• MeSH
• Blood Urea Nitrogen MeSH
• Research Support as Topic MeSH
• Risk Assessment methods   statistics & numerical data   utilization   MeSH
• Inpatients classification   statistics & numerical data   MeSH
• Creatinine diagnostic use   MeSH
• Humans MeSH
• Blood Pressure Determination methods   statistics & numerical data   utilization   MeSH
• Decision Support Techniques MeSH
• Hospital Mortality MeSH
• Heart Failure mortality   MeSH
• Check Tag
• Humans MeSH

PURPOSE: The purposes of this study are to identify the strongest clinical parameters in relation to in-hospital mortality, which are available in the earliest phase of the hospitalization of patients, and to create an easy tool for the early identification of patients at risk. MATERIALS AND METHODS: The classification and regression tree analysis was applied to data from the Acute Heart Failure Database-Main registry comprising patients admitted to specialized cardiology centers with all syndromes of acute heart failure. The classification model was built on derivation cohort (n = 2543) and evaluated on validation cohort (n = 1387). RESULTS: The classification tree stratifies patients according to the presence of cardiogenic shock (CS), the level of creatinine, and the systolic blood pressure (SBP) at admission into the 5 risk groups with in-hospital mortality ranging from 2.8% to 66.2%. Patients without CS and creatinine level of 155 μmol/L or less were classified into very-low-risk group; patients without CS, creatinine level greater than 155 μmol/L, and SBP greater than 103 mm Hg, into low-risk group, whereas patients without CS, creatinine level greater than 155 μmol/L, and SBP of 103 mm Hg or lower, into intermediate-risk group. The high-risk group patients had CS and creatinine of 140 μmol/L or less; patients with CS and creatinine level greater than 140 μmol/L belong to very-high-risk group. The area under receiver operating characteristic curve was 0.823 and 0.832, and the value of Brier's score was estimated on level 0.091 and 0.084, for the derivation and the validation cohort, respectively. CONCLUSIONS: The presented classification model effectively stratified patients with all syndromes of acute heart failure into in-hospital mortality risk groups and might be of advantage for clinical practice.

• MeSH
• Risk Assessment methods   MeSH
• Middle Aged MeSH
• Humans MeSH
• Hospital Mortality * MeSH
• Registries MeSH
• Risk Factors MeSH
• Aged, 80 and over MeSH
• Aged MeSH
• Heart Failure classification   mortality   MeSH
• Models, Statistical * MeSH
• Check Tag
• Middle Aged MeSH
• Humans MeSH
• Male MeSH
• Aged, 80 and over MeSH
• Aged MeSH
• Female MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH

Anémie je při chronickém srdečním selhání podobně jako při chronickém renálním selhání relativně častým jevem. O obou stavů představuje silný a nezávislý prediktor zvýšené morbidity a mortality. Etiologie této anémie je mutifaktoriální. V jejím vzniku hraje roli řada různých faktorů, např. neadekvátní produkce erytropoetinu v ledvinách, útlum kostní dřeně, deficience železa, ale také hemodiluce při retenci tekutin. Léčebné strategie jsou zaměřeny dvěma směry. Jedním je stimulace erytropoézy rekombinantním lidským erytropoetinem anebo jeho analogy, jako je darbepoetin a. Druhým pak substituce železa, pro vyšší účinnost a lepší toleranci především intravenózně. Dosud provedené klinické studie léčby anémie při chronickém srdečním selhání erytropoézu stimulujícími látkami byly menší, nebyly kontrolovány placebem a většinou hodnotily náhradní ukazatele. Jejich výsledky naznačovaly, že účinná léčba anémie u nemocných s chronickým srdečním selháním zlepšuje toleranci zátěže, zlepšuje klinický stav (třídu NYHA) i kvalitu života a snižuje nutnost podávání krevních transfuzí. Nedávno ukončená klinická studie TREAT byla první velká morbiditní a mortalitní studie srovnávající léčbu anémie analogem erytropoetinu proti placebu. U více než 4 000 nemocných s diabetes mellitus, chronickým renálním selháním a významnou anémií ukázala, že účinná léčba anémie darbepoetinem a vůbec neovlivnila výskyt ani kardiovaskulárních, ani renálních příhod, naopak, takřka na dvojnásobek zvýšila výskyt mozkových cévních příhod. Pochybnosti o bezpečnosti léčby erytropoézu stimulujícími látkami vznikly již v minulosti ze studií léčby anémie u onkologických i nefrologických nemocných. Odpověď, zda léčba anémie při chronickém srdečním selhání ovlivní příznivě prognózu nemocných, dostaneme až z výsledků probíhající morbiditně‑mortalitní studie RED‑ HF.

