Search

Despite improvements over recent years, morbidity and mortality associated with heart failure (HF) are higher in countries in the Central and Eastern Europe and Baltic region than in Western Europe. With the goal of improving the standard of HF care and patient outcomes in the Central and Eastern Europe and Baltic region, this review aimed to identify the main barriers to optimal HF care and potential areas for improvement. This information was used to suggest methods to improve HF management and decrease the burden of HF in the region that can be implemented at the national and regional levels. We performed a literature search to collect information about HF epidemiology in 11 countries in the region (Bulgaria, Croatia, Czechia, Estonia, Hungary, Latvia, Lithuania, Poland, Romania, Serbia, and Slovenia). The prevalence of HF in the region was 1.6-4.7%, and incidence was 3.1-6.0 per 1000 person-years. Owing to the scarcity of published data on HF management in these countries, we also collected insights on local HF care and management practices via two surveys of 11 HF experts representing the 11 countries. Based on the combined results of the literature review and surveys, we created national HF care and management profiles for each country and developed a common patient pathway for HF for the region. We identified five main barriers to optimal HF care: (i) lack of epidemiological data, (ii) low awareness of HF, (iii) lack of national HF strategies, (iv) infrastructure and system gaps, and (v) poor access to novel HF treatments. To overcome these barriers, we propose the following routes to improvement: (i) establish regional and national prospective HF registries for the systematic collection of epidemiological data; (ii) establish education campaigns for the public, patients, caregivers, and healthcare professionals; (iii) establish formal HF strategies to set clear and measurable policy goals and support budget planning; (iv) improve access to quality-of-care centres, multidisciplinary care teams, diagnostic tests, and telemedicine/telemonitoring; and (v) establish national treatment monitoring programmes to develop policies that ensure that adequate proportions of healthcare budgets are reserved for novel therapies. These routes to improvement represent a first step towards improving outcomes in patients with HF in the Central and Eastern Europe and Baltic region by decreasing disparities in HF care within the region and between the region and Western Europe., (© 2024 The Authors. ESC Heart Failure published by John Wiley & Sons Ltd on behalf of European Society of Cardiology.)

Background: Chronic heart failure (CHF) is a severe condition, often co-occurring with depression and anxiety, that strongly affects the quality of life (QoL) in some patients. Conversely, depressive and anxiety symptoms are associated with a 2-3 fold increase in mortality risk and were shown to act independently of typical risk factors in CHF progression. The aim of this study was to examine the impact of depression, anxiety, and QoL on the occurrence of rehospitalization within one year after discharge in CHF patients., Methods: 148 CHF patients were enrolled in a 10-center, prospective, observational study. All patients completed two questionnaires, the Hospital Anxiety and Depression Scale (HADS) and the Questionnaire Short Form Health Survey 36 (SF-36) at discharge timepoint., Results: It was found that demographic and clinical characteristics are not associated with rehospitalization. Still, the levels of depression correlated with gender (p ≤ 0.027) and marital status (p ≤ 0.001), while the anxiety values ​​were dependent on the occurrence of chronic obstructive pulmonary disease (COPD). However, levels of depression (HADS-Depression) and anxiety (HADS-Anxiety) did not correlate with the risk of rehospitalization. Univariate logistic regression analysis results showed that rehospitalized patients had significantly lower levels of Bodily pain (BP, p = 0.014), Vitality (VT, p = 0.005), Social Functioning (SF, p = 0.007), and General Health (GH, p = 0.002). In the multivariate model, poor GH (OR 0.966, p = 0.005) remained a significant risk factor for rehospitalization, and poor General Health is singled out as the most reliable prognostic parameter for rehospitalization (AUC = 0.665, P = 0.002)., Conclusion: Taken together, our results suggest that QoL assessment complements clinical prognostic markers to identify CHF patients at high risk for adverse events., Clinical Trial Registration: The study is registered under http://clinicaltrials.gov (NCT01501981, first posted on 30/12/2011), sponsored by Charité - Universitätsmedizin Berlin., (© 2023. The Author(s).)

Background: ST-segment-elevation myocardial infarction (STEMI) guidelines recommend pharmaco-invasive treatment if timely primary percutaneous coronary intervention (PCI) is unavailable. Full-dose tenecteplase is associated with an increased risk of intracranial hemorrhage in older patients. Whether pharmaco-invasive treatment with half-dose tenecteplase is effective and safe in older patients with STEMI is unknown., Methods: STREAM-2 (Strategic Reperfusion in Elderly Patients Early After Myocardial Infarction) was an investigator-initiated, open-label, randomized, multicenter study. Patients ≥60 years of age with ≥2 mm ST-segment elevation in 2 contiguous leads, unable to undergo primary PCI within 1 hour, were randomly assigned (2:1) to half-dose tenecteplase followed by coronary angiography and PCI (if indicated) 6 to 24 hours after randomization, or to primary PCI. Efficacy end points of primary interest were ST resolution and the 30-day composite of death, shock, heart failure, or reinfarction. Safety assessments included stroke and nonintracranial bleeding., Results: Patients were assigned to pharmaco-invasive treatment (n=401) or primary PCI (n=203). Median times from randomization to tenecteplase or sheath insertion were 10 and 81 minutes, respectively. After last angiography, 85.2% of patients undergoing pharmaco-invasive treatment and 78.4% of patients undergoing primary PCI had ≥50% resolution of ST-segment elevation; their residual median sums of ST deviations were 4.5 versus 5.5 mm, respectively. Thrombolysis In Myocardial Infarction flow grade 3 at last angiography was ≈87% in both groups. The composite clinical end point occurred in 12.8% (51/400) of patients undergoing pharmaco-invasive treatment and 13.3% (27/203) of patients undergoing primary PCI (relative risk, 0.96 [95% CI, 0.62-1.48]). Six intracranial hemorrhages occurred in the pharmaco-invasive arm (1.5%): 3 were protocol violations (excess anticoagulation in 2 and uncontrolled hypertension in 1). No intracranial bleeding occurred in the primary PCI arm. The incidence of major nonintracranial bleeding was low in both groups (<1.5%)., Conclusions: Halving the dose of tenecteplase in a pharmaco-invasive strategy in this early-presenting, older STEMI population was associated with electrocardiographic changes that were at least comparable to those after primary PCI. Similar clinical efficacy and angiographic end points occurred in both treatment groups. The risk of intracranial hemorrhage was higher with half-dose tenecteplase than with primary PCI. If timely PCI is unavailable, this pharmaco-invasive strategy is a reasonable alternative, provided that contraindications to fibrinolysis are observed and excess anticoagulation is avoided., Registration: URL: https://www., Clinicaltrials: gov; Unique identifier: NCT02777580., Competing Interests: Disclosures Dr Van de Werf reports institutional grants from Boehringer Ingelheim. Dr Ristić reports grants from Boehringer-Ingelheim and Novartis and travel fees from Astra Zeneca and Pfizer. Dr Arias-Mendoza reports grants from Merck and Novo Nordisk and personal fees from Novartis, Roche, Bayer, Boehringer Ingelheim, and Asofarma. Dr Saraiva received personal fees from Boehringer Ingelheim, Astra Zeneca, Novo Nordisk, Lily, Janssen, Daichii Sankyo, Bayer, Novartis, Nova Quimica Brazil, and Albert Einstein ARO Brazil. Dr Musić reports a grant from Boehringer Ingelheim and travel fees from Astra Zeneca and Pfizer. Dr Westerhout reports consulting fees from Bayer Canada. Dr Pagès is a senior medical advisor of Boehringer Ingelheim. Dr Danays reports consulting fees from Boehringer Ingelheim. Dr Bainey reports personal fees from Bayer, Astra Zeneca, Boehringer Ingelheim, and HLS Therapeutics. Dr Sinnaeve reports consulting fees to his institution (KU Leuven). Dr Welsh reports personal fees and travel fees from Boehringer Ingelheim. Dr Armstrong reports institutional and personal grants from Merck, Bayer, CLS Limited, Eli Lilly, and Boehringer Ingelheim and personal fees from Merck, Boehringer Ingelheim, Bayer, and Novo Nordisk. All other authors report no competing interests.

