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At least 991 records · Page 55Linked to original sources
PubMed2000

Physiological induction of a beta-adrenergic receptor kinase inhibitor transgene preserves ss-adrenergic responsiveness in pressure-overload cardiac hypertrophy.

BACKGROUND: Transgenic mice with constitutive myocardium-targeted expression of a peptide inhibitor of the ss-adrenergic receptor kinase (ssARKct) have increased in vivo cardiac function and enhanced ss-adrenergic receptor (ssAR) responsiveness. METHODS AND RESULTS: In the present study, we created transgenic mice with myocardium-targeted ssARKct transgene expression under control of the CARP (cardiac ankyrin repeat protein) promoter, which is active during cardiac development and inactive in the normal adult mouse heart. Consistent with this, adult CARP-ssARKct transgenic mice have normal in vivo cardiac contractility and ssAR responsiveness indistinguishable from their nontransgenic littermates (NLCs). However, because CARP is in a group of fetal genes activated in the adult ventricle during hypertrophy, we subjected animals to transverse aortic constriction (TAC) to induce pressure overload. Seven days after TAC, CARP-ssARKct hearts had elevations in left ventricular mass similar to those in NLCs; however, TAC did induce demonstrable ssARKct expression in the transgenic hearts. TAC in NLC mice resulted in an upregulation of myocardial ssARK1 and a loss of ssAR-mediated inotropic reserve. Importantly, although ssARK1 was increased in the hypertrophic CARP-ssARKct mice, the in vivo loss of ssAR responsiveness was not seen after induced ssARKct expression. CONCLUSIONS: These results demonstrate that acute ssARK1 inhibition can restore lost myocardial ssAR responsiveness and inotropic reserve in vivo. Furthermore, these mice demonstrate the novel utility of the CARP promoter as an inducible element responsive to pathophysiological conditions in the adult heart.

Animals↗
PubMed1985

Ventricular trabeculations in the chick embryo heart and their contribution to ventricular and muscular septal development.

Sixty-two chick embryo hearts were studied at incremental stages of development (Hamburger-Hamilton stages 16 to 39) by scanning electron microscopy following 3% glutaraldehyde fixation and critical point drying. Early in cardiac development, the primitive ventricle becomes homogeneously trabeculated with highly organized sheets of myocytes lined by endocardial cells, with the trabeculae generally oriented in the dorsoventral direction. Coalescence of these trabecular sheets begins at stage 26, initially at the area of the bulboventricular flange, and later proceeding caudally toward the floor of the ventricle. The fusion process is finished by stage 30, resulting in a muscular ventricular septum that has now divided the primitive ventricle into right and left ventricles. Further growth of the ventricular septum is by continued fusion of the adjoining trabecular sheets. Remnants of the apposing trabecular sheets are found in the solidified muscular septum in the form of endocardial channels. We suggest that persistent patency of these channels results in muscular ventricular septal defects.

Animals↗
PubMed2006

Role of p90 ribosomal S6 kinase-mediated prorenin-converting enzyme in ischemic and diabetic myocardium.

BACKGROUND: Epidemiological data strongly indicate that diabetes increases the incidence of heart failure. Although the benefit of angiotensin-converting enzyme inhibitor (ACE-I) treatment during and after myocardial infarction has been found to be greater in diabetics than nondiabetics and activation of the renin-angiotensin system (RAS) has been implicated, the molecular basis of these actions remains unclear. METHODS AND RESULTS: We generated transgenic mice with cardiac-specific overexpression of wild-type p90 ribosomal S6 kinase (WT-p90RSK-Tg) and a dominant-negative form of p90RSK (DN-p90RSK-Tg). Recovery of cardiac function after ischemia/reperfusion in WT-p90RSK-Tg isolated mouse hearts was significantly impaired. Matrix-assisted laser desorption/ionization time-of-flight mass spectrometry revealed specific induction of prorenin-converting enzyme (PRECE) in WT-p90RSK-Tg mice. mRNA induction of PRECE was confirmed with serial angiotensinogen protein reduction after perfusion in WT-p90RSK-Tg mice, suggesting an increase of angiotensinogen cleavage and subsequent RAS activation in WT-p90RSK-Tg mice. We investigated the role of the RAS in WT-p90RSK-Tg animals after ischemia/reperfusion with the use of an ACE-I (captopril) and an angiotensin II type 1 receptor blocker (olmesartan). We did not observe any effect of these inhibitors in non-Tg littermate controls, thus corroborating other reports in rodents. In contrast, both captopril and olmesartan significantly improved cardiac function and reduced infarct size in WT-p90RSK-Tg mice. At 8 months of age, WT-p90RSK-Tg mice developed cardiac dysfunction. p90RSK activity and PRECE mRNA were both increased by streptozotocin-induced hyperglycemia in non-Tg littermate controls, whereas DN-p90RSK-Tg animals exposed to streptozotocin did not have PRECE induction. CONCLUSIONS: This study demonstrates the critical role of p90RSK in hyperglycemia-mediated myocardial PRECE induction, which may explain the augmentation of the RAS in diabetic hearts and provide an alternative therapeutic approach to treat diabetic cardiomyopathy.