Anaemia is a relatively frequent co– morbidity of chronic heart as well as chronic renal failure. In both conditions, it represents a strong and independent predictor of increased morbidity and mortality. Aetiology of this anaemia is multi‑factorial. A number of various factors play a role in its development, e. g. inadequate erythropoietin production in the kidneys, bone marrow inhibition, iron deficiency as well as haemodilution associated with fluid retention. Treatment strategies aim at two directions. One is the stimulation of erythropoiesis with recombinant human erythropoietin or its analogues such as darbepoetin a. The other involves iron substitution, administered preferably intravenously for improved efficacy and tolerability. Clinical studies evaluating treatment of anaemia in chronic heart failure with erythropoiesis- stimulating agents conducted so far were of a small scale, were not controlled with placebo and usually assessed proxy parameters. Their results suggested that effective treatment of anaemia in patients with chronic heart failure improves exertion tolerance, clinical status (NYHA class) as well as the quality of life and reduces the need for blood transfusions. Recently completed TREAT study was the first large morbidity and mortality study evaluating treatment of anaemia with an erythropoietin analogue compared to placebo. On a sample of more than 4000 patients with diabetes mellitus, chronic renal failure and significant anaemia, this study has shown that effective treatment of anaemia with darbepoetin a did not affect at all the incidence of cardiovascular and renal events; on the other hand, it had lead to a nearly two‑fold increase in the incidence of cerebrovascular events. Some doubts about the safety of treatment with erythropoiesis-stimulating agents have occurred in the past based on the studies of anaemia treatment in patients with cancer and renal diseases. An answer to the question whether the treatment of anaemia associated with chronic heart failure affects positively the patient prognosis will be provided following the completion of the currently running morbidity and mortality RED- HF study.

• Keywords
• klinické studie TREAT, klinická studie FAIR-HF, erytropoéza stimulující látky, chronické renální selhání,
• MeSH
• Anemia etiology   MeSH
• Chronic Disease MeSH
• Erythropoietin adverse effects   MeSH
• Hematinics adverse effects   therapeutic use   MeSH
• Humans MeSH
• Heart Failure complications   blood   MeSH
• Iron therapeutic use   MeSH
• Check Tag
• Humans MeSH
• Publication type
• Review MeSH

Through linkage analysis and candidate gene sequencing, we identified three unrelated families with the autosomal-dominant inheritance of early onset anemia, hypouricosuric hyperuricemia, progressive kidney failure, and mutations resulting either in the deletion (p.Leu16del) or the amino acid exchange (p.Leu16Arg) of a single leucine residue in the signal sequence of renin. Both mutations decrease signal sequence hydrophobicity and are predicted by bioinformatic analyses to damage targeting and cotranslational translocation of preprorenin into the endoplasmic reticulum (ER). Transfection and in vitro studies confirmed that both mutations affect ER translocation and processing of nascent preprorenin, resulting either in reduced (p.Leu16del) or abolished (p.Leu16Arg) prorenin and renin biosynthesis and secretion. Expression of renin and other components of the renin-angiotensin system was decreased accordingly in kidney biopsy specimens from affected individuals. Cells stably expressing the p.Leu16del protein showed activated ER stress, unfolded protein response, and reduced growth rate. It is likely that expression of the mutant proteins has a dominant toxic effect gradually reducing the viability of renin-expressing cells. This alters the intrarenal renin-angiotensin system and the juxtaglomerular apparatus functionality and leads to nephron dropout and progressive kidney failure. Our findings provide insight into the functionality of renin-angiotensin system and stress the importance of renin analysis in families and individuals with early onset hyperuricemia, anemia, and progressive kidney failure.

