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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of thyroid hormones on vascular responses to various agents was examined in the coronary vascular bed perfused by the Langendorff's method at a fixed flow rate with Krebs-Henseleit solution in isolated rat hearts. In this study, ventricular fibrillation was induced by electrical stimulation to avoid secondary influences derived from alteration of ventricular contractility by agents. Vasodilator responses of coronary arteries to isoproterenol and methacholine were significantly enhanced in hyperthyroid preparations compared with those observed in euthyroid ones, though vasodilator responses to histamine and adenosine were not affected by hyperthyroidism. Vasoconstrictor response to 5-hydroxytryptamine (5-HT) was significantly potentiated by hyperthyroidism though that to balium chloride was not affected. So, these alterations in vascular responses by hyperthyroidism are assumed not to be nonspecific but to be mediator-specific events. As vasoconstriction in coronary arteries lowers oxygen supply to myocardium, enhanced vasoconstrictivity of coronary arteries to 5-HT by hyperthyroidism may be responsible for an exacerbation of heart disease in the case of patients having agglutinative thrombus, which should be a source of 5-HT, in their coronary arteries.
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PMID:Altered responsiveness of coronary arteries in hyperthyroid rats. 273 Feb 31

Sixteen patients with metastatic carcinoid tumors of ileal or cecal origin were studied in order to evaluate the frequency and degree of cardiac involvement in a nonselected patient group. We have also studied the correlation between plasma hormone levels (e.g., 5-hydroxytryptamine (5-HT) and substance P) and the degree of cardiac involvement. The patients underwent physical examinations, electrocardiograms, chest x-rays, cardiac catheterization, and echocardiography. Plasma levels of 5-HT and substance P were analyzed. Carcinoid heart involvement was found in 3 of 16 patients (19%) but no patient had subjective symptoms associated with heart disease. Four patients (25%) had slight pulmonary hypertension. No left-sided heart lesions were seen. No correlation between blood levels of 5-HT or substance P and heart involvement was found. Eight patients died during the follow-up period, but in none of these was the cause of death cardiac failure. Carcinoid heart disease is not as common in our patients as in patients selected on a cardiological basis described in earlier studies. Echocardiography appears to be the most efficient technique for detection of even subclinical heart involvement and a useful tool for following its progress.
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PMID:Heart involvement in metastatic carcinoid disease. 394 30

Thirty Nigerians with established endomyocardial fibrosis were studied. Basal serum 5-hydroxytryptamine levels were estimated on three different occasions at one-monthly intervals. Twentyfour hours before each estimation, dietary staples containing 5-hydroxytryptamine were excluded from the diet. Subsequently the patients were fed on a plantain diet and serum levels of 5-hydroxytryptamine were estimated at one- and three-hour intervals after plantain ingestion. 5-hydroxytryptamine was assayed on the fundal strip of rat's stomach. These values were compared with those obtained in an earlier study on healthy Nigerians. It was observed that, as in healthy Nigerians, no significant increase in serum 5-hydroxytryptamine levels occurred in these patients after plantain ingestion. The difference between endomyocardial fibrosis and carcinoid heart disease is underlined and it is emphasized that no correlation exists between the incidence of endomyocardial fibrosis and the high content of 5-hydroxytryptamine in the local dietary staples.
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PMID:The pathogenesis of endomyocardial fibrosis: the question of 5-hydroxytryptamine. 547 49

1 The cardiovascular effects of the tricyclic antidepressants (TCAs) are reviewed and compared with those of fluvoxamine, a new 5-hydroxytryptamine (5-HT) re-uptake inhibitor. 2 The TCAs have important effects on the heart, related to their anticholinergic and quinidine-like properties. The major side effects in therapeutic dosage include heart rate increase, postural hypotension and slight prolongation of the intraventricular conduction time and QT interval. In toxic dosage (or normal dosage in patients with severe heart disease) both advanced heart block and ventricular arrhythmias can occur, together with clinically important loss of myocardial contractile force. 3 Fluvoxamine has no effects on the heart except for a statistically (but not clinically) significant slowing of the heart rate.
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PMID:Cardiac effects of antidepressant drugs. A comparison of the tricyclic antidepressants and fluvoxamine. 640 5

