Effects of thyroid gland hormones on cardiovascular system have been known for many years. Thyroid gland hormones deficiency is connected with a range of metabolic and hemodynamic changes which can contribute to a genesis of heart failure. Recent works refer to an importance of connection of thyroid gland hormones metabolism with heart insufficiency pathophysiology. That is especially a syndrome of a low trijodthyronin level marked as euthyroid sick syndrome which is significantly more frequent in patients with chronic heart failure compared to a population of healthy individuals. Recent clinical works proved that treatment administration of thyroid gland hormones to patients with heart failure is connected with favourable hemodynamic changes and increased working capacity if the treatment is well tolerated.

• MeSH
• chronická nemoc MeSH
• hormony štítné žlázy fyziologie   MeSH
• hypotyreóza komplikace   MeSH
• lidé MeSH
• sick euthyroid syndrom komplikace   MeSH
• srdeční selhání etiologie   patofyziologie   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• anglický abstrakt MeSH
• časopisecké články MeSH
• přehledy MeSH
• Názvy látek
• hormony štítné žlázy MeSH

Hypothyroidism is frequently found in patients with heart disease. It is a risk factor for atherosclerosis and ischemic heart disease and has a direct negative effect on both the left and right ventricular functions (hypothyroidism-induced cardiomyopathy). The confirmed manifest hypothyroidism is always a reason for replacement therapy with levothyroxine; regarding patients with heart disease, we always begin treatment with a small dose and increase it gradually. The treatment of subclinical hypothyroidism in patients with heart disease is disputable and its benefits probably depend on age. At a higher age, the therapy-related risks often outweigh its benefits, so we make do with the target levels of the thyroid stimulating hormone being within the upper band of the normal range, or even slightly above it, rather than overdosing the patient. To summarize in a simplified way, the treatment of subclinical hypothyroidism in patients with heart disease is the most effective in younger individuals, mainly those aged below 65, while at a higher age > 80 years the risk usually outweighs the benefit.Key words: cardiovascular risk - hypothyroidism - ischemic heart disease - left ventricular dysfunction - right ventricular dysfunction - subclinical hypothyroidism - thyroid peroxidase antibodies.

• MeSH
• hormonální substituční terapie MeSH
• hypotyreóza komplikace   farmakoterapie   MeSH
• klinické rozhodování MeSH
• lidé MeSH
• nemoci srdce komplikace   MeSH
• rizikové faktory MeSH
• thyroxin terapeutické užití   MeSH
• věkové faktory MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• thyroxin MeSH

Genitopatellar syndrome (GPS) and Say-Barber-Biesecker-Young-Simpson syndrome (SBBYSS) are two distinct clinically overlapping syndromes caused by de novo heterozygous truncating mutations in the KAT6B gene encoding lysine acetyltransferase 6B, a part of the histone H3 acetyltransferase complex. We describe an 8-year-old girl with a KAT6B mutation and a combined GPS/SBBYSS phenotype. The comparison of this patient with 61 previously published cases with KAT6B mutations and GPS, SBBYSS or combined GPS/SBBYSS phenotypes allowed us to separate the KAT6B mutations into four groups according to their position in the gene (reflecting nonsense mediated RNA decay and protein domains) and their clinical outcome. We suggest that mutations in mid-exon 18 corresponding to the C-terminal end of the acidic (Asp/Glu-rich) domain of KAT6B may have more variable expressivity leading to GPS, SBBYSS or combined phenotypes, in contrast to defects in other regions of the gene which contribute more specifically to either GPS or SBBYSS. Notwithstanding the clinical overlap, our cluster analysis of phenotypes of all known patients with KAT6B mutations supports the existence of two clinical entities, GPS and SBBYSS, as poles within the KAT6B-related disease spectrum. The awareness of these phenomena is important for qualified genetic counselling of patients with KAT6B mutations.