• MeSH
• Anemia genetics   metabolism   MeSH
• Cell Line MeSH
• Kidney Failure, Chronic genetics   metabolism   MeSH
• Child MeSH
• Genes, Dominant MeSH
• Adult MeSH
• Genetic Linkage MeSH
• Hyperuricemia genetics   metabolism   MeSH
• Kidney cytology   ultrastructure   MeSH
• Middle Aged MeSH
• Humans MeSH
• Adolescent MeSH
• Young Adult MeSH
• Mutation MeSH
• Computer Simulation MeSH
• Child, Preschool MeSH
• Renin genetics   metabolism   MeSH
• Pedigree MeSH
• Sequence Analysis, DNA MeSH
• Age of Onset MeSH
• Check Tag
• Child MeSH
• Adult MeSH
• Middle Aged MeSH
• Humans MeSH
• Adolescent MeSH
• Young Adult MeSH
• Male MeSH
• Child, Preschool MeSH
• Female MeSH
• Publication type
• Research Support, Non-U.S. Gov't MeSH

Through linkage analysis and candidate gene sequencing, we identified three unrelated families with the autosomal-dominant inheritance of early onset anemia, hypouricosuric hyperuricemia, progressive kidney failure, and mutations resulting either in the deletion (p.Leu16del) or the amino acid exchange (p.Leu16Arg) of a single leucine residue in the signal sequence of renin. Both mutations decrease signal sequence hydrophobicity and are predicted by bioinformatic analyses to damage targeting and cotranslational translocation of preprorenin into the endoplasmic reticulum (ER). Transfection and in vitro studies confirmed that both mutations affect ER translocation and processing of nascent preprorenin, resulting either in reduced (p.Leu16del) or abolished (p.Leu16Arg) prorenin and renin biosynthesis and secretion. Expression of renin and other components of the renin-angiotensin system was decreased accordingly in kidney biopsy specimens from affected individuals. Cells stably expressing the p.Leu16del protein showed activated ER stress, unfolded protein response, and reduced growth rate. It is likely that expression of the mutant proteins has a dominant toxic effect gradually reducing the viability of renin-expressing cells. This alters the intrarenal renin-angiotensin system and the juxtaglomerular apparatus functionality and leads to nephron dropout and progressive kidney failure. Our findings provide insight into the functionality of renin-angiotensin system and stress the importance of renin analysis in families and individuals with early onset hyperuricemia, anemia, and progressive kidney failure.

• MeSH
• Anemia genetics   metabolism   MeSH
• Cell Line MeSH
• Kidney Failure, Chronic genetics   metabolism   MeSH
• Child MeSH
• Genes, Dominant MeSH
• Adult MeSH
• Financing, Organized MeSH
• Genetic Linkage MeSH
• Hyperuricemia genetics   metabolism   MeSH
• Kidney cytology   ultrastructure   MeSH
• Middle Aged MeSH
• Humans MeSH
• Adolescent MeSH
• Young Adult MeSH
• Mutation MeSH
• Computer Simulation MeSH
• Child, Preschool MeSH
• Renin genetics   metabolism   MeSH
• Pedigree MeSH
• Sequence Analysis, DNA MeSH
• Age of Onset MeSH
• Check Tag
• Child MeSH
• Adult MeSH
• Middle Aged MeSH
• Humans MeSH
• Adolescent MeSH
• Young Adult MeSH
• Male MeSH
• Child, Preschool MeSH
• Female MeSH

