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PubMed1992

Mechanisms involved in cardiac enlargement and congestive heart failure development after acute myocardial infarction.

For 3 months, we followed up 40 patients with acute myocardial infarction, 20 were randomly assigned to treatment with captopril and 20 to placebo, to elucidate mechanisms inducing left ventricular volume enlargement and development of congestive heart failure. Echocardiographic follow-up could be obtained in 28 patients, 11 of whom showed more than a 10% increase in left ventricular systolic and/or diastolic volumes (captopril n = 3/15, placebo n = 8/13, p = 0.05). Volume increase was significantly associated with an impairment in exercise capacity (VO2 max in patients with vs. without volume enlargement 24.7 +/- 1.7 vs. 29.5 +/- 1.9 ml O2/kg/min; p < 0.05). Plasma renin activity, angiotensin II and catecholamines were normal in the acute and chronic postinfarction phase in patients on placebo as well as in patients 12-24 h after captopril intake. Plasma atrial natriuretic peptide concentration (ANP) was increased immediately after myocardial infarction, but ANP levels almost normalized in patients with captopril treatment, while they continued to be elevated in patients on placebo. The only technical parameter able to predict left ventricular volume increases was the sphericity index (28.7 vs. 35.7; p = 0.07). We concluded that morphologic deformation and filling pressures as estimated from elevated ANP levels are major factors promoting remodelling following myocardial infarction. ACE inhibitors might exert their favorable effect predominantly by reducing filling pressure.

Atrial Natriuretic Factor↗
PubMed1991

Embryonic heart rates: development in early first trimester and clinical evaluation.

One hundred and forty-three women in the early first trimester of gestation were examined 364 times using transvaginal sonography, and the development of embryonic heart rate was studied. In each case gestational age was revised retrospectively by either recorded basal body temperature or ultrasound crown-rump length dating between 9 and 10 weeks. Embryonic cardiac activity could be detected as early as 37 days of gestation. In 133 continuing pregnancies, embryonic heart rate rose from an average of 97.7 beats per min at 36-38 days to 174.7 beats per min at 60-62 days. A significant correlation was seen between gestational age and embryonic heart rate (p less than 0.001). The regression equation for heart rate was as follows: heart rate = 3.850 x gestational age (days) -54.64 (r = 0.908, n = 347), in short, embryonic heart rate continued to rise about 4 beats per min every day until 8 weeks of gestation. In this series, 10 pregnancies resulted in spontaneous abortion in the first trimester, and all of them showed relative bradycardia. Embryonic heart rate measurements in 8 of them were below the 95% prediction intervals for normal heart rate plotted against gestational age. This study suggests that embryonic heart rate measurement by ultrasound may be a new method for dating early first trimester, and that first trimester bradycardia may be associated with a poor prognosis for the pregnancy.

Abortion, Spontaneous↗
PubMed2004

Growth of girls who later develop coronary heart disease.

OBJECTIVE: To determine the path of growth of girls who later develop coronary heart disease. DESIGN: Follow up study of girls whose body size at birth, during infancy, and childhood up to age 12 years was recorded. SETTING: Helsinki, Finland. PARTICIPANTS: 4130 girls who were born between 1934 and 1944, attended child welfare clinics in Helsinki, and were still resident in Finland in 1971. MAIN OUTCOME MEASURE: Hospital admission or death from coronary heart disease. RESULTS: In comparison with boys in the same cohort who later developed coronary heart disease the 87 girls were short at birth, rather than thin, had compensatory growth in height during infancy, became thin, and thereafter had a rapid increase in weight and body mass index. In a combined analysis the hazard ratios for coronary heart disease were 1.17 (95% confidence interval (CI) 1.03 to 1.32, p = 0.02) for each 1 cm decrease in length at birth, 1.52 (95% CI 1.23 to 1.89, p < 0.001) for each standard deviation score increase in body mass index after age 3 years, and 1.63 (95% CI 1.09 to 2.42, p = 0.02) for each decrease in level of education. CONCLUSIONS: Though broadly similar, the paths of growth associated with the later development of coronary heart disease differ in girls and boys. This may be because girls are less vulnerable to undernutrition in utero and are better able to sustain postnatal growth in an adverse environment.

