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 1,081 records · Page 60Linked to original sources
PubMed1983

Effects of myocardial infarction on perioperative cardiac complications.

Of 1104 consecutive noncardiac operations on 981 patients using general anesthesia, 63 were performed on 53 patients who had had a previous myocardial infarction. Patients with a previous infarct were compared to those with no prior infarct to determine the influence of a previous infarct on perioperative cardiac complications. Two of the 53 patients with a previous myocardial infarction (3.8%) had perioperative myocardial infarction, compared to 0.4% (4/928) of patients with no prior history of myocardial infarction (P less than 0.05). Ventricular tachycardia (P less than 0.05) and cardiac death (P less than 0.01) were more frequent in patients with a previous myocardial infarction compared to those with no prior infarct. All patients with a previous myocardial infarction who developed cardiac complications underwent vascular procedures (P less than 0.005) and were over 77 years of age. The two patients who reinfarcted experienced intraoperative hypotension (P less than 0.05). Fourteen of the 53 patients with a history of a myocardial infarction (26.4%) had previous coronary artery bypass surgery; no perioperative cardiac complications occurred in these patients.

Adult↗
PubMed1994

Clinical and echographic features of in utero cardiac dysfunction in the recipient twin in twin-twin transfusion syndrome.

OBJECTIVE: Fetal twin-twin transfusion syndrome (TTTS) presenting in the second trimester has been associated with almost no perinatal survival until recently, when serial drainage of amniotic fluid has improved the prognosis to 70%-80%. Most recipient twins now survive but develop cardiac dysfunction. The study was undertaken to evaluate the abnormal echocardiographic features and clinical complications of cardiac disease in the recipient twin of TTTS. DESIGN: Antenatal and postnatal echocardiographic and clinical observational study. SETTING: Antenatal studies in a tertiary referral centre. Postnatal management and follow up were performed by the same paediatric cardiologist, either at the obstetric hospital or at the regional referral centre. PATIENTS: Twin pregnancies complicated by TTTS with severe polyhydramnios diagnosed earlier than 25 weeks that proceeded until viability (n = 5). INTERVENTION: Serial fetal echocardiography with colour Doppler. Postnatal echocardiography in the first week and between two and seven months. Serial amnioreduction was performed in all pregnancies. Digoxin treatment, pericardiocentesis, paracentesis, or laser ablation of placental anastomoses was undertaken when there was hydrops. RESULTS: Increased cardiothoracic ratio and tricuspid regurgitation were seen in all recipient twins. High pulmonary artery velocities developed in three. One recipient twin died a week after delivery of endocardial fibroelastosis and infundibular pulmonary stenosis. Two other had balloon dilatation for pulmonary stenosis, one shortly after birth and one at four months. A further twin has apical thickening of the right ventricle at six months. The remaining recipient twin had normal echocardiographic findings at follow up. CONCLUSION: This report characterises for the first time a cardiac disease acquired in utero in the recipient twin in pregnancies complicated by TTTS. Clinical manifestations in utero range from mild to critical pulmonary stenosis or lethal cardiomyopathy. Although perinatal prognosis seems to be related to the severity of dysfunction when first diagnosed in utero, follow up in infancy is recommended in view of the possibility of progressive pulmonary stenosis.

Echocardiography, Doppler↗
PubMed1993

Inadvertent administration of rtPA to a patient with type 1 aortic dissection and subsequent cardiac tamponade.

Administration of thrombolytic agents to patients with misdiagnosis of acute myocardial infarction can result in serious side effects. A case of aortic dissection that was misdiagnosed as acute myocardial infarction and received rtPA is reported. Within 1 hour of rtPA infusion, the patient developed cardiac tamponade. Type 1 aortic dissection was diagnosed by aortic angiogram. The patient underwent emergency resection of the dissection and evacuation of the pericardial and anterior mediastinal hematoma. Although he required massive transfusion of blood products intraoperatively, he is doing well 22 months after his surgery.