Tree mortality is a key factor influencing forest functions and dynamics, but our understanding of the mechanisms leading to mortality and the associated changes in tree growth rates are still limited. We compiled a new pan-continental tree-ring width database from sites where both dead and living trees were sampled (2970 dead and 4224 living trees from 190 sites, including 36 species), and compared early and recent growth rates between trees that died and those that survived a given mortality event. We observed a decrease in radial growth before death in ca. 84% of the mortality events. The extent and duration of these reductions were highly variable (1-100 years in 96% of events) due to the complex interactions among study species and the source(s) of mortality. Strong and long-lasting declines were found for gymnosperms, shade- and drought-tolerant species, and trees that died from competition. Angiosperms and trees that died due to biotic attacks (especially bark-beetles) typically showed relatively small and short-term growth reductions. Our analysis did not highlight any universal trade-off between early growth and tree longevity within a species, although this result may also reflect high variability in sampling design among sites. The intersite and interspecific variability in growth patterns before mortality provides valuable information on the nature of the mortality process, which is consistent with our understanding of the physiological mechanisms leading to mortality. Abrupt changes in growth immediately before death can be associated with generalized hydraulic failure and/or bark-beetle attack, while long-term decrease in growth may be associated with a gradual decline in hydraulic performance coupled with depletion in carbon reserves. Our results imply that growth-based mortality algorithms may be a powerful tool for predicting gymnosperm mortality induced by chronic stress, but not necessarily so for angiosperms and in case of intense drought or bark-beetle outbreaks.

• MeSH
• Coleoptera * MeSH
• Stress, Physiological MeSH
• Droughts * MeSH
• Trees growth & development   MeSH
• Carbon MeSH
• Animals MeSH
• Check Tag
• Animals MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Research Support, U.S. Gov't, Non-P.H.S. MeSH

Nedepolarizující svalová relaxancia jsou dnes rutinně používána téměř u dvou třetin doplňovaných celkových anestezií. Jejich komplikací bývá pooperační reziduální kurarizace, která zvyšuje nebezpečí hypoventilace, pooperační aspirace a pneumonie. Kazuistika srovnává perioperační průběh u téhož pacienta, který byl operován v průběhu tří let dvakrát pro stejnou diagnózu. Při druhé operaci byl k antagonizaci nervosvalové blokády navozané rokuroniem použit sugammadex. Kazuistika potvrdila účinnost a spolehlivost sugammadexu.

Non-depolarizing muscle relaxing agents are routinely used in nearly two thirds of general anaesthetics. Residual neuromuscular blockade as a major side effect leads to hypoventilation and can contribute to the development of postoperative aspiration and pneumonia. This case report compares the peri-operative course of a patient who underwent the same surgical procedure within tree years. It corroborated the effectiveness and reliability of sugammadex.

• MeSH
• Abdominoplasty * MeSH
• Anesthesia, General MeSH
• Surgical Procedures, Operative MeSH
• Down Syndrome MeSH
• gamma-Cyclodextrins * MeSH
• Anesthesia, Intravenous MeSH
• Humans MeSH
• Young Adult MeSH
• Obesity, Morbid * MeSH
• Neuromuscular Nondepolarizing Agents * MeSH
• Perioperative Care MeSH
• Pulmonary Ventilation MeSH
• Respiratory Insufficiency MeSH
• Respiration, Artificial MeSH
• Check Tag
• Humans MeSH
• Young Adult MeSH
• Male MeSH
• Publication type
• Case Reports MeSH

• MeSH
• Heart Failure MeSH
• Heart-Lung Transplantation MeSH
• Publication type
• Monograph MeSH

• Conspectus
• Patologie. Klinická medicína
• NML Fields
• kardiologie
• transplantologie

Kardiovaskulární onemocnění (KVO) jsou celosvětově častým typem postižení vedoucího k úmrtí. Kaveolin je strukturální kaveolární protein se třemi izoformami (caveolin-1 [cav-1], cav-2 a cav-3]. Kaveoly hrají životně důležitou úlohu v přenášení signálů při přežití buněk v rámci kardioprotekce. Zvláště cav-1 ovlivňuje mnoho biologických pochodů (vyvážení buněčné energie, destrukce buněk a fibróza) v rozvoji srdečního selhání. Snížené hodnoty kaveolinu představují cíl léčby; budoucí studie by mohly ozřejmit řadu aspektů působení kaveolinu u starších a obézních pacientů. V tomto přehledu se zabýváme významem kaveol u kardiovaskulárních onemocnění. Zdůrazňujeme i úlohu kaveolinu u řady kardiovaskulárních onemocnění.

