Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Cardiac development”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 919 records · Page 51Linked to original sources
PubMed2000

Replacement of graft-resident donor-type antigen presenting cells alters the tempo and pathogenesis of murine cardiac allograft rejection.

BACKGROUND: Graft-resident antigen presenting cells (APCs) are potent stimulators of the alloresponse. To test whether replacement of graft-resident donor-type APCs with those of recipient-type alters allorecognition and the pathogenesis of both acute and chronic rejection, we created chimeric hearts for transplantation into naive recipients. METHODS: To replace donor-type APCs with those of recipient-type, chimeric animals were created by bone marrow transplantation (BMT) in fully allogeneic mouse and rat strain combinations. The degree of APC replacement in chimeric organs was assessed phenotypically and functionally. Chimeric hearts were transplanted heterotopically into untreated recipients. RESULTS: Flow cytometric and immunohistochemical analysis did not detect residual bone marrow recipient-type APCs in mouse BMT chimeras. Although semi-quantitative reverse transcription polymerase chain reaction detected 0.001-0.01% residual cells, APCs isolated from chimeric organs were functionally unable to stimulate donor-type cells. When transplanted into naive recipients, chimeric mouse hearts had significantly prolonged survival but were nevertheless rejected acutely. Similar results were obtained in the ACI --> LEW rat strain combination. However, in the PVG --> DA rat model, the majority of chimeric hearts survived >100 days and all long-surviving hearts developed cardiac allograft vasculopathy. CONCLUSIONS: BMT leads to near complete replacement of organ-resident APCs. The virtual absence of donor-type APCs in chimeric hearts delays or prevents acute rejection in a strain-dependent manner. In contrast, this type of graft modification does not prevent cardiac allograft vasculopathy. This suggests that, although the CD4+ direct pathway may play a role in acute rejection, it is not essential for the development of chronic rejection in rodent cardiac allografts.

Acute Disease↗
PubMed1998

A calcineurin-dependent transcriptional pathway for cardiac hypertrophy.

In response to numerous pathologic stimuli, the myocardium undergoes a hypertrophic response characterized by increased myocardial cell size and activation of fetal cardiac genes. We show that cardiac hypertrophy is induced by the calcium-dependent phosphatase calcineurin, which dephosphorylates the transcription factor NF-AT3, enabling it to translocate to the nucleus. NF-AT3 interacts with the cardiac zinc finger transcription factor GATA4, resulting in synergistic activation of cardiac transcription. Transgenic mice that express activated forms of calcineurin or NF-AT3 in the heart develop cardiac hypertrophy and heart failure that mimic human heart disease. Pharmacologic inhibition of calcineurin activity blocks hypertrophy in vivo and in vitro. These results define a novel hypertrophic signaling pathway and suggest pharmacologic approaches to prevent cardiac hypertrophy and heart failure.

Angiotensin II↗
PubMed1988

Cardiac tamponade complicating central venous catheter.

Cardiac tamponade complicating central venous catheters is usually fatal. We present a 23 year old woman who developed cardiac tamponade 12 hours after the insertion of a subclavian line. Early recognition of this complication and urgent pericardiocentesis led to her survival.

Adult↗
PubMedDate not supplied

Clinical and anatomic features of acardiac twins.

OBJECTIVE: To report 6 cases of acardiac twins, and to investigate prognostic factors that would lead to survival of the normal twin. SUBJECTS AND METHODS: During a 9-year period from 1993 to 2001, 6 cases of acardiac twins out of 109,000 deliveries at the Maternity Center, Tunis, Tunisia were studied. Detailed inspection, X-rays, ultrasound and autopsies were performed. RESULTS: Prenatal diagnosis was made in only 1 case at 33 weeks of gestation. Rudimentary cardiac tissue was observed in 2 of the 6 perfused twins, and the cephalic pole was less developed than other parts of the body. Severe agenesis or hypoplasia of the thoracoabdominal organs was commonly observed. Many limb malformations were observed, with arms the most affected. One of the pump twins was stillborn, 3 died between days 1 and 3 from respiratory distress, and 2 developed cardiac failure after birth and were treated with diuretics and digoxin, which led to a favorable outcome in only 1. The ratio of the weight of the acardiac to pump twin (TWR) ranged from 50 to 142%. CONCLUSION: The findings of this study indicate that acardia can be diagnosed by means of ultrasound in front of a monochorial twin pregnancy when one of the fetuses is deformed and has no cardiac activity. Heart failure and polyhydramnios, as well as a TWR greater than 50% are prognostic factors for the pump twin.

