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PubMed1997

[Hypoplasia of the left heart ventricle--casuistic contribution to the development of this heart malformation].

The case report describes and compares an univentricular heart of a calf with hypoplasias of left ventricles of two further calves and a newborn moufflon. In all cases there is also stenosis of the aortic arch. The functional effects of the malformations are discussed. The hypothesis is proposed that an univentricular heart may be the extreme variant of hypoplasia of the left heart when there is an additional aortic stenosis.

Animals↗
PubMed1997

Defective endogenous nitric oxide-mediated modulation of cellular respiration in canine skeletal muscle after the development of heart failure.

BACKGROUND: It is well documented that nitric oxide (NO) suppresses the function of a number of mitochondrial enzymes. Our recent studies found that endogenous NO may play an important role in the modulation of tissue oxygen (O2) consumption and cellular respiration both in vitro and in vivo. METHODS: Tissue O2 consumption was measured by a Clark-type O2 electrode at 37 degrees C in freshly isolated skeletal muscle segments from the accessory head of the triceps brachii (90% type I muscle fiber) and extensor carpi radialis (86% type II muscle fiber) from normal dogs and dogs with tachycardia-induced heart failure. RESULTS: S-nitroso-N-acetylpenicillamine (SNAP), carbachol, and bradykinin at doses of 10(-7) to 10(-4) mol/L concentration significantly suppressed tissue O2 consumption both in the absence and presence of 2,4-dinitrophenol (1 mmol/L), a mitochondrial uncoupler. These effects were not significantly different in the accessory head of the triceps brachii (90% type I muscle fiber) and extensor carpi radialis (86% type II muscle fiber). The effects of carbachol and bradykinin but not SNAP were attenuated by NG-nitro-L-arginine (10(-4) mol/L), indicating inhibition of the formation of endogenous NO. The inhibitory effect on tissue O2 consumption in response to carbachol and bradykinin became significantly smaller in skeletal muscle from dogs with pacing-induced heart failure, but the effects of SNAP were unchanged. CONCLUSIONS: Endogenous NO released from microvascular endothelium may play an important physiologic role in the modulation of cellular respiration in skeletal muscle, and the loss of this regulatory function may contribute to peripheral metabolic disorders and poor exercise tolerance during heart failure.

2,4-Dinitrophenol↗
PubMed1987

Effect of neural crest ablation on development of the heart and arch arteries in the chick.

Mesenchymal derivatives of the neural crest contribute to the connective tissues and blood vessels of the pharyngeal arches, and participate in the septation of the outflow tract of the heart. The present study was designed to determine the nature and timing of alterations in the development of the heart and arch arteries subsequent to diminished neural crest contributions. The neural crest contributing to the three caudalmost pharyngeal arches was ablated bilaterally in chick embryos and compared with sham or unoperated controls. Heart development was studied by scanning electron microscopy. Arch artery development was studied microscopically after intravascular injection of India ink and clearing of the specimen. Neural crest ablation caused morphological changes in most hearts. Hearts in experimental animals commonly were elongate and were subject to inappropriate development of ventricular and atrial areas. A surgical effect delayed the disappearance of arch arteries one and two, and removal of neural crest produced an additional delay. Neural crest ablation caused failure of arch arteries three, four (right), and six to develop to the proper size in some animals. Survival of those whose sixth arch arteries achieved the proper size caused group measurements to reach normal values again by stage 32. Closure of arch arteries in some animals and maintenance in others produced greater variability in experimental animals than in controls. It is significant that heart morphology was altered before septation of the outflow tract normally occurs. This indicates at the least that another factor, such as altered blood flow, contributes to the abnormal development. Altered flow may result from changes in pharyngeal arch mesenchyme and arch artery endothelium.

Animals↗
PubMed2003

Histological studies on embryonic development of the rabbit heart.