Aged↗
PubMed1993

Sudden cardiac arrest during adenotonsillectomy in a patient with subclinical Duchenne's muscular dystrophy.

We describe a four-year-old boy of Indian descent who had elective adenotonsillectomy for chronic sore throat and partial airway obstruction. About 10 minutes into the procedure, the patient suddenly developed cardiac asystole. After prolonged cardiac resuscitation, recovery was achieved. No permanent neurologic deficits resulted. The child was later found to have a strong family history of Duchenne's muscular dystrophy (DMD) and an elevated serum creatine kinase level documented since shortly after birth. We reviewed several case reports substantiating the risk for cardiac arrest during general anesthesia in DMD patients, and we concluded that DMD is a little-known risk for cardiac arrest during general anesthesia. The otolaryngologist must be aware of this potential complication, because tonsillectomy and adenoidectomy are commonly indicated for children at an age when DMD may be subclinical.

Adenoidectomy↗
PubMed1976

Systemic stress in the production of cardiac thrombosis in hypercholesterolaemic rats.

An experimental study to elucidate the effects of feeding a high fat diet, hypercholesterolaemia and superadded acute and chronic stress on the production of cardiac thrombosis was carried out in rats. The high fat diet contained 25 percent butter rat providing 45 percent calories from fat which produced significant increase of serum cholesterol and other lipids. Acute stress was induced by two injections of adrenaline on a single day which caused a marked transient alteration of haemodynamics. Chronic stress was of two types, physical and metabolic. The physical stress was induced by repeated exposure of the rats to electric shock or roller drum exercise, while metabolic stress was caused by repeated injection of ACTH. Rats of both acute and chronic stress groups showed variable degree of medial degeneration, hyaline and fibrinoid intimal deposits and calcification in coronary arteries. Cardiac thrombi were seen in 30 percent animals subjected to adrenaline shock. Among the chronic stress procedure 17 percent rats exposed to electric shock and only one rat of the ACTH group developed cardiac thrombosis but no thrombus was detected in those exposed to roller drum exercise. The myocardium showed patchy necrosis with or without calcification, Spontaneous mortality was maximum following acute adrenaline shock (25 %) while electric shock caused mortality in 17 percent animals. The other procedures did not lead to spontaneous mortality. This study highlights the significant role of high fat intake, hypercholesterolaemia and systemic stress in the pathogenesis of acute cardiac thrombosis and myocardial necrosis/infarction.

Adrenocorticotropic Hormone↗
PubMedDate not supplied

Cardiac involvement in HIV-infected people living in Africa: a review.

The primary objective of this study was to review and summarise the literature on the spectrum and management of cardiac disease in HIV-infected people living in Africa. We searched MEDLINE (January 1980 to February 2003), reference lists of papers, and reviews on the subject, and contacted experts working in the field for information on relevant references. The review was limited to papers that were published in peer-reviewed journals and indexed on MEDLINE. Seventeen of the 21 studies identified met the inclusion criteria for analysis. The studies confirmed that cardiac abnormalities are more common in HIV-infected people, compare to normal controls, and that about half of hospitalized patients and a significant proportion of patients followed up over several years develop cardiac abnormalities. The commonest HIV-related cardiac abnormalities were cardiomyopathy and pericardial disease. Tuberculosis was the major cause of large pericardial effusion in Africa. Myocarditis was the commonest pathological abnormality in HIV-associated cardiomyopathy, and non-viral opportunistic infections such as toxoplasmosis and cryptococcosis may account for up to 50% of cases of HIV-associated cardiomyopathy in Africa. Echocardiography is indicated in HIV-positive patients with cardiac symptoms or signs. If cardiomyopathy or pericardial disease is identified, further investigation must be considered to exclude potentially treatable opportunistic infections. Further research in large numbers of patients is needed to determine the value of endomyocardial biopsy in the management of patients with HIV-associated cardiomyopathy, and to establish the place of adjuvant steroids in the treatment of HIV-associated tuberculous pericarditis.