Abnormalities, Multiple↗
PubMed2005

Cardiomyocyte-specific knockout and agonist of peroxisome proliferator-activated receptor-gamma both induce cardiac hypertrophy in mice.

Peroxisome proliferator-activated receptor (PPAR)-gamma is required for adipogenesis but is also found in the cardiovascular system, where it has been proposed to oppose inflammatory pathways and act as a growth suppressor. PPAR-gamma agonists, thiazolidinediones (TZDs), inhibit cardiomyocyte growth in vitro and in pressure overload models. Paradoxically, TZDs also induce cardiac hypertrophy in animal models. To directly determine the role of cardiomyocyte PPAR-gamma, we have developed a cardiomyocyte-specific PPAR-gamma-knockout (CM-PGKO) mouse model. CM-PGKO mice developed cardiac hypertrophy with preserved systolic cardiac function. Treatment with a TZD, rosiglitazone, induced cardiac hypertrophy in both littermate control mice and CM-PGKO mice and activated distinctly different hypertrophic pathways from CM-PGKO. CM-PGKO mice were found to have increased expression of cardiac embryonic genes (atrial natriuretic peptide and beta-myosin heavy chain) and elevated nuclear factor kappaB activity in the heart, effects not found by rosiglitazone treatment. Rosiglitazone increased cardiac phosphorylation of p38 mitogen-activated protein kinase independent of PPAR-gamma, whereas rosiglitazone induced phosphorylation of extracellular signal-related kinase 1/2 in the heart dependent of PPAR-gamma. Phosphorylation of c-Jun N-terminal kinases was not affected by rosiglitazone or CM-PGKO. Surprisingly, despite hypertrophy, Akt phosphorylation was suppressed in CM-PGKO mouse heart. These data show that cardiomyocyte PPAR-gamma suppresses cardiac growth and embryonic gene expression and inhibits nuclear factor kappaB activity in vivo. Further, rosiglitazone causes cardiac hypertrophy at least partially independent of PPAR-gamma in cardiomyocytes and through different mechanisms from CM-PGKO.

Animals↗
PubMed2000

Early onset heart failure in transgenic mice with dilated cardiomyopathy.

In children, dilated cardiomyopathy is due to a variety of etiologies and usually carries a grave prognosis. The purpose of the present study was to carefully follow the progression of events leading to cardiac dilatation and congestive heart failure in a dilated cardiomyopathy model in neonatal and juvenile mice. These initial steps are often not well characterized. Furthermore, the loss of gap junctions and reduced electrical coupling of cardiomyocytes frequently found in human cardiomyopathies are also observed in these early stages. By 2 wk of age, molecular markers associated with hypertrophy were already altered. Cardiomyocyte hypertrophy, reduced connexin43 expression, and decreased conduction velocity were apparent by 4 wk, before overt cardiac dysfunction (decreased shortening fraction and chamber remodeling) that was not present until 12 wk of age. Our results show that in this model cardiomyopathic changes are present by 2 wk after birth and progress rapidly during the subsequent 2 postnatal weeks. Combined with the observations of other models of heart disease, we suggest that the first 2 wk of postnatal life are absolutely critical for normal cardiac development, and events that perturb homeostasis during this period determine whether the heart will continue to develop normally. These animals exhibit early symptoms of disease including reduced connexin43 and conduction defects before impaired cardiac function and demonstrate for the first time a temporal association between decreased connexin43 levels and the initiation of a contractility deficit that ends in heart failure.

Aging↗
PubMed1990

[Lyme borreliosis. The manifestations of the disease from the internal medicine and rheumatology viewpoints].

Lyme disease is an infectious syndrome transmitted by tick bites. Of the multiple manifestations, cardiac and joint involvement are of primary interest for internists and rheumatologists. Up to 10% of patients develop cardiac symptoms, most frequently a disturbance of atrioventricular conduction. The characteristic presentation of the disease, however, are of symptoms of arthritis in one or several large joints. This review summarizes Lyme disease with emphasis on presenting symptoms important to internists and rheumatologists.

Anti-Bacterial Agents↗
PubMed1996

[Successful repair of right atrial rupture due to nonpenetrating trauma of the chest].

A 24-year-old male was brought to our hospital after being injured in a traffic accident. On arrival, his blood pressure was 70/44 mmHg and his pulse rate was 135/min and regular. Chest X-p revealed cardiomegaly but there was no pleural effusion or bone fracture. Echocardiogram revealed cardiac tamponade and he was diagnosed as cardiac rupture due to non penetrating trauma. Under midline sternotomy, right atrial rupture was repaired. The patient developed cardiac arrest lasting approximately 8 minutes during anesthetic induction, so he needed to be ventilated for 8 days. However his postoperative course was not so eventful and he was discharged 38 days after surgery without any neurophysiological disturbance.

