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PubMed1979

Factors associated with cardiac mortality in developed countries with particular reference to the consumption of wine.

Deaths from ischaemic heart-disease in 18 developed countries are not strongly associated with health-service factors such as doctor and nurse density. There is a negative association with gross national product per capita and a positive but inconsistent association with saturated and monounsaturated fat intake. The principal finding is a strong and specific negative association between ischaemic heart-disease deaths and alcohol consumption. This is shown to be wholly attributable to wine consumption.

Adult↗
PubMed1975

Histometrical estimation of scar tissue in hypertrophied human heart muscle.

Histometrical estimation of scar tissue was made on 28 hypertrophied human hearts obtained at autopsy in order to know the significance of scar tissue in the process of cardiac hypertrophy and in the development of cardiac failure. Estimation was made on histological specimens of the anterior wall of the left ventricle and the posteromedial papillary muscle, according to Chalkley's point counting method, and the amount of scar tissue was expressed by percentages. The mean percentages were 4.6, 8.5 and 18.3 in the epicardial, endocardial part of the left ventricle, and the papillary muscle. There were very significant differences between these 3 mean percentages. There was a very significant correlation between the percentages of scar tissue in the endocardial part of the left ventricle and heart weight. There were no definite correlations between the percentages of scar tissue in the epicardial part or in the papillary muscle and heart weight. From these results, possible causes of scar formation and significance of scar tissue to the development of cardiac failure were discussed.

Adult↗
PubMed1979

Effect of a mild exercise program on myocardial function and the development of hypertrophy.

Cardiac function and the development of myocardial hypertrophy were studied in rats conditioned by an exercise program consisting of 8 wk of running on a treadmill. At the end of the training period a group of exercised and sedentary rats was subjected to hemodynamic evaluation under general anesthesia. Except for a slight elevation in the heart rates of the exercised animals there were no significant differences between the exercised and sedentary rats at rest. Following an increase in afterload or a period of hypoxia, the cardiac index of the exercised animals remained significantly higher than that of the sedentary controls. These differences were related to changes in stroke volume. Another group of exercised and sedentary animals underwent either constriction of the ascending aorta or a sham operation. Sedentary rats developed significant hypertrophy at 3 days but had no hypertrophy at 1 day after aortic constriction. Exercised rats, however, developed significant myocardial hypertrophy by 1 day after pressure overload. These data suggest that the heart from an exercised animal is better able to tolerate increases in afterload and hypoxia and can respond with compensatory myocardial hypertrophy more rapidly than the heart of a sedentary animal.

Animals↗
PubMedDate not supplied

The pathways of protein synthesis and degradation in normal heart and during development and regression of cardiac hypertrophy.

The half-life of cardiac myosin heavy chains (HC) was determined, with leucyl-tRNA as precursor, to be 5.4 days. Myosin HC are labeled more rapidly than actin; myosin light chains (LC1 and LC2) are labeled more slowly than HC. The observed differences are attributable to heterogeneity in the half-lives, e.g., actin, and to the effect of dilution by the existing macromolecular precursor pool (LC1 and LC2). Cardiac and skeletal muscle contain a population of filaments that can be released from myofibrils by ATP-relaxing solution. The easily released filaments (ERF) are devoid of alpha-actinin and M-protein. Labeling of ERF is more rapid than that of residual myofibrils. Cardiac and skeletal muscle contains calcium-activated neutral protease, which selectively removes alpha-actinin when incubated with isolated myofibrils. During development of pressure-induced cardiac hypertrophy, the labeling of LC2 is increased. In regressing cardiac hypertrophy the activities of free and total cathepsin D and of acidic RNase are unaltered.

Actins↗
PubMed1976

Effect of digitoxin on cardiac hypertrophy induced by pericardiectomy and exercise.

