Prediction of hospital readmission for heart failure: development of a simple risk score based on administrative data.
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Adult↗
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[Self-rated health as a predictor of ischemic heart disease development].
The study objective was to analyse the association between self-rated health and the incidence of fatal and non-fatal coronary heart disease in a Danish cohort followed up over 16 years. The study included 1052 men and women born in 1936. During the 16 years' follow-up 50 cases of coronary heart disease were registered either with the Danish register of deaths or the register of hospital admissions. Univariate analysis showed the following relative risks of coronary heart disease in the four self-rated health groups: "extremely good": 1.0, "good": 4.0, "poor": 5.8, "miserable": 12.1 (p = 0.02). After control for the conventional coronary risk factors and a substantial number of other potential confounders the relative risks were: 1.0, 4.2, 6.5, and 18.6 (p = 0.02) respectively. Self-rated health was an independent predictor of coronary heart disease in this recent cohort. If confirmed, the association between self-rated health and coronary heart disease may lead to new insights into psychosocial processes leading to this disease.
Aged↗
Comparison of amlodipine or nifedipine treatment with developing congestive heart failure: effects on myocyte contractility.
BACKGROUND: Past studies have suggested that amlodipine, a dihydropyridine L-type Ca(2+) channel antagonist, may exert useful effects in congestive heart failure (CHF). The present study examined the effects of amlodipine or nifedipine treatment in a model of developing CHF on left ventricular (LV) pump function and myocyte contractility. METHODS AND RESULTS: Pigs (25 kg) were randomly assigned to 1 of 4 groups: 1) pacing-induced CHF (rapid atrial pacing at 240 bpm) for 3 weeks (n = 9), 2) concomitant Ca(2+) channel blockade with amlodipine (1.5 mg/kg/day) and rapid pacing (n = 7), 3) concomitant Ca(2+) channel blockade with nifedipine (0.7 mg/kg twice daily) and rapid pacing (n = 7), and 4) sham controls (n = 7). LV fractional shortening fell with pacing CHF from baseline values (17% +/- 1% v 42% +/- 1%, P <.05). With rapid pacing and concomitant amlodipine treatment, LV fractional shortening increased from pacing CHF values (24% +/- 1%, P <.05) but was unchanged with concomitant nifedipine treatment (20% +/- 2%, P =.2). LV myocyte velocity of shortening, as measured by high speed videomicroscopy, was reduced with pacing CHF compared with controls (42 +/- 2 microm/s v 87 +/- 9 microm/s, P <.05), and increased from pacing CHF values with amlodipine or nifedipine treatment (62 +/- 8 microm/s, 64 +/- 4 microm/s, respectively; P <.05). Inotropic response to extracellular Ca(2+) (8 mmol/L) was reduced with pacing CHF (94 +/- 5 microm/s v 160 +/- 15 microm/s, P <.05) and increased from CHF values with amlodipine or nifedipine treatment (132 +/- 14 microm/s and 133 +/- 7 microm/s, respectively, P <.05) CONCLUSIONS: These results suggest that the primary mechanism for the effects of amlodipine on myocyte contractility in developing CHF is because of direct Ca(2+) channel blockade.
Amlodipine↗
Prediction of hospital readmission for heart failure: development of a simple risk score based on administrative data.
OBJECTIVES: The purpose of this study was to develop a convenient and inexpensive method for identifying an individual's risk for hospital readmission for congestive heart failure (CHF) using information derived exclusively from administrative data sources and available at the time of an index hospital discharge. BACKGROUND: Rates of readmission are high after hospitalization for CHF. The significant determinants of rehospitalization are debated. METHODS: Administrative information on all 1995 hospital discharges in New York State which were assigned International Classification of Diseases-9-Clinical Modification codes indicative of CHF in the principal diagnosis position were obtained. The following were compared among hospital survivors who did and did not experience readmission: demographics, comorbid illness, hospital type and location, processes of care, length of stay and hospital charges. RESULTS: A total of 42,731 black or white patients were identified. The subgroup of 9,112 patients (21.3%) who were readmitted were distinguished by a greater proportion of blacks, a higher prevalence of Medicare and Medicaid insurance, more comorbid illnesses and the use of telemetry monitoring during their index hospitalization. Patients treated at rural hospitals, those discharged to skilled nursing facilities and those having echocardiograms or cardiac catheterization were less likely to be readmitted. Using multiple regression methods, a simple methodology was devised that segregated patients into low, intermediate and high risk for readmission. CONCLUSIONS: Patient characteristics, hospital features, processes of care and clinical outcomes may be used to estimate the risk of hospital readmission for CHF. However, some of the variation in rehospitalization risk remains unexplained and may be the result of discretionary behavior by physicians and patients.