Accidents, Traffic↗
PubMedDate not supplied

Unsuccessful pericardiocentesis for cardiac tamponade during angiocardiography with nonionic contrast material.

Cardiac tamponade secondary to ventricular wall perforation is one of the possible complications of right-sided as well as left-sided cardiac catheterization. Ventriculography was performed on a patient with obstructive cardiomyopathy using a nonionic contrast medium. During the procedure, the right ventricle was accidentally perforated and the patient developed cardiac tamponade. Pericardiocentesis was unsuccessful and surgical drainage was needed after the patient developed progressive hemodynamic deterioration. At surgery, pericardial thrombus was found. We consider the reason for failure of pericardiocentesis was rapid coagulation of the extravasated blood in connection with nonionic contrast material.

Aged↗
PubMed1980

Development of a cardiac antiarrhythmic screening test utilizing theophylline in the rat.

Cardiac arrhythmias were produced in Sprague-Dawley-derived rats by chloroform challenge. The incidence of cardiac arrhythmias so induced increased with age and as a function of dose after pretreatment with theophylline. The dose-response and time-action parameters of theophylline's predisposing action to chloroform-hypoxia-induced cardiac arrhythmias were determined. This information has been utilized to develop a cardiac antiarrhythmic screening test in unanesthetized rats which is presented in the following paper.

Acetates↗
PubMed2006

GATA factors in vertebrate heart development and disease.

Vertebrate heart formation is dependent upon complex hierarchical gene regulatory networks, which effect both the specification and differentiation of cardiomyocytes and subsequently cardiac morphogenesis. GATA-4, -5 and -6 comprise an evolutionarily conserved subfamily of transcription factors, which are expressed within the precardiac mesoderm from early stages in its specification and continue to be expressed within the adult heart. We review here the functional roles of individual GATA transcription factors in cardiac development, normal homeostasis and disease. We also review the cellular mechanisms employed to regulate the expression and downstream targets of the different GATA factors.

Animals↗
PubMed1996

Pathophysiological analysis of serum troponin T release kinetics in evolving ischemic myocardial injury.

The present study measured cardiac troponin T(TnT) for the pathophysiological analysis of evolving ischemic myocardial injury in 35 patients with unstable angina (3: Class IB, 32: Class IIIB) and in 40 patients undergoing coronary reperfusion therapy for acute myocardial infarction. Serum TnT, creatine kinase (CK), CKMB, myoglobin (Mb), and myosin light chain 1 (MLC1) were measured every 2-24 h for 10 days after admission to the CCU. In patients with unstable angina, positive test results were detected in 65.7% for TnT, 20% for CK, 37.1% for CKMB, 60.9% for Mb, and 26% for MLC1. Of the 23 patients with positive TnT, 12 (52.2%) had cardiac events. Of the 12 patients with negative TnT, 11 (91.6%) were event-free. All of the patients who developed cardiac events showed a persistent (n = 10) or delayed elevation (n = 2) pattern 28-120 h beforehand. The sensitivity for predicting cardiac events was 92.3% for TnT, 80% for Mb, 53.8% for CKMB, and 50% for MLC1. In patients with acute myocardial infarction, TnT release kinetics showed 2 peaks after coronary reperfusion therapy. TnT values at the 1st peak significantly correlated with maximum CKMB (r = 0.70, p < 0.05) and early-stage left ventricular wall motion score (r = 0.60, p < 0.05), while 2nd-peak TnT values significantly correlated with maximum MLC1 (r = 0.59, p < 0.05), the T1-SPECT score (r = 0.78, p < 0.05) and left ventricular ejection fraction (r = -0.74, p < 0.05) in the convalescent stage. The 2nd/1st-peak TnT ratio significantly correlated with the nQ/nST elevation index (ratio of the number of leads developing abnormal Q-wave 1 week after the onset to the number of leads showing ST elevation of more than 1 mm at admission) (r = 0.63, p < 0.05) in patients with anterior myocardial infarction. These data indicate that persistent release of TnT reflects progressive irreversible myocardial damage in unstable angina and indicates a risk of future cardiac events. In acute myocardial infarction, the 2nd/1st-peak TnT ratio in patients undergoing coronary reperfusion therapy may be useful for the quantitative evaluation of myocardial salvage.