Cardiac tamponade is a medical emergency caused by the progressive accumulation of pericardial fluid (effusion), blood, pus or air in the pericardium, compressing the heart chambers and leading to haemodynamic compromise, circulatory shock, cardiac arrest and death. Pericardial diseases of any aetiology as well as complications of interventional and surgical procedures or chest trauma can cause cardiac tamponade. Tamponade can be precipitated in patients with pericardial effusion by dehydration or exposure to certain medications, particularly vasodilators or intravenous diuretics. Key clinical findings in patients with cardiac tamponade are hypotension, increased jugular venous pressure and distant heart sounds (Beck triad). Dyspnoea can progress to orthopnoea (with no rales on lung auscultation) accompanied by weakness, fatigue, tachycardia and oliguria. In tamponade caused by acute pericarditis, the patient can experience fever and typical chest pain increasing on inspiration and radiating to the trapezius ridge. Generally, cardiac tamponade is a clinical diagnosis that can be confirmed using various imaging modalities, principally echocardiography. Cardiac tamponade is preferably resolved by echocardiography-guided pericardiocentesis. In patients who have recently undergone cardiac surgery and in those with neoplastic infiltration, effusive-constrictive pericarditis, or loculated effusions, fluoroscopic guidance can increase the feasibility and safety of the procedure. Surgical management is indicated in patients with aortic dissection, chest trauma, bleeding or purulent infection that cannot be controlled percutaneously. After pericardiocentesis or pericardiotomy, NSAIDs and colchicine can be considered to prevent recurrence and effusive-constrictive pericarditis., (© 2023. Springer Nature Limited.)

Heart failure (HF) is a long-term clinical syndrome, with increasing prevalence and considerable healthcare costs that are further expected to increase dramatically. Despite significant advances in therapy and prevention, mortality and morbidity remain high and quality of life poor. Epidemiological data, that is, prevalence, incidence, mortality, and morbidity, show geographical variations across the European countries, depending on differences in aetiology, clinical characteristics, and treatment. However, data on the prevalence of the disease are scarce, as are those on quality of life. For these reasons, the ESC-HFA has developed a position paper to comprehensively assess our understanding of the burden of HF in Europe, in order to guide future policies for this syndrome. This manuscript will discuss the available epidemiological data on HF prevalence, outcomes, and human costs-in terms of quality of life-in European countries., (© 2022 The Authors. ESC Heart Failure published by John Wiley & Sons Ltd on behalf of European Society of Cardiology.)

In patients with heart failure, the beneficial effects of drug and device therapies counteract to some extent ongoing cardiac damage. According to the net balance between these two factors, cardiac geometry and function may improve (reverse remodelling, RR) and even completely normalize (remission), or vice versa progressively deteriorate (adverse remodelling, AR). RR or remission predict a better prognosis, while AR has been associated with worsening clinical status and outcomes. The remodelling process ultimately involves all cardiac chambers, but has been traditionally evaluated in terms of left ventricular volumes and ejection fraction. This is the second part of a review paper by the Study Group on Biomarkers of the Heart Failure Association of the European Society of Cardiology dedicated to ventricular remodelling. This document examines the proposed criteria to diagnose RR and AR, their prevalence and prognostic value, and the variables predicting remodelling in patients managed according to current guidelines. Much attention will be devoted to RR in patients with heart failure with reduced ejection fraction because most studies on cardiac remodelling focused on this setting., (© 2022 European Society of Cardiology.)

Cardiac remodelling refers to changes in left ventricular structure and function over time, with a progressive deterioration that may lead to heart failure (HF) development (adverse remodelling) or vice versa a recovery (reverse remodelling) in response to HF treatment. Adverse remodelling predicts a worse outcome, whilst reverse remodelling predicts a better prognosis. The geometry, systolic and diastolic function and electric activity of the left ventricle are affected, as well as the left atrium and on the long term even right heart chambers. At a cellular and molecular level, remodelling involves all components of cardiac tissue: cardiomyocytes, fibroblasts, endothelial cells and leucocytes. The molecular, cellular and histological signatures of remodelling may differ according to the cause and severity of cardiac damage, and clearly to the global trend toward worsening or recovery. These processes cannot be routinely evaluated through endomyocardial biopsies, but may be reflected by circulating levels of several biomarkers. Different classes of biomarkers (e.g. proteins, non-coding RNAs, metabolites and/or epigenetic modifications) and several biomarkers of each class might inform on some aspects on HF development, progression and long-term outcomes, but most have failed to enter clinical practice. This may be due to the biological complexity of remodelling, so that no single biomarker could provide great insight on remodelling when assessed alone. Another possible reason is a still incomplete understanding of the role of biomarkers in the pathophysiology of cardiac remodelling. Such role will be investigated in the first part of this review paper on biomarkers of cardiac remodelling., (© 2022 European Society of Cardiology.)

