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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thyroid hormones are essential to maintain normal function of many systems including the cardiovascular system. Their excess or deficiency may upset human body homeostasis. Hyperthyroidism leads to cardiovascular system's hyperdynamic status which is characterized by tachycardia, increased difference between systolic and diastolic arterial pressure, significant increase of the stroke volume and improvement of the left ventricular diastolic function. Long-lasting thyrotoxicosis in patient with heart disease may result in atrial fibrillation, deterioration of angina pectoris or congestive heart failure. Hypothyroidism leads to hemodynamic disturbances which are quite different than those observed in hyperthyroidism, but cardiac symptoms are scant in clinical practice. Hypothyroidism's clinical significance is limited to atherosclerosis progression and intensification of ischaemic heart disease symptoms. Both leads to symptomatic cardiovascular system failure or its deterioration. We should emphasize that cardiovascular system dysfunction associated with thyrometabolic disturbances subsides when euthyreosis is restored. It sounds promising that there are reports suggesting a potential advantage of thyroxin treatment in patients with acute or chronic cardiovascular system diseases. These hypotheses result from the observations that heart dysfunction in hypothyroidism is similar to that observed in heart failure.
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PMID:[Thyrometabolic disorders and heart failure]. 1794 Sep 89

Thyroid hormones have many effects on the heart and vascular system. Although cardiac output is reduced in hypothyroidism, heart failure is relatively rare because there is a lower demand for peripheral oxygen delivery. Hypothyroidism may also result in accelerated atherosclerosis and coronary artery disease. We report the case of a 55-year-old man with severe heart failure associated with severe longstanding untreated hypothyroidism. The patient was admitted for shortness of breath and chest pain. On presentation, signs and symptoms of severe hypothyroidism and heart failure were noticed. The electrocardiogram showed sinus bradycardia and ischemia. Thyroid stimulating hormone was extremely elevated and thyroid hormone levels were undetectable. A cardiac ultrasonography exam revealed abnormalities of the left ventricular dimensions and function consistent with dilated cardiomyopathy. Coronary angiography showed severe multivessel disease. Coronary by-pass was deemed necessary, but surgery was postponed because of severe heart failure. After an increasingly downhill clinical course, the patient died, eight month after his initial presentation, owing to severe heart failure. This patient represents an example of an overlooked diagnosis of severe hypothyroidism, rarely encountered nowadays, leading to dramatic consequences.
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PMID:Heart failure and dilated cardiomyopathy associated with severe longstanding untreated hypothyroidism. 1796 46

The discovery of four major water channels in the kidney, namely aquaporins (AQP) 1, 2, 3 and 4, has allowed a substantial increase in our understanding of renal water regulation in health and disease. This review discusses the renal aquaporin water channels in the urinary dilution and concentrating defects in cardiac failure, cirrhosis, syndrome of inappropriate hormone secretion, pregnancy, hypothyroidism, isolated glucocorticoid deficiency, isolated mineralocorticoid deficiency, primary polydipsia, acquired and genetic nephrogenic diabetes insipidus.
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PMID:Aquaporin-related disorders of water homeostasis. 1799 67

A case of hypothyroid cardiomyopathy secondary to hypopituitarism posed a diagnostic challenge. This lesson describes the patient's presentation with simultaneous acute heart failure and neurological signs; the investigations and imaging findings which initially suggested myocardial infarction (MI) and/or infiltration; and the response to treatment, with biochemical, sonographic and clinical resolution of the cardiomyopathy following thyroxine replacement therapy. This lesson illustrates the cardiovascular sequelae of severe hypothyroidism, and physicians are reminded of the difficulties involved in investigating putative coronary events in hypothyroid patients, since hypothyroidism itself may mimic MI.
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PMID:Hypothyroid cardiomyopathy due to hypopituitarism: a diagnostic dilemma. 1819 19