Acute Disease↗
PubMed2004

Determination of electrical properties of ES cell-derived cardiomyocytes using MEAs.

Pluripotent embryonic stem cells (ES cells) provide a novel tool to study cardiomyogenesis under in vitro conditions. This overview article focuses on the technical properties of extracellular recordings of ES cell-derived cardiomyocytes using Microelectrode Arrays (MEAs). It reviews recent experimental observations, in an effort to describe basic characteristics of field potentials (FPs) in the ES cell model of developing myocardium. ES cells kept in permanent culture are differentiated within aggregates ("embryoid bodies", EBs) in which among other cell types cardiomyocytes appear 3-4 days after plating. These form spontaneously beating clusters mostly consisting of expanded regions of cardiac cells connected with narrow tissue strands. To record the electrical activity of these contracting areas substrate-integrated MEAs consisting of 60 substrate-integrated electrodes can be used. We previously investigated the influence of Na+-, K+- and Ca2+ channel blockers on the electrical signal generation and propagation as well as on the shape of FPs. We also used ES cell-derived cardiac myocytes as a multicellular in vitro model for cardiac development. Long-term recordings with a MEA enabled the examination of electrophysiological properties during the ongoing differentiation process. During time in culture the beating aggregate of cardiac myocytes differentiating from ES cells increased in size (7-fold). This change was accompanied by an increase of the beating frequency from 1 to 5 Hz and a decrease of the FP duration. Furthermore a shortening of the FP upstroke velocity could be observed concomitant with a functional segregation of slow upstroke velocities in the area of the pacemaker. Our data indicate a functional differentiation and segregation of the cells into pacemaker and myocard-like regions. This in vitro development of a three-dimensional heart like structure closely follows the development known from mouse embryonic heart. The preparation thus forms an ideal model to monitor the development of electrical activity in embryonic cardiac myocytes for wild type and genetically modified ES cells, thereby taking into account the functional differentiation of the tissue. Our data suggest that EBs plated on MEAs provide a suitable tool for pre-screening of cardioactive substances.

Animals↗
PubMed1991

alpha-Actin proteins and gene transcripts are colocalized in embryonic mouse muscle.

The alpha-actins are among the earliest muscle-specific mRNAs to appear in developing cardiac and skeletal muscle. To determine if there is coexpression of the alpha-actin proteins at early stages of myogenesis, we have used an alpha-actin-specific polyclonal antibody and in situ hybridization with specific cRNA probes to cardiac and skeletal alpha-actin transcripts on serial slides of mouse embryo sections. As soon as we can detect alpha-actin mRNAs in embryonic striated muscle, we also detect the protein suggesting that alpha-actin transcripts are translated very rapidly after transcription during myogenesis. In skeletal muscle, this colocalization of alpha-actin mRNA and protein was observed both in the myotomes of somites and in developing muscles in the limbs. In cardiac muscle, alpha-actin transcripts and proteins are abundantly expressed as soon as a cardiac tube forms.

Actins↗
PubMed1992

Epidemiology of congenital heart disease in Louisiana: an association between race and sex and the prevalence of specific cardiac malformations.

We hypothesized that susceptibility to the genetic and environmental factors that disrupt cardiac development is associated with race and sex. To evaluate this hypothesis, we asked whether the prevalence of specific cardiac malformations differs by race and sex. We attempted to include all infants born alive in the State of Louisiana from January 1, 1988, through December 31, 1989, and diagnosed by echocardiography, catheterization and/or autopsy within a year of birth as having one of ten specific cardiac malformations. The prevalence of atrioventricular canal defects (AVCD) per 1,000 live births was significantly higher for black females (.744) compared to black males (.198) and for white females (.414) compared to white males (.116). Complete transposition of the great arteries (TGA) was significantly higher for white males (.559) compared to white females (.122); in contrast, TGA was not significantly different for black males (.198) and black females (.169). Obstructive left heart syndrome (OLHS)--aortic stenosis and/or coarctation of the aorta--was significantly higher for white males (.652) compared to white females (.317); in contrast, OLHS was not significantly different for black males (.264) and black females (.169). Single ventricle (SV) was significantly higher for whites (.202) compared to blacks (.067). We did not find that race and sex were associated with differences in the prevalence of tetralogy of Fallot and hypoplastic left heart syndrome. The numbers of infants with anomalous pulmonary venous return, tricuspid atresia, double outlet right ventricle, or truncus arteriosus were too small to measure an association with race and sex. These results demonstrate that the prevalence of a subset of cardiac malformations differs by race and sex.(ABSTRACT TRUNCATED AT 250 WORDS)

Female↗
PubMed1998

Selective induction of Na,K-ATPase alpha3 subunit mRNA abundance in cardiac myocytes by retinoic acid.