Adolescent↗
PubMed1996

Expression of exogenous protein and analysis of morphogenesis in the developing chicken heart using an adenoviral vector.

OBJECTIVES: Recombinant retroviral vectors have been shown to be useful tools for marking cells so as to follow their fates during development. The aim of this study was to determine the utility and advantages of an adenoviral vector as a tool to study the heart as it develops from a simple tube into a complex four-chambered organ. METHODS: Replication-defective adenovirus (10(7) pfu) expressing beta-galactosidase (beta-gal) under the control of the RSV-LTR was applied to the external surface of embryonic stage 13-21 chick hearts in ovo. Embryos were incubated for up to an additional 96 h. Hearts were harvested at 12-24 h intervals and (1) whole-mount-stained for beta-gal and sectioned, (2) examined by electron microscopy and (3) homogenized and beta-gal activity measured with a luminescent assay. RESULTS: beta-gal expression peaked at 48 h, when a significant percentage of the myocytes in the atrial and ventricular walls expressed the protein, and it comprised 0.5% of total heart protein. Significant levels were still expressed at 96 h. When applied to early-stage (13-16) embryos, expression occurred predominantly in cardiomyocytes. beta-gal marking of cells enabled us to identify the following morphogenic patterns: (1) cells of the conus region compact into the bulbis cordis; (2) by applying the virus at later stages, e.g. 21-22, it was evident that the epicardium invests the heart, after stage 17, in a dorsal to ventral and caudal to rostral direction; (3) at lower titers (10(5) pfu), the virus serves as a clonal marker through several cell divisions, with an estimated cell doubling time of 24 h. CONCLUSIONS: Application of an adenoviral vector to early-stage embryonic chick heart results in substantial expression of exogenous protein in a significant percentage of cardiomyocytes without grossly affecting heart development. Adenoviral vectors are useful for following the fate of cells as the heart develops from a simple tube into a complex four-chambered organ and hold promise for enabling the expression of exogenous proteins which might alter cell behavior.

Adenoviridae↗
PubMed1996

Differential expression of alpha-6 and other subunits of laminin binding integrins during development of the murine heart.

The development of the heart from a single heart tube to a four chambered organ with two separated unidirectional flows is a highly complex process. Events like looping, septation, tissue remodelling, and development of valves take place in a time period in which the heart already exerts its pump function. Adhesion of cells to each other and to their extracellular matrix as well as the capability to migrate in such a dynamic environment are extremely important. Integrins and extracellular matrix components have already been implicated in this process. In this report, we describe in detail the differential expression of the alpha-6 integrin subunit during late murine heart development, e.g., in the process from looping to the end of septation. We compare mRNA and protein expression patterns with those of beta-1 and other subunits of laminin-binding integrins, alpha-3 and alpha-7. We show a constant and high expression of alpha-6 in the atrial myocardium and a decrease in expression in the ventricular trabecular myocardium. The compact myocardial wall and the ventricular septum do not express alpha-6, except for the myocardium of the distal outflow tract at early stages. Moreover, we describe expression of this integrin subunit in the endocardial cushions that contribute to the development of the atrioventricular and semilunar valves. We propose a role for the alpha-6-beta-1 laminin receptor in the adhesion of cells to their extracellular matrix at sites of high stress due to cardiac contraction or blood flow induced shear stress. Moreover, site specific endothelial expression within the heart and surrounding extracardiac tissue is discussed. This study suggests a distinct role for alpha-6-beta-1 in the heart and provides insight concerning probably important roles of integrins and their extracellular matrix ligands during embryonic development.

Animals↗
PubMed2002

Expression of Peg1 (Mest) in the developing mouse heart: involvement in trabeculation.

Peg1 (Mest) is an imprinted gene of unknown function widely expressed in the mouse embryo, predominantly in cells of the mesodermal lineage. We have revealed a restricted expression pattern within the developing heart. Initial uniform expression throughout the linear heart tube subsequently becomes restricted, primarily to the developing myocardial trabeculae of both the atria and ventricles, where it persists into late development. Expression in the atrial appendage myocardium precedes the emergence of trabeculae (pectinate muscles), and occurs earlier and to a greater extent on the right than on the left, reflecting the spatial and temporal pattern of trabeculation. Analysis of myocardial morphology in mice lacking the Peg1 gene, which are viable and appear grossly normal, reveals a subtle alteration in the pattern of trabeculation: an increase in thickness and reduction in density of the compact myocardium, similar to that seen in the human cardiomyopathy ventricular noncompaction.