• Klíčová slova
• Genitopatellar syndrome, Genotype-phenotype correlation, KAT6B, Say-Barber-Biesecker-Young-Simpson syndrome,
• MeSH
• blefarofimóza diagnóza   genetika   MeSH
• dítě MeSH
• exony * MeSH
• faciální stigmatizace MeSH
• fenotyp MeSH
• histonacetyltransferasy genetika   MeSH
• kongenitální hypotyreóza diagnóza   genetika   MeSH
• kraniofaciální abnormality diagnóza   genetika   MeSH
• ledviny abnormality   MeSH
• lidé MeSH
• mentální retardace diagnóza   genetika   MeSH
• molekulární sekvence - údaje MeSH
• mutace * MeSH
• nestabilita kloubu diagnóza   genetika   MeSH
• patela abnormality   MeSH
• psychomotorické poruchy diagnóza   genetika   MeSH
• sekvence nukleotidů MeSH
• skrotum abnormality   MeSH
• urogenitální abnormality diagnóza   genetika   MeSH
• vrozené srdeční vady diagnóza   genetika   MeSH
• Check Tag
• dítě MeSH
• lidé MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• kazuistiky MeSH
• práce podpořená grantem MeSH
• Názvy látek
• histonacetyltransferasy MeSH
• KAT6B protein, human MeSH Prohlížeč

In patients with thyroid carcinoma who after thyroid elimination took thyroxine and triiodothyronine both hormones were discontinued and after 7 days a complex of peripheral and laboratory parameters was evaluated. Discontinuation of thyroid hormones led to a drop of their serum level and concurrent rise of the TSH level and serum cholesterol. The duration of the pre-ejection period of the systole, the Q-Kd interval and Achilles tendon reflex was protracted. The value of the index of the preejection time increased and that of the index of the expulsion time declined. The heart rate and systolic pressure declined and the body eight increased. Seven-day discontinuation of thyroid hormones did not affect the plasma level of noradrenaline, adrenaline and cyclic adenosine monophosphate. The diastolic pressure and index of electromechanical systole did not change.

• MeSH
• dospělí MeSH
• hormony štítné žlázy fyziologie   MeSH
• hypotyreóza krev   patofyziologie   MeSH
• katecholaminy krev   MeSH
• lidé středního věku MeSH
• lidé MeSH
• srdce patofyziologie   MeSH
• sympatický nervový systém patofyziologie   MeSH
• Check Tag
• dospělí MeSH
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• ženské pohlaví MeSH
• Publikační typ
• anglický abstrakt MeSH
• časopisecké články MeSH
• Názvy látek
• hormony štítné žlázy MeSH
• katecholaminy MeSH

Cardiovascular system is essentially affected by thyroid hormones by way of their genomic and non-genomic effects. Untreated overt thyroid dysfunction is associated with higher cardiovascular risk. Although it has been studied more than 3 decades, in subclinical thyroid dysfunction the negative effect on cardiovascular system is much more controversial. Large meta-analyses within last 10 years have shown that subclinical hyperthyroidism is associated with higher cardiovascular risk than subclinical hypothyroidism. Conversely, in patients of age > 85 years subclinical hypothyroidism was linked with lower mortality. Therefore, subclinical hyperthyroidism should be rather treated in the elderly while subclinical hypothyroidism in the younger patients and the older may be just followed. An important problem on the border of endocrinology and cardiology is amiodarone thyroid dysfunction. Effective and safe treatment is preconditioned by distinguishing of type 1 and type 2 amiodarone induced hyperthyroidism. The type 1 should be treated with methimazol, therapeutic response is prolonged, according to recent knowledge immediate discontinuation of amiodarone is not routinely recommended and patient should be usually prepared to total thyroidectomy, or rather rarely 131I radioiodine ablation may be used if there is appropriate accumulation. In the type 2 there is a promt therapeutic response on glucocorticoids (within 1-2 weeks) with permanent remission or development of hypothyroidism. If it is not used for life-threatening arrhytmias, amiodarone may be discontinuated earlier (after several weeks). Amiodarone induced hypothyroidism is treated with levothyroxine without amiodarone interruption.Key words: amiodarone induced thyroid dysfunction - atrial fibrillation - cardiovascular risk - heart failure - hyperthyroidism - hypothyroidism - thyroid stimulating hormone.

