Development of heart rate responses in early infancy [proceedings].
Explore the source record for details and available documents.
Acoustic Stimulation↗
SEARCH · Search PubMed
Results for “Heart 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.
Effects of age, light regimes and food removal on development of daily rhythmicity in chick heart rate.
Development of daily rhythms in the chick heart rate was investigated during the post-hatching period. The measurements were made in free-moving chicks at one-hour intervals under different light conditions. Clear daily rhythms were seen 3 days after hatching under LD (12:12 hr.) whereas no daily rhythm was observed under either constant illumination or constant dark. The present study demonstrated that while heart rate increased with age during the post-hatching period, the light-time heart rate increased more rapidly than the dark-time heart rate. It was also found that the daily rhythms in heart rate were not formed after food removal even under LD. These results indicate that the light and feeding play an important role in the development of the daily rhythms in chick heart rate.
Age Factors↗
[Tears in fibrotic heart valves and the mechanism of their development in acquired heart defect. Case report].
Explore the source record for details and available documents.
Adult↗
Disproportionate ventricular septal thickening in the developing normal human heart.
A disproportionately thickened ventricular septum containing numerous disorganized cardiac muscle cells is the most characteristic anatomic feature of hypertrophic cardiomyopathy. Since information concerning ventricular wall thicknesses and cellular arrangement in the developing heart may be pertinent to understanding the genesis of hypertrophic cardiomyopathy, morphologic observations were made in 151 normal human embryos, fetuses and term infants. Disproportionate ventricular septal thickening (septal-free wall ratio greater than or equal to 1.3) was present in 94% of embryos and young fetuses; in over one-third disproportionate thickening was particularly pronounced (septal-free ratio greater than or equal to 2.0). Disproportionate septal thickening was also present in 65% of older fetuses, but in only 12% of infants over two weeks of age. Septal-free wall ratio decreased in a curvilinear fashion with increasing age and apporixmated unity in the newborn. This phenomenon occurred because, while both ventricular septal and left ventricular free wall thicknesses increased directly with age, free wall thickness increased at a greater rate than septal thickness, particularly after birth. Marked cellular disorganization in the septum was not a feature of the hearts studied.
Female↗
Asymmetric septal hypertrophy and myocardial fiber disarray. Features of normal, developing, and malformed hearts.
The specificity and significance of the asymmetric septal hypertrophy (ASH) and myocardial fiber disarray of idiopathic hypertrophic subaortic stenosis (IHSS) is uncertain. To examine this we studied 215 hearts, including normal embryos, fetuses, children, and adults; and hearts with congenital and acquired disease. Disproportionate septal thickening was present in all embryos and in some abnormal hearts, particularly those with severe right ventricular hypertrophy due to congenital malformations. Some myocardial fiber disarray was present in all hearts at the junctions of interventricular septum and ventricular free wall. In hearts with semilunar valve atresia with intact ventricular septums, and in the infundibulum of some with tetralogy of Fallot, however, extensive fiber disarray was present. Thus, ASH occurs in the normal developing heart and in some malformed hearts with RVH; marked muscle fiber disarray may occur in certain congenital lesions with abnormal systolic contraction. Neither morphologic finding independently or in combination is pathognomonic of idiopathic hypertrophic subaortic stenosis.
Adult↗
The advantage of heterotopic cardiac transplantation over orthotopic cardiac transplantation in the management of severe acute rejection.
The major problems with organ transplantation are rejection of the allograft and the side effects of antirejection therapy. This report describes the successful treatment of a patient in whom rejection of the donor heart developed 10 months after implantation. The recipient's own heart had been left intact and was able to support the circulation during the period of rejection. Indications are that the "rest" period of 10 months was beneficial to the myopathic left ventricle of the recipient's heart.
Adult↗
Electron microscopic investigations on the differentiation of Purkinje cells in the ontogenetic development of the chicken heart.
