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PubMed1993

Expression of the helix-loop-helix factor Id during mouse embryonic development.

Expression and regulation of the helix-loop-helix (HLH) protein Id in cardiac cells and its negative effect on cardiac gene expression indicate that Id may play a role in cardiac development. To investigate this issue further, we have performed in situ analysis of Id mRNA in developing mouse embryos from Embryonic Days 7 to 15.5 and in neonatal heart. Consistent with its postulated role as an inhibitor of differentiation, Id mRNA was expressed in specific populations of proliferating mesenchymal and epithelial tissues, with its expression declining as differentiation progressed. In addition, patterns of Id mRNA hybridization overlapped considerably with those of two other developmentally important genes, twist and hox 7/7.1, of the HLH and homeobox family, respectively. Id mRNA hybridization was not observed in early epithelial somites or in the myotomal compartment of the somite, suggesting that Id is unlikely to play an inhibitory role in these early myogenic precursors. Id mRNA was expressed in specific regions of the developing nervous system. In the heart, Id mRNA was expressed at high levels in developing cardiac cushions and ridges of the outflow tract and continued to be expressed at high levels in valvular tissue of the neonatal heart.

Animals↗
PubMed1979

Low-pressure cardiac tamponade.

An elderly man developed cardiac tamponade from a tuberculous pericardial effusion but without such typical manifestations as pulsus paradoxus and jugular-vein distension. This case illustrates the difficulties in clinical recognition of low-pressure cardiac tamponade, which can develop in the presence of dehydration and hypovolemia. The hemodynamic factors that account for this phenomenon are discussed.

Aged↗
PubMed1980

Development of cardiac and behavioral responses to a three-dimensional toy stimulation in one- to six-month-old infants.

Concomitance between development of perceptual-motor behavior and cardiac-somatic association was evaluated in 1-6-month-old infants. The behavior was elicited by presenting 3-dimensional objects to 50 infants divided into 5 age groups. Each infant was presented with a sequence of 5 commercial toys on 2 immediately succeeding occasions. Each toy stimulation lasted 30 sec and was divided in 2 phases: distal and proximal to the infant. Cardiac responses during the distal phase (first 15 sec) differed as a function of maturing capability of infants to touch and grasp the toys when they subsequently became proximal (last 15 sec). In younger infants (aged 1-3 months), heart-rate (HR) response was consistently decelerative and indexed orienting and attention to the object. In older infants, HR response shifted to acceleration while they fixated the distal toys, before they could actually reach them. This difference in cardiac reaction was attributed to differing stages of perceptual-motor maturation which permit different transactions with external events: somatic activity (acceleration) or information-getting activity (deceleration).

Arousal↗
PubMedDate not supplied

[Duration-outcome relations in nonpharmacological treatment of chronic cardiac failure developed after acute myocardial infarction].

Left-ventricular (LV) systolic-diastolic function and cardiac rhythm variability, the rate of pathological LV remodeling and outcomes of the disease for 18 months were studied in 394 males at the age 35-68 years suffering from chronic cardiac failure (CCF) of NYHA functional class I-II consequent to myocardial infarction occurring 9.6-4.2 months before. It was found that long-term (12-24 weeks) taking sauna, underwater dousch-massage, general effervescent baths and exercise in combination with drug therapy in patients with asymptomatic CCF inhibit the rate of LV remodeling, decrease LV hypertrophy, improve diastolic function of the heart. This results in lowering a cumulative risk of unfavourable outcomes of the disease by 42% (p = 0.006). The best of effect of the combined therapy is not achieved in angina of effort, massive myocardial hypoperfusion zones, no viable myocardium in the zones of the lesion, marked LV hypertrophy.

Acute Disease↗
PubMed2004

Measuring continuity of care for cardiac patients: development of a patient self-report questionnaire.