Two experiments were performed to evaluate the normal development of the rabbit heart. In the first experiment the most intensive period of heart development was determined in rabbit embryos. The second experiment studied the most intensive period of heart development, determined in the first experiment, by concentrated sampling at 8-hour intervals. After cutting open the uterine wall opposite the discoid placenta, rabbit embryos were removed from the ampullae of the uterus using capillary tubes, under stereomicroscope at fivefold magnification. The embryos were subsequently placed into 4% formalin solution for 24 h. After fixation, slides stained with haematoxylin and eosin were made for histological examination. In the first experiment 51 embryos were examined, while during the second experiment a total of 113 embryos, representing different stages of development, were collected. Finally the data obtained on rabbits were compared with the well-known development of the heart in humans and mice.

Animals↗
PubMed2004

Angiopoietin 1 expression levels in the myocardium direct coronary vessel development.

Mutational studies in genetically engineered mice have shown that the angiopoietin/Tie2(Tek) signaling pathway is indispensable for vascular development. To further investigate the role of Angiopoietin 1 in heart development, we developed transgenic mice that express Angiopoietin 1 under control of doxycycline in cardiac myocytes. Ninety percent of all transgenic mice die between embryonic day 12.5 and 15.5. Beginning at embryonic day 12.5, transgenic mice exhibit dilated atria, a significant thinning of the myocardial wall, and eventual outflow tract collapse. In addition, hearts of the most severely affected transgenic embryos have no coronary arteries as a result of the defective development and maintenance of the epicardium. The subsequent lack of blood and nutrient delivery to the developing heart may account for decreases in N-cadherin expression and subsequent loss of cell-cell contact leading to cell death, and ultimately the collapse and hemorrhage of the heart. These results suggest a pivotal role for Angiopoietin 1 in cardiovascular development, specifically the development of the epicardium and coronary vasculature.

Angiopoietin-1↗
PubMed2000

Induction and differentiation of the zebrafish heart requires fibroblast growth factor 8 (fgf8/acerebellar).

Vertebrate heart development is initiated from bilateral lateral plate mesoderm that expresses the Nkx2.5 and GATA4 transcription factors, but the extracellular signals specifying heart precursor gene expression are not known. We describe here that the secreted signaling factor Fgf8 is expressed in and required for development of the zebrafish heart precursors, particularly during initiation of cardiac gene expression. fgf8 is mutated in acerebellar (ace) mutants, and homozygous mutant embryos do not establish normal circulation, although vessel formation is only mildly affected. In contrast, heart development, in particular of the ventricle, is severely abnormal in acerebellar mutants. Several findings argue that Fgf8 has a direct function in development of cardiac precursor cells: fgf8 is expressed in cardiac precursors and later in the heart ventricle. Fgf8 is required for the earliest stages of nkx2.5 and gata4, but not gata6, expression in cardiac precursors. Cardiac gene expression is restored in acerebellar mutant embryos by injecting fgf8 RNA, or by implanting a Fgf8-coated bead into the heart primordium. Pharmacological inhibition of Fgf signalling during formation of the heart primordium phenocopies the acerebellar heart phenotype, confirming that Fgf signaling is required independently of earlier functions during gastrulation. These findings show that fgf8/acerebellar is required for induction and patterning of myocardial precursors.

Animals↗
PubMed1998

The development of the Starr-Edwards heart valve.

Development of the Starr-Edwards heart valve marked a new era in the treatment of valvular heart disease. Until the development of the Starr-Edwards valve, there were no published reports of patients who had lived longer than 3 months with a prosthetic valve in the mitral position. This valve was the result of a unique partnership between a young surgeon, Dr. Albert Starr, and an experienced engineer, Mr. Lowell Edwards. Working as a team, these 2 men developed and successfully implanted the 1st Starr-Edwards valve within less than 2 years of their 1st meeting. Their key to success was their willingness and ability to make repeated modifications to their design to solve each clinical problem as it arose. Their constant focus on the clinical goal aided the rapid transformation of their design from a leaflet valve to a shielded ball valve, and finally to an unshielded ball valve suitable for implantation in a human being. Along the way, they abandoned the idea of imitating the appearance of native valves, in favor of developing valves that would be clinically successful. Their work has provided help and hope for patients who otherwise would have died from the complications of rheumatic heart disease and other valvular disorders for which valve replacement is the only treatment.

