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 757 records · Page 42Linked to original sources
PubMed2000

Cardiac abnormalities in SLE: pancarditis.

Many patients with systemic lupus erythematosus (SLE) develop cardiac manifestations during the course of their disease. Pericarditis is most commonly seen, with a reported prevalence of 60%. Myocardial involvement is present in only a minority of patients. In recent years, due to better noninvasive diagnostic techniques, valvular abnormalities can be demonstrated in an increasing number of patients. Depending on the technique used, valvulopathy can be demonstrated in up to 77% of SLE patients. Although most of the valvular lesions will be present without any symptoms, valve incompetence can result in congestive heart failure. Valvular lesions are associated with IgG anticardiolipin antibodies (aCL) and disease duration. We present a patient with SLE and secondary antiphospholipid syndrome (APS) who developed acute congestive heart failure due to pancarditis. Endocarditis, together with left ventricular dysfunction and pericardial effusion, were present. The endocarditis caused hemodynamically significant mitral valve insufficiency due to thickening of the mitral cusps. Just two weeks prior to the occurrence of congestive heart failure echocardiography had been normal. Treatment with high dose corticosteroids resulted in a gradual, almost complete recovery. Literature concerning cardiac manifestations in lupus is reviewed.

Adult↗
PubMed2006

Microarray analysis of Tbx5-induced genes expressed in the developing heart.

Tbx5 is a member of the T-box family of transcription factors and is associated with Holt-Oram syndrome (HOS), a congenital disorder characterized by heart and limb defects. Although implicated in several processes during development, only a few genes regulated by Tbx5 have been reported. To identify candidate genes regulated by Tbx5 during heart development, a microarray approach was used. A cardiac-derived mouse cell line (1H) was infected with adenoviruses expressing Tbx5 or beta-galactosidase and RNA was isolated for analysis using an Affymetrix gene chip representing over 39,000 transcripts. Real-time reverse transcriptase-polymerase chain reaction confirmed Tbx5 induction of a subset of the genes, including nppa, photoreceptor cadherin, brain creatine kinase, hairy/enhancer-of-split related 2, and gelsolin. In situ hybridization analysis indicated overlapping expression of these genes with tbx5 in the embryonic mouse heart. In addition, the effect of HOS-associated mutations on the ability of Tbx5 to induce target gene expression was evaluated. Together, these data identify several genes induced by Tbx5 that are potentially important during cardiac development. These genes represent new candidate gene targets of Tbx5 that may be related to congenital heart malformations associated with HOS.

Adenoviridae↗
PubMed2004

Heart morphogenesis is not affected by overexpression of the Sh3bgr gene mapping to the Down syndrome heart critical region.

Congenital heart disease (CHD) is the most common birth defect in humans and is present in 40% of newborns affected by Down syndrome (DS). The SH3BGR gene maps to the DS-CHD region and is a potential candidate for the pathogenesis of CHD, since it is selectively expressed in cardiac and skeletal muscle. To determine whether overexpression of Sh3bgr in the murine heart may cause abnormal cardiac development, we have generated transgenic mice using a cardiac- and skeletal-muscle-specific promoter to drive the expression of a Sh3bgr transgene. We report here that heart morphogenesis is not affected by overexpression of Sh3bgr.

Animals↗
PubMed1979

Hypertension with mineralocorticoid administration to the Long-Evans rat.

1. The Carworth Long-Evans rat has been reported to develop adrenal-regeneration hypertension but not deoxycorticosterone acetate (DOCA) hypertension. Deficiency of a hypothalamic receptor for deoxycorticosterone which mediates saline polydipsia has been postulated to underlie this resistance. Since a mineralocorticoid etiology for adrenal-regeneration hypertension has been postulated and all mineralocorticoids are thought to act on common receptors, these previous reports are difficult to reconcile. 2. To determine if an absolute or relative resistance to mineralocorticoids is present, Charles River Long-Evans and Sprague-Dawley rats were given 40 mg (107 micromol) of DOCA pellets/rat or 250 microgrms (0.65 micromol) of 2 alpha-methyl-9-alpha-fluorocortisol/day subcutaneously. 3. Saline polydipsia occurred with both steroids with both rat strains, though significantly less with the Long-Evans rats. Both types of rats became hypertensive and developed cardiac and renal enlargement with both steroids. Hypertension developed more rapidly with 2 alpha-methyl-9 alpha-fluorocortisol. 4. Thus mineralocorticoid hypertension can be produced in the Charles River Long-Evans rat, and the development of adrenal-regeneration hypertension in this rat strain is not incompatible with a mineralocorticoid etiology for adrenal-regeneration hypertension.

