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Long QT syndrome (LQTS) is characterised by both the depolarisation and repolarisation disorder of cardiac muscle cells. Cardiac resynchronising therapy (CRT) is an important treatment option for patients with chronic heart failure (CHF) when echocardiographic and electrocardiographic criteria are met. Although CRT was introduced in clinical practice 10 years ago, doubts related to application of this treatment method persist because of its potential proarrhythmogenic effect. This is a case describing a 66-year-old Caucasian female with LQTS coexisting with a left bundle branch branch block (LBBB) and an implantable single-cavity cardioverter-defibrillator (ICD VR), who had repeated appropriate high-energy treatments. The upgrade to resynchronisation therapy defibrillator (CRT-D) significantly reduced frequency of ventricular tachycardia and the need for electrical therapies. The normalisation of the left ventricle size, as seen on echo examination, and the improvement of heart failure symptoms were also observed.

Heart failure (HF) remains a major medical and social problem. The NT-pro-brain natriuretic peptide (NT-proBNP) and its active form, brain-type natriuretic peptide (BNP), in a simple blood test are the gold-standard biomarkers for HF diagnosis. However, even good biomarkers such as natriuretic peptides fail to predict all the risks associated with HF due to the diversity of the mechanisms involved. The pathophysiology of HF is determined by numerous factors, including oxidative stress, inflammation, neuroendocrine activation, pathological angiogenesis, changes in apoptotic pathways, fibrosis and vascular remodeling. High readmission and mortality rates prompt a search for new markers for the diagnosis, prognosis and treatment of HF. Oxidative-stress-mediated inflammation plays a crucial role in the development of subsequent changes in the failing heart and provides a new insight into this complex mechanism. Oxidative stress and inflammatory biomarkers appear to be a promising diagnostic and prognostic tool in patients with HF. This systematic review provides an overview of the current knowledge about oxidative stress and inflammation parameters as markers of HF. [ABSTRACT FROM AUTHOR]

The aim of this study was to analyze the relationship between levels of sST2, NT-proBNP and oxidative stress markers in patients with reduced ejection fraction (HFrEF) due to non-ischemic cardiomyopathy. A total of 88 patients with HFrEF were divided into four groups based on left ventricular ejection fraction (≤25% and >25%) and NYHA functional class (group 1—LVEF > 25% and NYHA class I or II; group 2—LVEF > 25% and NYHA class III or IV; group III—LVEF ≤ 25% and NYHA class I or II; group IV—LVEF ≤ 25% and NYHA class III or IV). In 39 (44.32%) patients LVEF was reduced below 25%, and 22 of them (56.41%) were in NYHA functional class III/IV. Of the 49 (55.68%) patients with LVEF ≥ 25%, only 18.37% were in NYHA functional class III/IV (p < 0.001). Patients with LVEF ≥ 25% had lower levels of NT-proBNP, total oxidant status (TOS), total antioxidant capacity (TAC), and oxidative stress index (OSI). The levels of NT-proBNP but not sST-2 correlated positively with NYHA functional class (p < 0.001) and negatively with LVEF (p < 0.001). The levels of sST-2 were associated with increased TAC (p = 0.009) and uric acid (p = 0.040). These findings indicate that only NT-proBNP was related to the severity of heart failure, whereas sST2 correlated with total antioxidant capacity. Therefore, in stable patients with HFrEF due to dilated cardiomyopathy, sST2 may be an additional biomarker reflecting the redox status, but not the severity of heart failure. [ABSTRACT FROM AUTHOR]

Objective: Despite several improvements in the management of heart failure (HF), it is still an incurable and a progressive disease. Several trials demonstrated that the process of inflammation may be responsible for initiation and progression of HF. The aim of the present study was to investigate the role of interleukin-33 (IL-33) in the pathogenesis of HF and to assess whether disease etiology and course of the disease affect the expression of cytokines. Methods: The study included 155 (106 male and 49 female) patients with systolic HF with a mean left ventricle ejection fraction of 32.13}12.8% and 60 (36 male and 24 female) healthy individuals. IL-33 concentrations were evaluated using enzyme-linked immunosorbent assay. Results: The concentration of IL-33 was statistically significantly lower in patients with HF than in healthy subjects, 16.91 (0-81.00) pg/mL and 92.51 (33.61-439.61) pg/mL, respectively. Patients with HF with ischemic etiology had lower concentration of IL-33 (10.75 pg/mL) than subjects with HF with non-ischemic etiology (21.05 pg/mL). Patients with stable HF (10.46 pg/mL) had lower IL-33 levels than those with unstable HF (19.02 pg/mL). Conclusion: The concentrations of IL-33 were lower in patients with HF than in healthy controls, which may play an important role of above cytokine in HF development and progression. In addition, interleukin concentrations varied depending on the etiology and severity of the course of the disease. [ABSTRACT FROM AUTHOR]

