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At least 811 records · Page 45Linked to original sources
PubMed1992

[Traumatic pneumopericardium with cardiac tamponade].

A 20 year old male motorist with multiple injuries, including bilateral lung laceration, developed cardiac tamponade 12 hours after injury. X-ray showed characteristic findings of pneumopericardium with air all around the cardiac silhouette, which was diminished in size. A chest tube was inserted intrapericardially through a subxiphoid incision. Blood pressure increased immediately, and central venous pressure became normal. Cardiac left ventricular stroke work increased by 86% to normal value. The drain was removed after three days. Another patient was a 15 year old male cyclist who had been overrun by a trailer. Left-sided emergency thoracotomy was performed during laparotomy for liver and vena cava injury, in the course of which procedures there was a sudden decrease in blood pressure with marked elevation of the central venous pressure. The pericardium was incised. Air hissed out, leading to normalisation of arterial and venous pressures. Both patients recovered. Pneumopericardium without symptoms may be treated by observation. Tension pneumopericardium is rare and is best treated by open drainage.

Accidents, Traffic↗
PubMedDate not supplied

Cardiac perforation after Kirschner wire migration.

A case report is described in which a patient developed cardiac tamponade after migration of a Kirschner wire, used for fixation of a luxated sternoclavicular joint, through the pericardium and into the pulmonary artery.

Bone Wires↗
PubMed1998

Cardiac physiology in transgenic mice.

By use of gene targeting and/or transgenesis, it is now possible to make defined changes in genes whose functions underlie mammalian cardiovascular function. Because of technical and economic considerations, these experiments are largely confined to the mouse. Genetic modification of the loci responsible for aspects of cardiac development, differentiation, and function via gene targeting, as well as modulation of the cardiac protein complement using transgenesis, has begun to provide mouse models of cardiac hypertrophy, dilated cardiomyopathy, and hypertrophic cardiomyopathies. In order to use these animal models fully and explore their phenotypes at the whole organ and whole animal levels, the extension of cardiovascular physiological methodologies to the mouse is imperative. Techniques for exploring aspects of cardiovascular function are well developed for larger animal models, but their modification for the small size of the mouse heart and for the animal's rapid cardiac cycle has proven to be a formidable challenge, requiring the combined efforts of the molecular biology, physiology, and cardiology communities. We review here the ability of present-day technology to obtain reproducible data on murine cardiac function at the whole organ and animal levels.

Animals↗
PubMed1989

Atrioventricular valves development in human heart: the Paris embryological collection revisited.

29 human embryos staging from stage 15 to stage 23 (post-somitic period, collection of the UER Biomedicale des Saints-Péres, Université René Descartes Paris V) have been studied. The most important morphological events of the atrioventricular valves development have been reinvestigated and photographed. This is a complementary information about cardiac development analysing this french collection of human embryos (Mandarim-de-Lacerda, in press). At stage 15, we can observe the gelatinous reticulum well organized when cardiac valves will become established; progressively the fused endocardial cushions and right and left lateral cushions encircle the atrioventricular channels indicating the site of the tricuspid valves. These cushions, however, have a temporary influence being replaced gradually by atrial and ventricular myocardium. At stage 23, the heart presents a complete atrioventricular valvular structure.

Humans↗
PubMed2006

Long-term administration of pirfenidone improves cardiac function in mdx mice.

Duchenne muscular dystrophy, an X-linked recessive neuromuscular disorder due to lack of the protein dystrophin, manifests as progressive muscle degeneration and cardiomyopathy with increased fibrosis. The exact mechanisms involved in fibrosis are unknown, but a cytokine, transforming growth factor-beta (TGF-beta), is a likely mediator. This study tested whether the TGF-beta antagonist, pirfenidone, could reduce cardiac fibrosis. Eight-month-old mdx mice were treated for 7 months with 0.4%, 0.8%, and 1.2% pirfenidone in drinking water; untreated water was given to control mdx and C57 mice. Mice treated with 0.8% and 1.2% pirfendone had lowered cardiac TGF-beta mRNA and improved in vitro cardiac contractility (P < 0.05) to levels consistent with C57 mice, yet without a change in cardiac stiffness or fibrosis. These results show that the TGF-beta antagonist, pirfenidone, can improve cardiac function in mdx mice, potentially providing a new avenue for developing cardiac therapies for patients with Duchenne muscular dystrophy.

Animals↗
PubMed2006

Heart development in Drosophila.