Adrenalectomy↗
PubMed2002

Development of heart failure and congenital septal defects in mice lacking endothelial nitric oxide synthase.

BACKGROUND: Nitric oxide (NO) produced by endothelial NO synthase (eNOS) plays an important role in the regulation of cell growth, apoptosis, and tissue perfusion. Recent studies showed that mice deficient in eNOS developed abnormal aortic bicuspid valves. The aim of the present study was to additionally investigate the role of eNOS in heart development. METHODS AND RESULTS: We examined postnatal mortality, cardiac function, and septum defects in eNOS(-/-), eNOS(+/-), and wild-type mice. Postnatal mortality was significantly increased in eNOS(-/-) (85.1%) and eNOS(+/-) (38.3%) compared with wild-type mice (13.3%, P<0.001). Postmortem examination found severe pulmonary congestion with focal alveolar edema in mice deficient in eNOS. Heart shortening determined by ultrasound crystals was significantly decreased in eNOS(-/-) compared with wild-type mice (P<0.05). Congenital atrial and ventricular septal defects were found in neonatal hearts. The incidence of atrial or ventricular septal defects was significantly increased in eNOS(-/-) (75%) and eNOS(+/-) (32.4%) neonates compared with those of the wild-type mice (4.9%). At embryonic days 12.5 and 15.5, cardiomyocyte apoptosis and myocardial caspase-3 activity were increased in the myocardium of eNOS(-/-) compared with wild-type embryos (P<0.01), and increases in apoptosis persisted to neonatal stage in eNOS(-/-) mice. CONCLUSIONS: Deficiency in eNOS results in heart failure and congenital septal defects during cardiac development, which is associated with increases in cardiomyocyte apoptosis. Our data demonstrate that eNOS plays an important role in normal heart development.

Animals↗
PubMed1994

Steady-state mRNA levels of the sarcolemmal Na(+)-Ca2+ exchanger peak near birth in developing rabbit and rat hearts.

To functionally compensate for an underdeveloped sarcoplasmic reticulum in immature cardiomyocytes, it has been proposed that the sarcolemmal Na(+)-Ca2+ exchanger may assume a more predominant role for regulating cytosolic Ca2+. Previous studies using sarcolemma prepared from developing rabbit hearts demonstrated that Na(+)-dependent Ca2+ uptake and exchanger protein content were highest at birth and declined postnatally. To further investigate the significance of the Na(+)-Ca2+ exchanger during normal myocardial development, steady-state mRNA levels of the cardiac Na(+)-Ca2+ exchanger were quantitated by Northern blot and slot-blot analyses using poly(A+) RNA isolated from rabbit and rat ventricles at various fetal and postnatal ages. Northern analyses were performed with a 1.35-kb guinea pig cardiac Na(+)-Ca2+ exchanger cDNA probe. Exchanger mRNA levels were quantitated by densitometric scans of the slot blots, and results were normalized by reprobing the same blots with 32P 5'-end-labeled oligo(dT). In both species, exchanger mRNA levels peaked near birth and declined postnatally. Maximal levels were approximately sixfold greater in the late fetal rabbit (gestational day 29) and eightfold greater in the early newborn rat (postnatal day 1) compared with adults of the respective species. The parallel changes in exchanger mRNA and protein levels suggest that developmental regulation of cardiac Na(+)-Ca2+ exchanger expression involves pretranslational control mechanisms. These results support the concept that during normal cardiac development, Na(+)-Ca2+ exchanger expression is maximal near the time of birth and then declines postnatally as Ca2+ regulation by the sarcoplasmic reticulum reaches functional maturity.

Aging↗
PubMed1988

[Cardiac mechanisms for the development of angina pectoris pain].

Despite numerous experimental and clinical investigations, the exact mechanisms involved in the development of cardiac pain are not completely understood. Sensory receptors for painful stimuli, presumably sympathetic sensory nerve endings, are located in the atria, the ventricles, and in the walls of the coronary arteries. These receptors fire at a background rate under normal hemodynamic conditions. They respond to chemical stimuli and are therefore similar to polymodal nociceptors. The afferent fibers (slow-conducting, unmyelinated group IV-fibers, or fast-conducting myelinated group III-fibers) run in the cardiac sympathetic nerves and converge with somatosensory fibers on the same ascending spinothalamic neurons, which may explain the phenomenon of "referred pain". Still unknown is the role of the afferent vagal fibers in pain perception; however, a modulating influence on pain threshold and characteristics seems possible. Two main mechanisms may be responsible for cardiac pain during ischemic periods: a) chemical excitation of free sensory nerve endings by substances such as bradykinin, PGE2, adenosine, histamine, serotonin, or K+; b) abnormal motion of ischemic segments (dyskinesia, bulging) during systole and excitation of mechanical receptors by passive stretching, and probably a combination of a) and b): the release of chemical substances sensitizes mechanical receptors and lowers their threshold for nociceptive stimuli. These can be suppressed at various spinal or supraspinal levels.

