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PubMed1999

p57Kip2 expression is enhanced during mid-cardiac murine development and is restricted to trabecular myocardium.

During embryonic development the heart is required to grow in size and cell number, undergo complex morphologic alterations, and function to circulate the blood. Between embryonic d 10.5 (E10.5) and E11.5, cardiac myocytes undergo rapid cell division, resulting in doubling of cardiac mass, while metabolic requirements are increased and contraction force is enhanced. Accelerated cardiomyocyte differentiation is accompanied by a significant increase in trabeculation of ventricular myocardium. Many single gene mutations in the mouse result in a "thinned myocardium" and embryonic lethality between E10.5 and E13.5 secondary to heart failure. This is the case in the Splotch mouse in which a mutation of the Pax3 gene results in neural crest and cardiac defects. Nevertheless, the molecular events governing these important developmental steps remain largely unknown. Here, we describe the use of suppression subtractive hybridization to identify mRNA transcripts whose expression is enhanced during this critical period in normal hearts. These genes encode functions related to maturation of the contractile apparatus, cardiomyocyte differentiation, altered cellular metabolism, and transcriptional regulation. One of the genes that we identified, p57Kip2, encodes a cyclin-dependent kinase inhibitor of the p21 family. We show that p57Kip2 is normally expressed in the inner trabecular layer of the developing heart. In Splotch embryos, expression of p57Kip2 is expanded to encompass the entire thickness of the myocardium. This result and further structural analysis suggests that the myocardial defect of Splotch embryos is associated with precocious cardiomyocyte differentiation.

Amino Acid Sequence↗
PubMed1995

Neonatal hypertension and cardiac failure.

Two newborn infants developed cardiac failure due to severe hypertension which was recognised as the heart failure was treated. Renal abnormalities were found in both infants who are normotensive off treatment at 18 months follow up. The finding of hypertension rather than hypotension in the presence of cardiac failure and the apparent absence of a cardiac abnormality should prompt a search for a renal or renovascular cause.

Female↗
PubMed1990

Cardiac hypertrophy developing during DOCA-salt treatment is dissociated from systemic and regional hemodynamics.

Systemic and regional hemodynamics were studied in DOCA-treated Sabra hypertensive (SBH) and normotensive (SBN) rats. In SBH rats, mean arterial pressure (MAP) and total peripheral resistance index (TPRI) increased significantly. In SBN rats, MAP remained stable and TPRI decreased. Cardiac output and heart rate were unchanged. Opposed changes in TPRI were mediated mainly by changes in vascular resistance of the skin, skeletal muscles and splanchnic organs. Both strains developed significant biventricular hypertrophy. We conclude that SBH and SBN rats' susceptibility or resistance to DOCA-salt hypertension are associated with opposed changes in TPRI. The development of biventricular hypertrophy is apparently dissociated from systemic hemodynamic changes.

Animals↗
PubMed2002

The challenges of developing a modern cardiac research program.

The development of a cardiac research program in the current health care setting can bring many challenges. The myriad of changing regulations involving research with vulnerable populations combined with the need to protect patient confidentiality is an issue that must be addressed in the initial stages of development. Also, the lack of an experienced workforce can often make the search for research staffing difficult at best. In 2001, Children's Healthcare of Atlanta initiated a cardiac research program. Over the last year, many obstacles have been overcome, and this experience has led to the appreciation of the challenges ahead.

Biomedical Research↗
PubMedDate not supplied

Heart size in inbred strains of rats. Part 2. Cardiovascular DNA and RNA contents during the development of cardiac enlargement in rats.

Enlargement and nucleic acid content of the cardiovascular system of several strains (SHRSP/N, SHR/N, OM/N, M520/N) of rats were compared with the WKY/N strain in an attempt to characterize cardiac enlargement. Cardiac enlargement in rats can be due to either hypertrophy (increase in myocyte size), hyperplasia (increase in cell number including supporting tissue), or a combination of both. The sum of the indices of the degree of hypertrophy and hyperplasia calculated from the difference of the heart and aorta deoxyribonucleic acid (DNA) concentration and total DNA content between each strain and the WKY/N was almost equal to the degree of heart and aorta enlargement. The SHRSP/N revealed a striking hypertrophy of myocardial cells from the prehypertensive stage, and hyperplasia appeared gradually with the elevation of blood pressure. In contrast, the SHR/N developed a marked hyperplasia with some hypertrophy at the prehypertensive stage. Cardiac enlargement of the OM/N was attributed to both hypertrophy and hyperplasia. A large heart weight of the M520/N was recognized at only a young age, and was due almost entirely to hyperplasia. Aortic enlargements were related to hyperplasia. An increased ribonucleic acid (RNA) concentration was observed in both ventricles of the SHRSP/N, SHR/N, and M520/N rats at 4 weeks of age, and in all of the four strains at 16 weeks of age. A significantly higher RNA concentration was indicated in the aorta of three hypertensive strains of SHRSP/N, SHR/N, and OM/N at established hypertensive stage. These changes might be related to manifestations of genetic or other factors such as the effect of elevated blood pressure.