BACKGROUND: Continuity of care can be a challenge for cardiac patients, many of whom require chronic and complex management from a variety of health care personnel in multiple settings. For health services research, measures are needed that encompass the multifaceted nature of continuity of care for cardiac patients. OBJECTIVE: To assess continuity of care from the patient's perspective, a comprehensive self-report instrument of continuity of care for patients with congestive heart failure and atrial fibrillation was developed and validated. METHODS: Based on published work, patient interviews and provider input, the Heart Continuity of Care Questionnaire (HCCQ) was developed to assess various aspects of care in the transition from hospital to home. The HCCQ covered a variety of content areas relevant to cardiac care. The HCCQ and either the Continuity of Care Index (CCI) or the Minnesota Living with Heart Failure Questionnaire (MLHFQ) were completed by 83 patients who had been discharged for at least six months. RESULTS: Most items had good response rates. The subscales, defined a priori, had good reliability (subscales alpha ranged from 0.80 to 0.93). The HCCQ and its subscales had strong correlations with the CCI but not the MLHFQ. The HCCQ subscales demonstrated better known group validity than the CCI. CONCLUSIONS: In this preliminary study, the HCCQ appears to be a comprehensive, reliable and valid measure of continuity of care from the patient perspective. Further studies of the validity, generalizability and use are needed.

Adult↗
PubMed2001

Accumulation of molecules involved in alpha1-adrenergic signal within caveolae: caveolin expression and the development of cardiac hypertrophy.

OBJECTIVE: Caveolin, a major protein component of caveolae, is now considered to be an inhibitor of cellular growth and proliferation. In this study, we examined the localization of the molecules involved in alpha1-adrenergic receptor signal relative to that of caveolin in the heart and the changes in caveolin expression during the development of hypertrophy in SHR. METHODS: We purified the caveolar protein fractions from rat cardiac tissues, H9C2 cells, and rat vascular smooth muscle cells. Using radioligand receptor binding assay and immunoblot analysis, we examined the distribution and the amount of alpha1-AR and caveolin. RESULTS: Caveolin-3, the alpha1-adrenergic receptor, Gq and PLC-beta subtypes (PLC-beta1, -beta3) were found exclusively in the caveolar fraction in the above tissues. Caveolin-3 were co-immunoprecipitated with alpha1-adrenergic receptor and Gq from the cardiac tissues. The amount of caveolin subtypes expression (caveolin-1 and -3) and the amount of the alpha1-adrenergic receptor were examined in the hearts of SHR and age-matched WKY (4- and 24-weeks-old). The amount of caveolin-3 expression was significantly smaller in SHR at 24-weeks-old than that in SHR at 4-weeks-old and that in WKY at 24-weeks-old. CONCLUSIONS: The molecules involved in alpha1-adrenergic signaling are confined to the same microdomain as caveolin. A decrease in caveolin-3 expression may play a role in the development of cardiac hypertrophy in SHR, presumably through de-regulating the inhibition of growth signal in the hearts of SHR in the hypertrophic stage.

Analysis of Variance↗
PubMed1990

The relation between EEG and mental development following cardiac surgery performed under simple deep hypothermia in children.

In order to assess the accuracy of electroencephalography (EEG), in children who have undergone cardiac surgery under simple deep hypothermia, the relation between IQ or schoolwork achievement and the duration of circulatory arrest was investigated in 75 such children. Abnormal preoperative EEG's were found in 16 per cent of the children while abnormal postoperative EEG's were found in 17 per cent. The children were divided into 4 groups, according to pre- and postoperative EEG results. Schoolwork achievement scores ranged between 3.0 and 3.2, the difference among the groups being insignificant. Moreover, no significant shift in IQ was found among the groups. Finally, regarding the number of children who were able to go on to a higher level of education, including high school then college or university, again no significant differences were found among the 4 groups. In a comparison with the number of such children in neighboring Nagasaki prefecture able to continue on to a higher level of education, no significant differences were seen either. The findings and statistics of this investigation therefore indicate that pre- and postoperative EEG's are not always a reliable reference for assessing the prognosis of cerebral activity.