Aims: Patients with heart failure (HF) have not been shown to benefit from statins. In a post hoc analysis, we evaluated outcomes in ODYSSEY OUTCOMES in patients with vs. without a history of HF randomized to the proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitor alirocumab or placebo., Methods and Results: Among 18 924 patients with recent acute coronary syndrome (ACS) receiving intensive or maximum-tolerated statin treatment, the primary outcome of major adverse cardiovascular events (MACE) was compared in patients with or without a history of HF. The pre-specified secondary outcome of hospitalization for HF was also analysed. Overall, 2815 (14.9%) patients had a history of HF. Alirocumab reduced low-density lipoprotein cholesterol and lipoprotein(a) similarly in patients with or without HF. Overall, alirocumab reduced MACE compared with placebo [hazard ratio (HR): 0.85; 95% confidence interval (CI): 0.78-0.93; P = 0.0001]. This effect was observed among patients without a history of HF (HR: 0.78; 95% CI: 0.70-0.86; P < 0.0001), but not in those with a history of HF (HR: 1.17; 95% CI: 0.97-1.40; P = 0.10) (Pinteraction = 0.0001). Alirocumab did not reduce hospitalization for HF, overall or in patients with or without prior HF., Conclusion: Alirocumab reduced MACE in patients without a history of HF but not in patients with a history of HF. Alirocumab did not reduce hospitalizations for HF in either group. Patients with a history of HF are a high-risk group that does not appear to benefit from PCSK9 inhibition after ACS., (Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2021. For permissions, please email: journals.permissions@oup.com.)

Guideline-directed medical therapy (GDMT) has the potential to reduce the risks of mortality and hospitalisation in patients with heart failure (HF) with reduced ejection fraction (HFrEF). However, real-world data indicate that many patients with HFrEF do not receive optimised GDMT, which involves several different medications, many of which require up-titration to target doses. There are many challenges to implementing GDMT, the most important being patient-related factors (comorbidities, advanced age, frailty, cognitive impairment, poor adherence, low socioeconomic status), treatment-related factors (intolerance, side-effects) and healthcare-related factors that influence availability and accessibility of HF care. Accordingly, international disparities in resources for HF management and limited public reimbursement of GDMT, coupled with clinical inertia for treatment intensification combine to hinder efforts to provide GDMT. In this review paper, authors aim to provide solutions based on available evidence, practical experience, and expert consensus on how to utilise evolving strategies, novel medications, and patient profiling to allow the more comprehensive uptake of GDMT. Authors discuss professional education, motivation, and training, as well as patient empowerment for self-care as important tools to overcome clinical inertia and boost GDMT implementation. We provide evidence on how multidisciplinary care and institutional accreditation can be successfully used to increase prescription rates and adherence to GDMT. We consider the role of modern technologies in advancing professional and patient education and facilitating patient-provider communication. Finally, authors emphasise the role of novel drugs (especially sodium-glucose co-transporter 2 inhibitors), and a tailored approach to drug management as evolving strategies for the more successful implementation of GDMT., (© 2021 European Society of Cardiology.)

Endomyocardial biopsy (EMB) is an invasive procedure, globally most often used for the monitoring of heart transplant rejection. In addition, EMB can have an important complementary role to the clinical assessment in establishing the diagnosis of diverse cardiac disorders, including myocarditis, cardiomyopathies, drug-related cardiotoxicity, amyloidosis, other infiltrative and storage disorders, and cardiac tumors. Improvements in EMB equipment and the development of new techniques for the analysis of EMB samples has significantly improved the diagnostic precision of EMB. The present document is the result of the Trilateral Cooperation Project between the Heart Failure Association of the European Society of Cardiology, Heart Failure Society of America, and the Japanese Heart Failure Society. It represents an expert consensus aiming to provide a comprehensive, up-to-date perspective on EMB, with a focus on the following main issues: (1) an overview of the practical approach to EMB, (2) an update on indications for EMB, (3) a revised plan for heart transplant rejection surveillance, (4) the impact of multimodality imaging on EMB, and (5) the current clinical practice in the worldwide use of EMB., (Copyright © 2021. Published by Elsevier Inc.)

Aim: Myocarditis is an inflammatory disease associated with increased glucose uptake. The hypothesis of this study assumes that 18F-2-fluoro-2-deoxy-d-glucose positron emission tomography/computed tomography (FDG-PET/CT) may improve specificity and sensitivity in the diagnosis of myocarditis and referral for endomyocardial biopsy (EMB), adding additional information for post-discharge risk stratification. The aim of the study is to assess the diagnostic and prognostic feasibility of FDG-PET/CT in comparison to cardiac magnetic resonance (CMR) (alone or in combination) in patients with clinically suspected myocarditis undergoing EMB., Methods: Fifty hospitalized patients with clinically suspected myocarditis who meet the inclusion/exclusion criteria will be enrolled in a prospective, observational, multicentre, cohort study (NCT04085718). The primary endpoint is the sensitivity and specificity of FDG-PET/CT imaging in the diagnosis of myocarditis. The main secondary endpoints include correlation of FDG-PET/CT imaging with CMR, echocardiography, and EMB results. The patients will undergo the following evaluations: clinical examination, blood tests (including biomarkers of fibrosis and anti-heart autoantibodies (AHA)), ECG, 24 h Holter ECG, echocardiography, CMR, as well as resting single photon emission computed tomography (SPECT) to assess possible myocardial perfusion defects, cardiac FDG-PET/CT and right ventricular EMB. After 6-months a follow-up visit will be performed (including 24 h Holter ECG, echocardiography and CMR). Investigators evaluating individual studies (CMR, SPECT, FDG-PET/CT and EMB) are to be blinded to the other tests' results., Conclusion: We believe that FDG-PET/CT alone or in combination with CMR may be a useful tool for improving diagnostic accuracy in patients with clinically suspected myocarditis., Competing Interests: Declaration of Competing Interest AT, KO, MK, ALPC, DSS, ADR, RM, PMS, RM, LK, GO, MG declare no conflict of interest., (Copyright © 2021 Elsevier B.V. All rights reserved.)

Endomyocardial biopsy (EMB) is an invasive procedure, globally most often used for the monitoring of heart transplant (HTx) rejection. In addition, EMB can have an important complementary role to the clinical assessment in establishing the diagnosis of diverse cardiac disorders, including myocarditis, cardiomyopathies, drug-related cardiotoxicity, amyloidosis, other infiltrative and storage disorders, and cardiac tumours. Improvements in EMB equipment and the development of new techniques for the analysis of EMB samples have significantly improved diagnostic precision of EMB. The present document is the result of the Trilateral Cooperation Project between the Heart Failure Association of the European Society of Cardiology, the Heart Failure Society of America, and the Japanese Heart Failure Society. It represents an expert consensus aiming to provide a comprehensive, up-to-date perspective on EMB, with a focus on the following main issues: (i) an overview of the practical approach to EMB, (ii) an update on indications for EMB, (iii) a revised plan for HTx rejection surveillance, (iv) the impact of multimodality imaging on EMB, and (v) the current clinical practice in the worldwide use of EMB., (© 2021 Elsevier Inc. and Journal of Cardiac Failure. [Published by Elsevier Inc.] All rights reserved.)