• MeSH
• amiodaron škodlivé účinky   MeSH
• dospělí MeSH
• fibrilace síní farmakoterapie   MeSH
• glukokortikoidy terapeutické užití   MeSH
• hormony štítné žlázy MeSH
• hypertyreóza chemicky indukované   terapie   MeSH
• hypotyreóza chemicky indukované   farmakoterapie   MeSH
• kardiologie MeSH
• kardiovaskulární systém MeSH
• lidé MeSH
• methimazol terapeutické užití   MeSH
• radioizotopy jodu terapeutické užití   MeSH
• rizikové faktory MeSH
• senioři nad 80 let MeSH
• srdeční selhání MeSH
• thyreostatika terapeutické užití   MeSH
• thyroxin terapeutické užití   MeSH
• Check Tag
• dospělí MeSH
• lidé MeSH
• senioři nad 80 let MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• amiodaron MeSH
• glukokortikoidy MeSH
• hormony štítné žlázy MeSH
• methimazol MeSH
• radioizotopy jodu MeSH
• thyreostatika MeSH
• thyroxin MeSH

• MeSH
• dospělí MeSH
• elektrokardiografie * MeSH
• fonokardiografie * MeSH
• hypertyreóza patofyziologie   MeSH
• hypotyreóza patofyziologie   MeSH
• kontrakce myokardu * MeSH
• lidé středního věku MeSH
• lidé MeSH
• minutový srdeční výdej * MeSH
• senioři MeSH
• systola * MeSH
• tepový objem * MeSH
• Check Tag
• dospělí MeSH
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• senioři MeSH
• ženské pohlaví MeSH
• Publikační typ
• anglický abstrakt MeSH
• časopisecké články MeSH

The paper examines the basic pathophysiologic mechanisms playing a role in the development of cardiovascular changes on thyroid hyper- and hypofunction. The haemodynamic changes typically associated with increased and decreased secretion of thyroid hormones are described and compared. Using echocardiography, the haemodynamics changes are documented in 12 patients with hyperthyroidism and 19 patients with myxoedema prior to thyrostatic and substitution therapy. Characteristic findings in florid hyperthyroidism include a significant rise in left ventricular end-diastolic volume as well as increases in stroke volume (SV) and cardiac index (CI). Mean velocity of circumferential fibre shortening (mVCF) is also significantly increased. Left ventricular myocardial weight shows a tendency towards an increase. Hypothyreosis is primarily associated with decreases in SV and CI; mVCF also declines. The paper underlines the importance of causative therapy as the above haemodynamics changes are fully reversible on attaining normal thyroid function.

• MeSH
• hemodynamika fyziologie   MeSH
• hormony štítné žlázy fyziologie   MeSH
• hypertrofie levé komory srdeční patofyziologie   MeSH
• hypertyreóza patofyziologie   MeSH
• hypotyreóza patofyziologie   MeSH
• kontrakce myokardu fyziologie   MeSH
• lidé MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• přehledy MeSH
• Názvy látek
• hormony štítné žlázy MeSH

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.