Black or African American↗
Prediction of hospital readmission for heart failure: development of a simple risk score based on administrative data
OBJECTIVES: The purpose of this study was to develop a convenient and inexpensive method for identifying and individual's risk for hospital readmission for congestive heart failure (CHF) using information derived exclusively from administrative data sources and available at the time of an index hospital discharge. BACKGROUND: Rates of readmission are higher after hospitalization for CHF. The significant determinants of rehospitalization are debated. METHODS: Administrative information on all 1995 hospital discharges in New York State which were assigned International Classification of Diseases--9--Clinical Modification codes indicative of CHF in the principal diagnosis position were obtained. The following were compared among hospital survivors who did and did not experience readmission: demographics, comorbid illness, hospital type and location, processes of care, length of stay and hospital charges. RESULTS: A total of 42,731 black or white patients were identified. The subgroup of 9,112 (21.3%) who were readmitted were distinguished by a greater proportion of blacks, a higher prevalence of Medicare and Medicaid insurance, more comorbid illnesses and the use of telemetry monitoring during their index hospitalization. Patients treated at rural hospitals, those discharged to skilled nursing facilities and those having echocardiograms or cardiac catheterization were less likely to be readmitted. Using multiple regression methods, a simple methodology was devised that segregated patients into low, intermediate and high risk for readmission. CONCLUSIONS: Patient characteristics, hospital features, processes of care and clinical outcomes may be used to estimate the risk of hospital readmission for CHF. However, some of the variation in rehospitalization risk remains unexplained and may be the result of discretionary behavior by physicians and patients.
Journal Article↗
Wnt-11 activation of a non-canonical Wnt signalling pathway is required for cardiogenesis.
Formation of the vertebrate heart requires a complex interplay of several temporally regulated signalling cascades. In Xenopus laevis, cardiac specification occurs during gastrulation and requires signals from the dorsal lip and underlying endoderm. Among known Xenopus Wnt genes, only Wnt-11 shows a spatiotemporal pattern of expression that correlates with cardiac specification, which indicates that Wnt-11 may be involved in heart development. Here we show, through loss- and gain-of-function experiments, that XWnt-11 is required for heart formation in Xenopus embryos and is sufficient to induce a contractile phenotype in embryonic explants. Treating the mouse embryonic carcinoma stem cell line P19 with murine Wnt-11 conditioned medium triggers cardiogenesis, which indicates that the function of Wnt-11 in heart development has been conserved in higher vertebrates. XWnt-11 mediates this effect by non-canonical Wnt signalling, which is independent of beta-catenin and involves protein kinase C and Jun amino-terminal kinase. Our results indicate that the cardiac developmental program requires non-canonical Wnt signal transduction.
3T3 Cells↗
Adrenergic innervation of the developing chick heart: neural crest ablations to produce sympathetically aneural hearts.
Ablation of various regions of premigratory trunk neural crest which gives rise to the sympathetic trunks was used to remove sympathetic cardiac innervation. Neuronal uptake of [3H]-norepinephrine was used as an index of neuronal development in the chick atrium. Following ablation of neural crest over somites 10-15 or 15-20, uptake was significantly decreased in the atrium at 16 and 17 days of development. Ablation of neural crest over somites 5-10 and 20-25 caused no decrease in [3H]-norepinephrine uptake. Removal of neural crest over somites 5-25 or 10-20 caused approximately equal depletions of [3H]-norepinephrine uptake in the atrium. Cardiac norepinephrine concentration was significantly depressed following ablation of neural crest over somites 5-25 but not over somites 10-20. Light-microscopic and histofluorescent preparations confirmed the absence of sympathetic trunks in the region of the normal origin of the sympathetic cardiac nerves following neural crest ablation over somites 10-20. The neural tube and dorsal root ganglia were damaged in the area of the neural-crest ablation; however, all of these structures were normal cranial and caudal to the lesioned area. Development of most of the embryos as well as the morphology of all of the hearts was normal following the lesion. These results indicate that it is possible to produce sympathetically aneural hearts by neural-crest ablation; however, sympathetic cardiac nerves account for an insignificant amount of cardiac norepinephrine. The adrenal medulla is the most likely source of cardiac norepinephrine in sympathetically aneural hearts.
