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PubMed2002

Approach to quantify the mechanical behavior of the intact embryonic chick heart.

The heart undergoes remarkable changes during embryonic development due to genetic programing and epigenetic influences such as mechanical loads. An important goal is to develop mathematical models that describe and predict the influence of mechanics on cardiac development, yet the data needed to develop such models remain scant. In particular, prior data from embryonic hearts have come from one-dimensional tests, which reveal well the general characteristic behaviors but are not sufficient for quantifying the complex material behavior exhibited by most soft tissues. We developed a computer-controlled system for quantifying in vitro the multiaxial, regionally dependent mechanical response of the intact embryonic chick heart to controlled distension pressures; such tests have not been accomplished heretofore but promise to contribute to our understanding for they better mimic the native loading conditions and geometry. Calibration of the device indicated that distending the hearts using low flow rates avoids significant viscous losses and thereby allows pressure to be measured directly over small ranges (0-2 mmHg) with good resolution (0.01 mm Hg). Likewise, an on-line video system allows two-dimensional strains to be measured regionally by tracking the motions of triplets of closely spaced (100 microm) microspheres to reasonable resolution (2.5 microm/pixel). Illustrative data from 18 hearts show the utility of the new system, confirm previous findings with regard to the strong viscoelastic response of the stage 18 embryonic chick heart, and provide guidance for the design of future experiments.

Animals↗
PubMed2002

Hypertrophic cardiomyopathy in cardiac myosin binding protein-C knockout mice.

Familial hypertrophic cardiomyopathy (FHC) is an inherited autosomal dominant disease caused by mutations in sarcomeric proteins. Among these, mutations that affect myosin binding protein-C (MyBP-C), an abundant component of the thick filaments, account for 20% to 30% of all mutations linked to FHC. However, the mechanisms by which MyBP-C mutations cause disease and the function of MyBP-C are not well understood. Therefore, to assess deficits due to elimination of MyBP-C, we used gene targeting to produce a knockout mouse that lacks MyBP-C in the heart. Knockout mice were produced by deletion of exons 3 to 10 from the endogenous cardiac (c) MyBP-C gene in murine embryonic stem (ES) cells and subsequent breeding of chimeric founder mice to obtain mice heterozygous (+/-) and homozygous (-/-) for the knockout allele. Wild-type (+/+), cMyBP-C(+/-), and cMyBP-C(-/-) mice were born in accordance with Mendelian inheritance ratios, survived into adulthood, and were fertile. Western blot analyses confirmed that cMyBP-C was absent in hearts of homozygous knockout mice. Whereas cMyBP-C(+/-) mice were indistinguishable from wild-type littermates, cMyBP-C(-/-) mice exhibited significant cardiac hypertrophy. Cardiac function, assessed using 2-dimensionally guided M-mode echocardiography, showed significantly depressed indices of diastolic and systolic function only in cMyBP-C(-/-) mice. Ca2+ sensitivity of tension, measured in single skinned myocytes, was reduced in cMyBP-C(-/-) but not cMyBP-C(+/-) mice. These results establish that cMyBP-C is not essential for cardiac development but that the absence of cMyBP-C results in profound cardiac hypertrophy and impaired contractile function.

Actin Cytoskeleton↗
PubMed1997

Consultation with the specialist. Chest pain in children.

Chest pain is a common complaint among children of all ages. It rarely is due to cardiac disease, but deserves careful evaluation for this possibility, with laboratory tests performed in limited cases. The child who has pain of acute onset that interferes with sleep, is precipitated by exercise, or is associated with dizziness, palpitations, syncope, or shortness of breath should be evaluated with the aid of laboratory tests. This includes at least a chest radiograph and electrocardiogram. Also, pain in the child who has a history of coin ingestion, trauma, previous cardiac disease, or conditions that put him or her at risk for developing cardiac pathology deserve further study. Likewise, those who have a history of conditions such as asthma, Marfan syndrome, or sickle cell disease warrant special consideration. Finally, most of those who have an abnormal physical examination (fever, respiratory distress, abnormal breath sounds, cardiac murmur, abnormal rhythm or heart sounds, palpable subcutaneous air, or obvious trauma) also require a chest radiograph and an electrocardiogram. However, the child who has chronic chest pain normal physical examination with no worrisome history needs reassurance and careful follow-up rather than extensive studies.

Adolescent↗
PubMed1965

THE CHEMOTHERAPY OF CARDIAC ARREST.