The ultrastructural development of subendocardial Purkinje cells of chicken left ventricle was investigated. In 9-day-old chick embryos the cell diameter and the organization of the cell organelles allow a distinction between Purkinje cells and ordinary myocardial cells In 14-day-old chick embryos, Purkinje cells show large accumulations of myosin filaments with interspersed ribosomes in addition to normomeric myofibrils. In these accumulations actin filaments seem to be absent. The deficiency of actin filaments is supposedly the reason for the random distribution of the myosin filaments. Purkinje cells of early chick embryos show areas with densely packed glycogen granules. In older embryos the glycogen concentration declines and only separate glycogen granules are visible. At hatching time the first subsarcolemmal leptomeric fibrils were observed in Purkinje cells. Leptomeric complexes arising in a close spatial relationship to the accumulations of myosin filaments and ribosomes can be seen in 2--4 week-old chickens. With the increasing age of the chickens, the size of these accumulations declines. Adult hens exhibit smaller accumulations, mainly in the neighborhood of leptomeric complexes. Purkinje cells show a distinct ontogenetic development. They are not simple embryonic remnants of ordinary myocardial cells.
Animals↗
Exploring genetic mapping and co-expression patterns to illuminate significance of Tbx20 in cardiac biology.
The transcription factor Tbx20 is integral to heart development and plays a significant role in various cardiac diseases. Despite its established importance, the regulatory mechanisms and functional significance of Tbx20 remain incompletely understood. To elucidate these mechanisms, we initially conducted eQTL mapping to identify genetic loci associated with Tbx20 expression in heart tissue from BXD mice. Co-expression and enrichment analyses revealed pathways linked to Tbx20, including dilated cardiomyopathy, hypertrophic cardiomyopathy, and FoxO signaling. Additionally, protein-protein interaction studies identified essential cardiac proteins, such as Myl2 and Myl7, along with upstream regulators like Mef2c. To validate our bioinformatic findings, we performed quantitative reverse transcription polymerase chain reaction (qRT-PCR) to assess the relative mRNA expression levels of TBX20 and Mef2c in the heart tissues of BXD mice compared to their parental strains (B6 and D2). Our results demonstrated significant up-regulation of both TBX20 and Mef2c in the BXD group relative to the parental strains. Conversely, both genes were down-regulated in B6, D2, Control, and Treatment groups when compared to BXD mice. These findings confirm the predicted regulatory roles of TBX20 and Mef2c in cardiac development as suggested by our initial analyses.This study not only reinforces the critical role of Tbx20 in cardiac gene regulation but also highlights its potential as a therapeutic target for cardiovascular disorders. Further investigations into Tbx20 and its interactions will enhance our understanding of heart biology and contribute to the development of targeted therapies for heart diseases.
Animals↗
Role of tropomyosin in actin filament formation in embryonic salamander heart cells.
Recessive mutant gene c in Ambystoma mexicanum embryos causes a failure of the heart to function even though initial heart development appears normal. An analysis of the constituent proteins of normal and mutant hearts by SDS-poly-acrylamide gel electrophoresis shows that actin (43,000 daltons) is present in almost normal amounts, while myosin heavy chain (200,000 daltons) is somewhat reduced in mutants. Both SDS-polyacrylamide gel electrophoresis and immunofluorescence studies reveal that tropomyosin is abundant in normal hearts, but very much reduced in mutants. Electron microscope studies of normal hearts show numerous well-organized myofibrils. Although mutant cardiomyocytes contain a few 60- and 150-A filaments, organized sacromeres are absent. Instead, amorphous proteinaceous collections are prominent. Previously reported heavy meromyosin (HMM)-binding experiments on glycerinated hearts demonstrate that most of the actin is contained within the amorphous collections in a nonfilamentous state, and the addition of HMM causes polymerization into F actin (Lemanski et al., 1976, J. Cell. Biol. 68:375-388). In the present study, glycerol-extracted hearts are incubated with tropomyosin, purified from rabbit or chicken skeletal muscle. This treatment causes the amorphous collections to disappear, and large numbers of distinct thin actin (60- to 80-A) filaments are seen in their place. Negative staining experiments corroborate this observation. These results suggest that the nonfilamentous actin located in the amorphous collections of mutant heart cells is induced to form into filaments with the addition of tropomyosin.
Actins↗
Empagliflozin and functional aerobic capacity in individuals with increased risk of heart failure: The Empire Prevent Cardiac trial.