Animals↗
Cardiac phenotypes in chromosome 4q- syndrome with and without a deletion of the dHAND gene.
PURPOSE: Terminal deletions of chromosome 4q are commonly associated with cardiovascular malformations (CVMs). The dHAND gene (HAND2 heart and neural crest derivative express 2), a basic helix-loop-helix transcription factor expressed in the developing heart, maps to 4q33. A targeted deletion in mouse shows that dHAND plays an important role in heart development, suggesting that haploinsufficiency of in patients with 4q deletions may be causal for CVMs. The purpose of this study is to examine the possible association between dHAND haploinsufficiency with the CVMs that occur in patients with 4q terminal deletions. METHODS: Fluorescence in situ hybridization (FISH) was performed with a dHAND human genomic probe on five patients with terminal deletion at 4q33 or 4q34. RESULTS: Of the three patients with a deletion of the dHAND locus, two had CVM (both valvar pulmonic stenosis). Of the two patients without a deletion of the dHAND gene, one had a small atrial septal defect noted on autopsy. In one of the patients with breakpoint on chromosome 4 assigned to 4q34.2 by GTG-banding, FISH revealed deletion of the dHAND gene. CONCLUSION: The results suggest that cardiac phenotypes are very variable in patients with the terminal deletion of chromosome 4q and that haploinsufficiency of the dHAND is not necessarily associated with CVMs. The correct cytogenetic interpretation of terminal chromosome deletions might be augmented by FISH.
Adult↗
Molecular cloning of rat cardiac troponin I and analysis of troponin I isoform expression in developing rat heart.
We have isolated and sequenced a cDNA encoding rat cardiac troponin I. The predicted amino acid sequence was highly identical with previously reported chemically derived amino acid sequences for rabbit and bovine cardiac troponin I. Clones for slow skeletal muscle troponin I were also obtained from neonatal rat cardiac ventricle by the polymerase chain reaction. The nucleotide sequences of these clones were determined to be more than 99% identical with a previously reported rat slow skeletal troponin I cDNA [Koppe et al. (1989) J. Biol. Chem. 264, 14327-14333]. The troponin I clones hybridized to RNA from the appropriate muscle from adult animals. However, RNA from fetal and neonatal rat heart also hybridized with the slow skeletal troponin I cDNA, demonstrating its expression in fetal and neonatal rat heart. Slow skeletal troponin I steady-state mRNA levels decreased with increasing age, but cardiac troponin I mRNA levels increased through fetal and early neonatal cardiac development. Thus, during fetal and neonatal development, slow skeletal and cardiac troponin I isoforms are coexpressed in the rat heart and regulated in opposite directions. The degree of primary sequence differences in these isoforms, especially at phosphorylation sites, may result in important functional differences in the neonatal myocardium.
Amino Acid Sequence↗
Selective regulation of cardiomyocyte gene expression and cardiac morphogenesis by retinoic acid.
Early heart development is known to be sensitive to retinoid concentrations; a specific pattern of malformations is observed in both vitamin A-deficiency and retinoid-toxicity states. While the influence of retinoids on early cardiac morphogenesis has been described previously, the effect of retinoids upon cardiomyocyte differentiation and gene expression is largely uncharacterized. We have established an in ovo chick embryo model in which slow-release retinoic acid (RA) induces four distinct cardiac malformations in a dose-dependent fashion. Late primitive streak-stage chick embryos were treated with all-trans-retinoic acid released from anion exchange beads placed on the embryo's left side and then allowed to develop further for 20-24 hr. At low doses (10 and 25 micrograms/ml RA) an abnormal loop structure was observed. At higher doses (50 and 100 micrograms/ml RA) cardia bifida and clustered heart tissue were noted. Situs inversus only occurred after treatment with 100 micrograms/ml RA. RA-treated embryos were subsequently analyzed for appropriate cardiac myocyte differentiation using antibody staining and ELISA analysis to detect sarcomeric myosin heavy chain, tropomyosin, titin, and alpha-actinin protein expression. Alpha-actinin expression was significantly decreased in RA-treated embryos, as compared to DMSO-treated controls. Also, heart contraction rate was depressed after RA exposure. RA exposure did not alter the protein expression levels of sarcomeric myosin heavy chain or tropomyosin. The observed alterations are consistent with suggestions that retinoids may affect both morphogenesis and myofibril formation in the developing heart.