Alleles↗
PubMed2003

Acute and chronic endothelial dysfunction: implications for the development of heart failure.

Heart failure has been characterized by a reduction in cardiac contractile function resulting in reduced cardiac output. The clinical symptoms including mild tachycardia, reduced arterial pressure, increased venous or filling pressure and exercise intolerance have conceptually, to a large degree, been attributed to cardiac myocyte dysfunction. More recently, a vascular component has been recognized to contribute to heart failure. Among the most studied vascular mechanisms that might contribute to the development of heart failure has been the reduced production of nitric oxide or the reduced bioactivity of NO associated with both basic models of heart failure and disease in patients. The still evolving concept that heart failure is a cytokine activated state has, in addition, focused attention on the possibility that the cytokine driven isoform of NO synthase (NOS), iNOS, may produce sufficient quantities of NO to actually suppress cardiac myocyte function contributing to the reduced inotropic state in the failing heart. Thus, our view of the role of NO in the development of heart failure has evolved from simply a reduction in production of NO in blood vessels, to altered substrate availability (i.e. L-arginine), to increased scavenging of NO by superoxide anion, to increased production of NO from iNOS. As these concepts develop, our approach to the therapeutics of heart failure has also progressed with the recognition of the need to develop treatments directed towards addressing one or more of these etiologies. This review will focus on these aspects of the involvement of NO in the development of heart failure and some of the treatments that have developed from our understanding of the basic biology of NO to address these pathohysiologic states.

Acute Disease↗
PubMed1999

Growth in utero and during childhood among women who develop coronary heart disease: longitudinal study.

OBJECTIVE: To examine whether women who develop coronary heart disease have different patterns of fetal and childhood growth from men in the same cohort who develop the disease. DESIGN: Follow up study of women whose body size at birth was recorded and who had an average of 10 measurements of height and weight during childhood. SETTING: Helsinki, Finland. SUBJECTS: 3447 women who were born in Helsinki University Central Hospital during 1924-33 and who went to school in Helsinki. MAIN OUTCOME MEASURES: Hazard ratios for hospital admission for or death from coronary heart disease. Results Coronary heart disease among women was associated with low birth weight (P=0.08 after adjustment for gestation, P=0.007 after adjustment for placental weight) and was more strongly associated with short body length at birth (P=0.001 and P<0.0001, respectively). The hazard ratio for women developing coronary heart disease increased by 10.2% (95% confidence interval 4.3 to 15.7) for each cm decrease in length at birth. The effect of short length at birth was greatest in women whose height "caught up" after birth so that as girls they were tall. Such girls tended to have tall mothers. In contrast, men in the same cohort who developed the disease were thin at birth rather than short, showed "catch up" growth in weight rather than height, and their mothers tended to be overweight rather than tall. CONCLUSION: Coronary heart disease among both women and men reflects poor prenatal nutrition and consequent small body size at birth combined with improved postnatal nutrition and "catch up" growth in childhood. The disease is associated with reductions in those aspects of body proportions at birth that distinguish the two sexes-short body length in women and thinness in men.

Adolescent↗
PubMed1998

Expression of retinol binding protein and transthyretin during early embryogenesis.