BACKGROUND: Higher maximal oxygen consumption (VO₂ max) is associated with lower risk of developing heart failure (HF). Empagliflozin improves VO2 max in HF with reduced ejection fraction, but the effect on VO2 max in individuals at risk of HF remain unknown. OBJECTIVE: This study aimed to evaluate the effect of 180 days treatment with empagliflozin compared to placebo on VO2 max, daily physical activity level, and quality of life (QoL) in individuals with overweight or obesity and risk of HF. METHOD: This investigator-initiated, double-blinded, randomized, placebo-controlled, multicenter trial included elderly individuals with body mass index >28 kg/m2 and at least one additional risk factor for HF, including hypertension, ischemic heart disease, stroke, or chronic kidney disease. Individuals with HF or type 2 diabetes mellitus were excluded. The primary endpoint was the mean difference in change of VO2 max. The secondary outcome was objectively measured physical activity level. QoL was an explorative outcome. RESULTS: Among 191 randomized individuals (94 empagliflozin, 97 placebo), 89% had hypertension and 66% ischemic heart disease. At baseline, 69% were male, median age was 68 years, median body mass index 31.9 kg/m², mean left ventricular ejection fraction 65 ± 9%, and mean VO₂ max 18.1 ± 4.3 mL/min/kg. Empagliflozin did not change VO2 max with an estimated treatment difference of -0.2 mL/min/kg (97.5% confidence interval -1.2 to 0.8), adjusted P = 1.00. No significant treatment differences were observed for neither daily physical activity nor QoL. CONCLUSIONS: Empagliflozin did not affect VO2 max, physical activity level, or QoL in elderly individuals with overweight or obesity and risk of HF.
Humans↗
Prediction of incident heart failure in established atherosclerotic cardiovascular disease: the SMART2-HF model.
BACKGROUND AND AIMS: Patients with established atherosclerotic cardiovascular disease (ASCVD) are at high risk of developing heart failure (HF). However, incident HF is not part of the risk assessment of current guideline-recommended models. The aim of this study was to develop and externally validate the SMART2-HF model for prediction of incident HF in patients with ASCVD. METHODS: SMART2-HF was developed in 7698 individuals with established ASCVD (coronary, cerebrovascular, or peripheral artery disease, or abdominal aortic aneurysm) but without prior HF from the UCC-SMART cohort. Cox proportional hazards models including sex-predictor interactions and with age as the time scale were derived to estimate the 10-year and lifetime risk of incident HF (hospitalization for HF or HF-related death), accounting for competing non-HF mortality. Predictors, limited to routinely available clinical characteristics, were aligned with the SMART2 risk model for recurrent cardiovascular (CV) risk in the same population. External validation was performed in 240 741 patients with ASCVD from six data sources: the Clinical Practice Research Datalink, the HUNT3 study, the SWEDEHEART Registry, the ASCVD-Particles cohort, the Estonian Biobank and the international REACH Registry. RESULTS: During a median follow-up of 11.2 years (interquartile range 6.1-16.4 years), 1031 incident HF events (13%) occurred in the UCC-SMART cohort. In the external validation data sources, a total of 24 885 incident HF events (10%) occurred. The pooled C-statistic was .696 (95% confidence interval .674-.717), with consistent performance in subgroups by sex and type of ASCVD. Predicted risks matched observed incidence in external validation. CONCLUSIONS: The SMART2-HF model enables the prediction of incident HF in patients with ASCVD. Aligned with the guideline-recommended SMART2 model for recurrent CV risk, SMART2-HF can be used as a complementary tool in this population.
Humans↗
Cellular growth of cardiac muscle after birth.
Present concepts concerning DNA synthesis in the heart have been reviewed, and a speculative theory presented involving control of DNA synthesis in the developing heart. Research describing DNA synthesis in myocytes of the weanling rat heart undergoing hypertrophy has been presented. Its possible use for testing the control theory is suggested.
Aging↗
Single-Cell Splicing Isoform Atlas of the Adult Human Heart and Heart Failure.
