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PubMed2004

Heart disease awareness among college students.

The purpose of this research was to explore college students' attitudes about heart disease risks and preventive strategies. The survey population consisted of students enrolled in selected lecture courses at Arizona State University. A total of 1481 surveys were used in data analysis. Respondents indicated a lower perception of heart disease risk for women than for men, and a majority of students incorrectly believed that breast cancer is a more significant health concern for women than heart disease. Respondents in most ethnic groups believed that whites are most at risk for developing heart disease. Students overall had relatively low levels of knowledge about heart disease and its risk factors compared to other health issues, such as sexually transmitted diseases (STDs) and psychological disorders. The results suggest that educational intervention is necessary to increase college students' knowledge about heart disease; and, in particular, efforts need to be made to raise awareness about heart disease among women and minorities. Guidelines for future educational intervention must address common misconceptions about which demographic groups are at risk for developing heart disease and address gaps in knowledge that young people have regarding heart disease prevention.

Ethnicity↗
PubMed1994

A time-insensitive predictive instrument for acute hospital mortality due to congestive heart failure: development, testing, and use for comparing hospitals: a multicenter study.

The purpose of this study was to develop a "time-insensitive" predictive instrument (TIPI) for acute hospital mortality due to congestive heart failure. In Phase 1, based on prospectively collected data on 401 congestive heart failure patients among 5,773 study patients who presented to six New England hospitals over a 2-year period whose chief complaints were chest pain, shortness of breath, or other cardiac symptoms, a multivariable logistic regression was used to develop the TIPI for acute mortality. Discrimination between patients who lived and those who died was reflected by receiver-operating characteristic (ROC) curve area of 0.90. Predicted mortality was found to not vary significantly from actual mortality rates across deciles of predicted probabilities from 0% to 100%. In Phase 2, the six hospitals' actual mortality rates for their congestive heart failure patients were compared to their respective rates predicted by the TIPI. Actual hospital mortality rates ranged from 3.6% to 11.3%, with no hospital having a statistically significantly higher rate. Predicted mortality rates ranged from 4% to 9%, with one hospital having a significantly lower predicted rate (P = .01), and one hospital having a borderline significantly higher predicted rate (P = .07). Individual hospitals' differences between actual and predicted mortality ranged from -3.8% to +4.7% (all NS). When grouped by hospital type, respectively for urban teaching, smaller city teaching, and rural non-teaching hospitals, the actual mortality rates were 5.1%, 10.5%, and 5.4%, (NS). The predicted mortality rates were 8.3%, 6.1%, and 5.4%, respectively, with the rate for urban major teaching centers being significantly higher (P = .03). No hospital type had significant differences between their actual and predicted mortality rates (NS). This congestive heart failure mortality TIPI (CHFM-TIPI) shows potential for risk-adjusted studies of hospitals, mortality for multi-hospital groups, hospital-to-hospital comparisons, and potentially for within-hospital assessment and if further validated, potentially also for real-time clinical use.

Acute Disease↗
PubMed1998

Differential expression of flectin in the extracellular matrix and left-right asymmetry in mouse embryonic heart during looping stages.

A novel extracellular matrix protein flectin (250 kD M(r)) shows specific left-right asymmetric expression before and throughout the looping process during heart development in avian embryos [Tsuda et al., 1996]. Flectin is a candidate molecule to provide directionality to the looping process in the avian model. In this study on mouse embryonic heart development, flectin is shown to be developmentally regulated and to be expressed in a specific asymmetric fashion, but in a different pattern from that observed in avian hearts. The molecules involved in development tend to be the same, but timing of expression, modulation, and asymmetry are different. In the mouse embryo, flectin is expressed symmetrically when the cardiogenic plate is formed. As looping progresses, flectin expression becomes asymmetric. There is right side predominance at the outflow tract and left side predominance at the ventricular portion of the tubular heart. The left side predominance of flectin develops in an anteroposterior direction, while right side predominance of the outflow tract remains relatively unchanged. These differential expression patterns of flectin decrease once the looping process is completed. After looping, flectin becomes restricted to the epicardium and subepicardial extracellular regions. In inv/inv mice, a known mouse model for human situs inversus, in which the directionality of heart looping is inverted, flectin expression pattern is mirror image of that of normal mouse embryos during looping stages. Our study indicates that, in the mouse, flectin shows a specific asymmetric expression pattern after initiation of heart looping and that this asymmetric expression pattern is related to the directionality of looping. The remodeling of the extracellular matrix (ECM) including specific flectin expression begins with the looping process. This morphogenetic change of the ECM coincides with the differentiation of each region of the tubular heart.