Animals↗
PubMed2002

Natriuretic peptides in the pathogenesis of cardiac dysfunction in the recipient fetus of twin-twin transfusion syndrome.

OBJECTIVE: Although serial amnioreduction has substantially improved the prognosis of twin-twin transfusion syndrome, the majority of recipient twins develop cardiac dysfunction in utero and some have structural abnormalities in the neonatal period. The mechanism of cardiac dysfunction is unclear. To test the hypothesis that this occurs as a result of preload or pressure overload, we determined atrial natriuretic peptide and brain natriuretic peptide levels and their association with endothelin-1 in monochorionic pregnancies with or without chronic twin-twin transfusion syndrome. PATIENTS AND METHODS: Matched maternal and fetal blood samples were obtained in utero from monochorial twin pregnancies complicated with (n = 14) and without twin-twin transfusion syndrome (n = 6). Serial fetal echocardiography assessment included cardiac anatomy, chamber size, cardiothoracic ratio, ventricular thickness, and the presence and severity of atrioventricular valve regurgitation. Postnatal echocardiograms were obtained on the surviving twins. The plasma levels of atrial natriuretic peptide, brain natriuretic peptide, and endothelin-1 were measured by use of radio-immunoassay. RESULTS: Levels of fetal atrial natriuretic peptide (P <.001), brain natriuretic peptide (P <.001), and endothelin-1 (P <.001) in the recipient fetuses were higher than in donor twins. Fetal concentrations of atrial natriuretic peptide, brain natriuretic peptide, and endothelin-1 in the donor twins were similar to those concentrations in twins that did not have twin-twin transfusion syndrome. Fetal brain natriuretic peptide (P <.01) and endothelin-1 (P <.01) levels were significantly higher in the recipient fetuses when compared to those without severe cardiac dysfunction. A significant positive correlation was present between levels of fetal brain natriuretic peptide and endothelin-1 (y = 230.9 LOG(x) - 264.1, r =.82; P <.01). In contrast, there was no association between levels of fetal atrial natriuretic peptide and the severity of cardiac dysfunction, or with levels of fetal brain natriuretic peptide and endothelin-1. CONCLUSION: Fetal natriuretic peptide levels were higher in the recipient twins than the co-twins, and the severity of cardiac dysfunction was related to levels of brain natriuretic peptide. These data, thereby, suggest that brain natriuretic peptide is a sensitive surrogate biochemical marker of cardiac dysfunction in the recipient twin.

Atrial Natriuretic Factor↗
PubMed2004

Early myocardial function affects endocardial cushion development in zebrafish.