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Background: The controversy over electrotherapy for patients aged >80 years occurs already at the stage of qualification for this treatment type and concerns optimal device selection, the implantation strategy, and the overall benefit from pacemaker therapy. The group also has a considerable number of cardiovascular risk factors, and the data from the literature on the impact of the pacing mode on the remote prognosis of this group are ambiguous.Objective: Assessment of the risk factors for death among patients with implanted pacemakers >80 years of age in a 4-year follow-up.Methods: The study group consisted of 140 consecutive patients (79 women) aged 84.48 ± 3.65 years with single- or dual-chamber pacemakers implanted >80 years of age because of symptomatic bradycardia. In univariate and multivariate Cox regression analyses, demographic, echocardiographic, and laboratory parameters, pharmacotherapy, and factors related to the implanted device - i.e., indications, pacemaker type, and the implantation position of the tip of the right ventricular lead - were included. The endpoint was death for any reason in a 4-year follow-up.Results: During follow-up, 68 patients (48.6%) died. Although atrial fibrillation with a slow ventricular response constituted 20% of the indications for implantation, 60.8% of the patients received a single-chamber system (VVI/VVIR). In the whole group, the multivariate Cox regression analysis showed both a favourable prognostic significance of DDD pacing system implantation (HR = 0.507; 95% CI: 0.294-0.876) and coexisting hypertension (HR = 0.520; 95% CI: 0.299-0.902). The risk factors were fasting glycaemia (HR = 1.180; 95% CI: 1.038-1.342) and, potentially, female sex (HR = 1.672; 95% CI: 0.988-2.830; p = 0.056). In the female subgroup a more favourable prognosis was related to the use of angiotensin-converting enzyme inhibitors (HR = 0.435; 95% CI: 0.202-0.933) and DDD pacemaker implantation (HR = 0.381; 95% CI: 0.180-0.806). In the male subgroup a more favourable prognosis was related to concerned patients with coexisting hypertension (HR = 0.349; 95% CI: 0.079-0.689).Conclusions: DDD mode pacing seems to serve as a factor which decreases mortality among patients aged >80 years in long-term follow-up. The potentially poorer prognosis for the female patients in this group may result from a combination of the dominant VVI pacing mode, potential propagation of atrial fibrillation, a low proportion of antithrombotic therapy, and sex-related predispositions to thromboembolic complications. [ABSTRACT FROM AUTHOR]

Background: The impact of myocardial viral persistence on the clinical outcome of patients with dilated cardiomyopathy (DCM) is still open to question. Methods: Fifty-two patients with DCM were enrolled and followed for a median of 3.8 years with respect to death or heart transplantation. Studied patients were clinically stable for at least 6 months before hospitalization. They underwent coronary angiography and endomyocardial biopsy. Specimens were examined by histo- and immunohistochemistry, and the viral genomes of parvovirus B19, cytomegalovirus (CMV), Coxsackie B virus (CVB), and hepatitis B and C viruses were studied by real-time polymerase chain reaction. Results: Forty-two out of 52 patients were available for clinical follow-up. The viral genome was detected in the myocardium of 32 out of 42 patients Among the viruses studied, CMV and CVB were the most frequently found. Nine out of 42 patients achieved the predefined study end point. No statistically significant correlation was found between the presence of a persistent viral genome and study end point. No statistically significant relationship between viral genomes studied and immunohistology results was detected. Conclusions: High prevalence of a viral genome in the myocardium of patients with DCM did not have an influence on their long-term clinical outcome. [ABSTRACT FROM AUTHOR]