Achievement↗
PubMed2002

Erk5 null mice display multiple extraembryonic vascular and embryonic cardiovascular defects.

Erk5 is a mitogen-activated protein kinase, the biological role of which is largely undefined. Therefore, we deleted the erk5 gene in mice to assess its function in vivo. Inactivation of the erk5 gene resulted in defective blood-vessel and cardiac development leading to embryonic lethality around embryonic days 9.5-10.5. Cardiac development was retarded largely, and the heart failed to undergo normal looping. Endothelial cells that line the developing myocardium of erk5-/- embryos displayed a disorganized, rounded morphology. Vasculogenesis occurred, but extraembryonic and embryonic blood vessels were disorganized and failed to mature. Furthermore, the investment of embryonic blood vessels with smooth muscle cells was attenuated. Together, these data define an essential role for Erk5 in cardiovascular development. Moreover, the inability of Erk5-deficient mice to form a complex vasculature suggests that Erk5 may play an important role in controlling angiogenesis.

Animals↗
PubMed2003

[A study on myocardial Pax-8 gene].

OBJECTIVE: Conventional deletion of ALK3, also termed as bone morphogenetic protein (BMP) receptor IA, in mice might result in early embryonic lethality. To investigate the function of ALK3 in cardiac development, the cardiac-specific deletion of ALK3 in mice was made by Dr. Schneider, using Cre recombinase driven by the alpha-MHC promoter that Dr. Fukushipe worked out. Such specific deletion of ALK3 caused death in mid-gestation with defects in the trabeculae, interventricular septum, and endocardial cushion. Since ALK3 is not a cardiac-specific gene, it is extremely important to identify ALK3 downstream genes. METHODS: Alpha-MHC Cre+/-, ALK3 F/- and alpha-MHC Cre+/-, ALK3 F/+ embryos were obtained after 20 alpha-MHC Cre+/-, ALK3 +/- mice and 20 ALK3 F/F mice were mating. The ALK3 downstream genes were screened using microarray made in Germany that could identify 25000 genes in mouse. Two populations of mRNA, one derived from the embryonic heart (11.5 days) of alpha-MHC Cre+/-, ALK3 F/- mice, and the other derived from the alpha-MHC Cre+/-, ALK3 F/+ mice, were compared. Cardiac-specific ALK3 downstream genes were identified using real time quantitative RT-PCR and in situ hybridization. RESULTS: The expression of 12 genes, such as Pax-8 and Hox-3.5 were down-regulated in alpha-MHC Cre+/-, ALK3 F/- mouse heart. The expression of 16 genes including Ras-related protein Rab-5b and EPS-8 protein was up-regulated in the group of alpha-MHC Cre+/-, ALK3 F/-. It was found that the Box protein Pax-8 gene was down-regulated by 7.1 fold (P < 0.001) in the alpha-MHC Cre+/-, ALK3 F/- mice by real time quantitative RT-PCR. It was also revealed that the Box protein Pax-8 gene was expressed stronger in alpha-MHC Cre+/-, ALK3 F/+ than alpha-MHC Cre+/-, ALK3 F/- E11.5 days mouse heart by means of in situ hybridization. CONCLUSION: The Box protein Pax-8 gene is an important and cardiac-specific ALK3 downstream gene in the BMP signaling pathway during inter-ventricular septum development.

Animals↗
PubMed2005

Cell biology of cardiac cushion development.