Objective: To explore glucose metabolism in rheumatoid arthritis (RA) and its association with insulin resistance (IR) risk factors and disease activity indicators, including matrix metalloproteinase-3 (MMP3)., Methods: This single-center study included 127 non-diabetic subjects: 90 RA patients and 37 matched controls. IR-related risk factors, disease activity (DAS28-ESR/CRP), concentrations of inflammation markers, MMP3, glucose, specific insulin, and C-peptide (a marker of β-cell secretion) were determined. Homeostasis Model Assessment was used to establish insulin resistance (HOMA2-IR) and sensitivity (HOMA2-%S). Associations of HOMA2 indices with IR-related risk factors, inflammation markers, and RA activity were tested using multiple regression analyses., Results: RA patients had significantly increased HOMA2-IR index than controls. In the RA group, multivariate analysis revealed DAS28-ESR, DAS28-CRP, tender joint counts, patient's global assessment, and MMP3 level as significant positive predictors for HOMA2-IR (β = 0.206, P = 0.014; β = 0.192, P = 0.009; β = 0.121, P = 0.005; β = 0.148, P = 0.007; β = 0.075, P = 0.025, respectively), and reciprocal negative for HOMA2-%S index. According to the value of the coefficient of determination (R 2 ), DAS28-ESR ≥ 5.1 has the largest proportion of variation in both HOMA2-IR indices. DAS28-ESR ≥ 5.1 and ESR were independent predictors for increased C-peptide concentration (β = 0.090, P = 0.022; β = 0.133, P = 0.022). Despite comparability regarding all IR-related risk factors, patients with DAS28-ESR ≥ 5.1 had higher HOMA2-IR than controls [1.7 (1.2-2.5) vs. 1.2 (0.8-1.4), P = 0.000]. There was no difference between patients with DAS28-ESR < 5.1 and controls [1.3 (0.9-1.9) vs. 1.2 (0.8-1.4), P = 0.375]., Conclusions: RA activity is an independent risk factor for impaired glucose metabolism. DAS28-ESR ≥ 5.1 was the main contributor to this metabolic disturbance, followed by MMP3 concentration, outweighing the impact of classic IR-related risk factors.

Aims: Impact of type 2 diabetes mellitus (T2DM) on non-thromboembolic outcomes in atrial fibrillation (AF) is insufficiently explored. This prospective cohort study of AF patients aimed (i) to analyse the association between T2DM and heart failure (HF) events (including new-onset HF), and all-cause and cardiovascular mortality, (ii) to assess the impact of baseline T2DM treatment on outcomes, and (iii) to explore characteristics of new-onset HF phenotypes in relation to T2DM status., Methods and Results: Of 1803 AF patients (515/1288, with/without prior HF), 389 (22%) had T2DM at baseline. After 5 years of median follow-up, T2DM patients had an 85% greater risk of HF events [adjusted hazard ratio (aHR) 1.85; 95% confidence interval (CI) 1.51-2.28; P < 0.001], including a 45% increased risk for new-onset HF (1.45; 1.17-2.28; P = 0.015). T2DM conferred a 56% higher all-cause (1.56, 1.22-2.01; P = 0.003) and a 48% higher cardiovascular mortality (1.48; 1.34-1.93; P = 0.007). Fine-Gray analysis, with mortality as a competing risk, confirmed greater HF risk among T2DM patients. All risks were highest among insulin-treated patients. The prevalence of new-onset HF phenotypes was as follows: 67% preserved ejection fraction (HFpEF), 20% mid-range ejection fraction (HFmrEF) and 13% reduced ejection fraction (HFrEF). On time-dependent Cox regression, adjusted for baseline characteristics and an interim acute coronary event, T2DM increased aHRs for new-onset HFpEF (2.38; 1.30-4.58; P <0.001) and the combined HFmrEF/HFrEF (1.77; 1.11-3.62; P = 0.017)., Conclusions: Atrial fibrillation patients with T2DM have independently increased risk of new-onset/recurrent HF events, cardiovascular and all-cause mortality, particularly when insulin-treated. The prevailing phenotype of new-onset HF was HFpEF; T2DM conferred higher risk of both HFpEF and HFmrEF/HFrEF., (© 2019 The Authors. European Journal of Heart Failure © 2019 European Society of Cardiology.)

Cardiomyopathies are a heterogeneous group of heart muscle diseases and an important cause of heart failure (HF). Current knowledge on incidence, pathophysiology and natural history of HF in cardiomyopathies is limited, and distinct features of their therapeutic responses have not been systematically addressed. Therefore, this position paper focuses on epidemiology, pathophysiology, natural history and latest developments in treatment of HF in patients with dilated (DCM), hypertrophic (HCM) and restrictive (RCM) cardiomyopathies. In DCM, HF with reduced ejection fraction (HFrEF) has high incidence and prevalence and represents the most frequent cause of death, despite improvements in treatment. In addition, advanced HF in DCM is one of the leading indications for heart transplantation. In HCM, HF with preserved ejection (HFpEF) affects most patients with obstructive, and ∼10% of patients with non-obstructive HCM. A timely treatment is important, since development of advanced HF, although rare in HCM, portends a poor prognosis. In RCM, HFpEF is common, while HFrEF occurs later and more frequently in amyloidosis or iron overload/haemochromatosis. Irrespective of RCM aetiology, HF is a harbinger of a poor outcome. Recent advances in our understanding of the mechanisms underlying the development of HF in cardiomyopathies have significant implications for therapeutic decision-making. In addition, new aetiology-specific treatment options (e.g. enzyme replacement therapy, transthyretin stabilizers, immunoadsorption, immunotherapy, etc.) have shown a potential to improve outcomes. Still, causative therapies of many cardiomyopathies are lacking, highlighting the need for the development of effective strategies to prevent and treat HF in cardiomyopathies., (© 2019 The Authors. European Journal of Heart Failure © 2019 European Society of Cardiology.)