Previous studies have shown that anterior lateral plate endoderm from stage 6 chicken embryos is necessary and sufficient to enable precardiac mesoderm to complete its cardiogenic program in vitro, culminating in a rhythmically contractile multicellular vesicle (Sugi and Lough [1994] Dev. Dyn. 200:155-162). To identify cardiogenic factors, we have begun to characterize proteins that are secreted by endoderm cell explants. Fluorography of proteins from endoderm-conditioned medium revealed 1-2 dozen bands, the most prominent of which migrated at approximately 17 and 25 kD. The bulk of the 17-kD band, which migrates near FGFs and subunits of the transforming growth factor-beta family, was identified by N-terminal sequencing as transthyretin (TTR). A component of the 25-kD band was identified by Western blotting as retinol binding protein (RBP). RT/PCR analysis revealed that mRNAs for both proteins are in the embryo as early as stage 3. In situ hybridization localized these mRNAs to the extraembryonic endoderm at stage 6, after which they were detected in endoderm overlying the embryo proper, including the developing heart. Later, RBP and TTR mRNA and protein were detected in cells associated with the developing heart. Western blotting of whole embryo proteins revealed the presence of RBP by stage 7, followed by sequential increases to stage 25; by contrast, content of RBP in isolated hearts peaked at stage 14, then declined. Immunohistochemistry revealed the presence of RBP protein in the extracellular matrix subjacent to lateral plate endoderm beginning at stage 8; upon formation of the definitive heart, intense staining was observed in the cardiac "jelly." By contrast TTR was intracellular, first detected as subtle deposits in stage 6 embryonic endoderm, which by stage 8 were prominent in the dorsally invaginated endoderm subjacent to the precardiac splanchnic mesoderm. At stages 11-14, TTR was detected only in myocardial cells. Such localization of RBP and TTR may indicate a role in the transport and distribution of retinol and thyroid hormone, respectively, from yolk to embryo prior to establishment of the circulatory system, and is suggestive of a subsequent role in heart development.

Amino Acid Sequence↗
PubMed1992

Sarcolemmal Na(+)-Ca2+ exchange activity and exchanger immunoreactivity in developing rabbit hearts.

It has been postulated that as a consequence of an underdeveloped sarcoplasmic reticulum, sarcolemmal Na(+)-Ca2+ exchange assumes relatively greater importance in modulating Ca2+ fluxes in the developing heart. To explore this concept, cardiac sarcolemmal vesicles were prepared from late fetal (28-day gestation), newborn (24-48 h), immature (14-16 days), and adult New Zealand White rabbits. Na(+)-dependent Ca2+ uptake was measured by diluting Na(+)-loaded (140 mM) vesicles into Na(+)-free buffer and measuring 45Ca2+ uptake (40 microM Ca2+) by timed quenching and rapid filtration. Vesicles from all four age groups demonstrated Ca2+ uptake curves characteristic of Na(+)-Ca2+ exchange with stimulation by valinomycin and inhibition by amiloride. Initial uptake velocity (measured at 2 s and corrected for the fraction of competent vesicles) was significantly higher in fetal (23.2 +/- 5.5 nmol/mg) and newborn (26.2 +/- 5.9 nmol/mg) than in adult sarcolemmal preparations (7.3 +/- 1.2 nmol/mg). Uptake was intermediate in the 2-wk-old group (13.7 +/- 1.7 nmol/mg). The relative amounts of exchanger protein were compared by quantitating immunoreactivity using a polyclonal antibody to the Na(+)-Ca2+ exchanger. Densitometric scanning of protein slot blots demonstrated approximately 2.5 times more exchanger protein in fetal and newborn sarcolemma than in adult preparations. The relative amount of exchanger protein detected immunologically corresponded with the age-related differences observed in exchanger activity. Thus the cardiac sarcolemmal Na(+)-Ca2+ exchanger is abundant and functionally well-developed in the late fetal/early newborn rabbit heart and appears to decline postnatally.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2001

ACC/AHA Guidelines for the Evaluation and Management of Chronic Heart Failure in the Adult: Executive Summary A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Revise the 1995 Guidelines for the Evaluation and Management of Heart Failure): Developed in Collaboration With the International Society for Heart and Lung Transplantation; Endorsed by the Heart Failure Society of America.

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Adult↗
PubMed2006

Sphingosine-1-phosphate inhibits cell migration and endothelial to mesenchymal cell transformation during cardiac development.

Sphingosine-1-phosphate (S1P) is a biologically active sphingolipid metabolite that exerts important effects on numerous cellular events via cell surface receptors, S1P(1-5). S1P influences differentiation, proliferation, and migration during vascular development. However, the effects of S1P signaling on early cardiac development are not well understood. To address this issue, we examined the expression of S1P regulatory enzymes and S1P receptors during cardiac development. We observed that enzymes that regulate S1P levels, sphingosine kinase and sphingosine-1-phosphate phosphatase, are expressed in the developing heart. In addition, RT-PCR revealed that four of the five known S1P receptors (S1P(1-4)) are also expressed in the developing heart. Next, effects of altered S1P levels on whole embryo and atrioventricular (AV) canal cultures were investigated. We demonstrate that inactivation of the S1P producing enzyme, sphingosine kinase, leads to cell death in cardiac tissue which is rescued by exogenous S1P treatment. Other experiments reveal that increased S1P concentration prevents alterations in cell morphology that are required for cell migration. This effect results in reduced cell migration and inhibited mesenchymal cell formation in AV canal cushion tissue. These data indicate that S1P, locally maintained within a specific concentration range, is an important and necessary component of early heart development.