The Drosophila heart, also called the dorsal vessel, is an organ for hemolymph circulation that resembles the vertebrate heart at its transient linear tube stage. Dorsal vessel morphogenesis shares several similarities with early events of vertebrate heart development and has proven to be an insightful system for the study of cardiogenesis due to its relatively simple structure and the productive use of Drosophila genetic approaches. In this review, we summarize published findings on Drosophila heart development in terms of the regulators and genetic pathways required for cardiac cell specification and differentiation, and organ formation and function. Emerging genome-based strategies should further facilitate the use of Drosophila as an advantageous system in which to identify previously unknown genes and regulatory networks essential for normal cardiac development and function.

Animals↗
PubMed2004

Novel NKX2-5 mutations in diseased heart tissues of patients with cardiac malformations.

NKX2-5 is a homeodomain-containing transcription factor important in cardiac development. Familial mutations in the NKX2-5 gene are associated with cardiac abnormalities, but mutations are rare in sporadic cases. We studied the pathology and molecular genetics of NKX2-5 in diseased heart tissues of 68 patients with complex congenital heart disease (CHD), particularly atrial (ASD), ventricular (VSD), and atrioventricular septal defects (AVSD). We also studied DNA extracted from 16 normal hearts, as well as lymphocytic DNA from 50 healthy volunteers, 7 families, and 4 unrelated individuals with CHD. Direct sequencing revealed 53 NKX2-5 mutations in the diseased heart tissues, including nonsynonymous substitutions in the homeodomain of NKX2-5. We found common mutations among unrelated patients, but certain mutations were specific to VSDs and AVSDs. Many patients had multiple NKX2-5 mutations, up to 14 nonsynonymous mutations per patient in VSDs. Importantly, these nonsynonymous mutations were mainly absent in normal heart tissues of the same CHD patients, thus indicating somatic origin and mosaicism of mutations. Further, observed mutations were completely absent in normal hearts and lymphocytic DNA of healthy individuals. Our findings provide new insights for somatic NKX2-5 mutations to be of importance in congenital heart disease.

Base Sequence↗
PubMed2000

Human protein tyrosine phosphatase-like gene: expression profile, genomic structure, and mutation analysis in families with ARVD.

The mouse protein tyrosine phosphatase-like gene (Ptpla) was recently cloned and data suggested that it plays a role in myogenesis and cardiogenesis. The human homologue (PTPLA) was mapped to chromosome 10p13-14, a region where we have mapped a locus responsible for arrhythmogenic right ventricular dysplasia (ARVD). As a positional candidate gene, we characterized PTPLA by determining its tissue expression, its genomic structure, and we also screened for mutations in the ARVD patients. Northern analysis demonstrated PTPLA is preferentially expressed in both adult and fetal heart. A much lower expression was detected in skeletal and smooth muscle tissues. Virtually no expression was observed in other tissues. The protein-encoding sequences of PTPLA consist of seven exons. A sequence variation (Lys64Gln) was found in all the affecteds in a large ARVD family. However, the same variant was also detected in normal control subjects (three alleles/100 chromosomes). Thus, the variant (Lys64Gln) is not responsible for ARVD in our family and is a benign polymorphism. Nevertheless, its tissue-specific expression in the developing and adult heart suggest PTPLA has a role in regulating cardiac development, differentiation, or other cellular events. The genomic structure and intragenic polymorphism of PTPLA should be useful for further clinical and genetic studies such as gene targeting of PTPLA.

Arrhythmogenic Right Ventricular Dysplasia↗
PubMed2003

A comparative study on cardiac ganglia in midday gerbil, Egyptian spiny mouse, chinchilla laniger and pigeon.

Using the thiocholine method and histological techniques, the topography and morphology of cardiac ganglia in midday gerbil, Egyptian spiny mouse, chinchilla laniger and pigeon were studied. The results demonstrated that cardiac ganglia in all investigated species are embedded in epicardial fat. They formed plexo-ganglionic structures. Each of them composed of many ganglia (from seven up to 36) different in size and shape, and interconnected by fascicles of nerve fibres. Comparative analysis showed that the density of neural network and cell aggregations was different in individual species. The richest plexo-ganglionic structure was in pigeon. It was organized in three plexo-ganglia with an average of 30 ganglia. The largest one was located along the anterior interventricular sulcus. The cardiac ganglia of investigated mammals were localized mainly on the epicardium of atria; in Egyptian spiny mouse and chinchilla laniger on the ventral surface of right atrium, but in midday gerbil on the dorsal surface of left atrium. Moreover, in midday gerbil and Egyptian spiny mouse the little plexo-ganglionic structure on the ventricle were noticed. Additionally, in midday gerbil the single nerve cells might be observed between cardiac muscle of atria. It can be said that, the strongly developed cardiac plexus in pigeon is probably connected with his behaviour and functional properties of the heart. The arrangement of neurones in cardiac ganglia of all examined mammals was uniform over the whole surface of the sections, while in the pigeon, neurones were located mainly in the peripheral part of the ganglion.