Interventional procedures for pericardial diseases include pericardiocentesis, drainage of pericardial effusion, intrapericardial therapy, and percutaneous balloon pericardiotomy or percutaneous pericardiostomy. Echocardiographic and fluoroscopic guidance have greatly increased safety and feasibility. Several devices for pericardiocentesis have been tested (PerDucer, PeriAttacher, visual puncture systems, Grasper, Scissors, and Reverse slitter), mainly to facilitate access to the pericardium in the absence of effusion for epicardial ablations or left atrial appendage ligation. In selected patients with pericardial effusions that cannot be managed medically or with prolonged drainage, various medications can be applied intrapericardially to prevent further recurrences or induce sclerosis of the pericardial space., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Advances in pharmacotherapy as well as device therapy in common cardiovascular diseases, especially implementation of rapid coronary reperfusion as a key management strategy in acute ischemic disease, improved overall survival. Yet, this success contributes to increased number of patients susceptible to heart failure development due to damaged myocardium. Although survival after heart failure diagnosis has improved over time, the death rate remains high: ≈50% of people diagnosed with this disease will die within 5 years. Thus, not only there is a space for novel concepts and strategies in the treatment of symptomatic heart failure, but also they are urgently needed. The mechanisms underlying the development of heart failure are multiple, complex, and not well understood. However, regardless of the cause of heart failure, or whether its presentation is acute or chronic, altered mitochondrial function/bioenergetics appears to play a substantial role in its pathophysiology. As such, the mitochondria are potentially promising, but still underused, target for new HF therapies. This review will focus on changes that occur in the mitochondria of failing myocardium, as well as on targets and approaches that suggest potential therapeutic effect in this ominous disease.

Full text available at: http://eurheartj.oxfordjournals.org/content/early/2015/08/28/eurheartj.ehv318., (Copyright © 2015 Sociedad Española de Cardiología. Published by Elsevier España, S.L.U. All rights reserved.)

Background: To evaluate association between von Willebrand factor (vWF) activity, inflammation markers, disease activity, and subclinical atherosclerosis in patients with rheumatoid arthritis (RA) and low cardiovascular risk., Methods: Above mentioned parameters were determined in blood samples of 74 non-diabetic, normotensive, female subjects, with no dyslipidemia(42 patients, 32 matched healthy controls, age 45.3±10.0 vs. 45.2±9.8 years). Intima-media thickness (IMT) was measured bilaterally, at common carotid, bifurcation, and internal carotid arteries. Subclinical atherosclerosis was defined as IMT>IMTmean+2SD in controlsat each carotid level and atherosclerotic plaque as IMT>1.5 mm. Majority of RA patients were on methotrexate (83.3%), none on steroids >10 mg/day or biologic drugs. All findings were analysed in the entire study population and in RA group separately., Results: RA patients with subclinical atherosclerosis had higher vWF activity than those without (133.5±69.3% vs. 95.3±36.8%, p<0.05). Predictive value of vWF activity for subclinical atherosclerosis was confirmed by logistic regression. vWF activity correlated significantly with erythrocyte sedimentation rate, fibrinogen, modified disease activity scores (mDAS28-ESR, mDAS28-CRP), modified Health Assessment Questionnaire (p<0.01 for all), duration of smoking, number of cigarettes/day, rheumatoid factor concentration (p<0.05 for all), and anti-CCP antibodies (p<0.01). In the entire study population, vWF activity was higher in participants with subclinical atherosclerosis (130±68% vs. 97±38%, p<0.05) or atherosclerotic plaques (123±57% vs. 99±45%, p<0.05) than in those without. Duration of smoking was significantly associated with vWF activity (β 0.026, p = 0.039)., Conclusions: We demonstrated association of vWF activity and subclinical atherosclerosis in low-risk RA patients as well as its correlation with inflammation markers, all parameters of disease activity, and seropositivity. Therefore, vWF might be a valuable marker of early atherosclerosis in RA patients.

This article describes the diagnostics, differential diagnostics, multimodal imaging, medicinal and invasive diagnostic therapy of acute and chronic pericarditis, constrictive pericarditis, pericardial effusion and cardiac tamponade under etiological aspects and on the basis of the guidelines of the European Society of Cardiology (ESC). The starting point of the decision tree is the symptomatic patient with echocardiographic evidence of pericardial effusion. The principle feature of the diagnostics is the etiopathogenetic allocation of the pericardial disease which influences the clinical picture, course therapy and prognosis. Infectious pericarditis (e.g. viral, bacterial and tuberculous) is differentiated from sterile autoreactive pericarditis and from neoplastic pericardial effusion by the cytology of the effusion and immunohistological and molecular investigations of the pericardial and epicardial biopsies. Pericardioscopy plays an important role in the recognition of suspicious areas. In many cases intrapericardial administration of cisplatin for neoplastic pericardial effusion and instillation of triamcinolone for autoreactive pericarditis prevent recurrence just as a treatment of several months with colchicine.

The epicardial halo delineates the heart shadow in fluoroscopy. To establish whether the sign is applicable to pericardiocentesis guidance, three investigators evaluated its intensity as absent = grade 0, indistinct = 0.5, clear = 1, intensive = 2 in posterior-anterior (PA) and lateral fluoroscopies recorded before pericardiocentesis or cardiac catheterization (Philips Integris-II BH3000). Three populations were studied: (a) 32 patients with pericardial effusion (PE group), 53.1 % males, aged 53.9 ± 13.9 years; (b) 14 patients with perimyocarditis (PM group), 64.3 % males, aged 51.6 ± 14.4 years; and (c) 46 coronary patients (CAD group), no PE, 95.6 % males, aged 67.3 ± 11.8 years. The intensity of the halo phenomenon was highest in patients with PE, lowest in patients with CAD, and intermediate in patients with PM (median sum of grades in PA/lateral view: 4/5 vs. 2/2.5 vs. 3/3, respectively) (p < 0.01). The halo phenomenon correlated well with HR and echocardiographic PE size in both angiographic views. The correlation with body mass index (BMI) and age was significant only in the lateral view and with PE volume only in the PA view. The sensitivity of the halo sign for PE was 84.1 % in PA and 92.0 % in lateral views. In 10/32 PE patients, the evaluation of the sign was repeated after PE drainage, revealing lower grades both in PA and in lateral views (p < 0.01). In conclusion, the epicardial halo sign is highly sensitive for the detection of a PE; it correlates well in at least one angiographic projection with the PE volume, HR, age, BMI, and the PE size in echocardiography and could be therefore applied as a safety guide for pericardiocentesis.