Africa↗
PubMed1985

[Cardiac insufficiency in infectious endocarditis].

The aim of this study of 101 cases of infective endocarditis was to determine the factors predisposing to cardiac failure, the prognostic factors of this complication and the therapeutic implications. A significant (p less than 0.05) Chi square test was the statistical reference. Fifty-two per cent of patients developed cardiac failure which was biventricular in 48 p. 100 of cases and the presenting symptom in 64 p. 100. The mean age of the patients with cardiac failure was 56.6 years with a clear male predominance. In 48 p. 100 of cases, cardiac failure complicated a pre-existing cardiac lesion which was usually acquired (84 p. 100). The commonest condition was valvular insufficiency of the aortic and mitral valves (70 p. 100 of cases with cardiac failure). Severe cardiac failure was observed more frequently and earlier in aortic than in mitral regurgitation. The commonest infecting organism was the streptococcus (53 p. 100 of cases with cardiac failure) and the most frequent presumed portal of entry was dental (25 p. 100). Arrhythmias were observed in 51 p. 100 of patients in cardiac failure, the commonest being atrial fibrillation (34 p. 100) complicating mitral valve disease in 56 p. 100 of cases; 17 p. 100 of arrhythmias were ventricular. Conduction defects were observed in 26 p. 100 of cases with cardiac failure, 55 p. 100 of which had aortic valve disease. Valvular vegetations were demonstrated by echocardiography in 43 p. 100 of cases with cardiac failure. Valve replacement had to be performed for resistant cardiac failure in 13 p. 100 of cases.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

Correction of serum electrolyte imbalance prevents cardiac arrhythmia during amphotericin B administration.

Arrhythmias and cardiac arrest have been reported during amphotericin B administration but no effective technique has been described to prevent them. I saw two patients with kala-azar resistant to sodium stibogluconate who developed cardiac arrest after amphotericin infusion (in spite of tolerating a test dose). Both had low levels of serum sodium, potassium and calcium. After these were corrected the amphotericin B was restarted and the course of treatment completed successfully. I suggest that prior to giving amphotericin B to patients with resistant kala-azar their electrolyte imbalance should be corrected.

Adult↗
PubMed1991

Hemodynamic changes and compensatory mechanisms during early cardiogenesis after neural crest ablation in chick embryos.

Microcinephotography was used to study early heart development in chick embryos with ablations of the neural crest known to result in persistent truncus arteriosus with associated aortic arch anomalies. The premigratory neural crest destined for the 3rd and 4th pharyngeal arches and the aorticopulmonary septum were ablated. When the embryos reached the looped cardiac tube stage (stage 18), 15 experimental and 15 control embryos were filmed at 100 frames/s under controlled environmental conditions. End-diastolic and end-systolic dimensions were determined for the conotruncus and presumptive right ventricle that together compose the bulbus cordis. The results showed that the shortening fractions and ejection fractions were significantly depressed in the experimental embryos. The experimental embryos exhibited dilation and decreased emptying of the ventricle. There was no difference in heart rate or stroke volume between the control and experimental embryos. Thus, the calculated cardiac output was the same in the control and experimental groups. It appeared that the experimental embryos compensated for decreased contractility by ventricular dilation. These functional compensations in very early cardiac development may play an etiologic role in the subsequent development of structural heart defects.

Animals↗
PubMed2003

Hypoxia and Rho/Rho-kinase signaling. Lung development versus hypoxic pulmonary hypertension.