Afferent Pathways↗
PubMed2003

Development of the cardiac conduction system as delineated by minK-lacZ.

INTRODUCTION: Due to the lack of good molecular markers, for decades the morphogenetic origin of the cardiac conduction system has been a matter of debate. More recently, the spatial expression of minK-lacZ in the adult mouse heart has been shown, for the larger part, to be coincident with the conduction tissues. METHODS AND RESULTS: To trace the embryonic development of this system, we performed an analysis of the expression of this construct throughout early cardiac development. Expression was first seen at the eighth embryonic day. Subsequently, discrete rings were found at the sinuatrial, atrioventricular, interventricular, and ventriculoarterial junctions. With time, the expression became restricted to boundary regions of the heart, such as the hinges of the leaflets of the pulmonary and aortic valves, the atrioventricular rings, and the venous valves, as well as becoming incorporated into the definitive conduction tissues themselves. In the postnatal heart, the areas retaining minK-lacZ positivity outside of the definitive conduction tissues are known to be the site of origin of abnormal cardiac rhythms, suggesting that ectopic foci may derive from tissues that share a common developmental pathway with the definitive conduction system. CONCLUSION: Our findings suggest that the boundary regions between compartments, along with the atrioventricular conduction axis, share a common developmental pathway.

Animals↗
PubMed2006

Deletion of angiotensin-converting enzyme 2 accelerates pressure overload-induced cardiac dysfunction by increasing local angiotensin II.

Angiotensin-converting enzyme 2 (ACE2) is a carboxypeptidase that cleaves angiotensin II to angiotensin 1-7. Recently, it was reported that mice lacking ACE2 (ACE2(-/y) mice) exhibited reduced cardiac contractility. Because mechanical pressure overload activates the cardiac renin-angiotensin system, we used ACE2(-/y) mice to analyze the role of ACE2 in the response to pressure overload. Twelve-week-old ACE2(-/y) mice and wild-type (WT) mice received transverse aortic constriction (TAC) or sham operation. Sham-operated ACE2(-/y) mice exhibited normal cardiac function and had morphologically normal hearts. In response to TAC, ACE2(-/y) mice developed cardiac hypertrophy and dilatation. Furthermore, their hearts displayed decreased cardiac contractility and increased fetal cardiac gene induction, compared with WT mice. In response to chronic pressure overload, ACE2(-/y) mice developed pulmonary congestion and increased incidence of cardiac death compared with WT mice. On a biochemical level, cardiac angiotensin II concentration and activity of mitogen-activated protein (MAP) kinases were markedly increased in ACE2(-/y) mice in response to TAC. Administration of candesartan, an AT1 subtype angiotensin receptor blocker, attenuated the hypertrophic response and suppressed the activation of MAP kinases in ACE2(-/y) mice. Activation of MAP kinases in response to angiotensin II was greater in cardiomyocytes isolated from ACE2(-/y) mice than in those isolated from WT mice. ACE2 plays an important role in dampening the hypertrophic response to pressure overload mediated by angiotensin II. Disruption of this regulatory function may accelerate cardiac hypertrophy and shorten the transition period from compensated hypertrophy to cardiac failure.

Angiotensin II↗
PubMed1995

[The cost-benefit of cardiac rehabilitation programs].

In the past 20 years there has been a steady improvement in the short-term prognosis of patients with myocardial infarction, following the introduction of beta blockers, thrombolysis, and aspirin. Cardiac rehabilitation and secondary prevention also has contributed to this improvement. However, the development cardiac rehabilitation is limited and not fully developed in Europe. Multiple reasons are related to the underuse of rehabilitation, between then the increase of economical cost associated rehabilitation services. The participation in comprehensive cardiac rehabilitation show and lower cardiac rehospitalization costs. Also, earlier return to work and less pension cost in patients included in cardiac rehabilitation. Several studies had confirmed rehabilitation programs are more cost-effective, in QALYs terms, that some drugs. Then, cardiac rehabilitation is an efficient health-care resource, and may be economically justified.

Cost-Benefit Analysis↗
PubMed2006

Diagnostic value of chest X-ray and echocardiography for cardiac tamponade in post cardiac surgery patients.