Animals↗
Transient expression of fast troponin C transcripts in embryonic quail heart.
Most myofibrillar proteins, including troponin I and troponin T subunits of troponin complex, undergo developmental stage-specific isoform transitions in vertebrate heart before attaining adult contractile and regulatory characteristics. Only the cardiac/slow skeletal muscle type isoform of troponin C, however, has been shown to be expressed in both adult and developing heart. The changes in troponin C could be functionally important as the TnC isoforms vary in their affinities for Ca(2+). For example, fast troponin C has two Ca(2+) binding sites while slow/cardiac troponin C has a single regulatory site. This study demonstrates the co-expression of both fast and slow transcripts of troponin C in not only quail embryonic skeletal muscle but also embryonic heart using two different analytical techniques of polymerase chain reaction and in situ hybridisation procedure. Fast troponin C expression in the quail heart using in situ hybridisation procedure was first observed at embryonic day 3, with maximum expression at day 5 after which its level in the developing heart was gradually down regulated. In situ hybridisation staining of sections at these developmental stages demonstrated the expression of both fast and slow transcripts of troponin C in all cardiomyocytes.
Animals↗
[The role of anti-beta1-adrenergic receptor autoantibodies in development of heart failure].
Epitopic analysis of anti-beta1-adrenergic receptor autoantibodies in the serum of patients with cardiomyopathy was performed. An immunoenzyme test system for detection of autoantibodies was developed using peptide containing 26 amino acids of the second extracellular loop of the beta1-adrenergic receptor as antigen. It was demonstrated that removal of autoantibodies against beta1-adrenergic receptor in patients with cardiomyopathy by immunoadsorption and plasmapheresis metodes led to improvement of the heart pumping capacity.
Amino Acid Sequence↗
Protective effects of dimethyl-propranolol (UM-272) during global ischemia of isolated feline hearts.
This study was designed to determine the effects of dimethyl-propranolol (UM-272) on myocardial injury after global ischemia of isolated feline hearts. Untreated ischemic hearts developed contracture, resulting in a leftward shift of the diastolic pressure-volume curve. Active pressure development in perfused ischemic hearts was significantly depressed compared to preischemic values. Untreated ischemic hearts exhibited increased water, sodium (Na+) and calcium (Ca++) contents and depletion of potassium (K+). The Ca++ accumulating ability of cardiac microsomal fractions isolated from untreated ischemic hearts was severely depressed. In hearts treated with UM-272, active ventricular pressure development after ischemia declined to the same extent as in untreated hearts, but ischemic contracture in treated hearts was delayed and completely reversed by reperfusion. Treated hearts were not depleted of K+ and changes in Na+ and Ca++ were significantly less than in untreated hearts. Microsomal Ca++ accumulation in the treated group was well preserved compared to that in untreated hearts. Experiments in which hearts were paced during UM-272 administration suggest that decreased myocardial oxygen consumption contributes substantially to the protective effects of UM-272. In addition, UM-272 may protect the ischemic heart through direct effects on myocardial Ca++ regulating mechanisms.
Animals↗
Structure and function of the developing zebrafish heart.