Animals↗
PubMed1984

Restriction of maternal food intake inhibits fatty acid activation in developing rat hearts.

We studied the effect of restricting the diet of pregnant and lactating rats on the beta-oxidation of fatty acids by the developing heart in suckling pups. Control pregnant rats were fed a stock diet ad libitum. For the experimental group, food was restricted to half of the control intake on the seventh day of pregnancy and continued through lactation. The pups on the restricted diet were significantly smaller than the controls. At postnatal days 5, 14 and 21, the beta-oxidation of [1-14C] palmitate by heart homogenates was determined in the presence of ATP, carnitine and CoA. At day 21, the production of 14CO2 was 60% lower in the group on the restricted diet. Consequently, the possibility of inhibiting activation or intramitochondrial transport of fatty acids by heart mitochondria was studied in vitro using [1-14C] palmitate, [1-14C] palmitoyl CoA and [1-14C] palmitoyl carnitine. With [1-14C] palmitate, the rate of 14CO2 produced was 2464 +/- 317 cpm/mg protein/min for the control and 1682 +/- 91 for the restricted diet group. With [1-14C] palmitoyl CoA and [1-14C] palmitoyl carnitine, the oxidation rate of the experimental group was similar to control values, showing clearly that the inhibition of oxidation was from a problem with activation. A significant decrease in palmitoyl CoA synthetase activity in the heart homogenates and mitochondria of the diet-restricted pups took place.

Animals↗
PubMed2005

Expression pattern of neuronal and skeletal muscle voltage-gated Na+ channels in the developing mouse heart.

In the mammalian heart, a variety of voltage-gated Na(+) channel transcripts and proteins have been detected. However, little quantitative information is available on the abundance of each transcript during development, or the contribution of TTX-sensitive Na(+) channels to the cardiac sodium current (I(Na)). Using competitive and real-time RT-PCR we investigated the transcription of six Na(+) channels (Na(v)1.1-Na(v)1.6) and the beta1 subunit during mouse heart development. Na(v)1.5 was predominantly expressed in the adult heart, whereas the splice variant Na(v)1.5a was the major Na(+) channel isoform in embryonic hearts. The TTX-resistant Na(+) channel transcripts (Na(v)1.5 and Na(v)1.5a) increased 1.7-fold during postnatal development. Transcripts encoding TTX-sensitive Na(+) channels (Na(v)1.1-Na(v)1.4) and the beta1 subunit gradually increased up to fourfold from postnatal day (P)1 to P126, while the Na(v)1.6 transcript level remained low and constant over the same period. In adults, TTX-sensitive channel mRNA accounted for 30-40% of the channel pool in whole-heart preparations (Na(v)1.3 > Na(v)1.4 > Na(v)1.2 >> Na(v)1.1 approximately Na(v)1.6), and 16% in mRNA from isolated cardiomyocytes (Na(v)1.4 > Na(v)1.3 > Na(v)1.2 > Na(v)1.1 > Na(v)1.6). Confocal immunofluorescence on ventricular myocytes suggested that Na(v)1.1 and Na(v)1.2 were localized at the intercalated disks and in the t tubules. Na(v)1.3 labelling predominantly produced a diffuse but strong intracellular signal. Na(v)1.6 fluorescence was detected only along the Z lines. Electrophysiological recordings showed that TTX-sensitive and TTX-resistant Na(+) channels, respectively, accounted for 8% and 92% of the I(Na) in adult ventricular cardiomyocytes. Our data suggest that neuronal and skeletal muscle Na(+) channels contribute to the action potential of cardiomyocytes in the adult mammalian heart.

Animals↗
PubMed1976

The cytochemical localization of cholinesterase activity in the developing chick heart.