Animals↗
PubMedDate not supplied

[Epidemiologic characteristics of nutrition of school children at high risk for developing ischemic heart disease and atherosclerosis].

The results of the investigation of a representative sample of Moscow schoolchildren, aged 11-14 years, are described. The investigation included a triple arterial pressure measuring, anthropometry, numerical score of sexual development, assay of cholesterol, triglycerides and high-density lipoprotein cholesterol levels in the blood serum. The character of nutrition of 250 (20% of the sample) schoolchildren was studied by the method of dietary inquiry (daily ration) with the use of food patterns. The data of the multivariative analysis have shown that sexual development, a low educational level of the parents (among them subjects engaged in the manual labor being predominant) influence the development of the risk factors of ischemic heart disease and atherosclerosis. Composition of food is of great importance, especially for boys with dislipoproteinemias (low consumption of starch per 1 kg bw, high consumption of total protein, low consumption of fat in cal %), and for those with excessive body mass and low physical activity (low consumption of total fat, polyunsaturated fat per 1 kg bw, as well as high consumption of total protein in cal %).

Adolescent↗
PubMed1983

Prenatal ethanol exposure alters development of heart ornithine decarboxylase response to insulin in rat. II. Daily dose.

Timed pregnant rats received daily a bolus of ethanol (4 g/kg, via stomach tube) from the 13th day of gestation and the development of cardiac sympathetic nerve function was determined in the offspring. Stimulation in sympathetic nerve activity was determined by an increase in heart ornithine decarboxylase (ODC) activity evoked by insulin-induced hypoglycemia. In controls, insulin-induced stimulation in heart ODC activity was maximal between 4 and 8 days of postnatal age. However, chlorisondamine pre-treatment decreased this stimulation starting from 6 days of age indicating that the induction in activity from this age is mediated via central stimulation of sympathetic nerves. In contrast, pups whose mothers received ethanol both during gestation and post-partum showed a decreased cardiac ODC response to insulin between 6 and 13 days of age. Withdrawal from ethanol at birth appeared to slow the development of neuronal reflex response to 8 days of age. Prenatal exposure to ethanol also altered the development of brain ODC response to insulin. In both heart and brain, basal ODC activity was increased after ethanol exposure. These data demonstrate that maternal exposure to ethanol even transiently produces alterations in the development of brain and cardiac sympathetic response to insulin in the offspring.

Animals↗
PubMed2006

Developmental stage-specific biphasic roles of Wnt/beta-catenin signaling in cardiomyogenesis and hematopoiesis.

Although Wingless (Wg)/Wnt signaling has been implicated in heart development of multiple organisms, conflicting results have been reported regarding the role of Wnt/beta-catenin pathway in cardiac myogenesis: Wg/armadillo signaling promotes heart development in Drosophila, whereas activation of Wnt/beta-catenin signaling inhibits heart formation in avians and amphibians. Using an in vitro system of mouse ES cell differentiation into cardiomyocytes, we show here that Wnt/beta-catenin signaling exhibits developmental stage-specific, biphasic, and antagonistic effects on cardiomyogenesis and hematopoiesis/vasculogenesis. Activation of the Wnt/beta-catenin pathway in the early phase during embryoid body (EB) formation enhances ES cell differentiation into cardiomyocytes while suppressing the differentiation into hematopoietic and vascular cell lineages. In contrast, activation of Wnt/beta-catenin signaling in the late phase after EB formation inhibits cardiomyocyte differentiation and enhances the expression of hematopoietic/vascular marker genes through suppression of bone morphogenetic protein signaling. Thus, Wnt/beta-catenin signaling exhibits biphasic and antagonistic effects on cardiomyogenesis and hematopoiesis/vasculogenesis, depending on the stage of development.

Animals↗
PubMed2002

Transcriptional regulation of vertebrate cardiac morphogenesis.

Transcription factors can regulate the expression of other genes in a tissue-specific and quantitative manner and are thus major regulators of embryonic developmental processes. Several transcription factors that regulate cardiac genes specifically have been described, and the recent discovery that dominant inherited transcription factor mutations cause congenital heart defects in humans has brought direct medical relevance to the study of cardiac transcription factors in heart development. Although this field of study is extensive, several major gaps in our knowledge of the transcriptional control of heart development still exist. This review will concentrate on recent developments in the field of cardiac transcription factors and their roles in heart formation.

Animals↗
PubMed2005

Mechanics and function in heart morphogenesis.