OBJECTIVE: To investigate the effectiveness of X-ray and echocardiography (ECHO) as a diagnostic tool for cardiac tamponade in adult cardiac surgery patients. METHODS: Thirty five coronary artery bypass and graft surgery patients who developed cardiac tamponade at Cleveland clinic foundation, were included in this study. Their diagnosis was confirmed at the time of re-exploration in the operating room. These patients were followed retrospectively for demographics, X-ray and echocardiography findings. Abnormal and enlarged cardiac silhouette which was different from first postoperative X-ray was used as radiological criteria for tamponade while echocardiographic diagnosis was left to the discretion of cardiologist. RESULTS: Twenty four males (69%) and 11 (31%) females with an average age of 60.7 +/- 15.2 years were included in this study. Only 7 (20%) patients met our criteria for radiological diagnosis of tamponade. All 35 patients showed pericardial effusion on ECHO while cardiac tamponade was present in 30 (86%) patients. Tamponade developed on an average on 4th postoperative day. CONCLUSION: Radiological diagnosis of cardiac tamponade based on changes in cardiac silhouette provide limited information while ECHO is a reliable diagnostic tool when combined with clinical findings.

Cardiac Tamponade↗
PubMed1998

Cardiac arrhythmias with external fixed-rate signal generators in shock wave lithotripsy with the Medstone lithotripter.

OBJECTIVES: To evaluate the incidence and outcome of cardiac arrhythmias associated with an external fixed-rate generator and the Medstone lithotripter with regard to stone location, anesthesia type, patient age, and gender. METHODS: Data were obtained on 933 patients who underwent shock wave lithotripsy (SWL) with the Medstone lithotripter. Patients were randomly divided into two study groups, including those with pre-existing cardiac disease, hypertension, and cardiac medications. Group 1 (576 patients) were treated with the external fixed-rate signal generator (cardiac simulator). Group 2 (357 patients) underwent electrocardiogram-gated SWL (no simulator). All patients were monitored for arrhythmias during SWL. Patients who developed arrhythmias on the simulator were converted to gated SWL. RESULTS: In group 1, 463 patients (80%) had no arrhythmias during treatment, whereas 113 patients (20%) developed cardiac arrhythmias (primarily premature ventricular contractions [PVCs]) and were successfully converted to gated SWL. Only 1 patient in group 2 (0.3%) had a documented arrhythmia (PVC). Group 1 patients who developed arrhythmias with a cardiac simulator were more likely to have renal rather than ureteral stones. Chi-square analysis showed a significant correlation between patients with and without arrhythmias in group 1 with regard to stone location (P <0.0001). In group 1, regional anesthesia, intravenous anesthesia, and general anesthesia had an arrhythmia rate of 14%, 27%, and 38%, respectively. The only patient in group 2 who developed arrhythmias was under general anesthesia. The differences between groups 1 and 2, with regard to anesthesia type and arrhythmia, were statistically significant (P <0.001). No patients required additional medical therapy or hospitalization for cardiac events, and all patients safely completed the SWL treatment. CONCLUSIONS: With careful monitoring and adequate precautions, external fixed-rate signal generators are safe, effective methods for pacing the Medstone shock wave lithotripter and probably other extracorporeal shock wave lithotripters.

Arrhythmias, Cardiac↗
PubMed1991

In vitro clonal analysis of quail cardiac neural crest development.

The developmental potentials of cardiac neural crest cells were investigated by in vitro clonal analysis. Five morphologically distinct types of clones were observed: (1) "pigmented" clones contained melanocytes only; (2) "mixed" clones consisted of pigmented and unpigmented cells; (3) "unpigmented dense" clones consisted of flattened, closely aligned unpigmented cells; (4) "unpigmented loose" clones consisted of a few loosely arranged, flattened cells; and (5) "unpigmented large" clones included a large number of small, stellate cells that were highly proliferative. The binding patterns of antibodies against lineage-specific markers showed that cells in the different clones expressed characteristic phenotypes. The following phenotypes were expressed in addition to pigment cells: smooth muscle cells, connective tissue cells, chondrocytes, and cells in the sensory neuron lineage. Mixed clones expressed all five phenotypes. Unpigmented dense clones contained smooth muscle cells, connective tissue cells, chondrocytes, and sensory neurons. Unpigmented loose clones exclusively consisted of smooth muscle cells, whereas unpigmented large clones contained chondrocytes and sensory neuron precursors. Based on these results, the following conclusions can be drawn: (1) Pigmented and unpigmented loose clones are most likely formed by precursors that are committed to the melanogenic and myogenic cell lineages, respectively. (2) Mixed and unpigmented dense clones are derived from pluripotent cells with the capacity to give rise to four or five phenotypes. (3) Unpigmented large clones originate from progenitor cells that appear to have a partially restricted developmental potential, that is, these cells are capable of generating two phenotypes in clonal cultures. Thus, the data indicate that the early migratory cardiac neural crest is a heterogeneous population of cells, consisting of pluripotent cells, cells with a partially restricted developmental potential, and cells committed to a particular cell lineage.