Function of the heart begins long before its formation is complete. Analyses in mouse and zebrafish have shown that myocardial function is not required for early steps of organogenesis, such as formation of the heart tube or chamber specification. However, whether myocardial function is required for later steps of cardiac development, such as endocardial cushion (EC) formation, has not been established. Recent technical advances and approaches have provided novel inroads toward the study of organogenesis, allowing us to examine the effects of both genetic and pharmacological perturbations of myocardial function on EC formation in zebrafish. To address whether myocardial function is required for EC formation, we examined silent heart (sih(-/-)) embryos, which lack a heartbeat due to mutation of cardiac troponin T (tnnt2), and observed that atrioventricular (AV) ECs do not form. Likewise, we determined that cushion formation is blocked in cardiofunk (cfk(-/-)) embryos, which exhibit cardiac dilation and no early blood flow. In order to further analyze the heart defects in cfk(-/-) embryos, we positionally cloned cfk and show that it encodes a novel sarcomeric actin expressed in the embryonic myocardium. The Cfk(s11) variant exhibits a change in a universally conserved residue (R177H). We show that in yeast this mutation negatively affects actin polymerization. Because the lack of cushion formation in sih- and cfk-mutant embryos could be due to reduced myocardial function and/or lack of blood flow, we approached this question pharmacologically and provide evidence that reduction in myocardial function is primarily responsible for the defect in cushion development. Our data demonstrate that early myocardial function is required for later steps of organogenesis and suggest that myocardial function, not endothelial shear stress, is the major epigenetic factor controlling late heart development. Based on these observations, we postulate that defects in cardiac morphogenesis may be secondary to mutations affecting early myocardial function, and that, in humans, mutations affecting embryonic myocardial function may be responsible for structural congenital heart disease.

Actins↗
PubMed2006

Mechanisms of cardiac fibrosis induced by urokinase plasminogen activator.

Human hearts with end-stage failure and fibrosis have macrophage accumulation and elevated plasminogen activator activity. However, the mechanisms that link macrophage accumulation and plasminogen activator activity with cardiac fibrosis are unclear. We previously reported that mice with macrophage-targeted overexpression of urokinase plasminogen activator (SR-uPA+/o mice) develop cardiac macrophage accumulation by 5 weeks of age and cardiac fibrosis by 15 weeks. We used SR-uPA+/o mice to investigate mechanisms through which macrophage-expressed uPA causes cardiac macrophage accumulation and fibrosis. We hypothesized that: 1) macrophage accumulation and cardiac fibrosis in SR-uPA+/o mice are dependent on localization of uPA by the uPA receptor (uPAR); 2) activation of plasminogen by uPA and subsequent activation of transforming growth factor-beta1 (TGF-beta1) and matrix metalloproteinase (MMP)-2 and -9 by plasmin are critical pathways through which uPA-expressing macrophages accumulate in the heart and cause fibrosis; and 3) uPA-induced cardiac fibrosis can be attenuated by treatment with verapamil. To test these hypotheses, we bred the SR-uPA+/o transgene into mice deficient in either uPAR or plasminogen and measured cardiac macrophage accumulation and fibrosis. We also measured cardiac TGF-beta1 protein (total and active), Smad2 phosphorylation, and MMP activity after the onset of macrophage accumulation but before the onset of cardiac fibrosis. Finally, we treated mice with verapamil. Our studies revealed that plasminogen is necessary for uPA-induced cardiac fibrosis and macrophage accumulation but uPAR is not. We did not detect plasmin-mediated activation of TGF-beta1, MMP-2, or MMP-9 in hearts of SR-uPA+/o mice. However, verapamil treatment significantly attenuated both cardiac fibrosis and macrophage accumulation.

Animals↗
PubMed2005

Managing a fateful alliance: anaemia and cardiovascular outcomes.

Cardiovascular disease (CVD) is a significant complication in chronic kidney disease (CKD) and a major cause of death in dialysis patients. Clinical studies have shown that anaemia is associated with reduced survival in patients with renal disease, heart failure or both. There is also evidence that, even in otherwise healthy individuals, anaemia is independently associated with an increased risk of CVD. The body adapts to anaemia by increasing cardiac output, which may result in cardiac remodelling and progression of left ventricular (LV) growth. Indeed, low haemoglobin (Hb) has been identified as an independent risk factor for LV growth in CKD patients, suggesting that there is a direct link between anaemia and adverse cardiac outcomes. This suggests that correction of anaemia with recombinant human erythropoietin (rhEPO; epoetin) may improve prognosis. Partial correction of anaemia produces partial regression of LV hypertrophy, while complete correction of anaemia can help to prevent LV dilatation in haemodialysis patients with normal LV volumes. Moreover, in non-dialysis patients with advanced CVD, pilot studies showed that a moderate increase in Hb improved cardiac function and reduced hospitalization rates. In addition, consistent epoetin treatment before the start of dialysis was associated with a reduced risk of developing cardiac disease in CKD patients. In contrast, in dialysis patients with advanced cardiac disease, Hb normalization increased mortality risk. Therefore, early correction of anaemia appears important. The Cardiovascular risk Reduction by Early Anaemia Treatment with Epoetin beta (CREATE) study is investigating whether this approach is associated with a measurable reduction in cardiovascular risk.