Despite a myriad of causes, pericardial diseases present in few clinical syndromes. Acute pericarditis should be differentiated from aortic dissection, myocardial infarction, pneumonia/pleuritis, pulmonary embolism, pneumothorax, costochondritis, gastroesophageal reflux/neoplasm, and herpes zoster. High-risk features indicating hospitalization are: fever >38 °C, subacute onset, large effusion/tamponade, failure of non-steroidal anti-inflammatory drugs (NSAIDs), previous immunosuppression, trauma, anticoagulation, neoplasm, and myopericarditis. Treatment comprises 10-14-days NSAID plus 3 months colchicine (2 × 0.5 mg; 1 × 0.5 mg in patients <70 kg). Corticosteroids are avoided, except for autoimmunity, as they facilitate the recurrences. Echo-guided pericardiocentesis (±fluoroscopy) is indicated for tamponade and effusions >2 cm. Smaller effusions are drained if neoplastic, purulent or tuberculous etiology is suspected. In recurrent pericarditis, repeated testing for autoimmune and thyroid disease is appropriate. Pericardioscopy and pericardial/epicardial biopsy may clarify the etiology. Familial clustering was recently associated with tumor necrosis factor receptor-associated periodic syndrome (TNFRSF1A gene mutation). Treatment includes 10-14 days NSAIDs with colchicine 0.5 mg bid for up to 6 months. In non-responders, low-dose steroids, intrapericardial steroids, azathioprine, and cyclophosphamide can be tried. Successful management with interleukin-1 receptor antagonist (anakinra) was recently reported. Pericardiectomy remains the last option in >2 years severely symptomatic patients. In constriction, expansion of the heart is impaired by the rigid, chronically inflamed/thickened pericardium (no thickening ~20 %). Chest radiography, echocardiography, computerized tomography, magnetic resonance imaging, hemodynamics, and endomyocardial biopsy indicate the diagnosis. Pericardiectomy is the only treatment for permanent constriction. Predictors of poor survival are prior radiation, renal dysfunction, high pulmonary artery pressures, poor left ventricular function, hyponatremia, age, and simultaneous HIV and tuberculous infection.

Pericardial cytokine patterns in various diseases are not well established. We have analyzed pericardial proinflammatory (interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha) and immunoregulatory cytokines (transforming growth factor (TGF)-beta1 and interferon (IFN)-gamma) in patients with pericarditis, myocarditis, and ischemic heart disease. Pericardial fluid was obtained in 30 subsequent patients undergoing pericardiocentesis (Group 1: 60 % males, 52.4 ± 14.2 years) and in 21 patients during aortocoronary bypass surgery (Group 2: 42.9 % males, age 67.2 ± 7.4 years). After clinical, laboratory, echocardiography examination, fiberoptic pericardioscopy (Storz-AF1101Bl, Germany) and pericardial/epicardial biopsy Group 1 was subdivided to 40 % neoplastic, 36.6 % autoreactive, 10 % iatrogenic, and 13.3 % viral pericarditis. Samples were promptly aliquoted, frozen, and stored at -70 °C. The cytokines were estimated using quantikine enzyme amplified-sensitivity immuno-assays (R&D Systems, USA) and the results compared between neoplastic, viral, iatrogenic, and autoreactive pericarditis and surgical groups. IL-6 was significantly increased in PE versus serum in all forms of pericarditis (except in autoreactive) and increased in comparison with pericardial fluid of surgical patients. TNF-alpha was increased only in PE of patients with viral pericarditis in comparison with Group 2. TGF-beta1 was strikingly lower in the PE than in the serum of all pericarditis patients. However, TGF-beta1 levels in PE were significantly higher in Group 1 than in Group 2, except in viral pericarditis. IFN-gamma levels did not significantly differ between PE and serum or in comparison with Group 2. The cytokine pattern "high TNF-alpha/low TGF-beta1" was found in viral pericarditis and low IL-6 in autoreactive PE. Different etiologies of pericardial inflammation did not influence the IFN-gamma levels. IL-6 pericardial to serum ratio was significantly higher in autoreactive PE than in viral and neoplastic forms. However, TNF-alpha and IFN-gamma pericardial to serum ratios were significantly higher in viral than in autoreactive and neoplastic PE.

Diabetic cardiomyopathy is a controversial clinical entity that in its initial state is usually characterized by left ventricular diastolic dysfunction in patients with diabetes mellitus that cannot be explained by coronary artery disease, hypertension, or any other known cardiac disease. It was reported in up to 52-60% of well-controlled type-II diabetic subjects, but more recent studies, using standardized tissue Doppler criteria and more strict patient selection, revealed a much lower prevalence. The pathological substrate is myocardial damage, left ventricular hypertrophy, interstitial fibrosis, structural and functional changes of the small coronary vessels, metabolic disturbance, and autonomic cardiac neuropathy. Hyperglycemia causes myocardial necrosis and fibrosis, as well as the increase of myocardial free radicals and oxidants, which decrease nitric oxide levels, worsen the endothelial function, and induce myocardial inflammation. Insulin resistance with hyperinsulinemia and decreased insulin sensitivity may also contribute to the left ventricular hypertrophy. Clinical manifestations of diabetic cardiomyopathy may include dyspnea, arrhythmias, atypical chest pain, and dizziness. Currently, there is no specific treatment of diabetic cardiomyopathy that targets its pathophysiological substrate, but various therapeutic options are discussed that include improving diabetic control with both diet and drugs (metformin and thiazolidinediones), the use of ACE inhibitors, beta blockers, and calcium channel blockers. Daily physical activity and a reduction in body mass index may improve glucose homeostasis by reducing the glucose/insulin ratio and the increase of both insulin sensitivity and glucose oxidation by the skeletal and cardiac muscles.

Introduction: Several cardiovascular manifestations in patients with diabetes may be asymptomatic. Left ventricular diastolic dysfunction (LVDD) is considered to be the earliest metabolic myocardial lesion in these patients, and can be diagnosed with tissue Doppler echocardiography. Silent myocardial ischemia (SMI) is a characteristic and frequently described form of ischemic heart disease in patients with diabetes. Objective The aim of the study was to assess the prevalence of LVDD and SMI in patients with type 2 diabetes, as well as to compare demographic, clinical, and metabolic data among defined groups (patients with LVDD, patients with SMI and patients with type 2 diabetes, without LVDD and SMI)., Methods: We investigated 104 type 2 diabetic patients (mean age 55.4 +/- 9.1 years, 64.4% males) with normal blood pressure, prehypertension and arterial hypertension stage I. Study design included basic laboratory assessment and cardiological workup (transthoracic echocardiography and tissue Doppler, as well as the exercise stress echocardiography)., Results: LVDD was diagnosed in twelve patients (11.5%), while SMI was revealed in six patients (5.8%). Less patients with LVDD were using metformin, in comparison to other two groups (chi2 =12.152; p=0.002). Values of HDL cholesterol (F=4.515; p=0.013) and apolipoprotein A1 (F=5.128; p= 0.008) were significantly higher in patients with LVDD., Conclusion: The study confirmed asymptomatic cardiovascular complications in 17.3% patients with type 2 diabetes.