Animals↗
PubMed1983

Cardiac metastases from osteosarcoma. A report of two cases.

Two children who developed cardiac metastases from osteogenic sarcoma are described, and the value of computed tomography in making an antemortem diagnosis is illustrated. Computed tomographic images with a narrow window width will reveal the presence of calcification within the cardiac metastases. Images in this mode should always be studied in patients with osteogenic sarcoma who are undergoing chest computed tomography scans to detect pulmonary metastases.

Adolescent↗
PubMed2002

Identification and characterization of two novel zinc finger genes, ZNF359 and ZFP28, in human development.

Transcription factors play an essential role in controlling gene expression during cardiac and vascular pathogeneses. Identification of regulatory genes in the cardiovascular system is a necessary step toward an understanding of the pathogenesis of congenital heart disease and acquired cardiovascular diseases. The Cys2/His2 type zinc finger genes are the single largest class of transcription factors in the human genome and many numbers of these krüpple-like zinc finger genes have been found to be involved in cardiac development or cardiovascular diseases. In this study, we have identified two novel human krüpple-like zinc finger genes named ZNF359 and ZFP28 from the human heart cDNA library. The complete human ZNF359 cDNA sequence is 3270bp and contains a 1932-bp open reading frame (ORF) that encodes a 643 amino acid protein with an N-terminal KRAB domain and 16 C-terminus zinc finger C2H2 motifs. The ZFP28 cDNA sequence is 4104bp and contains a 2076-bp ORF that encodes an 868 amino acid protein with an N-terminal signal peptide, two KRAB domains, and 14 C-terminal C2H2 zinc finger motifs. Northern blot analyses showed a strong expression of ZNF359 and ZFP28 in various tissues of adult human. A further analysis using human embryonic tissues (18-23 weeks) showed a development-specific expression pattern in heart, skeletal muscle, liver, lung, kidney, and brain, suggesting a role for these genes in embryonic development.

Amino Acid Motifs↗
PubMed1992

Post-cardiac surgery tamponade mimicking acute hepatitis. Report of two cases.

Two patients developed cardiac tamponade from delayed hemorrhage into the pericardial sac following open heart surgery. The initial clinical manifestations of tamponade included nausea and dramatic elevations of serum aminotransferases, simulating acute hepatitis. To our knowledge, this presentation of cardiac tamponade has not been previously reported.

Acute Disease↗
PubMed1996

[Emergency percutaneous cardiopulmonary support for patients with cardiac arrest or severe cardiogenic shock].

A total of 20 patients who developed cardiac arrest or severe cardiogenic shock were resuscitated with percutaneous cardiopulmonary support system (PCPS). The etiology of shock was acute myocardial infarction (n = 8), post-infarction left ventricular (LV) free wall rupture (n = 9) and others (n = 3). After successful resuscitation with PCPS, 17 patients underwent therapeutic interventions: either closure of an LV rupture (n = 9), coronary artery bypass grafting (n = 4), percutaneous transluminal angioplasty (n = 1) and percutaneous transluminal coronary recanalization (n = 1). Of the 20 patients, 17 were weaned from PCPS or standard cardiopulmonary bypass. Nine patients survived longer than 30 days and 6 patients were discharged from the hospital. In nine patients with LV free wall rupture, one could be discharged from the hospital. Even though our experience is still small in number, it can be concluded that cardiopulmonary resuscitation using PCPS improves survival in fatally ill patients.

Adolescent↗
PubMed1990

Cardiac tumors and dysrhythmias in transgenic mice.

Transgenic mice expressing atrial natriuretic factor-SV40 T-antigen fusion genes (ANF-TAG) developed cardiac tumors asymmetrically in the right atrium. Features associated with cardiac failure, including increased plasma creatine kinase activity (MM and MB) and ventricular dysrhythmias, also were associated with atrial tumor growth. These atrial tumors were able to grow at histocompatible sites (subcutaneously in syngeneic animals) for protracted periods of time yielding a series of transplantable atrial tumor lineages. The transplantable tumors displayed several cardiac-specific characteristics, such as endogenous electrical activity and expression of cardiac-specific proteins. These transplantable atrial tumors constitute a novel experimental resource for developing cell lines which display an adult cardiac phenotype.

Animals↗