Animals↗
PubMed2001

Bone morphogenetic protein-2 inhibits serum deprivation-induced apoptosis of neonatal cardiac myocytes through activation of the Smad1 pathway.

Bone morphogenetic protein (BMP)-2 has been shown to induce ectopic expression of cardiac transcription factors and beating cardiomyocytes in non-precardiac mesodermal cells, suggesting that BMP-2 is an inductive signaling molecule that participates in cardiac development. However, direct evidence of the effects of BMP-2 on cardiac myocytes has not been reported. To examine the role of BMP-2 and its receptors, we studied the ability of BMP-2 to promote survival of isolated neonatal rat cardiac myocytes. BMP receptors IA, IB, and II and activin receptor I were found to be expressed in myocytes, and BMP-2 phosphorylated Smad1 and p38 MAPK. Interestingly, BMP-2 promoted survival and inhibited apoptosis of serum-deprived myocytes, although it did not strongly induce hypertrophic growth. To explore the mechanisms for this protective effect, an adenovirus-based vector system was used. Similar to BMP-2, Smad1 promoted survival that was repressed by Smad6. Moreover, BMP-2 and Smad1 enhanced the expression of the anti-apoptotic molecule Bcl-x(L). Antisense oligonucleotides to bcl-x(L) attenuated the survival effected by BMP-2. Overall, our findings suggest that BMP-2 prevents apoptosis of myocytes by induction of Bcl-x(L) via a Smad1 pathway and might be a novel survival factor without any hypertrophic effect on myocytes.

Animals↗
PubMedDate not supplied

On the role of shear stress in cardiogenesis.

The relative contribution of physical and chemical factors in organogenesis in general and in cardiogenesis in particular is an old and still unsolved question in developmental biology (Chang 1932, Anatomical Record, 51, 253-265). A recent Nature paper (Hove et al. 2003, Nature, 421, 172-177) strongly suggests (but does not prove) the important role of blood flow and associated shear stress in cushion tissue morphogenesis. However, another elegantly designed study (Bartman et al. 2004, Public Library of Science-Biology, 2, E129) raises questions as to the validity of the shear stress hypothesis and the role of physical factors in cardiogenesis. Although these studies advance our understanding of cardiac development, other possible explanations for the role of blood flow in cardiac organogenesis remain to be addressed.

Animals↗
PubMed1998

Adult T cell leukemia/lymphoma with massive involvement of cardiac muscle and valves.

An autopsy case of a 58-year-old woman with massive cardiac involvement of adult T cell leukemia/lymphoma (ATLL) is reported. She developed cardiac failure due to aortic and mitral regurgitation with cardiac infiltration of ATLL cells, and underwent replacement of both aortic and mitral valves. Studies of the cut-surfaces revealed diffuse thickening of the subendocardial wall of the left chamber with widespread whitish-brown tumor infiltrates. In the regions surrounding the replaced aortic and mitral valves there was also massive tumor cell infiltration. The tumor cells infiltrating the cardiac muscle wall were T cell in origin and exhibited Leu-3a (CD4)-positive immunoreaction. Ultrastructurally, tumor cells contained markedly indented nuclei and some were attached directly to the muscle cells. These findings suggest that this was an unusual form of ATLL with widespread involvement of the heart.

Biomarkers, Tumor↗
PubMed2005

Dilated cardiomyopathy in Erb-b4-deficient ventricular muscle.

The neuregulin receptor tyrosine kinase Erb-b4, initially linked to early cardiac development, is shown here to play a critical role in adult cardiac function. In wild-type mice, Erb-b4 protein localized to Z lines and to intercalated disks, suggesting a role in subcellular and intercellular communications of cardiomyocytes. Conditional inactivation of erb-b4 in ventricular muscle cells led to a severe dilated cardiomyopathy, characterized by thinned ventricular walls with eccentric hypertrophy, reduced contractility, and delayed conduction. This cardiac dysfunction may account for premature death in adult erb-b4-knockout mice. This study establishes a critical role for Erb-b4 in the maintenance of normal postnatal cardiac structure and function.

Animals↗
PubMed1996

Ablation of the murine alpha myosin heavy chain gene leads to dosage effects and functional deficits in the heart.

The alpha-myosin heavy chain (alpha-MyHC) is the major contractile protein expressed in the myocardium of adult mice. We have produced mice carrying a null mutation of alpha-MyHC by homologous recombination in murine ES cells. Homozygous null animals die between 11 and 12 d in utero of gross heart defects, while alpha-MyHC+/- heterozygotes survive and appear externally normal. The presence of a single functional alpha-MyHC+ allele in heterozygous animals results in reduced levels of the transcript and protein as well as fibrosis and alterations in sarcomeric structure. Examination of heart function using a working heart preparation revealed severe impairment of both contractility and relaxation in a subset of the alpha-MyHC+/- animals. Thus, two alpha-MyHC+ alleles are necessary for normal cardiac development, and hemizygosity for the normal allele can result in altered cardiac function.