1 The hypothesis that magnesium deficiency, linked to the magnesium content of drinking water, induces major tone increases in coronary arteries and enhances their responses to vasoactive agents to an extent sufficient to explain sudden death associated with ischaemic heart disease was examined in an in vitro preparation. 2 The spontaneous tone of cattle coronary arteries was not increased during a 30 min exposure to Mg2+-deficient Krebs until the mineral was omitted entirely from the bathing medium, and even then the observed increase was small. Only in strips maintained under extremely deficient conditions for a prolonged period, namely Mg2+ concentration of 0.2 mM and 0.0 mM for 3 h, was tone substantially greater than in controls in standard (1.2 mM) Mg2+-Krebs. 3 Responses to acetylcholine and to noradrenaline were not increased in Mg2+-free Krebs but those to potassium and to 5-hydroxytryptamine were enlarged over the lower parts of their concentration-response curves. Responses to potassium and to 5-hydroxytryptamine were also examined in Krebs containing very low concentration of Mg2+ (0.4 and 0.2 mM) and only modest increases in contraction size were detected. Increases in the Mg2+ concentration of the Krebs (to 4.8 mM) depressed responses to potassium and 5-hydroxytryptamine. 4 It is concluded that Mg2+ deficiency must be nearly complete (0.4-0.0 mM) to induce even moderate tone increases in coronary vessels, or to sensitize them to agonist responses, and that there is no reason to link marginally subnormal Mg2+ levels, occasionally reported in humans with heart disease, to marked changes in coronary dynamics.
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PMID:The effect of magnesium deficiency and excess on bovine coronary artery tone and responses to agonists. 685 Jan 65

A total of 29 subjects were studied which included 18 heart failure and 11 matched control cases. The underlying heart disease in heart failure cases was mostly chronic rheumatic valvular disease. The diagnosis of heart disease and heart failure was made on the basis of clinical examination, supplemented by electrocardiography, chest skiagram and echo cardiography. The serotonin status was assessed by measuring platelet serotonin uptake, intraplatelet serotonin content and whole blood 5-hydroxytryptamine (5-HT) levels. Blood platelet count was also done. In heart failure cases, platelet count were significantly less, the platelet 5-HT uptake and blood 5-HT levels remain unaltered. These findings indicate that platelet pool of serotonin does not contribute to raised serotonin blood levels in heart failure. The high blood serotonin levels may be due to either clearance defect or enhanced secretion from the gut or both. The altered serotonin kinetics in platelets also indicate a state of platelet activation in heart failure.
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PMID:Serotonergic mechanisms in heart failure. 787 2

There are a number of dimensions to the complex relationship between cardiovascular disease and affective disorders including: (i) patients with depression are at an increased risk of dying from sudden cardiovascular death compared with the general population; (ii) patients with depression over the course of a lifetime have a higher rate of symptomatic and fatal ischaemic heart disease compared with a control group without depression; and, (iii) patients after either a myocardial or a cerebrovascular infarction who are depressed have a higher mortality rate than their medically comparable nondepressed counterparts. The deleterious impact of depression on the prognosis of cardiac disease and the suggestion that treatment of depression may reduce cardiac mortality has led clinicians to seek safe and effective treatment for patients with comorbid depression and ischaemic disease. Though they are robustly effective, the tricyclic antidepressants are type 1A antiarrhythmic agents and presumably carry the same risk in patients with ischaemic disease as treatment with other type 1 antiarrhythmics such as moricizine. Short term studies of the safety of other antidepressant agents, specifically amfebutamone (bupropion) and the selective serotonin (5-hydroxytryptamine; 5-HT) reuptake inhibitors (SSRIs) fluoxetine, paroxetine and sertraline, suggest that these medications have a benign cardiovascular profile in patients with depression and pre-existing cardiac disease. However, given the methodological limitations of study design and the relatively small number of patients included, it is premature to conclude that SSRIs are a 'safe' treatment in patients with heart disease. Thus, clinicians must still make treatment decisions on a case by case basis, considering the type and severity of depression and cardiovascular disease, as well as what is known about the cardiovascular effects and therapeutic profile of the different classes of antidepressant medications.
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PMID:Treating depression in patients with ischaemic heart disease: which agents are best to use and to avoid? 1034 96