Cardiovascular diseases (CVDs) are common diseases that cause many deaths around the world. Caveolin is a structural caveolae protein with three isoforms (Caveolin-1 [Cav-1], Cav-2, and Cav-3). Caveolae has a vital role in generating survival signals for cardiac protection. In particular, Cav-1 influences many biological processes (cellular energy balance, cellular destruction, and fibrosis) in the development of heart failure (HF). Decreased caveolin levels are a therapeutic target and could shed light on future studies in elderly and obese patients. In this review, we discussed the significance of caveolae in cardiovascular diseases. We have also emphasized the role of caveolin in many cardiovascular diseases.

• MeSH
• Myocardial Infarction etiology   MeSH
• Caveolin 1 deficiency   therapeutic use   MeSH
• Humans MeSH
• Hypertension, Pulmonary etiology   MeSH
• Heart Disease Risk Factors MeSH
• Heart Failure etiology   drug therapy   MeSH
• Check Tag
• Humans MeSH
• Publication type
• Research Support, Non-U.S. Gov't MeSH
• Review MeSH

Aim: Retrospective analysis of the prescribing practice and cost of ambulatory treatment of hypertension and its common complications – heart failure, sequelae of cerebrovascular disease, and angina pectoris. Methods: Analysis of 3,240 reimbursable ambulatory prescriptions for hypertension, heart failure, sequelae of cerebrovascular disease and angina pectoris according to the complexity of the therapy and frequency of the prescribed medicines. Modeling and calculation of the expected monthly cost for outpatient therapy by using the “decision tree model”. Sensitivity analysis is performed within the ±30% interval. Results: 65% of the prescription were for the hypertension, and 35% for the observed complications. 1,297 prescriptions for hypertension include one medicine, 647 include two medicines, and only 8% of prescriptions were for three medicines. ACE inhibitors have been prescribed in 41% of all hypertension prescriptions, followed by beta-blockers (19%), Ca channel blockers (16%), diuretics (15%) etc. The prescriptions for hypertension complications are more diverse as therapeutic groups. The expected monthly cost of prescribed medicines per patient with hypertension alone is 6.90 € and in case of complications it is 10.71 € according to the prevalence of the complexity of therapy, and weighted monthly cost of medicines. The overall ambulatory cost is expected to be around 148 million € per year for near 1.5 million patients with 44% reimbursement. The cost of the therapy is sensitive more to changes in the medicine’s prices than to its complexity. Conclusion: This study is a first step in providing information for evidence-based cost containment measures or policy decisions at ambulatory level in Bulgaria and for the assessment of the share of complications’ therapy on the overall hypertension cost.

• MeSH
• Angina Pectoris economics   drug therapy   prevention & control   MeSH
• Adrenergic beta-Antagonists administration & dosage   economics   MeSH
• Calcium Channel Blockers administration & dosage   economics   MeSH
• Cerebrovascular Disorders economics   drug therapy   prevention & control   MeSH
• Diuretics administration & dosage   economics   MeSH
• Models, Economic MeSH
• Economics, Pharmaceutical statistics & numerical data   MeSH
• Hypertension economics   drug therapy   complications   MeSH
• Angiotensin-Converting Enzyme Inhibitors administration & dosage   economics   MeSH
• Prescriptions economics   statistics & numerical data   MeSH
• Humans MeSH
• Drug Costs statistics & numerical data   MeSH
• Outpatients statistics & numerical data   MeSH
• Heart Failure economics   drug therapy   prevention & control   MeSH
• Check Tag
• Humans MeSH
• Geographicals
• Bulgaria MeSH