Alleles↗
PubMed1990

[The treatment of acute heart failure].

Acute cardiac failure is a symptom of a defined heart disease. Therapeutic efforts will only be successful, if the casual disease can be recognized. The clinical picture of cardiac failure is composed of a lot of pathophysiological and pathobiochemical developments. Some of them are still today completely or partly unknown. Each pharmacological intervention influences these regulations and reacts in every situation not only in the desirable but also in an unexpected way. Since we do not know the speed and direction of the developing cardiac failure, patients in NYHA II-III have to be sent to hospital. Starting the efficient treatment in time success can be expected without expensive diagnostics and monitoring techniques. But in some cases highly specialized equipment will be necessary and must be available.

Acute Disease↗
PubMed1994

Prolonged asystolic hyperkalemic cardiac arrest with no neurologic sequelae.

We report the case of a 70-year-old man who developed cardiac arrest secondary to hyperkalemia that complicated severe chronic renal failure due to obstructive uropathy. The patient experienced electromechanical dissociation and approximately 26 minutes of asystole after which the resuscitation was suspended. However, 8 to 10 minutes after declaration of death, the patient was noted to have developed spontaneous return of circulation as the emergency department personnel were preparing to transport him to the morgue. The patient survived and was discharged without apparent neurologic sequelae. This case demonstrates the challenges facing physicians to predict the outcome of hyperkalemic cardiac arrest based on usual parameters. It also highlights the relative paucity of resuscitation guidelines to assist in the management of this medical emergency.

Aged↗
PubMed2005

Multiple stem cell populations contribute to the formation of the myocardium.

Owing to the very rapid growth of the vertebrate embryo following fertilization, an efficient circulatory system needs to be established during the initial stages of development. For that reason, the first functional organ that develops in both the bird and mammalian embryo is the heart. Until recently, the narrative of cardiac development was portrayed in a straightforward manner, with all the myocardium in the mature heart being generated from the expansion of an original pool of myocardial cells present in the early gastrula. It is now known that the story of the developing myocardium is more dynamic, as it is comprises cellular components of multiple ancestries. The de novo addition of myocytes to the developing heart occurs at various points during embryogenesis, as cardiac muscle takes on new members by the absorption of cells that either reside in neighboring nonmuscle tissue or come into contact with the myocardium by entering the heart upon migration or via the circulation. This article reviews what is presently known about cellular populations that contribute to the myocardium and examine reasons why the embryo utilizes multiple cellular sources for forming the cardiac muscle.

Animals↗
PubMedDate not supplied

Decreased susceptibility to arrhythmias in hypertrophied hearts of physically trained rats.

The aim of this study was to investigate the propensity to develop cardiac arrhythmias during an acute period of ischemia between normal and hypertrophied (by means of a swimming training regimen) rat hearts. We used the coronary artery ligation in vivo technique which induced the occurrence of cardiac arrhythmias in rats that was followed by the determination of the occluded zone size. This study was coupled to an in vitro study using a two-compartment tissue bath in which half of the ventricular preparation was exposed to normal conditions and the other to ischemic conditions (low pH, hypoxia, and hyperkalemia). We also measured the collagen content and the DNA/protein ratio of the hearts. Twenty-eight male Wistar rats submitted to an eight-week swimming training (SWT) and twenty-eight cage-confined matched rats were used for the studies. SWT resulted in a 14% decrease in mean body weight and an 8% increase in absolute heart weight. We also observed a resting bradycardia in the trained animals and blood pressure remained unchanged between the two groups. Collagen content was unchanged and DNA/protein ratio was lower in the left ventricle of trained animals. During a 30-min period of coronary artery ligation, SWT rats demonstrated fewer ischemia-induced arrhythmias as compared to controls. The size of the zone affected by the vasal occlusion was lower in trained animals. Electrophysiological data recorded in the two-compartment bath showed a marked prolongation of action potential duration and refractory period in the SWT rat hearts. During the 15-min period of in vitro ischemia there was a global alteration of all electrophysiological parameters which did not differ between the two groups. Our data support the hypothesis that resting bradycardia and decrease in ischemic zone size may be involved in the arrhythmogenic protection observed in hypertrophied hearts of swimming rats after an acute ligation of the left coronary artery. Our results also indicate that cardiac hypertrophy, as defined by quantitative changes in cardiac mass or by the electrophysiological alterations that are related to its development, is not necessarily associated with an increased risk for the occurrence of arrhythmias.

Action Potentials↗