• Keywords
• NT-proBNP, 2-ST2,
• MeSH
• Acute Disease MeSH
• Biomarkers * blood   MeSH
• Interleukin-1 Receptor-Like 1 Protein blood   MeSH
• Calcitonin blood   MeSH
• Humans MeSH
• Natriuretic Peptide, Brain blood   MeSH
• Peptide Fragments blood   MeSH
• Prognosis * MeSH
• Procalcitonin MeSH
• Heart Failure * diagnosis   blood   MeSH
• Troponin blood   MeSH
• Emergency Medical Services MeSH
• Check Tag
• Humans MeSH

Srdeční selhání (SS) je komplexní klinický syndrom, který se manifestuje typickými příznaky a objektivními známkami srdeční nedostatečnosti. Výskyt SS, zejména v chronické podobě, je odhadován ve státech střední a západní Evropy na 0,4–2 % s nárůstem ve vyšších věkových skupinách, ve věku > 80 let postihuje 10–20 % populace. S ohledem na jeho narůstající incidenci i prevalenci jsou stále vyvíjeny nové postupy farmakologické i nefarmakologické léčby s cílem zlepšit kvalitu života a přežití postižených pacientů. V rámci tohoto souhrnného článku nejprve stručně, vycházejíce ze současných guidelines, popíšeme možnosti diagnostiky srdečního selhání, včetně novinek ze současných klinických a preklinických studií (např. solubilní ST2, FSTL1 apod) a poté se zaměříme na novinky ve farmakologické terapii chronického (ivabradin, ARNI, glifloziny) i akutního (ularitid, serelaxin, nesiritid) srdečního selhání. V poslední části poté podáme přehled možné nefarmakologické terapie (modulace srdeční kontrakce, ovlivnění aktivity sympatiku a parasympatiku a základní možnosti trvalé i dočasné přístrojové podpory).

Heart failure (HF) is a complex clinical syndrome which is manifested by characteristic symptoms and objective signs of cardiac insufficiency. The incidence of HF, particularly its chronic form, is estimated 0.4–2 % in the central and western Europe, with an increase in higher age groups, affecting 10–20 % of the population aged over 80. With respect to its growing incidence and prevalence, novel modalities of pharmacological and non-pharmacological treatment are being developed in order to improve quality of life and survival of the affected patients. This review based on up-to-date guidelines focuses in the first part on brief description of the possibilities of diagnosing heart failure, including the novelties arising out from the latest clinical and preclinical studies (such as soluble ST2, FSTL1, etc), further it concentrates on innovations in pharmacological treatment of chronic (ivabradine, ARNI, gliflozins) and acute (ularitide, serelaxin, nesiritide) HF. The last part provides an overview of available non-pharmacological HF therapeutics options (modulation of cardiac contraction, influencing the activity of sympathetic and parasympathetic nervous systems and permanent and temporary device support).

• MeSH
• Aminobutyrates therapeutic use   MeSH
• Atrial Natriuretic Factor therapeutic use   MeSH
• Benzazepines therapeutic use   MeSH
• Adrenergic beta-Antagonists therapeutic use   MeSH
• Defibrillators, Implantable utilization   MeSH
• Diagnosis, Differential MeSH
• Sodium-Glucose Transporter 2 Inhibitors MeSH
• Hypoglycemic Agents therapeutic use   MeSH
• Clinical Trials as Topic MeSH
• Myocardial Contraction MeSH
• Humans MeSH
• Extracorporeal Membrane Oxygenation MeSH
• Neprilysin antagonists & inhibitors   physiology   therapeutic use   MeSH
• Receptors, Angiotensin physiology   therapeutic use   MeSH
• Renin-Angiotensin System MeSH
• Heart Rate MeSH
• Cardiac Resynchronization Therapy utilization   MeSH
• Heart Failure * diagnosis   etiology   therapy   MeSH
• Sympathetic Nervous System MeSH
• Valsartan MeSH
• Check Tag
• Humans MeSH
• Publication type
• Overall MeSH