The combination of optical clarity and large scale of mutants makes the zebrafish vital for developmental biologists. However, there is no comprehensive reference of morphology and function for this animal. Since study of gene expression must be integrated with structure and function, we undertook a longitudinal study to define the cardiac morphology and physiology of the developing zebrafish. Our studies included 48-hr, 5-day, 2-week, 4-week, and 3-month post-fertilization zebrafish. We measured ventricular and body wet weights, and performed morphologic analysis on the heart with H&E and MF-20 antibody sections. Ventricular and dorsal aortic pressures were measured with a servonull system. Ventricular and body weight increased geometrically with development, but at different rates. Ventricle-to-body ratio decreased from 0.11 at 48-hr to 0.02 in adult. The heart is partitioned into sinus venosus, atrium, ventricle, and bulbus arteriosus as identified by the constriction between the segments at 48-hr. Valves were formed at 5-day post-fertilization. Until maturity, the atrium showed extensive pectinate muscles, and the atrial wall increased to two to three cell layers. The ventricular wall and the compact layer increased to three to four cell layers, while the extent and complexity in trabeculation continued. Further thickening of the heart wall was mainly by increase in cell size. The bulbus arteriosus had similar characteristics to the myocardium in early stages, but lost the MF-20 positive staining, and transitioned to smooth muscle layer. All pressures increased geometrically with development, and were linearly related to stage-specific values for body weight (P < 0.05). These data define the parameters of normal cardiac morphology and ventricular function in the developing zebrafish.
Animals↗
[Why does the heart not develop after extirpation of the entoblast in the larva of Urodela?].
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Animals↗
Blood pressure and heart rate development in young spontaneously hypertensive rats.
The course of hypertension development in young spontaneously hypertensive rats (SHR) was studied by the measurement of changes in systolic blood pressure (BP), body weight, and heart rate (HR) at 2, 3, 4, and 6 wk of age. To achieve this, we compared inbreeding lines of SHR and Wistar-Kyoto rats (WKY) to determine if differences in BP, body weight, or HR were present among inbreeding lines of the same strain or between strains. The effect of these differences on the eventual level of BP was then assessed. We found that BP began to diverge between SHR and WKY at 4 wk of age. Significant differences in systolic BP (24 mmHg) between SHR inbreeding lines at 4 wk of age did not affect the BP at 8 wk (172 vs. 170 mmHg). Pulse pressure was significantly higher in SHR than in WKY at 4 wk of age. HR was elevated in SHR over age-matched WKY at 3 wk of age and positively correlated to the level of BP attained by individual animals at 6 wk (P = 0.037). Moreover, WKY inbreeding lines showing elevated HR developed higher BP (145 vs. 127 mmHg) at 10-12 and 20 wk of age. The prehypertensive tachycardia in SHR was investigated further and found to result from an increased intrinsic HR. Because HR at 3 wk is a genetic trait that can be partitioned into inbreeding lines, and inbreeding lines most expressive of this trait showed the highest eventual BP, we conclude that prehypertensive tachycardia may be an important first step during hypertension development in SHR. Moreover, early elevations in HR are highly predictive (r = 0.41) of hypertension occurrence in the animal population studied.
Age Factors↗
Effects of taxol on endothelial cells of the developing semilunar heart valves in the chick embryo.
Recent ultrastructural studies have revealed that there are differences in endothelial cell shape and cytoskeletal architecture between the arterial and ventricular faces of developing semilunar valves. In the present work we have analyzed valvular endothelial cell response to taxol in the chick embryo. Following taxol administration, abnormal mitotic cells appear in the endothelium of both faces of the cusps. Interphase cells show few structural alterations. No differential response of the valvular endothelium to the drug was observed in the arterial or ventricular faces of the cusps.
Alkaloids↗
Effects of colchicine administration on the endothelial cells of the developing semilunar heart valves of the chick embryo.
Recent ultrastructural studies have revealed that differences exist in endothelial cell shape and cytoskeletal architecture between the arterial and ventricular faces of developing semilunar valves. In the present work we analyzed the morphologic response of the valvular endothelial cells of chick embryos to colchicine by light microscopy, scanning electron microscopy and transmission electron microscopy. The results show that colchicine administration during the stages of valve morphogenesis causes a very conspicuous disruption of the endothelial layer of the arterial face of the valves. The cells appear rounded and show massive surface blebbing. These alterations were not present in the endothelial cells on the ventricular face of the valves at the same stages. On the basis of these results we suggest that a difference in the degree of cell differentiation exists between the endothelial cells of the arterial and ventricular faces of the cusps and that this difference may have morphogenetic significance.
Animals↗