Animals↗
PubMed2003

Cardiac developmental onomatology: the real heart of the matter.

There has been much controversy regarding Cardiac Embryology since the 19th Century; this has brought up contradictions over many studies on Cardiac Development, and stems mainly from semantic differences rather than from scientific observations. In 1998, FCAT published the 1st Edition of Terminologia Anatomica, which did not include Terminologia Embryologica, and to this day, we do not have a thorough compilation of Terminology related to Cardiac Development (O'Rahilly and Müller 1996). In the present study we have reviewed the literature from the 19th and 20th Centuries gathering the terms proposed by those scientists who influenced Prenatal Cardiac Terminology. Our aim is to bring to the attention of clinicians and researchers of cardiac morphogenesis the need to undertake a reform of the Developmental Cardiac Terminology. We believe an International Consensus on the terminology to be used during the developmental stages is urgent; it should be meaningful both to the experimental embryologist and to the cardiologist, without being ambiguous or controversial. We must not forget that a terminology is of value only when it is properly used.

Anatomy↗
PubMed2004

[Suicidal fatal beta-blocker intoxication].

We report on the case of a 45-year-old female with beta receptor antagonist intoxication after swallowing about 30 tablets of Cordanum (Talinolol) with suicidal intent. The out of hospital and clinical management is discussed. Prior to admission to hospital the patient only showed a few signs of intoxication such as hypotension, central symptoms and cyanosis. There was no bradycardia but during treatment she developed cardiac arrest. Out of hospital it was possible to stabilise the circulation with catecholamines (norepinephrin) and the transport to hospital was uneventful but only a few minutes after hospital admission the patient developed cardiac arrest. After initially successful CPR the patient died some hours later in the intensive care unit.

Adrenergic alpha-Agonists↗
PubMed2000

MesP1 and MesP2 are essential for the development of cardiac mesoderm.

The transcription factors, MesP1 and MesP2, sharing an almost identical bHLH motif, have an overlapping expression pattern during gastrulation and somitogenesis. Inactivation of the Mesp1 gene results in abnormal heart morphogenesis due to defective migration of heart precursor cells, but somitogenesis is not disrupted because of normal expression of the Mesp2 gene. To understand the cooperative functions of MesP1 and MesP2, either a deletion or sequential gene targeting strategy was employed to inactivate both genes. The double-knockout (dKO) embryos died around 9.5 days postcoitum (dpc) without developing any posterior structures such as heart, somites or gut. The major defect in this double-knockout embryo was the apparent lack of any mesodermal layer between the endoderm and ectoderm. The abnormal accumulation of cells in the primitive streak indicates a defect in the migratory activity of mesodermal cells. Molecular markers employed to characterize the phenotype revealed a lack of the cranio-cardiac and paraxial mesoderm. However, the axial mesoderm, as indicated by brachyury (T) expression, was initially generated but anterior extension was halted after 8.5 dpc. Interestingly, a headfold-like structure developed with right anterior-posterior polarity; however, the embryos lacked any posterior neural properties. The persistent and widely distributed expression of Cerberus-like-1(Cer1), Lim1 and Otx2 in the anterior endoderm might be responsible for the maintenance of anterior neural marker expression. We also performed a chimera analysis to further study the functions of MesP1 and MesP2 in the development of mesodermal derivatives. In the chimeric embryos, dKO cells were scarcely observed in the anterior-cephalic and heart mesoderm, but they did contribute to the formation of the somites, notochord and gut. These results strongly indicate that the defect in the cranial-cardiac mesoderm is cell-autonomous, whereas the defect in the paraxial mesoderm is a non-cell-autonomous secondary consequence.

Animals↗
PubMed2006

A tyrosine-rich domain within homeodomain transcription factor Nkx2-5 is an essential element in the early cardiac transcriptional regulatory machinery.

Homeodomain factor Nkx2-5 is a central component of the transcription factor network that guides cardiac development; in humans, mutations in NKX2.5 lead to congenital heart disease (CHD). We have genetically defined a novel conserved tyrosine-rich domain (YRD) within Nkx2-5 that has co-evolved with its homeodomain. Mutation of the YRD did not affect DNA binding and only slightly diminished transcriptional activity of Nkx2-5 in a context-specific manner in vitro. However, the YRD was absolutely essential for the function of Nkx2-5 in cardiogenesis during ES cell differentiation and in the developing embryo. Furthermore, heterozygous mutation of all nine tyrosines to alanine created an allele with a strong dominant-negative-like activity in vivo: ES cell<-->embryo chimaeras bearing the heterozygous mutation died before term with cardiac malformations similar to the more severe anomalies seen in NKX2.5 mutant families. These studies suggest a functional interdependence between the NK2 class homeodomain and YRD in cardiac development and evolution, and establish a new model for analysis of Nkx2-5 function in CHD.