Biomedical Engineering↗
PubMed2002

Transcriptional activation of energy metabolic switches in the developing and hypertrophied heart.

1. The present review focuses on the gene regulatory mechanisms involved in the control of cardiac mitochondrial energy production in the developing heart and following the onset of pathological cardiac hypertrophy. Particular emphasis has been given to the mitochondrial fatty acid oxidation (FAO) pathway and its control by members of the nuclear receptor transcription factor superfamily. 2. During perinatal cardiac development, the heart undergoes a switch in energy substrate preference from glucose in the fetal period to fatty acids following birth. This energy metabolic switch is paralleled by changes in the expression of the enzymes and protein involved in the respective pathways. 3. The postnatal activation of the mitochondrial energy production pathway involves the induced expression of nuclear genes encoding FAO enzymes, as well as other proteins important in mitochondrial energy transduction/production pathways. Recent evidence indicates that this postnatal gene regulatory effect involves the actions of the nuclear receptor peroxisome proliferator-activated receptor alpha (PPARalpha) and its coactivator the PPARgamma coactivator 1 (PGC-1). 4. The PGC-1 not only activates PPARalpha to induce FAO pathway enzymes in the postnatal heart, but it also plays a pivotal role in the control of cardiac mitochondrial number and function. Thus, PGC-1 plays a master regulatory role in the high-capacity mitochondrial energy production system in the adult mammalian heart. 5. During the development of pathological forms of cardiac hypertrophy, such as that due to pressure overload, the myocardial energy substrate preference shifts back towards the fetal pattern, with a corresponding reduction in the expression of FAO enzyme genes. This metabolic shift is due to the deactivation of the PPARalpha/PGC-1 complex. 6. The deactivation of PPARalpha and PGC-1 during the development of cardiac hypertrophy involves regulation at several levels, including a reduction in the expression of these genes, as well as post-translational effects due to the mitogen-activated protein kinase pathway. Future studies aim at defining whether this transcriptional 'switch' and its effects on myocardial metabolism are adaptive or maladaptive in the hypertrophied heart.

Animals↗
PubMed1991

Analysis of proteins synthesized by 9.5 day mouse embryos: determination of cardiac and noncardiac proteins.

To catalog polypeptides that were specific to developing hearts, we separated 35S-methionine-labeled 9.5 day mouse embryos into cardiac and noncardiac (carcass) components. Two-dimensional gels were then used to analyze the polypeptides synthesized in these two fractions. As a result, we were able to distinguish polypeptides that were specific to or increased in the heart as well as those polypeptides that were specific to or increased in the embryo minus the dissected heart. Using this analysis, there were two polypeptides that were cardiac-specific and 17 that were expressed at increased levels by at least twofold in the heart. The cardiac-specific polypeptides may be used in further studies to identify early cardiac tissue. Conversely, there were 26 polypeptides unique to noncardiac structures and an additional 15 that were increased in the carcass more than twofold relative to the heart. The noncardiac-specific polypeptides may be used to define contamination of putative cardiac tissue with noncardiac material. Two of the polypeptides expressed more abundantly in the carcass appeared to correspond to known proteins in the mouse fibroblast database, cyclin and tropomyosin 4. Thus the heart at 9.5 days of murine development can be distinguished readily from the remainder of the embryonic mouse both macroscopically and on two-dimensional gels.

Animals↗
PubMed2006

Aldosterone blockade in post-acute myocardial infarction heart failure.