Direct-air ventilation, external cardiac compression, and external defibrillation are established techniques for patients who unexpectedly develop cardiac arrest. The proper use of drugs can increase the incidence of successful resuscitation. Intracardiac adrenaline (epinephrine) acts as a powerful stimulant during cardiac standstill and, in addition, converts fine ventricular fibrillation to a coarser type, more responsive to electrical defibrillation. Routine use of intravenous sodium bicarbonate is recommended to combat the severe metabolic acidosis accompanying cardiac arrest. Lidocaine is particularly useful when ventricular fibrillation or ventricular tachycardia tends to recur. Analeptics are contraindicated, since they invariably increase oxygen requirements of already hypoxic cerebral tissues. The following acrostic is a useful mnemonic for recalling the details of the management of cardiac arrest in their proper order: A (Airway), B (Breathing), C (Circulation), D (Diagnosis of underlying cause), E (Epinephrine), F (Fibrillation), G (Glucose intravenously), pH (Sodium bicarbonate), I (Intensive care).

Acidosis↗
PubMed1990

[Hemorrhagic cardiac tamponade without heart rupture during a myocardial infarct. A clinical case].

Cardiac tamponade during acute myocardial infarction is a life-threatening complication that can be confounded with right ventricular infarction. The most frequent cause of this complication is cardiac rupture. We report here a patient with acute myocardial infarction that developed cardiac tamponade on day 7, after receiving late systemic thrombolysis. The diagnosis was suspected with echocardiography and confirmed with hemodynamic measurements. The tamponade was partially relieved with pericardiocentesis but afterwards required emergency surgery. No cardiac rupture was found but an hemorrhagic infarction. We conclude that in this case the hemorrhagic tamponade was probably related both to late thrombolysis and to post infarction pericarditis.

Adult↗
PubMed1982

The development of the atrioventricular bundle and its branches in the avian heart.

A light microscopic study of serial sections of the hearts of 64 avian embryos (chicken, turkey, duck and goose) was undertaken in order to elucidate the development of the atrioventricular bundle and its branches. The developing atrioventricular bundle and its branches were shown to appear simultaneously (at about a third of the way through incubation) as relatively large, discrete fasciculi, which were dark-staining when compared with developing cardiac muscle. Prior to the appearance of the bundle and branches, the developing conducting tissue was found to be present as a widespread precursor tissue, which was distributed as a complete, dark-staining subendocardial sleeve, lining the whole of the ventricular canal, ventriculobulbar loop, and extending into the common atrial cavity. From these observations, it is concluded that, with septation and chamber formation, the tissue of the sleeve is partly incorporated within the chamber walls to give origin to diffuse Purkinje tissue, and is partly retained as the bundle and branches. The manner of derivation of the bundle and branches is discussed, and it is stressed that the definitive positions of the bundle and branches denote the junctional zones of the components of septation.

Animals↗
PubMed1990

Simple, rapid, and effective method of producing aortocaval shunts in the rat.

STUDY OBJECTIVE - The aim of the study was to develop a new procedure to produce abdominal aortocaval shunts in the rat without vascular microsurgery. PROCEDURE - The inferior vena cava and abdominal aorta were exposed by laparotomy. The aorta was punctured caudal to the left renal artery with an 18 gauge disposable needle which was advanced into the vessel, perforating the adjacent wall between aorta and vena cava and penetrating the latter. A bulldog vascular clamp was placed across the aorta cephalic to the puncture, the needle was withdrawn, and the aortic puncture point was sealed with a drop of cyanoacrylate glue. The clamp was removed 30 s later. Patency of the shunt was verified visually by swelling of the vena cava and admixture of arterial and venous blood. No local haemorrhages were seen. The laporatomy was then closed. The procedure takes less than 10 min. RESULTS - Of 11 rats which received this procedure, only one died within 24 h. All the other animals were killed 4 weeks after operation. Nine of these 10 animals had developed cardiac hypertrophy of about the same magnitude. There were no changes in sham operated controls. CONCLUSIONS - This is a reproducible, simple and rapid method of developing high output heart failure and cardiac hypertrophy in the rat which could be useful in many laboratories.

Animals↗
PubMed1994

Cardiac arrhythmia after infusion of cryopreserved stem cells.