Anemia↗
PubMed1992

[Infectious endocarditis in parenteral drug addicts: study of 57 cases].

We present 57 cases of infectious endocarditis (IE) in 51 parenterally drug addicts (PDA) admitted at the Internal Medicine Service of the Hospital Clínico of Valencia between January ist, 1988 and January 15th, 1992. The disease affected young patients, 84% of them being HIV-1+ and 86% presenting CD4+ lymphocytes lower than 200 cells/mm3. Fever was the most constant symptom, with radiological disorders and presence of vegetations by echocardiogram in 65% and 53% of episodes, respectively, and affectation of the tricuspid valve in 59% of patients. The diagnosis of endocarditis was definitive in 51% of cases, possible in 15% and probable in 22%, being cardiac failure the most severe complication, present in 23% of episodes. The detection of significant valve regurgitation in patients with IE and without developing cardiac failure is not predictive of future complications, nor its absence identifies patients with a favourable prognosis. Staphylococcus aureus was the most frequently isolated germ (48%), being methicillin-resistant in 15% of cases and with a slower response to the treatment with vancomycin than the methicillin-sensitive. Five patients died, all of them with CD4+ lower than 50 cells/mm3, which may have a predictive value in the follow-up of these patients.

Adolescent↗
PubMed1977

The effect of propranolol upon chick embryo cardiogenesis.

The teratogenic effects of propranolol HCl on cardiac development were studied in chick embryos of days 3 and 4 of incubation. Propranolol was injected into the yolk sac at doses ranging from 0.05 to 0.6 mg per egg. All the treated and control embryos were examined on day 7. The LD50 for the embryos treated on the 3rd and 4th day was 0.15 and 0.35 mg per embryo, respectively. Cardiac anomalies such as aortic stenosis ventricular septal defects and common truncus arteriosus were observed. Other malformations included atrial septal defects, thin atrial wall and defects of the pulmonic, aortic and atrioventricular valves. The incidence of cardiac anomalies in the controls was very low. Propranolol was observed to slow the heart rate in the experimental embryos. It is suggested that slowing of heart rate at the early stages of heart development caused aberrant bloodstream flow patterns which probably resulted in the genesis of cardiac anomalies. The results of this study indicate that propranolol has teratogenic effects on chick embryo cardiogenesis.

Abnormalities, Drug-Induced↗
PubMed2004

Prevalence and development of additional cardiac abnormalities in 1448 patients with congenital ventricular septal defects.

OBJECTIVE: To determine by modern echocardiographic techniques the prevalence and development of cardiac abnormalities associated with ventricular septal defect (VSD). METHODS: Consecutive patients referred to a tertiary centre for paediatric cardiology and attenders at an adult congenital heart disease clinic had details of clinical outcome prospectively recorded. Patients with VSD in association with conotruncal abnormalities, atrioventricular septal defects, and univentricular heart were not included in the study. RESULTS: 1448 patients with VSD were assessed between 1991 and 1998. 1127 (78%) patients had isolated defects; of these 862 (76%) were perimembranous and 265 (24%) were muscular. Of the remainder, 284 (19.6% of the total population) patients had VSD associated with one other significant cardiac abnormality: 35 (2.4%) with two and two (0.1%) with three other abnormalities. The most common associated cardiac abnormalities were infundibular pulmonary stenosis (5.8%), aortic valve prolapse (3.6%), pulmonary valvar stenosis (2.7%), osteum secundum atrial septal defect (2.2%), persistent ductus arteriosus (1.9%), and coarctation of the aorta (1.5%). In the cohort of 743 patients followed up from birth, cumulative mortality was 4% by the age of 8 years and most deaths occurred within the first year of life in infants with associated genetic abnormalities such as trisomy 13 or 18. Of the 594 patients attending the adult congenital clinic with VSD, aortic regurgitation due to aortic root prolapse developed in 45 (7.6%) patients. Most of these cases were detected before the patient was 30 years old. CONCLUSIONS: In 22% of patients with congenital VSD there were significant associated cardiac abnormalities. Some of these abnormalities, such as aortic prolapse and regurgitation or infundibular pulmonary stenosis, may develop or progress subsequently and therefore should be sought during the initial assessment and monitored during follow up. Follow up to the age of 30 years allows the detection of most cases of aortic regurgitation. The prognosis from VSD is excellent and the risk of endocarditis in a population informed of the need for antibiotic prophylaxis is small.