For years, biomechanical engineers have studied the physical forces involved in morphogenesis of the heart. In a parallel stream of research, molecular and developmental biologists have sought to identify the molecular pathways responsible for embryonic heart development. Recently, several studies have shown that these two avenues of research should be integrated to explain how genes expressed in the heart regulate early heart function and affect physical morphogenetic steps, as well as to conversely show how early heart function affects the expression of genes required for morphogenesis. This review combines the perspectives of biomechanical engineering and developmental biology to lay out an integrated view of the role of mechanical forces in heart development.

Animals↗
PubMed1988

Ryanodine and caffeine prevent ventricular arrhythmias during acute myocardial ischemia and reperfusion in rat heart.

This study investigates the possible role of oscillatory release of calcium from sarcoplasmic reticulum in the genesis of ventricular arrhythmias during acute myocardial ischemia and reperfusion in isolated rat hearts. We used ryanodine and caffeine, which are known to modulate the oscillatory release of calcium from sarcoplasmic reticulum. During 30 minutes of left main coronary artery ligation, all 13 control hearts developed ventricular premature beats (number of beats, 225 +/- 51) and ventricular tachycardia (duration, 123 +/- 21 seconds); five hearts developed ventricular fibrillation. In a separate series of experiments, reperfusion after 15 minutes of coronary artery ligation caused ventricular fibrillation to occur within 15 seconds in all 12 hearts. Ryanodine (10(-9) to 10(-7) M) abolished ventricular arrhythmias during coronary artery ligation and prevented reperfusion ventricular fibrillation. Ryanodine (10(-9), 10(-8), and 10(-7) M) caused 15%, 23%, and 74% decreases in the maximal rate of rise of left ventricular pressure development and 20%, 32%, and 85% decreases in the maximal rate of fall of left ventricular pressure development, respectively, prior to coronary artery ligation. During acute myocardial ischemia, ryanodine 10(-9) M maintained and 10(-8) M impaired left ventricular function; 10(-7) M caused left ventricular failure. Coronary perfusion rate did not increase during ischemia. Antiarrhythmic activity occurred independent of preservation of high energy phosphates, reduction in tissue lactate, or tissue cyclic adenosine monophosphate in the ischemic myocardium. Caffeine 10(2) M decreased the incidence of ventricular arrhythmias during ischemia and upon reperfusion; protection occurred coincident with development of diastolic contracture. Caffeine increased ischemic tissue cyclic adenosine monophosphate content and worsened tissue energy status.(ABSTRACT TRUNCATED AT 250 WORDS)

Alkaloids↗
PubMed1995

Morphological changes in the normal pattern of ventricular myoarchitecture in the developing human heart.

BACKGROUND: The aim of the present study was to describe the morphological changes in the normal pattern of ventricular myoarchitecture in the prenatal and adult human heart, to understand the three-dimensional organization of the muscle fibers and their active functional role in valvular dynamics. METHODS: We used dissection and histological techniques in 56 human hearts from fetuses and adults of both sexes. RESULTS: In all hearts, the ventricular wall was arranged in three different layers: superficial (subepicardial), middle, and deep (subendocardial) myocardium. The superficial and deep layers are present in both ventricles, whereas the middle layer is found only in the left ventricle. Age-related differences were noted in the pattern of myoarchitecture of the superficial layer, mainly in the fetal period, and especially in the right ventricle; however, the middle layer always shows a circumferential pattern, which is specially evident in elderly hearts. The ventricular fibers in the superficial and deep layers are anchored in the ventricular orifices. CONCLUSIONS: Our findings reveal that muscle fiber architecture showed age- but not sex-related differences. These variations may reflect a mechanism of adaptation of the heart to functional demands throughout life.

Adolescent↗
PubMed1984

Development of enzymes of energy metabolism in rat heart.

The behavior of several enzymes was studied during rat heart development (4 days before birth to adult stage). Hexokinase has its highest activity during the fetal period; it decreases at birth and remains with low activity in the adult. The alpha-glycerophosphate dehydrogenase and alpha-glycerophosphate oxidase profiles are similar up to the 15th day of development. From there onwards, both profiles diverge, the cytoplasmic activity increasing 3-fold, while the mitochondrial activity remains unchanged. The developmental profiles of the malate dehydrogenases are almost parallel. The development of citrate synthase and succinate dehydrogenase results in a 2- to 4-fold increase in their activities. However, ATPase increases dramatically (20-fold) over the same period. With respect to the enzymes of the adenine nucleotide metabolism, adenylate kinase is fully expressed throughout all ages examined, showing no variation during development. AMP deaminase and creatine kinase increase during development, the cytoplasmic creatine kinase reaching a high level at birth whereas the increases of the mitochondrial enzymes take place gradually during development.