Amino Acid Sequence↗
PubMed1998

Relevance of delayed hospital admission on development of cardiac rupture during acute myocardial infarction: study in 225 patients with free wall, septal or papillary muscle rupture.

OBJECTIVES: We analyzed the possible relation between the presence of a hospital admission delay (> or =24 h), undue physical effort or recurrence of anginal pain, alone or in combination, with the development of free wall rupture (FWR), septal rupture (SR) or papillary muscle rupture (PMR) in patients with an acute myocardial infarction (AMI). BACKGROUND: Physical activity as a trigger of FWR in AMI remains controversial, and its contribution to SR or PMR remains unknown. Moreover, the role of ischemia or reinfarction as an additional cause of rupture has not been explored. METHODS: The incidence of hospital admission delay > or =24 h with maintenance of some ambulatory activity and the incidence of postinfarction angina were analyzed in consecutive patients with a first AMI with (n = 225) or without rupture (n = 1,012 [control group]) over different time periods. RESULTS: An admission delay > or =24 h occurred in 27 (27.6%) of 98 patients with FWR, 47 (47.0%) of 100 with SR and 14 (51.9%) of 27 with PMR but in only 81 (8%) of 1,012 control patients (p < 0.0001). Information on undue in-hospital effort preceding rupture was available for 111 patients and was present in 17 (32.7%) of 52 with FWR, 9 (18.4%) of 49 with SR and 3 (30%) of 10 with PMR versus only 76 (7.5%) of 1,012 control patients (p < 0.001). Information on postinfarction anginal pain was available for 114 patients with rupture and occurred in 30 (56.6%) of 53 with FWR, 30 (60%) of 50 with SR and 4 (36.4%) of 11 with PMR versus 120 (11.9%) of 1,012 control patients (p < 0.0001). Mean age and incidence of male gender, hypertension, absence of heart failure, single-vessel disease or occlusion of the infarct-related artery were comparable among the groups with FWR, SR or PMR. CONCLUSIONS: Delayed hospital admission or undue in-hospital physical activity appears to increase the risk of rupture in patients prone to this complication (i.e., a first transmural AMI, absence of overt heart failure and advanced age); recurrence of ischemia/infarction emerges as a potential additional trigger in a proportion of these patients.

Age Factors↗
PubMed2003

Gap junctional connexins in the developing mouse cardiac conduction system.

Gap junctional channels which couple myocytes mediate conduction phenomena in the heart. These channels are dodecamers of transmembrane proteins belonging to the connexin family (Cx). Three Cxs, Cx43, -40 and -45, have been found to be expressed in cardiomyocytes. Each of them has a distinct spatiotemporal pattern of expression, which is regulated during development. In the adult mouse heart, Cx43 is expressed in all the working myocytes and most of the conductive myocytes; Cx45 is weakly expressed in all conductive myocytes, including those of the nodal tissues; Cx40 expression is restricted to the atria and ventricular conduction system. Analysis of mice with deletions of Cx genes has provided evidence that Cx43, -40 and -45, and consequently the gap junctional channels they form, are involved in both heart function and development. For example, Cx40 deficiency results in sinoatrial conduction impairments, a significant decrease of the conduction velocity in the atria, and a delay of the propagation of impulse in the His bundle. Transgenic mouse lines with modified Cx40 genes are now being used to draw up a detailed map of the conduction system in the adult and developing heart, and to identify the regulatory elements involved in the transcriptional regulation of the Cx40 gene. Some preliminary results of these studies are described.

Animals↗
PubMed2006

Cardiac valvulopathy associated with pergolide use.

OBJECTIVE: To review the risk of pergolide associated cardiac valvulopathy in patients with Parkinson's disease. DATA SOURCES: MEDLINE, Embase, and the Cochrane Library. Reference lists were reviewed and librarians were consulted to identify additional trials. STUDY SELECTION: All studies and case reports in the English literature on pergolide and cardiac valvulopathy. DATA EXTRACTION: Demographics of patients, study duration, dose and duration of pergolide use, echocardiogram results, length of follow-up, and clinical outcome. RESULTS: Twenty-two published articles were identified. There were no randomized controlled trials. Follow-up time varied between a few months and four years. Three case reports and four studies (three case control and one observational) assessed 246 patients. Evidence for valvulopathy was found in all studies. Variable methods were used to assess the degree of valvular regurgitation making comparisons between studies difficult. Little clinical correlation is available for echocardiogram results. Variable improvement was shown in the few patients in whom the drug was stopped. There is insufficient data to determine whether dose and duration or other comorbities have an effect on the risk of developing cardiac valvulopathy. CONCLUSION: Pergolide therapy is associated with an increased risk of developing cardiac valvulopathy but the true incidence and importance of this remains unknown. Further prospective studies are needed with standardized assessments of echocardiograms.