Development of heart failure (HF) or left ventricular systolic dysfunction (LVSD) significantly increases mortality post acute myocardial infarction (AMI). Aldosterone contributes to the development and progression of HF post AMI, and major guidelines now recommend aldosterone blockade in this setting. However, lack of practical experience with aldosterone blockade may make clinicians hesitant to use these therapies. This review is based on a consensus cardiology conference that occurred in May 2005 (New York City) concerning these topics. Potential barriers to the use of aldosterone blockade are discussed and an algorithm for appropriate in-hospital pharmacologic management of AMI with LVSD and/or HF is presented.

Algorithms↗
PubMed1983

Heart failure in Nigerian hypertensives.

A study of 209 consecutive cases of hypertension, seen at the cardiac unit of the University College Hospital, Ibadan, Nigeria, showed that heart failure occurred more commonly in patients who were in the low socio-economic class. All those who had a haematocrit below 30% had heart failure. The lower the serum albumin, the greater the likelihood of developing heart failure. Hypertensives who were heavy alcohol drinkers were very prone to heart failure while a significant proportion of those who had cardiomegaly or cardiomegaly with aortic unfolding on chest x-ray had heart failure. Age, sex, Hb genotype, obesity and retinal changes had no influence on the development of heart failure. It is concluded that there are other factors, besides hypertension, which precipitate heart failure in Nigerian hypertensives. This may be responsible for the high incidence of heart failure among Nigerian with hypertension.

Adult↗
PubMed1993

Minute-by-minute association of heart rate variation with basal heart rate in developing infants.

Particular types of heart rate variation are enhanced during periods of slow heart rate and diminished when heart rate is high. We examined how the correlations between heart rate and various types of heart rate variation developed in normal infants. Polygraphic recordings were obtained from 25 infants at 1 week and at 1, 2, 3, 4 and 6 months of age. Median heart rate and the extents of heart rate variation at three distinct frequencies were determined for each 1-minute epoch. Pearson's r was used to assess the correlation of median heart rate in each epoch with each of three types of heart rate variation. For each recording, correlations were assessed separately for quiet sleep, rapid eye movement (REM) sleep and waking. The maturational patterns of heart rate by heart rate variation correlations were strongly influenced by sleep-waking state and were dissimilar to those previously reported for correlations between cardiac and respiratory measures. The findings suggest dissimilar developmental patterns for autonomic and somatic motor systems, and include a discontinuity in autonomic development at approximately 1 month of age. We speculate that these trends reflect a change in the nature of sleep states as forebrain connections develop.

Aging↗
PubMed2005

Postnatal consequences of prenatal cocaine exposure and myocardial apoptosis: does cocaine in utero imperil the adult heart?

Cocaine use is common among pregnant women with a history of substance abuse, and has been shown to cause abnormalities in the heart during fetal and postnatal development. However, mechanisms underlying the detrimental effects of cocaine on the developing heart are not fully understood. In this issue, Bae and Zhang show that prenatal cocaine exposure increases the susceptibility of the postnatal heart to ischemia and reperfusion injury. Their results suggest that myocardial apoptosis induced by cocaine during fetal development may represent one of the mechanisms by which prenatal cocaine exposure exerts its long-term, deleterious consequences on postnatal cardiac function.

Adult↗
PubMed1997

Regulation of post-translationally modified microtubule populations during neonatal cardiac development.

Microtubules have been implicated in a number of muscle-specific functions, including sarcomerogenesis and the regulation of heart cell beating rate. Post-translationally modified microtubules (MTs) have been correlated, in other cell types, with MTs of increased stability and possibly distinct functions. This study was begun in order to determine whether neonatal heart development is associated with changes in MT populations, as a prelude to assaying their role in cardiac development and function. Biochemical and morphological studies were performed on heart tissues and cells, over the developmental range from embryonic Day 19 through neonatal Day 20, as well as only fully grown adults. The specific activity of the detyrosinating enzyme, tubulin carboxypeptidase, was high in early neonatal hearts but then decreased progressively to adulthood. Levels of tyrosinated, detyrosinated, and total tubulin varied in a complex manner over the same time period, while levels of acetylated tubulin in detergent-extracted homogenates were low in all age groups. Immunofluorescence analysis of heart sections revealed non-uniform levels of Glu and acetylated tubulin between cells over that period. Cultured, neonatal day 3 myocytes exhibited much more prominent populations of both Glu and acetylated MTs than were present in the co-isolated nonmyocytes, while cell cultures from older animals showed more restricted staining for both MT types. The immunostaining pattern for 7-tubulin, a marker for MT-organizing centers, was diffuse in the cardiomyocytes throughout this period, while the staining in the non-myocytes was much more focused and punctate. These results reveal that individual MT populations are present in developing heart tissue, and may be required for specific functions during myocyte differentiation.

