in the untrained horses with heart diseases, this correlation was remarcable (r = 0.99).
Clinical observations indicate that in heart-lung grafting the heart is less frequently rejected than in heart grafting alone. In addition, our results of allograft experiments indicated that the graft survival period is longer in the former (11.8 +/- 0.8 days versus 6.6 +/- 0.5 days, p < 0.05), suggesting that the simultaneous grafting of the lung in heart-lung allografts suppressed the rejection of the grafted heart. We assessed the effect of simultaneous lung xenografting, splenectomy, and FK506 treatment on the survival of the xenografted heart in a concordant model. With Wistar rats as recipients and golden hamsters as donors, cardiac survival was compared between en bloc heart-lung and heart heterotopic xenografts. The cardiac survival of heart-lung and heart xenografts was not prolonged by FK506 treatment alone but was prolonged by splenectomy. Splenectomy plus FK506 (1.0 mg/kg/day) showed suppression of antibody production and a remarkable synergistic effect in prolongation (33.2 +/- 7.4 days versus 36.8 +/- 8.1 days) in heart-lung and heart xenografts. Simultaneous lung xenografting significantly shortened the survival period of the xenografted heart in splenectomy plus FK506 (0.5 mg/kg/day) recipients (4.8 +/- 0.8 days versus 9.0 +/- 3.5 days, p < 0.05), in contrast to the prolongation of the survival period of the grafted heart in heart-lung allografting.
BACKGROUND: Heart transplantation is the surgical procedure of choice for treatment of refractory heart failure. However, it benefits a small number of patients because of the limited number of donors and selection criteria of recipients. Cardiomyoplasty is an alternative surgical procedure for heart failure. The aim of this investigation was to report our experience with heart transplantation, cardiomyoplasty, and clinical treatment of heart failure caused by idiopathic dilated cardiomyopathy. METHODS: Ninety patients with refractory heart failure caused by idiopathic dilated cardiomyopathy were observed from May 1988 to March 1993. The patients had New York Heart Association functional class III or IV symptoms. The patients were divided in three groups according to the treatment received: heart transplantation (33 patients), cardiomyoplasty (25 patients), or medical treatment (32 patients). We studied the event-free curve, the New York Heart Association functional class, the left ventricular ejection fraction, and the morbidity of the groups in the follow-up of 19 +/- 16 months. We considered as an event death or crossover to another group because of severe symptoms. RESULTS: The event-free rate in the cardiomyoplasty group was 92%, 88%, 79%, 74%, and 62% at 3, 9, 12, 18, and 24 months of follow-up, respectively. The event-free rate after heart transplantation was 82%, 78%, 82%, 75%, and 69% at 3, 9, 12, 18, and 24 months, respectively. The event-free rate in the medical treatment group was 78%, 65%, 61%, 48%, and 48% at 3, 9, 12, 18, and 24 months, respectively. All surviving patients in the heart transplantation group had functional class I symptoms. After cardiomyoplasty 90% of surviving patients had class I or II symptoms and 10% had class III symptoms. However, in the medical treatment group 27% of surviving patients had class I or II symptoms and 67% had class III or IV symptoms. In the cardiomyoplasty group left ventricular ejection fraction increased from 20% +/- 3% to 24.4% +/- 6.3% at 6 months (p < 0.05). In the heart transplantation group the left ventricular ejection fraction normalized, and the mean value of the left ventricular ejection fraction did not change in the medical treatment group. The need for endomyocardial biopsy and the incidence of rejection and infection were characteristics of the heart transplantation group. CONCLUSIONS: In properly selected patients, cardiomyoplasty and heart transplantation seem to be associated with improvement in survival and functional class at mid-term follow-up. Heart transplantation was more effective than cardiomyoplasty for functional class improvement.
UNLABELLED: Cardiovascular diseases are the major cause of death not only in Germany. Coronary heart diseases result in substantial disability and loss of productivity and contribute to escalating costs of health care. OBJECTIVE: It was our objective to estimate the costs of CHD for the German population from the perspective of the society. The characteristic of this approach is the calculating of costs until the approximated end of life. METHODS: In the study, all health care costs concerning CHD in Germany were allocated to age, sex, health care sector and primary diagnosis on the basis of comprehensive data on morbidity, mortality, direct and indirect costs. For the estimate of indirect costs the human capital approach was taken. Considered as cases were all patients hospitalized in the reference year (1996). The costs of this cohort in 1996 and up to their protected end of life were estimated. It was taken into account that, in comparison to the general population, life expectancy of cases with risk factors or CHD would have been reduced. In calculating indirect costs, gender and age specific unemployment rates were considered. All future costs were discounted by 4% from the reference year onward. RESULTS: Direct costs are approximately 39 billion DM discounted at 4%, indirect costs total 73 billion DM. The average cost per case (including morbidity and mortality) until the approximated end of life is nearly 125,000 DM. CONCLUSION: In our cost analysis, the indirect costs are higher than the direct costs. For the future, it will be important to estimate the costs of prevalent cases until the end of life and to compare the influence of different interventions on these parameters and on the whole budget of the social security system.