A retrospective study of the cardiovascular side-effects of 17 patients during and after receiving unpurged cryopreserved autologous bone marrow and/or peripheral blood stem cells was performed. Fourteen (82%) patients developed cardiac arrhythmia, of which 11 (65%) developed sinus bradycardia, four (24%) second degree heart block and one patient had complete heart block. The onset of sinus bradycardia occurred at 15-513 (median 56) min and the onset of heart block ranged from 30 to 680 (median 234) min after starting the stem cell infusion. Hypertension was noted in seven patients (41%) and usually occurred within 2 hours of infusion. There was no mortality or symptoms associated with these findings. Since some of these arrhythmias could be quite severe as assessed electrophysiologically, continuous cardiac monitoring should be considered during and after the infusion of cryopreserved stem cells.

Adolescent↗
PubMed2006

Atrial and ventricular myosin heavy-chain expression in the developing chicken heart: strengths and limitations of non-radioactive in situ hybridization.

Myosin heavy-chain (MHC) isoforms are major structural components of the contractile apparatus of the heart muscle. Their spatio-temporal patterns of expression have been used as a tool to dissect cardiac development and differentiation. Although extensively investigated, controversy still exists concerning the expression patterns of atrial (AMHC), ventricular (VMHC), and cardiac myosin heavy-chain (CMHC) during development in the heart. In this study, we describe that probe length, probe concentration, and staining time in the non-radioactive in situ hybridization procedure seriously influence the observed pattern of MHC expression and the subsequent interpretation, explaining the divergent opinions in the field. Using a variety of external and internal controls for the in situ hybridization procedure, we demonstrate that both AMHC and VMHC are expressed throughout the entire heart tube during early development. During subsequent development, VMHC becomes restricted to the ventricles, whereas AMHC remains expressed in the atria, and, at substantially lower levels, is detected in the ventricles. These results are discussed in the context of methodological constraints of demonstrating patterns of gene expression. This manuscript contains online supplemental material at http://www.jhc.org. Please visit this article online to view these materials.

Animals↗
PubMedDate not supplied

Sudden cardiac arrest in a neonate with congenital adrenal hyperplasia.

We describe a 6-day-old male who developed cardiac arrest due to hyperkalemia secondary to congenital adrenal hyperplasia and was successfully resuscitated. This case illustrates the importance of considering congenital adrenal hyperplasia as one of the causes of sudden cardiac arrest in a neonate. A literature review revealed only one similar case in a 3-month-old with a fatal outcome.

Adrenal Hyperplasia, Congenital↗
PubMed1992

Benefits and weaknesses of a cardiac rehabilitation programme.

The British Heart Foundation and the Chest, Heart and Stroke Association have allocated funds to develop cardiac rehabilitation programmes. We have recently completed and now evaluate an exercise-based rehabilitation course reinforced with advice about return to normal activity for 110 patients who had suffered acute myocardial infarction. Patients admitted to the Plymouth cardiac care unit were randomised into groups: a control group to receive standard hospital care, and a rehabilitation group who, in addition, received an exercise programme reinforced with advice. Patients were assessed at entry to the study and at intervals thereafter. Assessment was by questionnaire and objective tests consisting of a 12-minute walking test and weekly outpatient pedometry. In the rehabilitation group patients were able to walk further and faster, return to work earlier, undertake more housework, and resume normal sexual activity; they were less short of breath and did not experience more angina. However, the rehabilitation course brought little benefit to the patients' perception of well-being and their anxiety about health or their outlook on life. Exercise and advice are important components of a rehabilitation programme, but more attention needs to be given to the psychological aspects of recovery from a heart attack.

Adult↗
PubMed2000

Programmed cell death in the developing heart: regulation by BMP4 and FGF2.

Programmed cell death, or apoptosis, plays an important role in embryonic development. To provide new insights into the role of programmed cell death in cardiac development, we examined the hearts of the murine embryos from E9.5 to postnatal day 3. Using terminal transferase-mediated dUTP nick end-labeling assays, apoptosis was detected in the endocardial cushions and myocardium from E11.5 to postnatal day 3 (P3). In the ventricular myocardium, more apoptotic cells were observed in the left than right ventricles throughout embryonic and early postnatal development. Apoptosis was also present in the trabeculae and papillary muscles of the ventricles. In the outflow tract, cell death was present in the endocardial cushions before they fuse to form the conotruncal septum (E11.5-E12. 5) and reached a peak intensity when the conotruncal septum formed (E13.5). In the atrioventricular (AV) endocardial cushions, cell death was detected in the fusion seam of the cushion tissues at E12. 5 and E13.5 during AV septation. When the patterns of apoptosis were compared with patterns of cell division, we found that programmed cell death occurred in the areas in the endocardial cushions and trabeculae where rates of cell proliferation were low. We also found that programmed cell death was regulated by the growth factors, BMP4 and FGF2, in vitro. BMP4 induced, whereas FGF2 inhibited, apoptosis in both endocardial cushions and ventricular myocardium. Overall, our observations show that there is apoptosis in the regions where fusion or remodeling of tissues occurs. We also show that cardiac programmed cell death can be influenced by growth factors.