Hemodynamic instability is the major concern in surgical patients with pericardial diseases, since general anesthesia and positive pressure ventilation may precipitate cardiac tamponade. In advanced constriction diastolic impairment and myocardial fibrosis/atrophy may cause low cardiac output during and after surgery. Elective surgery should be postponed in unstable patients with pericardial comorbidities. Pericardial effusion should be drained percutaneously (in local anesthesia) and pericardiectomy performed for constrictive pericarditis before any major surgical procedure. In emergencies, volume expansion, catecholamines, and anesthetics keeping cardiac output and systemic resistance should be applied. Etiology of pericardial diseases is an important issue is the preoperative management. Patients with neoplastic pericardial involvement have generally poor prognosis and any elective surgical procedure should be avoided. For patients with acute viral or bacterial infection or exacerbated metabolic, uremic, or autoimmune diseases causing significant pericardial effusion, surgery should be postponed until the causative disorder is stabilized and signs of pericarditis have resolved.

Background: Renal function frequently deteriorates in decompensated heart failure (DHF) patients, and one determinant is reduced renal blood flow. This may, in part, result from low cardiac output (CO), reduced mean arterial pressure (MAP), and venous congestion. The combined impact of both venous congestion (elevated right atrial pressure [RAP]) and low MAP are reflected by a reduced pressure gradient MAP-RAP. This study investigated the renal effects of ularitide, a synthetic version of the renal natriuretic peptide urodilatin in DHF patients., Methods: In SIRIUS II, a double-blind phase II trial, 221 patients hospitalized for DHF (with dyspnea at rest or minimal activity, cardiac index or=18 mm Hg) were randomized to a single 24-hour infusion of ularitide (7.5, 15, or 30 ng/kg per minute) or placebo added to standard therapy., Results: Estimated glomerular filtration rate, serum creatinine, creatinine clearance, and blood urea nitrogen (BUN) were not impaired by ularitide throughout infusion and during a 2-day follow-up period. At 24 hours, 15 ng/kg per minute ularitide reduced BUN levels (-4.07 +/- 12.30 vs -0.20 +/- 7.50 for placebo, P < .05). Ularitide at 15 and 30 ng/kg per minute rapidly elevated CO with sustained effects. Although 15 ng/kg per minute ularitide preserved the pressure gradient MAP-RAP, 30 ng/kg per minute ularitide reduced MAP-RAP by -7.8 +/- 10.6 mm Hg vs -2.4 +/- 9.8 mm Hg for placebo (P < .01, at 6 hours). A strong inverse correlation between MAP-RAP and BUN levels (Corr = -0.50579, P = .00015) was observed with 15 ng/kg per minute ularitide., Conclusions: Single 24-hour infusions of ularitide at 15 ng/kg per minute preserved short-term renal function in DHF patients possibly by both elevating CO and maintaining the MAP-RAP pressure gradient.

Cardiovascular manifestation of diabetes has remarkable therapeutic and prognostic implications. Diabetic cardiomyopathy is a distinct heart muscle disease in patients with well-controlled diabetes mellitus that cannot be ascribed to coronary artery disease, hypertension or any other known cardiac disease. It is characterized by left ventricular diastolic dysfunction that can be detected in 52-60% of well-controlled type II diabetic subjects using contemporary Doppler techniques. Pathophysiologically, hyperglycaemia causes myocardial necrosis and fibrosis, as well as the increase of myocardial free radicals and oxidants, which decrease nitric oxide levels, worsen the endothelial function and induce myocardial inflammation. Insulin resistance with hyperinsulinaemia and decreased insulin sensitivity are responsible for left ventricular hypertrophy. Clinical manifestations of diabetic cardiomyopathy are dispnoea, arrhythmias, atypical chest pain or dizziness. The treatment of diabetic cardiomopathy should be initiated as early as diastolic dysfunction is identified. Various therapeutic options include improving diabetic control with both diet and drugs (metformin and thiazolidinediones), use of ACE inhibitors, beta blockers and calcium channel blockers. Daily physical activity and reduction in body mass index may improve glucose homeostasis by reducing the glucose/insulin ratio, and the increase of both insulin sensitivity and glucose oxidation by the skeletal and cardiac muscles. Metformin and thiazolidinendiones are used to treat insulin resistance, but have different mechanisms of action. Metformin reduces free fatty amino acids effluvium from fat cells, thereby suppressing hepatic glucose production and indirectly improving peripheral insulin sensitivity and the endothelial function. In contrast, thiazolidinediones improve peripheral insulin sensitivity by reducing circulating free fatty amino acids, but also increasing production of adiponectin, which improves insulin sensitivity. Beta-adrenoceptor blocking agents are effective in preventing or reversing myocardial dilatation and remodelling, while ACE inhibitors facilitate blood flow through microcirculation in coronary vascular bed, fat and skeletal muscle, as well as improve insulin action at the cellular level.

Introduction: Autonomic dysfunction is present early in the course of heart failure, and has a direct role on deterioration of cardiac function and prognosis. Heart rate variability (HRV) estimates sympathovagal control of heart frequency. The influence of respiratory pattern on HRV is clinically important. Breathing disorders are common in heart failure and highly affect HRV and autonomic evaluation. It was previously shown that slow and deep breathing increased parasympathetic tone, but effects of this respiratory pattern on HRV were not evaluated., Objective: The aim of the study was to estimate effects of slow and deep breathing (SDB) on HRV in heart failure patients., Method: In 55 patients with heart failure (78% male, mean age 57.18 +/- 10.8 yrs, mean EF = 34.12 +/- 10.01%) and 14 healthy controls (57.1% male, mean age 53.1 +/- 8.2 yrs), short term HRV spectral analysis was performed (Cardiovit AT 60, Schiller). VLF, LF, HF and LF/HF were determined during spontaneous and deep and slow breathing at 0.1 Hz (SDB)., Results: LF, HF and LF/HF significantly increased during SDB compared with spontaneous breathing both in controls (LF 50.71 +/- 61.55 vs. 551.14 +/- 698.01 ms2, p < 0.001; HF 31.42 +/- 29.98 vs. 188.78 +/- 142.74 ms2, p < 0.001 and LF/HF 1.46 +/- 0.61 vs. 4.21 +/- 3.23, p = 0.025) and heart failure patients (LF 27.37 +/- 36.04 vs. 94.50 +/- 96.13 ms2, p < 0.001; HF 12.13 +/- 19.75 vs. 41.58 +/- 64.02 ms2, p < 0.001 and LF/HF 3.77 +/- 3.79 vs. 6.38 +/- 5.98, p = 0.031). Increments of LF and HF induced by SDB were significantly lower in patients than healthy controls. Heart failure patients had lower HRV compared to healthy controls both during spontaneous breathing and SDB. During spontaneous breathing, only HF was significantly lower between healthy controls and patients (p = 0.002). During SDB VLF (p = 0.022), LF (p < 0.001) and HF (p < 0.001) were significantly lower in heart failure patients compared to controls., Conclusion: These data suggest that SDB increases HRV both in healthy and heart failure patients; the highest increment is in LF range. Differences in spectral profile of HRV between healthy controls and heart failure patients become more profound during SDB. Controlled respiration during HRV analysis might increase sensitivity and reliability in detection of autonomic dysfunction in heart failure patients.