Several lines of evidence suggest that the serotonin (5-hydroxytryptamine, 5-HT) regulates cardiovascular functions during embryogenesis and adulthood. 5-HT binds to numerous cognate receptors to initiate its biological effects. However, none of the 5-HT receptor disruptions in mice have yet resulted in embryonic defects. Here we show that 5-HT(2B) receptor is an important regulator of cardiac development. We found that inactivation of 5-HT(2B) gene leads to embryonic and neonatal death caused by heart defects. 5-HT(2B) mutant embryos exhibit a lack of trabeculae in the heart and a specific reduction in the expression levels of a tyrosine kinase receptor, ErbB-2, leading to midgestation lethality. These in vivo data suggest that the Gq-coupled receptor 5-HT(2B) uses the signaling pathway of tyrosine kinase receptor ErbB-2 for cardiac differentiation. All surviving newborn mice display a severe ventricular hypoplasia caused by impaired proliferative capacity of myocytes. In adult mutant mice, cardiac histopathological changes including myocyte disarray and ventricular dilation were consistently observed. Our results constitute genetic evidence that 5-HT via 5-HT(2B) receptor regulates differentiation and proliferation of developing and adult heart. This mutation provides a genetic model for cardiopathy and should facilitate studies of both the pathogenesis and therapy of cardiac disorders in humans.
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PMID:Serotonin 2B receptor is required for heart development. 1094 20

Long-term hyperserotoninemia induces heart valve disease in rats, and cases of cardiac valvulopathies have been reported in patients using ergolines, possibly through activation of the 5-hydroxytryptamine(2B) (5HT(2B)) receptor. The ergoline terguride (transdihydrolisuride) is a 5HT(2B/2C) receptor antagonist. Using a rat model, we have investigated whether terguride could prevent serotonin-induced changes in general and heart disease specifically. During 4 months, twelve Sprague-Dawley rats were given daily subcutaneous serotonin injections; twelve rats received a combination of serotonin injections and terguride by gavage, whereas ten rats were untreated controls. Using echocardiography, rats with aortic insufficiency were found in all 3 groups, while pulmonary insufficiency was only found in two rats injected with serotonin alone. Animals given serotonin alone had significantly higher heart weights compared to the controls (p=0.029) and rats given terguride (p=0.034). Rats injected with serotonin alone developed macroscopic skin changes at the injection sites, histologically identified as orthokeratosis and acanthosis. Terguride completely prevented these changes (p=0.0001, p=0.0003). Liver weights were higher in the animals given serotonin alone compared to controls (p=0.014) and terguride treated animals (p=0.009). Stomach weights were higher in animals given serotonin alone compared to rats given terguride (p=0.012). In the mesenchymal cell-line MC3T3-E1, terguride almost completely inhibited serotonin-induced proliferation (p<0.01). Serotonin increases heart, liver and stomach weights, possibly through enhanced proliferation. Terguride inhibits these effects. We propose that terguride may have beneficial effects in the treatment of diseases such as carcinoid syndrome, where serotonin plays an important pathogenic role.
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PMID:Long-term serotonin effects in the rat are prevented by terguride. 1739 82

Using the Tph1-invalidated mouse line, in which blood is depleted in serotonin (5-hydroxytryptamine, 5-HT), we have demonstrated previously that maternal 5-HT is required for normal embryonic development. Here, we address the issue of the influence of the maternal 5-HT concentration on the cardiac function of the offspring as adults. We investigated the cardiac phenotype of Tph1-invalidated mice born to Tph1 heterozygous and null mothers. Functionally, all mutants display a significant decrease of cardiac contractility, indicative of impaired left ventricular function. They exhibit progressive dilated cardiomyopathy and are unable to adapt appropriately to a pharmacological stress. Moreover, we show that the cardiopathy is more severe in adult Tph1(-/-) mice born to homozygous mothers than to heterozygous mothers. Importantly, the severity of the cardiac phenotype is inversely correlated with the plasma 5-HT concentration but not the whole-blood 5-HT concentration. Thus, plasma 5-HT concentration may be a useful index of heart failure. These findings show that cardiac function, through the plasma 5-HT concentration, is influenced by the maternal serotonergic status.
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PMID:Maternal serotonin influences cardiac function in adult offspring. 1826 82


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