The valves of the heart develop in the embryo from precursor structures called endocardial cushions. After cardiac looping, endocardial cushion swellings form and become populated by valve precursor cells formed by an epithelial-mesenchymal transition (EMT). Endocardial cushions subsequently undergo directed growth and remodeling to form the valvular structures and the membranous septa of the mature heart. The developmental processes that mediate cushion formation include many prototypic cellular actions including adhesion, signaling, migration, secretion, replication, differentiation, and apoptosis. Cushion morphogenesis is unique in that these cellular possesses occur in a functioning organ where the cushions act as valves even while developing into definitive valvular structures. Cardiovascular defects are the most common congenital defects, and one of the most common causes of death during infancy. Thus, there is significant interest in understanding the mechanisms that underlie this complex developmental process. In this regard, substantial progress has been made by incorporating an understanding of cardiac morphology and cell biology with the rapidly expanding repertoire of molecular mechanisms gained through human genetics and research using animal models. This article reviews cardiac morphogenesis as it relates to heart valve formation and highlights selected growth factors, intracellular signaling mediators, and extracellular matrix components involved in the creation and remodeling of endocardial cushions into mature cardiac structures.

Emigration and Immigration↗
PubMed1999

Development of cardiac sensitivity to oxygen deficiency: comparative and ontogenetic aspects.

Hypoxic states of the cardiovascular system are undoubtedly associated with the most frequent diseases of modern times. They originate as a result of disproportion between the amount of oxygen supplied to the cardiac cell and the amount actually required by the cell. The degree of hypoxic injury depends not only on the intensity and duration of the hypoxic stimulus, but also on the level of cardiac tolerance to oxygen deprivation. This variable changes significantly during phylogenetic and ontogenetic development. The heart of an adult poikilotherm is significantly more resistant as compared with that of the homeotherms. Similarly, the immature homeothermic heart is more resistant than the adult, possibly as a consequence of its greater capability for anaerobic glycolysis. Tolerance of the adult myocardium to oxygen deprivation may be increased by pharmacological intervention, adaptation to chronic hypoxia, or preconditioning. Because the immature heart is significantly more dependent on transsarcolemmal calcium entry to support contraction, the pharmacological protection achieved with drugs that interfere with calcium handling is markedly altered. Developing hearts demonstrated a greater sensitivity to calcium channel antagonists; a dose that induces only a small negative inotropic effect in adult rats stops the neonatal heart completely. Adaptation to chronic hypoxia results in similarly enhanced cardiac resistance in animals exposed to hypoxia either immediately after birth or in adulthood. Moreover, decreasing tolerance to ischemia during early postnatal life is counteracted by the development of endogenous protection; preconditioning failed to improve ischemic tolerance just after birth, but it developed during the early postnatal period. Basic knowledge of the possible improvements of immature heart tolerance to oxygen deprivation may contribute to the design of therapeutic strategies for both pediatric cardiology and cardiac surgery.

Aging↗
PubMed1984

Cardiac rehabilitation: developing a successful program.

The Downriver Treadmill Team, a Phase II and Phase III outpatient cardiac rehabilitation program, is presented as a prototypical successful program. The qualities and attributes of this program are discussed as a means to actively promote cardiac rehabilitation directly to the consumer.

Cardiac Care Facilities↗
PubMed1988

Cilazapril prevents the development of cardiac hypertrophy and the decrease of coronary vascular reserve in spontaneously hypertensive rats.

Cilazapril is a new inhibitor of angiotensin converting enzyme which has been shown to prevent development of high blood pressure and cardiac hypertrophy in spontaneously hypertensive (SHR) rats. The goal of the present experiment was to evaluate the effects of a chronic treatment with cilazapril on the decrease of coronary reserve in SHR rats. For this purpose, a group of 10 SHR rats which received by oral gavage 10 mg/kg/day of cilazapril for 9 weeks was compared with a control group of 9 SHR rats which received distilled water. Coronary reserve was evaluated by measuring coronary blood flow with the radioactive microspheres method before and after a dose of dipyridamole (2 mg/kg/min) which induces maximal coronary vasodilation. The left ventricular weight/body weight ratio was decreased in the cilazapril group compared to the placebo-treated group (p less than 0.001). Moreover, minimal coronary vascular resistance of the left ventricle and the right ventricle were 33% and 39%, respectively, lower in the cilazapril group as compared with the control group (p less than 0.01). We conclude that chronic treatment with cilazapril can prevent the development of left ventricular hypertrophy and the decrease of coronary vascular reserve in the left and right ventricles of spontaneously hypertensive rats.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2004

A cardiac myosin-specific autoimmune response is induced by immunization with Trypanosoma cruzi proteins.