There is accumulating evidence showing that ischemic preconditioning (PC) may lose its cardioprotective effect in the diseased states. The present study investigated whether PC can be effective in hypothyroidism, a clinical condition which is common and often accompanies cardiac diseases such as heart failure and myocardial infarction. Hypothyroidism was induced in rats by 3-week administration of 6n-propyl-2-thiouracil in water (0.05 %). Normal and hypothyroid hearts (HYPO) were perfused in Langendorff mode and subjected to 20 min of zero-flow global ischemia and 45 min of reperfusion. A preconditioning protocol (PC) was also applied prior to ischemia. HYPO hearts had significantly improved post-ischemic recovery of left ventricular developed pressure, end-diastolic pressure and reduced lactate dehydrogenase release. Furthermore, phospho-JNK and p38 MAPK levels after ischemia and reperfusion were 4.0 and 3.0 fold lower in HYPO as compared to normal hearts (P<0.05). A different response to PC was observed in normal than in HYPO hearts. PC improved the post-ischemic recovery of function and reduced the extent of injury in normal hearts but had no additional effect on the hypothyroid hearts. This response, in the preconditioned normal hearts, resulted in 2.5 and 1.8 fold smaller expression of the phospho-JNK and phospho-p38 MAPK levels at the end of reperfusion, as compared to non-PC hearts (P<0.05), while in HYPO hearts, no additional reduction in the phosphorylation of these kinases was observed after PC. Hypothyroid hearts appear to be tolerant to ischemia-reperfusion injury. This response may be, at least in part, due to the down-regulation of ischemia-reperfusion induced activation of JNKs and p38 MAPK kinases. PC is not associated with further reduction in the activation of these kinases in the hypothyroid hearts and fails to confer added protection in those hearts.
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PMID:Ischemic preconditioning fails to confer additional protection against ischemia-reperfusion injury in the hypothyroid rat heart. 1819 89

Interest in the role of thyroid hormones (TH) in heart failure is steadily increasing due to evidence for a physiological, homeostatic role of TH and the effects of altered TH metabolism on the cardiovascular system, particularly in presence of heart failure. Experimental studies have shown that altered TH metabolism modifies cardiovascular homeostasis by inducing alterations of cardiac histology, cardiomyocyte morphology and gene expression and consequently, of diastolic and systolic myocardial function. Clinical studies have shown that mild forms of thyroid dysfunction, both primary (subclinical hypothyroidism and subclinical hyperthyroidism) and secondary (low T(3) syndrome) have negative prognostic impact in patients with heart failure. In these patients, the administration of synthetic triiodothyronine (T(3)) was well tolerated and induced significant improvement in cardiac function without increased heart rate and metabolic demand. Large multicenter, placebo-controlled prospective studies are necessary to evaluate the safety and prognostic effects of chronic treatment with TH replacement therapy in patients with heart failure. The article also discusses recent patents in this field.
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PMID:Triiodothyronine (T3) effects on cardiovascular system in patients with heart failure. 1822 Nov 25

E Natriuretic peptides represent a novel diagnostic tool in the assessment of heart failure. N-terminal-pro-B-type natriuretic peptide (NT-proBNP), a member of the natriuretic peptid family, is produced and released from cardiac ventricles. Changes in cardiac functions are observed in thyroid dysfunctions. The aim of this study was to assess the changes in serum NT-proBNP levels and to evaluate impact of thyroid hormones on serum NT-proBNP in patients with hyperthyroidism and hypothyroidism. Serum NT-proBNP levels were measured in 21 patients with hyperthyroidism and in 24 patients with hypothyroidism and compared with 20 healthy control subjects. Patients without cardiac disease were included into the study as well. Serum NT-proBNP levels were measured by electrochemiluminescence immunoassay. Serum NT-proBNP levels were higher in hyperthyroid patients than in hypothyroid patients and in control subjects, with mean values of 239.03 +/- 47.33, 45.97 +/- 13.48, 55.57 +/- 13.01 pg/ml, respectively (p < 0.0001). Serum NT-proBNP and thyroid hormones were correlated in all patients. Moreover, there was a significant positive correlation between serum NT-proBNP and serum free T4 (FT4) levels (r = 0.549, p = 0.012) in hyperthyroidic patients. Multiple regression analyses demonstrated that increasing FT4 was independently associated with a high serum NT-proBNP levels, whereas heart rate was not in hyperthyroid patients. Serum NT-proBNP levels are higher in the hyperthyroid state as compared with the hypothyroid and euthyroid state. Thyroid dysfunction affects serum NT-proBNP levels, possibly influencing the secretion of the peptide. Therefore, thyroid function has to be considered when evaluating high serum NT-proBNP levels in patients without cardiac dysfunction.
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PMID:Serum N-terminal-pro-B-type natriuretic peptide (NT-pro-BNP) levels in hyperthyroidism and hypothyroidism. 1827 1