Intracellular signaling via the small GTP-binding protein RhoA and its downstream effector Rho-kinase plays a role in regulating diverse cellular functions, including cell contraction, migration, gene expression, proliferation, and differentiation. Rho/Rho-kinase signaling has an obligatory role in embryonic cardiac development, and low-level chemical activation of Rho promotes branching morphogenesis in fetal lung explants. Gebb has found that hypoxia markedly augments branching morphogenesis in fetal rat lung explants, and our preliminary results suggest this is associated with activation of RhoA. Whereas hypoxia-induced activation of Rho/Rho-kinase may promote fetal lung development, other evidence indicates it has adverse effects in the lungs of neonates and adults. When exposed at birth to the mild hypoxia of Denver's altitude (5,280 ft), the neonatal fawn-hooded rat (FHR) develops severe pulmonary hypertension (PH) associated with impaired lung alveolarization and vascularization. We have observed that administration via the drinking water of the Rho-kinase inhibitor fasudil to the nursing, Denver FHR mother for the first 2 to 3 weeks, and then directly to the Denver FHR pups for the next 7 to 8 weeks, ameliorates the lung dysplasia and PH. The adult Sprague-Dawley rat develops PH when exposed for 3 to 4 wk to a simulated altitude of 17,000 ft. We have found that this hypoxic PH is associated with activation of pulmonary artery Rho/Rho-kinase and is almost completely reversed by acute intravenous administration of the Rho-kinase inhibitor Y-27632. In addition, chronic in vivo treatment with Y-27632 reduces development of the hypoxic PH. In summary, hypoxic activation of Rho/Rho-kinase signaling may be important for fetal lung morphogenesis, but continued activation of this pathway in the neonate impairs postnatal lung development and re-activation in the adult contributes to development of PH.

Altitude↗
PubMed2005

[Development and cardiomyopathy: serum response factor, a key protein].

Serum response factor (SRF) is a widely expressed transcription factor involved in the transcription of various genes linked to muscle differentiation and cellular growth. Recent studies show the pivotal role of SRF in orchestrating genetic programs essential for cardiac development and function. Dominant negative isoforms of SRF resulting from caspase cleavage or alternative splicing have been identified in different forms of cardiomyopathies. This review summarizes the role of SRF, its structure, function and its role in human cardiopathies. Finally, we discuss the results of recently developed murine models which address the role of SRF in the adult heart in vivo. The existing biological data suggest that SRF could be a target of neurohumoral activation which is involved in myocardial hypertrophy. Conversely, inhibition of SRF activity in different murine models leads to dilated cardiomyopathy.

Animals↗
PubMed1989

Cardiac tamponade complicating leukaemia: immediate chemotherapy or pericardiocentesis?

Although leukaemic infiltration of the pericardium is frequently observed at post-mortem, clinically evident cardiac tamponade is rare. Two cases of cardiac tamponade complicating leukaemia are presented. One patient had cardiac tamponade as the initial presentation of acute lymphoblastic leukaemia and experienced complete resolution of the pericardial effusion within 6 days after chemotherapy without therapeutic pericardiocentesis. The other patient with chronic myeloid leukaemia developed cardiac tamponade requiring pericardiocentesis as the first sign of acute blastic transformation. The roles of early chemotherapy and pericardiocentesis in managing this complication are discussed.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1994

Angiotensin II induced alteration of cyclic adenosine 3',5'-monophosphate generation in the hypertrophic myocardium of Dahl salt-sensitive rat on a high-salt diet.