Animals↗
PubMed2002

Angiotensin converting enzyme inhibition decreases cell turnover in the neonatal rat heart.

The renin angiotensin system plays an important role in growth and development. Exposure of the neonate to an ACE inhibitor increases mortality and results in growth retardation and abnormal development. We have demonstrated that ACE inhibition in the developing kidney increases apoptosis and decreases cell proliferation, which may account for renal growth impairment. To evaluate the role of endogenous angiotensin in cardiac development, the relationship between ACE inhibition, cell proliferation, apoptosis, several modulators of apoptosis (bcl-2, bcl-xl, and clusterin) was examined in the developing rat heart. Thirty-five newborn rat pups were treated with enalapril (30 mg/kg/d) or a vehicle (control group) for 7 d, and hearts were removed for rt-PCR and Western blotting of bcl-2, bcl-xl, and clusterin. An additional 10 rat pups were treated with hydralazine (10 mg/kg/d) or a vehicle, to serve as a hypotensive control. Cell proliferation was determined by PCNA immunostaining, and apoptosis was detected using the total TUNEL technique. Enalapril treatment resulted in a 24% mortality, reduced body weight, and decreased heart weight (p < 0.05). Enalapril decreased proliferating myocytes by 23%, and reduced proliferating cardiac interstitial cells by 8.1% (p < 0.05). Enalapril also decreased myocytes apoptosis by 60%, but the proportion of myocytes undergoing apoptosis was 10-fold less than that of proliferating cells. Cardiac bcl-2 mRNA, clusterin mRNA, bcl-2 protein, and bcl-xl protein content were not changed, but clusterin protein expression was decreased by enalapril treatment. Hydralazine did not alter cardiac cell proliferation or apoptosis. We conclude that ACE inhibition decreases cell turnover in the developing rat heart, which may contribute to cardiac growth impairment. The loss of myocytes may lead to greater myocyte hypertrophy and myocardial damage during later life.

Angiotensin II↗
PubMed2005

GATA factors and transcriptional regulation of cardiac natriuretic peptide genes.

The A- and B-natriuretic peptides (ANP and BNP) are the heart major secretory products. ANF and BNP expression is a marker of cardiomyocyte differentiation, and is regulated spatially, developmentally and hormonally. Analysis of the ANP and BNP promoters has contributed in a major way to our present understanding of the key regulators of cardiac development. It has also started to unravel the complex combinatorial interactions required for proper regulation of the cardiac genetic program. The GATA family of transcription factors initially identified as essential regulators of the two natriuretic peptide genes appears to be at the heart of the molecular circuits governing cardiac growth and differentiation. In particular, GATA-4 has emerged as the nuclear effector of several signaling pathways which modulate its function through post-translational modifications and protein-protein interactions. This review will cover our current knowledge of cardiac transcription and the role of GATA factors in embryonic and postnatal heart development.

Animals↗
PubMed2006

Transcatheter closure of atrial septal defects in adults using two devices: an angiographic overview.

Atrial septal defects are a common congenital cardiac abnormality in adults. lndividuals with atrial septal defects carry the risk to develop cardiac problems such as right ventricle volume overload, pulmonary hypertension, atrial fibrillation, and more rarely paradoxical embolic events. Surgery was the standard treatment for symptomatic patients with atrial septal defects for decades. More recently, percutaneous transcatheter closure of atrial septal defects in adults using a closure device has become an alternative to surgery in selected patients.

Adult↗
PubMed1995

Cardiac failure and dysrhythmias 6-19 years after anthracycline therapy: a series of 15 patients.