The link between thyroid dysfunction and cardiovascular diseases has been recognized for more than 100 years. Although overt hypothyroidism leads to impaired cardiac function and possibly heart failure, the cardiovascular consequences of borderline low thyroid function are not clear. Establishment of a suitable animal model would be helpful. In this study, we characterized a rat model to study the relationship between cardiovascular function and graded levels of thyroid activity. We used rats with surgical thyroidectomy and subcutaneous implantation of slow release pellets with three different T(4) doses for 3 wk. In terminal experiments, cardiac function was evaluated by echocardiograms and hemodynamics. Myocardial arteriolar density was also quantified morphometrically. Thyroid hormone levels in serum and heart tissue were determined by RIA assays. Thyroidectomy alone led to cardiac atrophy, severe cardiac dysfunction, and a dramatic loss of arterioles. The low T(4) dose normalized serum T(3) and T(4) levels, but cardiac tissue T(3) and T(4) remained below normal. Low-dose T(4) failed to prevent cardiac atrophy or restore cardiac function and arteriolar density to normal values. All cardiac function parameters and myocardial arteriolar density were normalized with the middle dose of T(4), whereas the high dose produced hyperthyroidism. Our results show that thyroid hormones are important regulators of cardiac function and myocardial arteriolar density. This animal model will be useful in studying the pathophysiological consequences of mild thyroid dysfunction. Results also suggest that cardiac function may provide valuable supplemental information in proper diagnosis of mild thyroid conditions.
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PMID:Serum thyroid hormone levels may not accurately reflect thyroid tissue levels and cardiac function in mild hypothyroidism. 1831 May 9

The literature on the effect of excess thyroid hormone on ventricular repolarization is controversial. To study whether free thyroxine (T(4)) and TSH are associated with QTc prolongation we conducted population-based cohort study. This study was conducted as part of the Rotterdam Study and included 365 men and 574 women aged 55 years and older with an electrocardiogram, who were randomly sampled for the assessment of thyroid status (free T(4)/TSH) at baseline, after exclusion of participants with hypothyroidism, use of antithyroid drugs, thyroid hormones or digoxin, left ventricular hypertrophy, and left and right bundle branch block. Endpoints were the length of the QTc interval and risk of borderline QTc prolongation. The associations were examined by means of linear and logistic regression analysis, adjusted for age and gender, diabetes mellitus, myocardial infarction, hypertension, and heart failure. Overall, there was no significant association between TSH and QTc interval (0.8 ms (95% confidence interval (CI) -3.5, 5.2) in the first quintile compared with the fifth quintile). Subjects in the fifth quintile of free T(4) did not have an increased QTc interval (3.2 ms (95% CI -1.1, 7.6)); stratification on gender showed an increment of 10.9 ms (95% CI 3.4, 18.3) in the fifth quintile in men and 1.1 ms (95% CI -4.2, 6.3) in the fifth quintile of free T(4) in women. When compared with subjects in the first quintile, male subjects in the fifth quintile of free T(4) had a significantly increased risk of a borderline QTc interval and QTc prolongation (odds ratio 2.40 (95% CI 1.20, 4.80)). High levels of free T(4) are associated with substantial QTc prolongation in men of up to 10 ms. The fact that free T(4) is also associated with a significantly increased risk of borderline and prolonged QTc values with its risk of sudden cardiac death, endorses the clinical importance of our findings.
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PMID:High free thyroxine levels are associated with QTc prolongation in males. 1846 46

Impaired urinary dilution leading to water retention and hyponatremia may occur in patients with cardiac failure, cirrhosis, pregnancy, oxytocin administration, hypothyroidism, glucocorticoid, and mineralocorticoid deficiency. The mechanisms for these defects predominantly involve the nonosmotic stimulation of arginine vasopressin release with up-regulation of aquaporin 2 water channel expression and trafficking to the apical membrane of the principal cells of the collecting duct. These perturbations are reversed by V2 vasopressin receptor antagonists. In contrast, urinary concentration defects leading to polyuria are vasopressin resistant. They may involve several factors, such as impaired countercurrent concentration secondary to down-regulation of Na-K-2Cl cotransporter. Vasopressin-resistant down-regulation of aquaporin 2 expression has also been described as a factor in impaired urinary concentration.
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PMID:Vasopressin and aquaporin 2 in clinical disorders of water homeostasis. 1851 89


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