Trypanosoma cruzi is the protozoan parasite that causes Chagas' heart disease, a potentially fatal cardiomyopathy prevalent in Central and South America. Infection with T. cruzi induces cardiac myosin autoimmunity in susceptible humans and mice, and this autoimmunity has been suggested to contribute to cardiac inflammation. To address how T. cruzi induces cardiac myosin autoimmunity, we investigated whether immunity to T. cruzi antigens could induce cardiac myosin-specific autoimmunity in the absence of live parasites. We immunized A/J mice with a T. cruzi Brazil-derived protein extract emulsified in complete Freund's adjuvant and found that these mice developed cardiac myosin-specific delayed-type hypersensitivity (DTH) and autoantibodies in the absence of detectable cardiac damage. The induction of autoimmunity was specific since immunization with extracts of the related protozoan parasite Leishmania amazonensis did not induce myosin autoimmunity. The immunogenetic makeup of the host was important for this response, since C57BL/6 mice did not develop cardiac myosin DTH upon immunization with T. cruzi extract. Perhaps more interesting, mice immunized with cardiac myosin developed T. cruzi-specific DTH and antibodies. This DTH was also antigen specific, since immunization with skeletal myosin and myoglobin did not induce T. cruzi-specific immunity. These results suggest that immunization with cardiac myosin or T. cruzi antigen can induce specific, bidirectionally cross-reactive immune responses in the absence of detectable cardiac damage.

Animals↗
PubMed1996

Molecular pathways controlling heart development.

Heart formation requires complex interactions among cells from multiple embryonic origins. Recent studies have begun to reveal the genetic pathways that control cardiac morphogenesis. Many of the genes within these pathways are conserved across vast phylogenetic distances, which has allowed cardiac development to be dissected in organisms ranging from flies to mammals. Studies of cardiac development have also revealed the molecular defects underlying several congenital cardiac malformations in humans and may ultimately provide opportunities for genetic testing and intervention.

Animals↗
PubMed1993

Dietary sunflower, linseed and fish oils affect phospholipid fatty acid composition, development of cardiac lesions, phospholipase activity and eicosanoid production in Atlantic salmon (Salmo salar).

Atlantic salmon (Salmo salar) post-smolts were fed practical-type diets in which the lipid was supplied either as fish oil (FO), sunflower oil (SFO) or linseed oil (LO) for 12 weeks. In general, the heart phospholipids from SFO-fed fish had increased 18:2n-6, 20:2n-6, 20:3n-6 and 20:4n-6 but decreased 20:5n-3 compared to both other dietary treatments. This was reflected in a decreased n-3/n-6 polyunsaturated fatty acid (PUFA) ratio and an increased 20:4n-6/20:5n-3 or eicosanoid precursor ratio in SFO-fed fish. While heart phospholipids of fish fed LO had increased levels of 18:2n-6, 20:2n-6 and 20:3n-6 compared to fish fed FO, 20:4n-6 levels were reduced, although only significantly in phosphatidylcholine (PC). Dietary-induced changes in phospholipid fatty acid compositions of blood leucocytes were similar to those in heart, although fish fed LO had increased 20:5n-3 compared to fish fed FO. Thromboxane B2 (TXB2) produced by stimulated blood cells was reduced in fish fed LO compared to those fed SFO. Prostaglandin E2 (PGE2) production was reduced in LO-fed fish compared to both other dietary treatments. Fish fed LO had reduced PC in heart membranes compared to the other two dietary treatments, resulting in a ratio of PC:PE (phosphatidylethanolamine) less than unity. Fish fed SFO developed a marked cardiac histopathology which, while present in FO-fed fish albeit in a less severe form, was virtually absent in fish fed LO. Fish fed SFO had increased heart phospholipase A activity compared to those given either FO or LO.

Animals↗