The objective of this study was to explore the action of angiotensin II (AII) on cardiac contractility and cyclic AMP (cAMP) generation by forskolin and isoproterenol in the hypertrophic myocardium of the salt-sensitive Dahl rat. Inbred Dahl S and Dahl R rats that had been on a diet supplemented with 6% NaCl were studied. The functional effects of the interaction of AII and forskolin on cardiac contractility were assessed in the isolated heart preparation. The effect on the cAMP signal transduction pathway was assessed in cardiomyocytes isolated from hearts of Dahl S and R rats. Dahl S rats developed cardiac hypertrophy on a high-salt diet, whereas Dahl R rats did not. Forskolin increased cardiac contractility, which was differently affected by AII, depending on whether the heart was from hypertrophied Dahl S rat or from the control Dahl R rat. AII accentuated forskolin-induced increases in cardiac contractility in hypertrophic hearts but diminished forskolin-induced increases in contractility in the nonhypertrophied hearts. This response was reflected in the cAMP response to forskolin, in that AII decreased forskolin-induced increases in cAMP in the nonhypertrophic heart. AII had the reverse effect in cardiomyocytes from hypertrophied hearts, as AII increased forskolin-induced cAMP production. This was shown to be due to an AII receptor mediated effect, as it was antagonized by the AII receptor antagonist saralasin. The same effects of AII were found on isoproterenol-induced increases in cAMP. Similar results occurred in the presence of the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX), suggesting that the effect was on cAMP production rather than cAMP degradation. This was attributed to an inhibitory G protein (Gi) mechanism, as the muscarinic agonist carbachol, which acts through Gi, produced the same effects as AII. Furthermore, the effects of AII were abolished by pertussis toxin, which inactivates Gi. These data indicate a reversal of control by AII in the hypertrophic Dahl S heart in response to forskolin, which activates adenylyl cyclase directly on the catalytic subunit, converting the substrate, ATP, to cAMP, independent of the guanine nucleotide activated protein, and in response to isoproterenol, which activates adenylyl cyclase through G protein mechanisms. All accentuated the forskolin-induced increase in cardiac contractility and cAMP generation in the hypertrophied ventricle but decreased both contractility and cAMP generation in nonhypertrophied hearts, suggesting that the process of cardiac hypertrophy in salt-sensitive Dahl rat may compensate for the reduction in intracellular cAMP by altering its regulatory control by AII.

1-Methyl-3-isobutylxanthine↗
PubMed1989

Expression of the fibronectin gene.

Fibronectin (FN) is an extracellular matrix protein that acts as a substrate for cell migration and adhesion during development. FN adheres to cells through a dimeric membrane protein, the FN receptor. Antibodies to FN and synthetic peptides that inhibit FN-receptor interaction inhibit gastrulation, block neural crest cell migration, arrest cardiac development, and block the fusion of myoblasts to form myotubes. FN and its receptor also appear to be important for lung development, where their expression coincides with the onset of branching morphogenesis, but drops to barely detectable levels in adult lung, indicating developmental specificity. FN expression is generally low in most adult tissues. However, synthesis is drastically increased during injury and wound healing, a process that in many ways mimics development. FN synthesis is also drastically increased in fibroproliferative lung lesions associated with major architectural changes in the lung. Expression of FN is regulated by a variety of growth factors and hormones. Several of these inducers (cAMP, transforming growth factor-beta, epidermal growth factor, platelet-derived growth factor, glucocorticoids, and vitamin D3) have themselves been implicated in developmental processes, and both cAMP and transforming growth factor-beta are known to stimulate expression of other matrix genes. One role of these hormones and growth factors in development may be to control expression of matrix genes, thereby controlling cell migration and adhesion. In the following report, the effect of hormones and growth factors on expression of the FN gene is reviewed.

Animals↗
PubMed2002

Erythropoietin receptor signalling is required for normal brain development.