AMP Deaminase↗
PubMed2000

Heart failure development in rats with ascending aortic constriction and angiotensin-converting enzyme inhibition.

It remains unknown whether angiotensin-converting enzyme (ACE) inhibition can prevent heart failure in rats with a fixed high pressure load of the left ventricle and if this effect could be attributed to normalization of contractile protein phenotype and cardiac collagen content. Rats with constriction of the ascending aorta were treated with the ACE inhibitor quinapril (6 mg kg(-1) day(-1)) (n=95) or placebo (n=96) (starting 6 weeks post surgery. Quinapril treatment improved survival markedly (P<0.0000001) during the 24 weeks observation period. There were 69 deaths with placebo and only 25 deaths with quinapril. At the end of the observation period signs of left ventricular backward failure were, however, detected in 75 rats with placebo and in 67 rats treated with quinapril (P=0.229). Cox proportional hazard model with time-dependent covariates was used to document that the effect of quinapril treatment had been dependent on time. Quinapril had no significant effect on the development of morphological signs of left ventricular dysfunction after the first 54 days of treatment. The increased isomysin V(3) proportion of hypertrophied non-failing hearts was also not affected by quinapril treatment. Irrespective of treatment, failing hypertrophied hearts were characterized by an increase in left ventricular volume (P<0.05), percentage of the 'foetal' isomyosin V(3) (P<0.05), and hydroxyproline concentration (P<0.05). While the cause of the improved survival remains unknown, quinapril did apparently not interfere with the restitution of 'foetal' gene expression of pressure overloaded cardiomyocytes leading to depressed myocardial performance, ventricular dysfunction and the consecutive myocardial fibrosis.

Analysis of Variance↗
PubMed1995

Studies of hypoxemic/reoxygenation injury: without aortic clamping. III. Comparison of the magnitude of damage by hypoxemia/reoxygenation versus ischemia/reperfusion.

The immature heart is more tolerant to ischemia than the adult heart, yet infants with cyanosis show myocardial damage after surgical correction of congenital cardiac defects causing hypoxemia. This study tested the hypothesis that the hypoxemic developing heart is susceptible to oxygen-mediated damage when it is reoxygenated during cardiopulmonary bypass and that this hypoxemic/reoxygenation injury is more severe than ischemic/reperfusion stress. Fifteen Duroc-Yorkshire piglets (2 to 3 weeks old, 3 to 5 kg) underwent 60 minutes of 37 degrees C cardiopulmonary bypass. Five piglets (control) were not made ischemic or hypoxemic. Five underwent 30 minutes of normothermic ischemia (aortic clamping) and 25 minutes of reperfusion before cardiopulmonary bypass was discontinued. Five others underwent 30 minutes of hypoxemia (bypass circuit primed with blood with oxygen tension 20 to 30 mm Hg) and 30 minutes of reoxygenation during cardiopulmonary bypass. Functional (left-ventricular contractility) and biochemical (levels of plasma and tissue conjugated dienes and antioxidant reserve capacity) measurements were made before ischemia/hypoxemia and after reperfusion/reoxygenation. Cardiopulmonary bypass (no ischemia or hypoxemia) caused no changes in left-ventricular function or coronary sinus levels of conjugated dienes. The tolerance to normothermic ischemia was confirmed, inasmuch as left-ventricular function returned to 108% of control values and coronary sinus levels of conjugated dienes did not rise after reperfusion. Conversely, reoxygenation raised plasma levels of conjugated dienes in coronary sinus blood in the hypoxic group 57% compared with end-hypoxic levels (p < 0.05 versus end-hypoxic levels and versus ischemia, by analysis of variance). Antioxidant reserve capacity showed the lowest levels (highest production of malondialdehyde) in the hypoxemic group (51% higher than control values; p < 0.05 by analysis of variance). These biochemical changes were associated with a 62% depression of left-ventricular function after bypass because end-systolic elastance recovered only 38% of control levels (p < 0.05 by analysis of variance). These data confirm the tolerance of the immature heart to ischemia and reperfusion and document a hypoxemic/reoxygenation injury that occurs in immature hearts reoxygenated during bypass. Hypoxemia seems to render the developing heart susceptible to reoxygenation damage that depresses postbypass function and is associated with lipid peroxidation. These findings suggest that starting bypass in cyanotic immature subjects causes an unintended reoxygenation injury that may potentially be counteracted by adding antioxidants to the prime of the extracorporeal circuit.