BACKGROUND: Right ventricular pacing (RVP) can result in pacing-induced cardiomyopathy (PICM). It is unknown whether specific biomarkers reflect differences between His bundle pacing (HBP) and RVP and predict a decrease in left ventricular function during RVP. AIMS: We aimed to compare the effect of HBP and RVP on the left ventricular ejection fraction (LVEF) and to study how they affect serum markers of collagen metabolism. METHODS: Ninety-two high-risk PICM patients were randomized to HBP or RVP groups. Their clinical characteristics, echocardiography, and serum levels of transforming growth factor β1 (TGF-β1), matrix metalloproteinase 9 (MMP-9), suppression of tumorigenicity 2 interleukin (ST2-IL), tissue inhibitor of metalloproteinase 1 (TIMP-1), and galectin 3 (Gal-3) were studied before pacemaker implantation and six months later. RESULTS: Fifty-three patients were randomized to the HBP group and 39 patients to the RVP group. HBP failed in 10 patients, who crossed over to the RVP group. Patients with RVP had significantly lower LVEF compared to HBP patients after six months of pacing (-5% and -4% in as-treated and intention-to-treat analysis, respectively). Levels of TGF-β1 after 6 months were lower in HBP than RVP patients (mean difference -6 ng/ml; P = 0.009) and preimplant Gal-3 and ST2-IL levels were higher in RVP patients, with a decline in LVEF ≥5% compared to those with a decline of <5% (mean difference 3 ng/ml and 8 ng/ml; P = 0.02 for both groups). CONCLUSION: In high-risk PICM patients, HBP was superior to RVP in providing more physiological ventricular function, as reflected by higher LVEF and lower levels of TGF-β1. In RVP patients, LVEF declined more in those with higher baseline Gal-3 and ST2-IL levels than in those with lower levels.

• MeSH
• Biomarkers MeSH
• Electrocardiography MeSH
• Ventricular Function, Left * physiology   MeSH
• Bundle of His MeSH
• Interleukin-1 Receptor-Like 1 Protein MeSH
• Cardiomyopathies * MeSH
• Cardiac Pacing, Artificial adverse effects   MeSH
• Collagen MeSH
• Humans MeSH
• Stroke Volume physiology   MeSH
• Tissue Inhibitor of Metalloproteinase-1 MeSH
• Transforming Growth Factor beta1 MeSH
• Treatment Outcome MeSH
• Check Tag
• Humans MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Randomized Controlled Trial MeSH

BACKGROUND: Dilated cardiomyopathy (DCM) is a major cause of heart failure and carries a high mortality rate. Myocardial recovery in DCM-related heart failure patients is highly variable, with some patients having little or no response to standard drug therapy. A genome-wide association study may agnostically identify biomarkers and provide novel insight into the biology of myocardial recovery in DCM. METHODS: A genome-wide association study for change in left ventricular ejection fraction was performed in 686 White subjects with recent-onset DCM who received standard pharmacotherapy. Genome-wide association study signals were subsequently functionally validated and studied in relevant cellular models to understand molecular mechanisms that may have contributed to the change in left ventricular ejection fraction. RESULTS: The genome-wide association study identified a highly suggestive locus that mapped to the 5'-flanking region of the CDCP1 (CUB [complement C1r/C1s, Uegf, and Bmp1] domain containing protein 1) gene (rs6773435; P=7.12×10-7). The variant allele was associated with improved cardiac function and decreased CDCP1 transcription. CDCP1 expression was significantly upregulated in human cardiac fibroblasts (HCFs) in response to the PDGF (platelet-derived growth factor) signaling, and knockdown of CDCP1 significantly repressed HCF proliferation and decreased AKT (protein kinase B) phosphorylation. Transcriptomic profiling after CDCP1 knockdown in HCFs supported the conclusion that CDCP1 regulates HCF proliferation and mitosis. In addition, CDCP1 knockdown in HCFs resulted in significantly decreased expression of soluble ST2 (suppression of tumorigenicity-2), a prognostic biomarker for heart failure and inductor of cardiac fibrosis. CONCLUSIONS: CDCP1 may play an important role in myocardial recovery in recent-onset DCM and mediates its effect primarily by attenuating cardiac fibrosis.

• MeSH
• Antigens, Neoplasm therapeutic use   MeSH
• Genome-Wide Association Study MeSH
• Cardiomyopathy, Dilated * metabolism   MeSH
• Fibrosis MeSH
• Ventricular Function, Left MeSH
• Humans MeSH
• Cell Adhesion Molecules metabolism   MeSH
• Heart Failure * MeSH
• Stroke Volume MeSH
• Check Tag
• Humans MeSH
• Publication type
• Journal Article MeSH

• MeSH
• Acute Disease MeSH
• Anticoagulants therapeutic use   MeSH
• Biomarkers MeSH
• Diagnostic Techniques, Cardiovascular MeSH
• Clinical Medicine MeSH
• Comorbidity MeSH
• Heart Failure diagnosis   epidemiology   drug therapy   classification   prevention & control   therapy   MeSH
• Telemedicine MeSH
• Heart Transplantation MeSH

• Conspectus
• Patologie. Klinická medicína
• NML Fields
• kardiologie
• NML Publication type
• kolektivní monografie

• Conspectus
• Patologie. Klinická medicína
• NML Fields
• patologie