Removal of the pericardium in combination with a mild exercise programme of swimming resulted in a significant increase in heart weight and heart weight/body weight ratio of young rats. Heart weight/body weight ratios were 3.46+/-0.25 in the sedentary control animals, 4.16+/-0.26 in pericardiectomized animals swimming 2 h each day, and 4.60+/-0.22 in pericardiectomized animals swimming 6h/d. The effect of pericardiectomy on the development of cardiac hypertrophy is additive to that of mild exercise (2h/d) but not to prolonged exercise (6h/d). The administration of digitoxin significantly decreased the development of cardiac hypertrophy in pericardiectomized animals that were exercised for 2 h/d but not those exercised for 6 h/d. These findings further substantiate the physiological effect on the heart of the pericardium. The effects of pericardiectomy should be considered in experimental studies of cardiac hypertrophy and in clinical studies involving cardiac surgery.

Animals↗
PubMed1979

Cardiac specific antigen and antibody in immunopathogenesis of cardiac disease.

Antibody to human cardiac extracts was detected in the sera of many patients undergoing open heart surgery. A passive hemagglutination assay using cardiac extracts as antigen coated onto erythrocytes showed the development of cardiac antibody in the patients, with peak titers usually one to three weeks after the surgery. Radioimmunoassay revealed the presence of cardiac specific myoglobin antigen antigen in the sera of many patients, with peak levels 1-3 days after the procedure. A correlation was observed between development of circulating serum antibody and appearance of cardiac myoglobin antigen. These results support the view that immunologic disease related to release of cardiac antigen in patients undergoing heart surgery may be a factor in post-cardiotomy disease.

Antibodies↗
PubMed1976

Biochemical changes associated with development and reversal of cardiac hypertrophy in spontaneously hypertensive rats.

This study is the first report describing the sequence of biochemical alterations of myocardium during the progression of naturally occurring hypertrophy in spontaneously hypertensive rats (SHRs) and then with its reversal by alpha-methyldopa therapy. Changes in DNA, RNA, hydroxyproline, as well as incorporation of 14C lysine into cardiac myosin, were compared with the pattern found in suitably matched controls. A significant increase in RNA, hydroxyproline, and 14C incorporation was observed in SHRs. Antihypertensive treatment caused reversal of hypertrophy and normalization of all biochemical parameters except hydroxyproline, the concentration of which increased significantly as myocardial weight decreased. These compositional changes may help explain the conflicting result of the haemodynamic effects of cardiac hypertrophy.

Animals↗
PubMed1976

Heart volume and myocardial connective tissue during development and regression of thyroxine-induced cardiac hypertrophy in rats.

To determine whether development and regression of cardiac hypertrophy are accompanied by changes in heart volume and to learn whether a change in heart volume is associated with changes in the myocardial connective tissue, cardiac hypertrophy was induced in rats by administration of thyroxine. Rats were given L-thyroxine for 4 weeks. Heart volume was estimated radiologically in vivo at the start of the experiment and at 1- or 2-week intervals for 7 weeks. At each of these stages a number of rats were killed, their hearts were weighed and determinations were made of the myocardial contents of DNA, of collagen measured as hydroxyproline, and of glycosaminoglycans, measured as uronic acid. After thyroxine treatment the ratio of left heart ventricle weight to body weight and of heart volume to body weight rose significantly. The increase in heart weight was greater than the increase in heart volume. At the same time, there was a significant decrease in the concentration of hydroxyproline. After discontinuation of thyroxine treatment heart volume, heart weight and the concentration of myocardial collagen returned to normal within 2 weeks. However, the total amount of myocardial collagen was still less than normal at 2 weeks. The results suggest that the decrease in the amount of myocardial collagen associated with thyroxine-induced cardiac hypertrophy--because it results in a weakening of the supporting properties of the myocardial connective tissue framework--might contribute to a slight increase in in vivo heart volume.

Animals↗
PubMed1975

Nicotine effects on the acid mucopolysaccharide content of chick embryo cardiac jelly.