• MeSH
• fosforylace MeSH
• funkce levé komory srdeční MeSH
• hypotyreóza chemicky indukované   komplikace   metabolismus   patofyziologie   MeSH
• ischemické přivykání * MeSH
• JNK mitogenem aktivované proteinkinasy metabolismus   MeSH
• komorový tlak (srdce) MeSH
• kontrakce myokardu MeSH
• krysa rodu Rattus MeSH
• L-laktátdehydrogenasa metabolismus   MeSH
• mitogenem aktivované proteinkinasy p38 metabolismus   MeSH
• modely nemocí na zvířatech MeSH
• myokard enzymologie   MeSH
• neúspěšná terapie MeSH
• obnova funkce MeSH
• perfuze MeSH
• potkani Wistar MeSH
• propylthiouracil MeSH
• reperfuzní poškození myokardu komplikace   metabolismus   patofyziologie   prevence a kontrola   MeSH
• sarkoplazmatická Ca2+-ATPáza metabolismus   MeSH
• srdeční myosiny metabolismus   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• JNK mitogenem aktivované proteinkinasy MeSH
• L-laktátdehydrogenasa MeSH
• mitogenem aktivované proteinkinasy p38 MeSH
• propylthiouracil MeSH
• sarkoplazmatická Ca2+-ATPáza MeSH
• srdeční myosiny MeSH

• MeSH
• elektrokardiografie MeSH
• hypotyreóza chemicky indukované   MeSH
• kardiostimulátor MeSH
• kombinovaná farmakoterapie MeSH
• lidé středního věku MeSH
• lidé MeSH
• prokainamid terapeutické užití   MeSH
• propranolol terapeutické užití   MeSH
• srdeční arytmie farmakoterapie   MeSH
• srdeční blokáda terapie   MeSH
• trijodthyronin terapeutické užití   MeSH
• Check Tag
• lidé středního věku MeSH
• lidé MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• prokainamid MeSH
• propranolol MeSH
• trijodthyronin MeSH

Thyroid hormones are powerful modulators of heart function and susceptibility to arrhythmias via both genomic and non-genomic actions. We aimed to explore expression of electrical coupling protein connexin-43 (Cx43) in the heart of rats with altered thyroid status and impact of omega-3 polyunsaturated fatty acids (omega-3) supplementation. Adult male Lewis rats were divided into following six groups: euthyroid controls, hyperthyroid (treated with T(3)) and hypothyroid (treated with methimazol) with or without six-weeks lasting supplementation with omega-3 (20 mg/100 g/day). Left and right ventricles, septum and atria were used for immunoblotting of Cx43 and protein kinase C (PKC). Total expression of Cx43 and its phosphorylated forms were significantly increased in all heart regions of hypothyroid rats compared to euthyroid controls. In contrast, the total levels of Cx43 and its functional phosphorylated forms were decreased in atria and left ventricle of hyperthyroid rats. In parallel, the expression of PKC epsilon that phosphorylates Cx43, at serine 368, was increased in hypothyroid but decreased in hyperthyroid rat hearts. Omega-3 intake did not significantly affect either Cx43 or PKC epsilon alterations. In conclusion, there is an inverse relationship between expression of cardiac Cx43 and the levels of circulating thyroid hormones. It appears that increased propensity of hyperthyroid while decreased of hypothyroid individuals to malignant arrhythmias may be in part attributed to the changes in myocardial Cx43.

• MeSH
• fosforylace MeSH
• hormony štítné žlázy krev   MeSH
• hypertyreóza metabolismus   MeSH
• hypotyreóza metabolismus   MeSH
• konexin 43 metabolismus   MeSH
• matrixová metaloproteinasa 2 metabolismus   MeSH
• myokard enzymologie   MeSH
• náhodné rozdělení MeSH
• omega-3 mastné kyseliny farmakologie   MeSH
• potkani inbrední LEW MeSH
• potravní doplňky MeSH
• proteinkinasa C metabolismus   MeSH
• srdce účinky léků   MeSH
• zvířata MeSH
• Check Tag
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• Gja1 protein, rat MeSH Prohlížeč
• hormony štítné žlázy MeSH
• konexin 43 MeSH
• matrixová metaloproteinasa 2 MeSH
• Mmp2 protein, rat MeSH Prohlížeč
• omega-3 mastné kyseliny MeSH
• proteinkinasa C MeSH