Antiparkinson Agents↗
PubMed1998

Quantification of aortic regurgitant volume by a newly developed automated cardiac flow measurement method: an in vitro study.

BACKGROUND: Quantifying regurgitant volumes is important for treatment of patients with valvular aortic regurgitation. Simple, reliable methods to quantify aortic regurgitation have been sought both in the catheterization laboratory and the echocardiography laboratory. OBJECTIVES: The aim of our study was to investigate the applicability of a new automated cardiac flow measurement method with color Doppler velocity data for quantifying retrograde flow volumes of aortic regurgitation in an ascending aorta model. METHODS AND RESULTS: A 2-chamber pulsatile flow system with a modeled ascending aorta and a regurgitant aortic valve orifice was developed. The model could generate "aortic regurgitation-like" waveforms through the use of an electrically controlled valve. The regurgitant flows through the orifice (8.5 to 28.1 mL/beat) were measured by an ultrasound flowmeter; they were also calculated in the ascending aorta 1.0 cm above the orifice by the automated cardiac flow measurement method, which integrated spatially distributed digital flow velocity data through "diastole." Calculated regurgitant volumes measured with the low color Doppler filter (5.4 cm/s) agreed well with those measured with the flowmeter (r=.99, P < .001, mean difference=2.2+/-3.7 mL). However, the regurgitant volume was underestimated when 2 higher filter settings were used (9.6 and 10.9 cm/s). Although there was no significant difference in mean volume, higher frame rate (19 frames/s) provided more reproducible results with smaller standard deviation as compared with lower frame rate (7 frames/s). CONCLUSIONS: This new automated cardiac flow measurement method appears to be promising for semiautomatic quantification of aortic regurgitant volume. Appropriate choice of filter setting and high frame rate assists reliable data acquisition.

Aorta↗
PubMed1976

Chemical transmission between rat sympathetic neurons and cardiac myocytes developing in microcultures: evidence for cholinergic, adrenergic, and dual-function neurons.

Electrophysiological studies were made on microcultures (300-500 mum in diameter) in which solitary sympathetic principal neurons from newborn rats grew on previously dissociated rat heart cells. Some neurons inhibited,some excited, and others first inhibited and then excited the cardiac myocytes. Application of drugs provided evidence for secretion of acetylcholine by the first group, catecholamines by the second, and both acetylcholine and catecholamines by the third. Solitary neurons which inhibited themyocytes usually excited themselves at nicotinic synapses (autapses).

Acetylcholine↗
PubMed1983

Possible adrenergic effects on heart protein metabolism.

It is known that the heart will adapt to actual demand by increasing or decreasing its size through different mechanisms. In this presentation, the possible role of catecholamines in regulating heart protein synthesis and developing cardiac hypertrophy and cardiomyopathy is discussed. Injecting animals with catecholamines has been found to induce cardiac hypertrophy. In vitro perfusion of rat heart in the presence of catecholamines has been found to induce a time-dependent and dose-dependent stimulation of amino acid transport and incorporation into proteins. Acute haemodynamic effects of catecholamines increase cardiac performance while long-term treatment seems to cause depression of cardiac function, especially during ischaemic conditions. Chronic beta-blockade in patients with primary congestive cardiomyopathy improved both cardiac function and clinical condition in more than half the patients. Furthermore, a beneficial effect on survival was also found, when compared with a matched control group. It is hypothesised that catecholamines may play a role in developing cardiac hypertrophy as well as congestive cardiomyopathy.

Adrenergic beta-Antagonists↗
PubMed1998

Expression of vascular endothelial growth factor during the development of cardiac hypertrophy in spontaneously hypertensive rats.

Left ventricular hypertrophy (LVH) is often associated with an impaired maximal coronary blood flow and increases the vulnerability of the heart tissue to ischaemia. In this study, the correlation between coronary blood flow and expression of the vascular endothelial growth factor (VEGF) mRNA was investigated. Using both haemodynamic measurements and analysis of mRNA, we have demonstrated that during development of LVH, in spontaneously hypertensive rats (SHR), an impaired maximal coronary flow at 12 weeks of age is associated with low levels of VEGF mRNA. However, in older SHR (32 weeks) with stabilised hypertrophy and a normal maximal coronary flow response, VEGF mRNA levels are increased 3-fold. These results suggest that the mechanism for the impaired flow, observed in some types of cardiac hypertrophy, might involve an inadequate growth of the coronary vessels due to insufficient activation of the VEGF gene.

Animals↗