Histochemical studies were made on the developing chick embryo heart to determine the effects of nicotine on acid mucopolysaccharide content during the critical stages of the cardiac morphogenesis. Two-day old embryos were injected with the dosages of nicotine ranging from 1.5 to 3 mg per embryo. The embryos were studied on the 3rd and 4th days of incubation. For an evaluation of acid mucopolysaccharides, the staining procedures of Mowry (1958) and Saunders (1964) were employed. It was found that nicotine decreases the content of acid mucopolysaccharide in the developing cardiac jelly. In the control embryos, the cardiac tissues picked up very intense coloration. At lower dosages (Group A; 1.5 mg/egg), the staining response of the treated heart tissues containing acid mucopolysaccharides was moderate as compared to the control embryos. At higher dosages (Group B; 3 mg/egg), the cardiac tissues were faintly colored as compared to the embryos of Group A. It is possible that the cardiac lesions previously reported in the chick embryos following the administration of nicotine (Gilani, 1971) are due to the reduction of the amount of acid mucopolysaccharides in the developing cardiac jelly--a susceptible period of the genesis of heart.

Animals↗
PubMed2025

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↗
PubMed1978

Idiopathic cardiomyopathy, age, and suppressor-cell dysfunction as risk determinants of lymphoma after cardiac transplantation.

A review of lymphomas developing in recipients of cardiac allografts has yielded significant risk factors. Frequency varied strikingly according to original cardiac disease: lymphoma developed in 6 of 37 patients with prior idiopathic cardiomyopathy (I.C.M.) but in one of 54 patients with prior coronary-artery disease (C.A.D.). All patients who developed lymphomas were aged under 40. Combination of both risk factors (I.C.M. and age less than 40) produces a sub-group with a highly significantly increased risk of lymphoma. I.C.M., but not C.A.D., is characterised by a defect in mitogen-induced mononuclear-cell suppressor activity. It is postulated that defective regulation in the immune systems of younger patients under chronic alloantigen stimulation may allow lymphoid proliferation to proceed to lymphoreticular malignancy. Immunosuppressive agents such as azathioprine may exert a co-oncogenic effect.

Adolescent↗
PubMed1976

Quantitative analysis of cardiac hypertrophy due to pressure load in reference to the relations of blood pressure, left ventricular weight and left ventricular capacity.

In almost all of the cases of cardiac hypertrophy due to sustained hypertension, left ventricular capacity is increased in proportion to increased left ventricular weight, even in the absence of manifest cardiac insufficiency. The condition is regarded as the general expression of cardiac response to pressure load, and the concept of "isomorphic hypertrophy" is proposed. Concentric hypertrophy of the current concept is observed only on rare special occasions, and its role in cardiac adaptation to pressure load is obscure. The increase in myocardial mass is sufficient to maintain the work done by a unit myocardial volume at a normal level. However, the calculation on pertinent models demonstrates that hypertrophied hearts of any type expel the normal stroke volume with smaller shortening of muscle fibers under larger stress, which is further elevated with the progress of cardiac contraction. Because the maximum force generated by muscle fibers declines with advancing cardiac contraction, hypertrophied hearts harbor a latent risk of mechanical insufficiency. Even under pressure load, ventricular dilation seems to precede the re-inforcement of ventricular wall in the development of cardiac hypertrophy. A common mechanism may be therefore assumed underlying the development and performance of all types of hypertrophied hearts, regardless of the difference in the character of physical loads.

Adult↗
PubMed1975

[Pathogenesis of cardiac insufficiency in thyrotoxicosis].