BACKGROUND: Alternative splicing plays crucial roles in normal heart development and cardiac disease by influencing protein-coding sequences, functional domains, and molecular networks. However, a detailed characterization of the human heart isoform landscape remains incomplete. METHODS: Leveraging long-read single-nucleus RNA sequencing and computational analysis, we dissected full-length isoform heterogeneities, expression patterns, and usage shifts across cell types, cell states, and cardiac conditions of the adult left ventricle. We applied in silico approaches to assess the functional relevance of identified isoforms; validated isoform compositions of representative cardiac genes using reverse transcription quantitative polymerase chain reaction and targeted amplicon sequencing; and developed a web server for interactive navigation of our results. RESULTS: The data revealed that isoform heterogeneity is widespread in the cardiac cellular system, serving as a posttranscriptional buffer mechanism that calibrates the molecule reservoirs in human hearts. In healthy left ventricles, ≈30% of cell type-specific genes were polyform, using multiple isoforms tailored to cell type-specific programs. Among ubiquitously expressed genes, >300 showed differential isoform usage with cell type specificity in normal hearts. Comparisons of cardiomyocytes across conditions uncovered 379 genes with marked isoform usage shifts, most of which are predicted to change protein coding outcomes through direct changes in protein coding sequences and switches between intron retention and non-protein-coding biotypes. In contrast, cell state-specific programs tend to operate on monoform genes associated with changes among cell states. In addition, our data revealed heart failure-associated differential isoform usage events in stromal and immune cell types in the cardiac microenvironment. CONCLUSIONS: We present a comprehensive atlas of splicing isoforms in the normal adult heart and heart failure through long-read single-nucleus RNA sequencing and computational analyses. The results suggest crucial roles of isoforms in buffering core cellular programs and contributing to disease-associated cell states. The full-length details of these cell-specific isoforms serve as an important reference for downstream translational and mechanistic studies and are available on our online data portal at https://github.com/gaolabtools/heart-isoform-atlas.
Humans↗
[Functional, morphologic and histochemical changes in the myocardium and their role in the development of cor pulmonale following pulmonary resection].
Functional, morphological and histochemical alterations were studied in 32 dogs within the period of 5 days--18 months after resection of 32-80% of the pulmonary tissue. According to the presence of hypertrophy of the heart right ventricle wall, morphological changes of the myocardium and disorders in the functional features of the cardiovascular activity all the animals were divided into 4 groups: 1--control animals; 2--experimental animals without hypertrophy of the right ventricle wall; 3--experimental animals with hypertrophy of the right ventricle wall in the stage of compensation; 4--experimental animals with hypertrophy of the right ventricle wall in the stage of decompensation. In the myocardium of the second group animals a decrease of aerobic processes and an increase of anaerobic ones were found to take place. The aerobic processes increased and the anaerobic processes decreased in the myocardium of dogs having hypertrophy of the right ventricle wall in the stage compensation. In the muscle of the decompensated pulmonary heart there occurred a pronounced decrease of aerobic and anaerobic processes, a disturbance of the protein and fat metabolism. All this resulted in a decreased contractive function of the myocardium with distrubed hemodynamics. The investigations have shown the interrelationships of morphological, histochemical and ECG alterations in the dynamics of the pulmonary heart development after resection of lungs.
Animals↗
Combination of delta9-tetrahydrocannabinol with oxymorphone or pentobarbital: Effects on ventilatory control and cardiovascular dynamics.
Marijuana is widely used, yet few data concerning its actions combined with other drugs exist. Psychologic, respiratory and cardiovascular effects of delta9-tetrahydrocannabinol (THC), the active component of marijuana, combined with oxymorphone (OXM) or with pentobarbital (PBL), were studies in 15 healthy volunteers. Oxymorphone, 1.0 mg/70 kg, iv, caused sedation and ventilatory depression (minute ventilation: 24.9 plus or minus 11.9 SD to 14.1 plus or minus 4.9 1/min with PETCO2 held at 50 torr) in eight volunteers. TCH (27, 40, 60, 90, and 134 mug/kg, iv) increased sedation and further decreased ventilation with each TCH dose to 6.6 plus or minus 3.7 1/min after 134 mug/kg. The combination of OXM and THC decreased the CO2-ventilation slope from 2.23 to 0.88 1/min/torr. When THC, 134 mug/kg, was added to OXM, which alone caused no significant cardiovascular change, cardiac index (4.1 plus or minus 1.3 to 5.0 plus or minus 2.2 1/min/m-2) and heart rate (66 plus or minus 12 to 107 plus or minus 31 beats/min) significantly increased and total peripheral resistance (1,030 plus or minus 260 to 660 plus or minus 200 dynes-sec/cm-5) decreased. Heart rates exceeded 150 beats/min in two subjects after 27 and 134 mug/kg THC. Pentobarbital alone, 100 mg/70 kg, iv, caused no significant ventilatory or cardiovascular change. THC, after PBL pretreatment, induced hallucinations and anxiety in five of seven volunteers; four failed to complete all five doses of THC becuase of the severe psychologic effects. The combination of PBL and 40 to 134 mug/kg THC did not affect ventilation significantly. After PBL pretreatment, THC significantly increased heart rate (76 plus or minus 17 to 130 plus or minus 32 beats/min). Cardiac index also increased (3.8 plus or minus 0.8 to 5.6 plus or minus 1.9 1/min/m-2) and total peripheral resistance decreased (1,070 plus or minus 240 to 720 plus or minus 300 dynes-sec/cm-5). Three subjects developed heart rates esceeding 150 beats/min after 27, 27, and 90 mug/kg THC; in all three, heart rates fell from maximal value with a further dose of THC.