Alkadienes↗
PubMed2000

Chronic exercise training preserves prostaglandin-induced dilation of epicardial coronary artery during development of heart failure in awake dogs.

Although it has been shown that long-term exercise training preserves endothelium-mediated nitric oxide vasodilator function in chronic heart failure (CHF), whether exercise training exerts similar beneficial effects on endothelial/prostaglandin-mediated vasodilator capacity in coronary circulation during the development of CHF has not been determined. Fifteen mongrel dogs were surgically instrumented for measurement of left ventricular pressure, aortic pressure, coronary blood flow and left circumflex coronary artery diameter. Dogs (n = 5) who underwent 4 weeks of cardiac pacing (210 b/min for 3 weeks and 240 b/min for the 4th week) developed CHF as characterized by significant reduction in left ventricular systolic pressure, mean arterial pressure and left ventricular dP/dt, increases in left ventricular end-diastolic pressure and heart rate, as well as clinical signs of CHF. Endothelial prostaglandin-mediated vasodilation of the epicardial coronary artery was impaired, as manifested by an attenuated arachidonic acid (AA)-induced dilation of the artery (epicardial artery diameter increased by: 0.78 +/- 0. 84% in CHF versus 4.6 +/- 0.89% in normal, P < 0.05); however, prostacyclin (PGI(2))-induced and nitroglycerin-induced vasodilation of the coronary circulation were not altered. In contrast, dogs (n = 6) with cardiac pacing plus daily exercise training (4.4 +/- 0.3 km/h, 2 h/day) only developed mild cardiac dysfunction, and the response of the epicardial coronary artery diameter to AA was preserved (epicardial artery diameter increased by 4.2 +/- 0.98% from baseline, P 0.05 compared to its respective control). Thus, long-term exercise training preserves endothelial/prostaglandin-mediated dilation of epicardial coronary artery during development of CHF.

Animals↗
PubMed1986

Ultrastructural quantitative characterisation of sinus and atrioventricular nodal cells in the developing caprine heart compared with ordinary atrial and ventricular myocardial cells.

Cellular growth and changes in subcellular components as well as in intercellular junction structure were investigated quantitatively in sinus and atrioventricular nodes in comparison with right atrial and left ventricular myocardial cells of the goat heart in fetuses aged 6, 8, 10, 12, 14, 16 and 18 gestational weeks, young animals aged 1 and 3 postnatal weeks, and adults. At the earliest stage examined (sixth gestational week) no clear difference was recognised, in the patterns of star diagrams representing cellular characteristics, between nodal cells and ordinary cardiac muscle cells, except for a larger number of myofibrils in the ordinary cells. Atrial specific granules also appeared in the atrial cells at this stage. In general, initial signs of differentiation in ordinary cardiac muscle cells were detected at the sixteenth gestational week when transverse tubule formation occurred in the ventricular muscle cells. Throughout the developmental period, no appreciable alterations in the ultrastructural features were found in the sinus nodal cells whereas the atrioventricular nodal cells revealed slight changes at the later fetal and adult stages.

Animals↗
PubMed1997

The chicken GATA-6 locus contains multiple control regions that confer distinct patterns of heart region-specific expression in transgenic mouse embryos.

The GATA-6 transcription factor is expressed in cardiogenic cells and during subsequent stages of heart development in diverse vertebrate species. To gain insights into the molecular events that govern this heart-restricted expression, we isolated the chicken GATA-6 gene and used several approaches to screen for associated control regions. Our analysis of two chicken GATA-6/lacZ constructs in transgenic mouse embryos was particularly revealing. One GATA-6/lacZ construct, which has 1.5 kilobase pairs of upstream sequences along with the promoter and first intron, was expressed exclusively in the atrioventricular canal region of the heart. This expression pattern is novel and appears to mark specialized myocardial cells that induce underlying endocardial cells to initiate valve formation. The other GATA-6/lacZ construct, which has an additional 7.7 kilobase pairs of upstream sequences, was expressed in the ventricle and outflow tract in addition to the atrioventricular canal. The failure of these GATA-6 control regions to function as enhancers in transfected cardiac myocyte cultures underscores the importance of using transgenic approaches to elucidate transcriptional controls that function in the developing heart. Although the endogenous GATA-6 gene is expressed throughout the heart, our results indicate that this is effected in a heart region-specific manner.

Animals↗