Retinoic acid (RA) is a high affinity ligand for a nuclear receptor which regulates transcription in target cells. Specific effects of RA on cardiac development and myocardial cell hypertrophy have been demonstrated; however, little information exists concerning RA-mediated regulation of cardiac genes. This study was initiated to investigate whether RA regulates Na,K-ATPase subunit gene expression in primary cultures of neonatal rat cardiac myocytes. Northern blot analyses demonstrated that NA, K-ATPase alpha3 subunit mRNA content was stimulated three-fold by RA. The effect of RA on alpha3 subunit gene expression was selective as RA treatment had no effect on either Na,K-ATPase alpha1, alpha2 or beta1 subunit mRNAs. A stimulatory effect of RA on Na,K-ATPase alpha3 gene transcription was not evident in either transient transfection or nuclear run-on studies, suggesting that augmentation of alpha3 mRNA content by RA was due to a post-transcriptional mechanism. Finally, RA diminished the magnitude of the thyroid hormone (T3)-mediated increase in Na,K-ATPase beta1 subunit mRNA, while RA had no effect on the stimulation of alpha3 mRNA content by T3.

Animals↗
PubMed1992

Diagnosis and management (by subxiphoid pericardiotomy) of large pericardial effusions causing cardiac tamponade.

To determine the clinical features, course and outcome of patients with cardiac tamponade, 57 consecutive patients with new, large pericardial effusions were prospectively studied. Twenty-five patients (44%) developed cardiac tamponade with venous hypertension and a pulsus paradoxus greater than 10 mm Hg. Electrocardiography, radiographic studies and echocardiography did not differentiate patients with and without tamponade. All 57 patients underwent thorough diagnostic evaluation followed by subxiphoid pericardial biopsy and drainage. A diagnosis was obtained in 53 patients (93%). Collagen vascular disease was significantly more frequent in the 25 patients with than in the 32 without cardiac tamponade (24 vs 3%; p less than 0.05). The frequency of malignant and uremic effusions was equal in both groups, whereas radiation-induced effusions seldom produced tamponade. At 1-year follow-up, 3 patients (12%) with tamponade had recurrent effusions, and 1 needed reoperation. This was not significantly different from the 32 patients without tamponade. Twelve-month mortality was also similar in both groups (36 vs 44%). This prospective series disclosed several unexpected findings: (1) Cardiac tamponade occurred in almost 50% of patients with new large pericardial effusions; (2) both malignancy and collagen vascular disease occurred with equal frequency as etiologies, whereas radiation-induced tamponade was unusual; (3) thorough clinical evaluation resulted in few idiopathic etiologies; and (4) subxiphoid pericardiotomy was effective for both diagnosis and therapy of tamponade.

Cardiac Tamponade↗
PubMed2000

Alterations in exon 4 of the p53 gene in gastric carcinoma.

BACKGROUND & AIMS: Our long-term goal was to evaluate the role of p53 in the prognosis of gastric cancer. We previously showed a discrepancy between p53 expression and the presence of mutations when only exons 5-9 were examined. We then evaluated exon 4. METHODS: DNA was sequenced from 217 gastric cancers to detect exon 4 alterations. Codon 72 was examined by restriction enzyme digestion. RESULTS: Mutations were present in 3.2% of tumors. In addition, 2 polymorphic sites were found at codons 36 and 72. Polymorphisms at codon 36 were only found in 2 patients. In contrast, the codon 72 polymorphism was very frequent. The genotype frequency was arg/arg (54%), arg/pro (33%), and pro/pro (14%). The genotype of the polymorphic site varied with race (P = 0.001): 64% of whites had the arg/arg genotype, compared with 24% of blacks. The difference in genotype by site, sex, or histological tumor type was not statistically significant (P = 0.067). CONCLUSIONS: There are several exon 4 alterations in gastric cancers. These include the rare mutations and the very rare codon 36 polymorphism. The most common change is the codon 72 polymorphism, the genotype of which differs significantly with race. The more common arg/arg genotype in whites may explain why whites are more prone to develop cardiac cancer, whereas the more common proline allele in blacks may explain why they are more prone to develop antral cancers. Further studies are required to determine whether the codon 72 polymorphism affects patient predisposition to gastric cancer.

Adenocarcinoma, Mucinous↗