Adult↗
Two-years' study with a combination of pindolol and clopamide ('Viskaldix') in patients with moderate hypertension.
A study was carried out to evaluate the long-term effects and side-effects of a combination product containing the beta-blocker pindolol (10 mg) and the diuretic clopamide (5 mg) in 15 patients with moderate hypertension. All patients completed the 2-years' study. The dose of the combination was increased until blood pressure normalized or a maximum dose of 3 tablets (equivalent to 30 mg pindolol and 15 mg clopamide) daily was reached. Blood pressure and heart rate were recorded monthly and detailed medical examinations were done regularly throughout the study. A mean dose of 2 tablets of the combination product (20 mg pindolol and 10 mg clopamide) produced a significant reduction in blood pressure. In all but 1 patient, blood pressure control was achieved and maintained. No tolerance developed. Heart volume showed a marked decrease. No side-effects of clinical importance were noted.
Adult↗
Heart adaptation to acute pressure overload: an involvement of endogenous prostaglandins.
The purpose of this investigation was to study the relationships between the contractile behavior of the heart and myocardial prostaglandins. Using an open-chest model in rabbits, we assayed the left ventricular tissue content to prostaglandins (PG) E and F2 alpha at various intervals following acute pressure overload created by graduated aortic stenosis. The results suggest that the rabbits could be divided into two distinct groups based on specific hemodynamic changes following coarctation (systolic and diastolic pressure, dP/dt, and contractility index). The first group included rabbits whose adaptation to pressure overload was expressed as a gradual increase in the contractility index. The second group was comprised of rabbits that developed heart failure following coarctation. The increase in contractility in response to overload in the first group was paralleled by an increase in the content of PGE and PGF 2 alpha in the left ventricle, whereas, in rabbits with heart failure, the prostaglandin level did not rise above that of the control hearts. It is suggested that an increased endogenous prostaglandin content may be an important factor in adaptation to acute overload.
Animals↗
New Genetic Loci Implicated in Cardiac Morphology and Function Using Three-Dimensional Population Phenotyping.
BACKGROUND: Cardiac remodeling occurs in the mature heart and is a cascade of adaptations in response to stress, which are primed in early life. A key question remains as to the processes that regulate the geometry and motion of the heart and how it adapts to stress. METHODS: We performed spatially resolved phenotyping using machine learning-based analysis of cardiac magnetic resonance imaging in 47 549 UK Biobank participants. We analyzed 16 left ventricular spatial phenotypes, including regional myocardial wall thickness and systolic strain in both circumferential and radial directions. In up to 40 058 participants, genetic associations across the allele frequency spectrum were assessed using genome-wide association studies with imputed genotype participants, and exome-wide association studies and gene-based burden tests using whole-exome sequencing data. We integrated transcriptomic data from the GTEx project and used pathway enrichment analyses to further interpret the biological relevance of identified loci. To investigate causal relationships, we conducted Mendelian randomization analyses to evaluate the effects of blood pressure on regional cardiac traits and the effects of these traits on cardiomyopathy risk. RESULTS: We found 42 loci associated with cardiac structure and contractility, many of which reveal patterns of spatial organization in the heart. Whole-exome sequencing revealed 3 additional variants not captured by the genome-wide association study, including a missense variant in CSRP3 (minor allele frequency 0.5%). The majority of newly discovered loci are found in cardiomyopathy-associated genes, suggesting that they regulate spatially distinct patterns of remodeling in the left ventricle in an adult population. Our causal analysis also found regional modulation of blood pressure on cardiac wall thickness and strain. CONCLUSIONS: These findings provide a comprehensive description of the pathways that orchestrate heart development and cardiac remodeling. These data highlight the role that cardiomyopathy-associated genes have on the regulation of spatial adaptations in those without known disease.
Humans↗