This cross-sectional study investigated the association of hostility and social support to coronary heart disease (CHD) in 2 groups of men and women: those with a familial predisposition for CHD (high-risk sample) and a randomly selected group. The hypothesis was that hostility and low social support would be associated with CHD, and would have a greater effect in the high-risk group. The random sample contained 2,447 individuals (47.1% male) from 576 families, and the high-risk sample consisted of 2,300 people (45.5% male) from 542 families. Odds ratios (OR) and their 95% confidence intervals were calculated using generalized estimating equations (GEE) for logistic regression. Family was specified as the clustering variable, and robust SEEs were obtained to account for dependence of the data within families. After controlling for age, education, body mass index, exercise, smoking history, drinking history, and drinking >5 drinks a day, hostility was associated with a history of coronary bypass surgery or coronary angioplasty in high-risk men (OR 1.21) and a history of myocardial infarction in high-risk women (OR 1.39). High-risk women with high social support had reduced odds of a previous myocardial infarction (OR 0.76), whereas women with high network adequacy in the random sample had reduced risk of myocardial infarction (OR 0.41) and angina (OR 0.49). A ratio of high hostility to low social support was associated with past myocardial infarction in high-risk women (OR 2.47) and a history of angina (OR 2.02) in the random sample men. These results suggest that high hostility and low social support are associated with some manifestations of CHD after controlling for adverse health behaviors.
BACKGROUND: Secondary prevention of coronary heart disease (CHD) among older individuals is associated with considerable benefit. METHODS: In this study, we have examined the extent of secondary prevention among British women and men aged 60-79 years who were surveyed and examined between 1998 and 2001. RESULTS: Among 483 women (12.1% of the whole sample) and 831 men (19.5%) with CHD, >90% of both sexes had at least one modifiable risk factor, with over two-fifths having high blood pressure and over three-quarters high cholesterol. For total cholesterol and body mass index, mean values in both male and female subjects were above recommended levels, and a large shift in the population distributions would be required for targets to be met. Less than one-quarter of subjects of either sex were on a statin, and whilst the majority of men were taking an antiplatelet medication, only 40% of women were. CONCLUSIONS: Most older women and men in Britain were failing to meet National Service Framework standards for secondary prevention in the period immediately before its implementation. Large shifts in the population distributions of some risk factors would be required in this group to meet these standards.
BACKGROUND: Heart failure treatment guidelines emphasize daily weight monitoring for patients with heart failure, but data to support this practice are lacking. Using a technology-based heart failure monitoring system, we determined whether daily reporting of weight and symptoms in patients with advanced heart failure would reduce rehospitalization and mortality rates despite aggressive guideline-driven heart failure care. METHODS: This was a randomized, controlled trial. Patients hospitalized with New York Heart Association class III or IV heart failure, with a left ventricular ejection fraction < or =35% were randomized to receive heart failure program care or heart failure program care plus the AlereNet system (Alere Medical, Reno, Nev) and followed-up for 6 months. The primary end point was 6-month hospital readmission rate. Secondary end points included mortality, heart failure hospitalization readmission rate, emergency room visitation rate, and quality of life. RESULTS: Two hundred eighty patients from 16 heart failure centers across the United States were randomized: 138 received the AlereNet system and 142 received standard care. Mean age was 59 +/- 15 years and 68% were male. The population had very advanced heart failure, New York Heart Association class III (75%) or IV (25%), as evidenced by serum norepinepherine levels, 6-minute walk distance and outcomes. No differences in hospitalization rates were observed. There was a 56.2% reduction in mortality (P <.003) for patients randomized to the AlereNet group. CONCLUSIONS: This is the largest multicenter, randomized trial of a technology-based daily weight and symptom-monitoring system for patients with advanced heart failure. Despite no difference in the primary end point of rehospitalization rates, mortality was significantly reduced for patients randomized to the AlereNet system without an increase in utilization, despite specialized and aggressive heart failure care in both groups.
In patients awaiting heart transplantation, end-stage disease of a second organ may occasionally require consideration of simultaneous multiorgan transplantation. Outcome statistics in multiorgan transplant recipients are needed to define optimal utilization of scarce donor resources. Incidence of cardiac allograft rejection, actuarial recipient survival, and cardiac allograft rejection-free survival were evaluated in 82 recipients of 84 simultaneous heart and kidney transplants. Twenty-three of the 82 dual-organ recipients have died with 1, 6, 12, and 24-month actuarial survival rates of 92%, 79%, 76%, and 67%, respectively. The actuarial survival rates in the heart-kidney recipients were similar to those observed in 14,340 isolated heart recipients (United Network for Organ Sharing Scientific Registry) during the same period (92%, 86%, 83%, and 79%, respectively; P=0.20). Clinical data on all episodes of treated rejection in either organ and on immunosuppressive regimens were available on 56 patients; 48% of these patients have had no rejection in either organ, 27% experienced heart rejection alone, 14% experienced kidney rejection alone, and 11% had both heart and kidney allograft rejection. Heart allograft rejection was less common in heart-kidney recipients, as compared with isolated heart transplant recipients; 0, 1, and > or = 2 treated cardiac allograft rejection episodes occurred in 63%, 20%, and 18% of heart-kidney recipients compared with 46%, 27%, and 28% of 911 isolated heart recipients reported by Transplant Cardiologists' Research Database (P=0.02). The rejection-free survival rates at 1, 3, and 6 months were 88%, 74%, and 71% in the double-organ recipients, as compared with 66%, 44%, and 39%, respectively, in the single-organ recipients. Compared with isolated heart transplantation, combined heart-kidney transplantation does not adversely affect intermediate survival and results in a lower incidence of treated cardiac allograft rejection. The findings suggest that combined heart-kidney transplantation may be an acceptable option in a small subset of potential heart transplant recipients with severe renal dysfunction.