Adolescent↗
PubMed1979

Cardiac tamponade resulting from pericardial extramedullary hematopoiesis: a case report and review of the literature.

A patient with an unusual myeloproliferative disorder, characterized by hepatosplenomegaly, myelofibrosis, ringed sideroblasts, and conversion to acute myeloblastic leukemia developed cardiac tamponade secondary to pericardia extramedullary hematopoiesis. Diagnostic criteria are discussed. Irradiation and systemic chemotherapy were successful in controlling the effusion.

Adolescent↗
PubMed1996

Expression of the smooth muscle cell calponin gene marks the early cardiac and smooth muscle cell lineages during mouse embryogenesis.

Although several genes are considered markers for vascular smooth muscle cell (SMC) differentiation, few have been rigorously tested for SMC specificity in mammals, particularly during development where considerable overlap exists between different muscle gene programs. Here we describe the temporospatial expression pattern of the SMC calponin gene (formerly h1 or basic calponin) during mouse embryogenesis and in adult mouse tissues and cell lines. Whereas SMC calponin mRNA expression is restricted exclusively to SMCs in adult tissues, during early embryogenesis, SMC calponin transcripts are expressed throughout the developing cardiac tube as well as in differentiating SMCs. Transcription of the SMC calponin gene initiates at two closely juxtaposed sites in the absence of a consensus TATAA or initiator element. Transient transfection assays in cultured SMC demonstrated that high level SMC calponin promoter activity required no more than 549 nucleotides of 5 sequence. In contrast to the strict cell type-specificity of SMC calponin mRNA expression, the SMC calponin promoter showed activity in several cell lines that do not express the endogenous SMC calponin gene. These results demonstrate that SMC calponin responds to cardiac and smooth muscle gene regulatory programs and suggest that the cardiac and smooth muscle cell lineages may share a common gene regulatory program early in embryogenesis, which diverges as the heart matures. The finding that the isolated SMC calponin promoter is active in a wider range of cells than the endogenous SMC calponin gene also suggests that long-range repression or higher order regulatory mechanism(s) are involved in cell-specific regulation of SMC calponin expression.

Animals↗
PubMed2005

Cardiac tamponade due to pneumopericardium.

We describe a newborn with acute respiratory distress syndrome, subjected to mechanical ventilatory assistance with high level of peak inspiratory pressure (PIP) and positive end expiratory pressure (PEEP), who developed cardiac tamponade due to pneumopericardium. Tension pneumopericardium produces the same physiological derangement as cardiac tamponade secondary to accumulated blood or other fluids. This life-threatening complication demands immediate diagnosis and treatment.

Cardiac Tamponade↗
PubMed2006

Identification of differentially expressed genes in human heart with ventricular septal defect using suppression subtractive hybridization.

Ventricular septal defect (VSD) accounts for the largest number of birth congenital heart defects in human, but the genetic programs that control ventricular septation are poorly understood. To identify differentially expressed genes between ventricular septal defect and normal ventricular septum myocardium, we have undertaken suppression subtractive hybridization (SSH) and generated reciprocal cDNA collections of representative mRNAs specific to human heart with ventricular septal defect versus normal control. Following SSH, 1378 clones were sequenced and found to derive from 551 different genes. These predominately expressed genes included genes involved in energy metabolism, cell cycle and growth, cytoskeleton and cell adhesion, LIM protein, zinc finger protein, and development. It is anticipated that further study of genes identified will provide insights into their specific roles in the etiology of VSD, even in cardiac development, aging, and disease.

Adult↗
PubMed2003

Mitochondrial DNA mutations activate the mitochondrial apoptotic pathway and cause dilated cardiomyopathy.