The clinical course of late symptomatic anthracycline cardiomyopathy, and resultant changes of cardiac function, were described in 15 patients. They represented a subset of 300 patients who had cardiac evaluations to identify the prevalence of late cardiotoxicity more than 4 years after anthracycline therapy in these patients. The clinical course and all available cardiac evaluations including electrocardiography, continuous taped electrocardiography, echocardiography, radionuclide cardiac angiography, cardiac catheterization, and endomyocardial biopsy, of the 15 patients were reviewed. The patients had received 285-870 (median 540) mg/M2 of daunorubicin and/or doxorubicin 6-19 (median 12) years prior to the onset of late symptoms. Seven patients also had 2,100-4,000 cGy mediastinal radiotherapy. Five patients had required treatment for cardiac symptoms at the end of chemotherapy but 10 patients had no cardiac problems anteceding their late decompensation. Fractional shortening on echocardiogram at late decompensation was 8-20% (median 17%) and radionuclide left ventricular ejection fraction was 8-59% (median 38%). All were treated with digitalis and diuretics and 13/15 with afterload reduction, with at least transient improvement of symptoms. They were followed for 1-9 (median 3) years after late decompensation. One died of uncontrollable cardiac failure. Another underwent successful cardiac transplantation. Conduction abnormalities and dysrhythmias were present in 14/15 patients and 3 died suddenly. Two more had syncope, one requiring an automatic cardiac defibrillator. Endomyocardial biopsy or autopsy revealed hypertrophy and fibrosis in 10/10 patients. Our patients with early cardiac symptoms improved transiently but decompensated later and patients with no early symptoms developed cardiac symptoms more than 10 years after anthracycline therapy. Therefore, patients who have received anthracyclines should have continued cardiac evaluation.

Adolescent↗
PubMed1999

C-reactive protein as a marker for cardiac ischemic events in the year after a first, uncomplicated myocardial infarction.

The prognostic role of C-reactive protein levels in patients with a first acute myocardial infarction, an uncomplicated in-hospital course, and the absence of residual ischemia on a predischarge ergometer test and with an echocardiographic ejection fraction > or = 50% has not been described. C-reactive protein was determined during hospitalization in 64 patients (55 men, mean age 64.6 +/- 10.4 years). The patients were followed up for 13 +/- 4 months and the following cardiac events were recorded: cardiac death, new-onset angina pectoris, and recurrent myocardial infarction. Patients who developed cardiac events during the follow-up period had significantly higher C-reactive protein values than patients without events (3.61 +/- 2.83 vs 1.48 +/- 2.07 mg/dl, p <0.001). The probability of cumulative end points was: 6%, 12%, 31%, and 56% (p = 0.006; RR 3.55; confidence interval 1.56 to 8.04), respectively, in patients stratified by quartiles of C-reactive protein (< 0.45, 0.45 to 0.93, 0.93 to 2.55 and > 2.55 mg/dl). In the Cox regression model, only increased C-reactive protein levels were independently related to the incidence of subsequent cardiac events (chi-square 9.8, p = 0.001). Thus, increased C-reactive protein levels are associated with a worse outcome among patients with a first acute myocardial infarction, an uncomplicated in-hospital course without residual ischemia on the ergometer test, and with normal left ventricular function.

Aged↗
PubMed1988

Cellular electrophysiologic responses of isolated neonatal and adult cardiac fibers to d-sotalol.

The short-term cellular electrophysiologic actions of d-sotalol on isolated neonatal and adult canine ventricular myocardium and Purkinje fibers were evaluated using standard microelectrode techniques. d-Sotalol, 10(-6) to 10(-4)M, had no effects on action potential amplitude, maximal diastolic potential or action potential upstroke velocity (Vmax) in any neonatal or adult preparation. In five adult myocardial preparations, d-sotalol produced concentration-dependent increases in action potential duration at 50% (APD50) and 90% (APD90) repolarization and effective refractory period. In six neonatal myocardial preparations, d-sotalol produced a biphasic response; APD50, APD90 and effective refractory period decreased at 10(-6) and 10(-5)M. At 10(-4)M, these values increased significantly but to a lesser extent compared with values in adults. In seven adult Purkinje fibers, d-Sotalol significantly increased APD50, APD90 and effective refractory period in a concentration-dependent manner. All six neonatal Purkinje fibers responded in a biphasic manner, with values for APD50, APD90 and effective refractory period being less than control at 10(-6)M and near control values at 10(-5)M. At 10(-4)M, these variables were significantly increased, but to a lesser extent than in adult preparations. Our data confirm the typical class III effects of d-sotalol in adult cardiac tissues. The shortening of repolarization and refractoriness at lower drug concentrations in developing cardiac tissues may relate to age-dependent differences in cellular ionic function and basic electrophysiology.

Action Potentials↗