Erythropoietin, known for its role in erythroid differentiation, has been shown to be neuroprotective during brain ischaemia in adult animal models. Although high levels of erythropoietin receptor are produced in embryonic brain, the role of erythropoietin during brain development is uncertain. We now provide evidence that erythropoietin acts to stimulate neural progenitor cells and to prevent apoptosis in the embryonic brain. Mice lacking the erythropoietin receptor exhibit severe anaemia and defective cardiac development, and die at embryonic day 13.5 (E13.5). By E12.5, in addition to apoptosis in foetal liver, endocardium and myocardium, the erythropoietin receptor null mouse shows extensive apoptosis in foetal brain. Lack of erythropoietin receptor affects brain development as early as E10.5, resulting in a reduction in the number of neural progenitor cells and increased apoptosis. Corresponding in vitro cultures of cortical cells from Epor(-/-) mice also exhibited decreases in neuron generation compared with normal controls and increased sensitivity to low oxygen tension with no surviving neurons in Epor(-/-) cortical cultures after 24 hour exposure to hypoxia. The viability of primary Epor(+/+) rodent embryonic cortical neurons was further increased by erythropoietin stimulation. Exposure of these cultures to hypoxia induced erythropoietin expression and a tenfold increase in erythropoietin receptor expression, increased cell survival and decreased apoptosis. Cultures of neuronal progenitor cells also exhibited a proliferative response to erythropoietin stimulation. These data demonstrate that the neuroprotective activity of erythropoietin is observed as early as E10.5 in the developing brain, and that induction of erythropoietin and its receptor by hypoxia may contribute to selective cell survival in the brain.

Animals↗
PubMed2004

Neuroendocrine evaluation of cardiac disease.

Current evidence favors the view that regardless of etiology, there is a predictable sequence of neuroendocrine activation that operates in most dogs and cats with progressive heart disease and that it is largely, but not entirely, independent of etiology. The natriuretic peptides and sympathetic nervous system seem to be early responders to developing cardiac and hemodynamic perturbations in both species. BNP plays a particularly prominent role in cats, possibly as a reflection of disease etiology. Shortly thereafter, plasma endothelin concentrations rise, reflecting the impact of the hemodynamic alterations on the vasculature. Endothelin and the natriuretic peptides directly suppress plasma renin release but have divergent effects on aldosterone. Activation of the tissue RAAS may operate early on to further the progression of heart failure, but evidence of plasma RAAS activation occurs comparatively late and near the time of development of overt CHF. Finally, in animals with severe CHF that are prone to hypotension,vasopressin levels may also rise, contributing to the retention of free water and congestion that is refractory to diuretics. Although oversimplified, this scenario seems to be consistent with data obtained in human, canine, and feline patients. These observations provide some impetus for evaluating ACE inhibitors in cats and beta-receptor-blocking drugs in dogs and cats. Perhaps we are also a little closer to identifying useful biochemical markers that can aid in the diagnosis of heart disease, guide therapy, and improve our understanding of the biologic processes occurring in our patients.

Animals↗
PubMedDate not supplied

Cyclins that don't cycle--cyclin T/cyclin-dependent kinase-9 determines cardiac muscle cell size.

A subset of cyclin-dependent protein kinases--Cdk7, Cdk8, and Cdk9--participates directly, in complex ways, with the fundamental machinery for gene transcription, as elements of general transcription factors whose substrate is the C-terminal domain (CTD) of RNA polymerase II. Here, we review recent data implicating the CTD kinase Cdk9 as a critical determinant of cardiac hypertrophy, in vitro and in vivo. Diverse trophic signals that increase cardiac mass all activated Cdk9 (work load, the small G-protein Gaq, and the calcium-dependent phosphatase calcineurin in mouse myocardium; endothelin-1, a hypertrophic agonist, in cultured cardiomyocytes). Little or no change occurred in levels of the kinase or its activator, cyclin T. Instead, in all four hypertrophic models, Cdk9 activation involves the dissociation of 7SK small nuclear RNA (snRNA), an endogenous inhibitor. In culture, dominant-negative Cdk9 blocked ET-1-induced hypertrophy, whereas an anti-sense "knockdown" of 7SK snRNA provoked spontaneous cell growth. In trans-genie mice, concordant with these results, activation of Cdk9 activity via cardiac-specific overexpression of cyclin Tl suffices to provoke hypertrophy. Together, these findings implicate Cdk9 activity as a pivotal regulator of pathophysiological heart growth. Because hypertrophy, in turn, is a cardinal risk factor for developing cardiac pump failure, these results support the logic of examining Cdk9 as a potential drug target in heart disease.

Animals↗