OBJECTIVE: To determine whether low frequency mitochondrial DNA (mtDNA) mutations are pathogenic. METHODS: We studied mice that express a proofreading-deficient mitochondrial DNA polymerase in the heart and develop cardiac mtDNA mutations. RESULTS: At 4 weeks of age, when point mutation levels had risen to on average two per mitochondrial genome, these mice developed severe dilated cardiomyopathy. Interstitial fibrosis first became apparent at 4 weeks of age and progressed with age. Sporadic myocytic death occurred in all regions of the heart, apparently due to apoptosis as assessed by histological analysis and TUNEL staining. The frequency of TUNEL-positive cells peaked at 4-5 weeks of age and then gradually declined. While mitochondrial respiratory function, ultrastructure, and number remained normal, cytochrome c was released from mitochondria, a known apoptotic signal. CONCLUSION: mtDNA mutations therefore are pathogenic, and seem to trigger apoptosis through the mitochondrial pathway.

Animals↗
PubMed2002

Identification, tissue expression and chromosomal localization of human Obscurin-MLCK, a member of the titin and Dbl families of myosin light chain kinases.

Members of the Dbl family of guanine nucleotide exchange factors (GEFs) have important roles in the organization of actin-based cytoskeletal structures of a wide variety of cell types. Through the activation of members of the Rho family of GTP signaling molecules, these exchange factors elicit cytoskeletal alterations that allow cellular remodeling. As important regulators of RhoGTPase activity, members of this family are candidates for mediating the RhoGTPase activation and cytoskeletal changes that occur during cardiac development and during the myocardial response to hypertrophic stimuli. In this study, we characterize a novel human gene that is expressed in skeletal and cardiac muscle and has putative functional domains similar to those found in members of both the Dbl family of GEFs and the titin family of myosin light chain kinases (MLCK). The cDNA sequence of this gene, which has been designated Obscurin-myosin light chain kinase (Obscurin-MLCK), would be predicted to encode for at least 68 immunoglobulin domains, two fibronectin domains, one calcium/calmodulin binding domain, a RhoGTP exchange factor domain, and two serine-threonine kinase domains. The combination of the putative Rho GEF and two kinase domains has not been noted in any other members of the titin or Dbl families. Alternative splicing allows the generation of a number of unique Obscurin-MLCK isoforms that contain various combinations of the functional domains. One group of isoforms is comparable to Unc-89, a Caenorhabditis elegans sarcomere-associated protein, in that they contain a putative RhoGEF domain and multiple immunoglobulin repeats. Other isoforms more closely resemble MLCK, containing one or both of the putative carboxy-terminal serine-threonine kinase domains. The modular nature of the Obscurin-MLCK isoforms indicates that it may have an array of functions important to cardiac and skeletal muscle physiology.

Alternative Splicing↗
PubMed2004

Cardiac adverse effects associated with psychotropic drugs.

Within the drug safety program in psychiatry AMSP ( Arzneimittelsicherheit in der Psychiatrie), severe adverse drug reactions (ADRs) in psychiatric inpatients are assessed in the naturalistic setting of routine treatment. Currently, 35 psychiatric hospitals and departments are participating. This paper focuses on severe cardiovascular ADRs due to psychotropic medications. Related to the number of patients surveyed (122,562 from 1993 to 2000), these are rare events (68 cases or 0.055 %). Imputed drug classes for probable cases were antidepressants in 0.03 % and neuroleptics in 0.019 %, but other drugs were also involved. Within the group of antidepressants, the risk for a cardiac ADR depends much on the class: SSRIs were never imputed alone, but tricyclic antidepressants were imputed alone in 0.05 %. In the group of antipsychotics, the lowest rate of cardiac ADRs was found for the group of phenothiazines (0.003 %). Cardiovascular risk factors elevated the risk for a cardiac ADR from 0.04 % to 0.14 %. Age as an independent factor did not contribute substantially to the risk for a cardiac ADR. The data of the drug safety program in psychiatry allow some estimate of differential risk rates for cardiac ADRs with different psychotropic drug groups. The results of the project can help clinicians select the appropriate drug for patients at risk to develop cardiac ADRs.

Adult↗
PubMed1993

Cardiac rupture during coronary angioplasty.

Cardiac rupture is a catastrophic complication of acute myocardial infarction. We describe a patient with acute myocardial infarction who received thrombolytic therapy and then developed cardiac rupture and tamponade during rescue angioplasty.

Angioplasty, Balloon, Coronary↗