The electronhistochemical localization of the cholinesterases of developing chick heart muscle cells has been studied with the aid of a substrate which incorporates an enzyme-susceptible thiolester group and a diazonium group into the same molecule. The embryonic chick heart exhibits cholinesterase activity from Hamilton-Hambruger stage 3 through to four days post hatching. Although enzyme activity is not demonstrated in every location at all stages studied, it has been observed on the nuclear envelope, golgi complex, rough and smooth endoplasmic reticulum, mitochondria and myofilaments. A change in the type of activity has been demonstrated, acetylcholinesterase is found during the first fourteen days of development but thereafter, non-specific cholinesterase is seen instead. As nerves have not been found in relation to the working myocardium, further support is given to the concept that an acetylcholine-cholinesterase system of myogenic origin is involved in spontaneous contraction. Consideration of the distribution of enzyme within the myocardial cell, raises the possibility that cholinesterase may be concerned in a regulatory mechanism of protein synthesis, a suggestion made previously in connection with liver cells.

Animals↗
PubMed1985

Characterization of a myosin heavy chain in the conductive system of the adult and developing chicken heart.

A monoclonal antibody (anterior latissimus dorsi 58 [ALD58]; antimyosin heavy chain, MHC) directed against myosin from slow tonic muscle was found to react specifically with the striated muscle cells of the conductive system in the adult chicken heart. This monoclonal antibody was used to study the expression of myosin in the conductive system of the adult and developing heart. Using immunofluorescence microscopy with ALD58, muscle cells of the conductive system were demonstrated in both the atria and ventricles of the adult heart as previously shown by Sartore et al. (Sartore, S., S. Pierobon-Bormioli, and S. Schiafinno, 1978, Nature (Lond.), 274: 82-83). Radioactive myosin from adult atria and ventricles was precipitated with ALD58 and subjected to limited proteolysis and subsequent peptide mapping. Peptide maps of ALD58 reactive myosin from atria and ventricles were very similar, if not identical, but differed from peptide maps of ordinary atrial and ventricular myosin. The same antibody was used to study cardiac myogenesis in the chick embryo. When ALD58 was reacted with myosin isolated from atria and ventricles at selected stages of development in radioimmunoassays, reactivity was not observed until the last week of embryonic life (greater than 15 d of egg incubation). Thereafter concomitant and progressively increased reactivity was observed in atrial and ventricular preparations. Also, no ALD58 positive cells were observed in immunofluorescence studies of embryonic hearts until 17 d of egg incubation. Primary cell cultures of embryonic hearts also proved to be negative for this antibody. This study demonstrates that an epitope recognized by ALD58 associated with an antimyosin heavy chain of striated muscle cells of the adult heart conductive system is absent or present in only small amounts in the early embryonic heart.

Aging↗
PubMed2002

Retinoic acid influences the expression of the neuronal regulatory genes Mash-1 and c-ret in the developing rat heart.

We analyzed the expression of neuronal regulatory genes Mash-1 and c-ret by immunohistochemistry and reverse transcriptase-polymerase chain reaction in the developing heart of rat embryos following exogenous retinoic acid (RA) treatment of the pregnant dams. On E12, expression of Mash-1 and c-ret was confined to cells migrating via the common cardinal vein. On E16.5, Mash-1 and c-ret expression were restricted to cardiac ganglia around the great vessels and posterior atrial wall. While Mash-1 expression was down-regulated at birth, that of c-Ret was maintained. RA-treated hearts showed a down-regulation of both Mash-1 and c-Ret at the mRNA as well as at the protein level on E16.5. The present results show that differentiation of cardiac ganglionic cells is affected after RA treatment, by the down-regulation of Mash-1 and c-Ret.

Animals↗
PubMed1986

Development of heart and aortic lesions in DBA/2NCrj mice.

The development of heart and aortic lesions was investigated in 3- to 8-week-old DBA/2NCrj mice. In the heart, small foci of myocardial calcification and severe calcification with subsequent inflammation were observed. Severe lesions were restricted to the myocardium below the right ventricular epicardium. Small foci of myocardial calcification were found from 4 to 8 weeks of age with almost the same frequency. The incidence of severe calcification showed a drastic increase between 6 and 7 weeks of age. Aortic lesions were observed from 3 weeks of age and characterized by focal calcification of the smooth muscle cells and elastic laminae. The frequency of aortic calcification was about 50% and not age-related.

Animals↗