The purpose of the work was to study some problems relating to the pathogenesis of cardiac insufficiency in patients with thyrotoxicosis. To do this a total of 108 patients suffering from thyrotoxicosis with varying degree of severity and aged from 17 to 59 were examined. In addition to the general clinical examination vectoro-, poly- and mechanocardiography was employed. The resulting findings ascertained two possible ways for the development of cardiac insufficiency in patients under consideration. One of them is cardiac hyperfunction that comes to the forefront. In this case the myocardial changes are of a stage-wise nature. The myocardial contractility at the onset of the affection is up, a slight hypertrophy is developing, chiefly, of the outflow passages. As the disease progresses further hypertrophy gains in intensity and dilation of the heart comes in as an intercurrent factor. At this time the contractile function of the myocardium is still unaffected and the patients are at a stage of compensation. With progressing dystrophy and wearing away of the myocardium its contractility is declining and signs of cardiac incompetence appear. Such a development is characteristic of patients with severe course of thyrotoxicosis, long-standing disease and frequent relapses. Of the other way is typical cardiac hyperfunction of low intensity. To the forefront come dystrophic alterations in the myocardium unaccompanied by hypertrophy, and in this case cardiac insufficiency is of latent nature. Such alterations are seen to occur with a milder course of thyrotoxicosis, with the disease of short duration. Dynamic observations bear proof to a reversible nature of hypertrophy and dystrophy of the myocardium.

Adolescent↗
PubMed2025

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↗
PubMed1977

Development of SHR hypertension and cardiac hypertrophy during prolonged beta blockade.

Spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats were treated with beta-adrenergic receptor inhibiting drugs (either propranolol or timolol) from conception until 12 weeks of age to determine if this therapy would alter the development of systemic hypertension or left ventricular hypertrophy. Therapy (propranolol or timolol, 500 mg/liter drinking water) was initiated with breeding parents and continued throughout the pregnancy, nursing, and postweaning periods. Although the heart rates of beta-adrenergic receptor inhibited WKY and SHR rats were consistently reduced with respect to their respective tap-water controls, this therapy did not alter body growth. Hemodynamic studies demonstrated reduced central venous pressure, cardiac index, and maximum acceleration of aortic flow in the beta-adrenergic inhibited rats. In spite of these findings, the arterial pressure of the treated rats and the degree of left ventricular hypertrophy of the SHR were unaltered by treatment. Thus, administration of the beta-adrenergic receptor blocking agents, propranolol or timolol, from conception through the developmental stage of SHR hypertension, failed to alter either the progressive rise in arterial pressure or the development of hypertensive vascular disease and left ventricular hypertrophy.

Adrenergic beta-Antagonists↗
PubMed1975

Coronary blood flow in rats native to simulated high altitude and in rats exposed to it later in life.

In rats exposed to a simulated high altitude of 3500 m for their whole prenatal and postnatal life a severe cardiac hypertrophy develops. In rats born and first staying 5 weeks at sea level and then being exposed to simulated high altitude, only a unilateral right cardiac hypertrophy occurs. In both groups nutritional coronary blood flow was estimated in left ventricle, right ventricle, and septum and was compared with control animals of similar age. Coronary blood flow was measured at hypoxia in all groups. At first cardiac output was determined by the Fick principle, then 86Rb was applied and the animals were killed after 55 sec. Activity of 86Rb was measured in both cardiac ventricles and septum and the fractional uptake was calculated. According to Sapirstein (1956, 1958) the distribution of 86-RB follows the distribution of cardiac output and from both these data the nutritional blood flow to the parts of the heart may be estimated. Cardiac output was similar in rats exposed to simulated high altitude later in life ('newcomers') and in control animals, but it was significantly lower in rats born in the low pressure chamber ('natives'). Fractions of cardiac output supplying cardiac ventricles and septum in rats from both hypoxic groups were significantly higher than in control animals. In the 'natives' they were significantly higher than in the 'newcomers'. The fractions of cardiac output in both 'newcomers' and 'natives' remained significantly higher than those of the control animals, also when calculated per gram of heart tissue. Nutritional coronary blood flow (in ml/min) was higher in both ventricles and septum of the 'newcomers' and in the right ventricle of the 'natives', and lower in the septum of the 'natives', when compared with control animals. Coronary blood flow per gram of heart tissue (in ml/min.g) was significantly higher in all cardiac parts of the 'newcomers', but it was about the same in all cardiac parts of the 'natives' when compared with controls. The importance of observed changes concerning myocardial tissue oxygenation is analyzed by using Krogh's cylindrical tissue model.

Age Factors↗