Animals↗
PubMed1997

N-cadherin is crucial for heart formation in the chick embryo.

The developing heart primordium strongly expresses N-cadherin. In order to investigate the role of this adhesion molecule in heart morphogenesis, chicken embryos were cultured at stages 5-12, and injected with anti-N-cadherin antibodies that can specifically block the activity of this cadherin. In the injected embryos, the epimyocardial layers, which develop bilaterally from the splanchnic mesoderm, did not fuse to form a single cardiac tube. Moreover, each of the unfused layers became fragmented into epithelioid clusters. At the cellular level, large intercellular gaps were observed in the antibody-treated myocardial layers. These disorganized myocardial layers beat to some extent, suggesting that their differentiation was not blocked; however, their contraction was not coordinated. Morphogenesis of other tissues, not only N-cadherin-negative but also N-cadherin-positive tissues, such as the neural tube and notochord, proceeded normally even in the presence of anti-N-cadherin antibodies. These results suggest that N-cadherin is indispensable for heart formation, but not for morphogenesis of the other tissues, at the developmental stages examined. For the latter processes, expression of other cadherin subtypes presumably compensated for the loss of N-cadherin activity.

Animals↗
PubMed1996

Prolonged enteroviral infection in a patient who developed pericarditis and heart failure after bone marrow transplantation.

We described a patient who developed heart failure and pericarditis after bone marrow transplantation for a hematologic malignancy. The patient died of heart failure complicated by pneumonia. Despite extensive surveillance, an infectious cause for the heart failure was not found while he was alive. In addition, cultures of specimens obtained at autopsy did not reveal a cause for the heart failure. Enterovirus was detected by the polymerase chain reaction (PCR) in two samples of pleural fluid that were obtained 21 days apart while he was alive. After the patient died, enteroviral RNA was also detected in his lungs, liver, and spleen, indicating a generalized infection. Analysis of the PCR products revealed sequences sharing close homology with the coxsackie B-like group of enteroviruses. In addition to reporting this case, we review the literature regarding enteroviral infections after transplantation.

Adult↗
PubMed1991

Immunolocalization of basic fibroblast growth factor during chicken cardiac development.

Basic fibroblast growth factor (bFGF) has been identified in cultured cardiac myocytes as well as in myocardial tissue of both embryonic and adult organisms; bFGF has also been demonstrated to regulate proliferation and differentiation of these cells in culture. Such studies suggest a possible role for bFGF in cardiac myogenesis. In vitro studies using cultured endothelial and neuronal cells also suggest that myocyte-derived bFGF may be involved in the regulation of vascularization and/or innervation of the developing heart. We have generated a spatial and temporal map for bFGF in the developing chick heart using immunohistochemical techniques and our monospecific polyclonal rabbit antihuman bFGF IgG. A progressive decrease in bFGF expression was seen in the highly trabeculated region of the ventricular myocardium, relative to the myocardium directly underlying the epicardial tissue, with increasing developmental age. bFGF expression was limited to the cytoplasm of cardiac myocytes; neither vascular endothelium nor smooth muscle contained anti-bFGF immunoreactive material. A correlation between the temporal and spatial pattern of bFGF expression seen here, with the pattern of myocyte proliferation and differentiation reported by others, suggests a role for bFGF in the autocrine regulation of myocyte proliferation and differentiation.

Animals↗