Pericardial cysts are uncommon and caused by an incomplete coalescence of fetal lacunae forming the pericardium. The paper presents two cases of pericardial cyst and literature review. The first is a case of a female patient with progressive dispnoa and spherical mass located in the right cardiophrenic angle on a chest x-ray. A pericardial cyst with low signal intensity was noted on T1w, high signal intensity on T2w in TSE (turbo spin echo) sequence on magnetic resonance images (MRI) which was suggestive of serous content. The patient underwent pericardial puncture and was thereafter free of symptoms. Histologic study of the cyst confirmed hydatid cyst diagnosis. Another patient is with echocardiographic evidence of cystic formation which was confirmed on MRI, with high signal intensity on SSFP (steady state free precession) sequence. The cyst was without septa and without communication with pericardial space. Since there were no significant hemodynamic changes, the patient is on regular follow up.

Background: The most frequent pericardial emergency is cardiac tamponade, but complications of an acute coronary syndrome and aortic dissection may also involve the pericardium. Acute pericarditis can also represent a medical emergency due to chest pain of upsetting intensity. Decompensations in chronic advanced constriction and in the clinical course of purulent pericarditis necessitate critical care as well., Diagnosis and Management: The diagnosis of cardiac tamponade is based on clinical presentation and physical findings, confirmed by echocardiography and cardiac catheterization. Tamponade is an absolute indication for urgent drainage, either by pericardiocentesis or surgical pericardiotomy. The approach for pericardiocentesis can be subxiphoid or intercostal using echocardiographic or fluoroscopic guidance. Urgent drainage, combined with intravenous antibiotics, is also mandatory in suspected purulent pericarditis. If confirmed, it should be combined with intrapericardial rinsing (best by a surgical drainage). Pericardiocentesis is contraindicated in cardiac tamponade complicating aortic dissection. This condition should immediately lead to cardiac surgery. Although pericardiectomy is the only treatment for permanent constriction, this procedure is contraindicated when extensive myocardial fibrosis and/or atrophy are demonstrated., Case Study: Iatrogenic tamponade may occur during percutaneous mitral valvuloplasty, implantation of pacemakers, electrophysiology and radiofrequency ablation procedures, right ventricular endomyocardial biopsy, percutaneous coronary interventions, and rarely during Swan-Ganz catheterization. The authors report on a 79-year-old who suffered coronary perforation and cardiac tamponade during elective stent implantation. Tamponade was successfully treated with pericardiocentesis and implantation of a membrane-covered graft stent. Subsequent recurrent pericarditis/postpericardial injury syndrome with moderate pericardial effusion was initially treated with aspirin and then with aspirin and colchicine. At 6 months, the patient is in stable remission even after withdrawal of colchicine., Conclusion: Natural history of pericardial diseases can be complicated with pericardial emergencies requiring prompt diagnosis, intensive care with hemodynamic monitoring, and early aggressive management. Medical supportive measures, drainage of pericardial effusion, surgical pericardiotomy, and pericardiectomy should be applied when needed with no delay. This procedural approach also applies to iatrogenic interventions leading to tamponade.

Percutaneous ablation for electrical disconnection of the arrhythmogenic foci using various forms of energy has become a well-established technique for treating atrial fibrillation (AF). Success rate in preventing recurrence of AF episodes is high although associated with a significant incidence of pulmonary vein (PV) stenosis and other rare complications. Clinical workup of AF patients includes imaging before and after ablative treatment using different noninvasive and invasive techniques such as conventional angiography, transoesophageal and intracardiac echocardiography, computed tomography (CT) and magnetic resonance imaging (MRI), which offer different information with variable diagnostic accuracy. Evaluation before percutaneous ablation involves assessment of PVs (PV pattern, branching pattern, orientation and ostial size) to facilitate position and size of catheters and reduce procedure time as well as examining the left atrium (presence of thrombi, dimensions and volumes). Imaging after the percutaneous ablation is important for assessment of overall success of the procedure and revealing potential complications. Therefore, imaging methods enable depiction of PVs and the anatomy of surrounding structures essential for preprocedural management and early detection of PV stenosis and other ablation-related procedures, as well as long-term follow-up of these patients.

Invasive diagnostic and therapeutic techniques are indispensable for the diagnosis and interventional treatment of coronary artery disease, valvular involvement and, in particular, if the specific components of the inflammatory or degenerative processes in rheumatic disease are to be identified in the different components of the heart. Although impairment of cardiac function and ischaemia can be suspected also by non-invasive techniques, coronary involvement needs the final proof by angiography. Endomyocardial or epicardial biopsy identifies the key players of autoreactivity: the infiltrating cells and the bound and circulating antibodies. Before corticoid treatment is started, a viral or microbial aetiology has to be excluded at the site of cardiac inflammation. This again can only be done by the analysis of cardiac tissue samples.

Rhythm and conduction disturbances and sudden cardiac death (SCD) are important manifestations of cardiac involvement in autoimmune rheumatic diseases (ARDs). In patients with rheumatoid arthritis (RA), a major cause of SCD is atherosclerotic coronary artery disease, leading to acute coronary syndrome and ventricular arrhythmias. In systemic lupus erythematosus (SLE), sinus tachycardia, atrial fibrillation and atrial ectopic beats are the major cardiac arrhythmias. In some cases, sinus tachycardia may be the only manifestation of cardiac involvement. The most frequent cardiac rhythm disturbances in systemic sclerosis (SSc) are premature ventricular contractions (PVCs), often appearing as monomorphic, single PVCs, or rarely as bigeminy, trigeminy or pairs. Transient atrial fibrillation, flutter or paroxysmal supraventricular tachycardia are also described in 20-30% of SSc patients. Non-sustained ventricular tachycardia was described in 7-13%, while SCD is reported in 5-21% of unselected patients with SSc. The conduction disorders are more frequent in ARD than the cardiac arrhythmias. In RA, infiltration of the atrioventricular (AV) node can cause right bundle branch block in 35% of patients. AV block is rare in RA, and is usually complete. In SLE small vessel vasculitis, the infiltration of the sinus or AV nodes, or active myocarditis can lead to first-degree AV block in 34-70% of patients. In contrast to RA, conduction abnormalities may regress when the underlying disease is controlled. In neonatal lupus, 3% of infants whose mothers are antibody positive develop complete heart block. Conduction disturbances in SSc are due to fibrosis of sinoatrial node, presenting as abnormal ECG, bundle and fascicular blocks and occur in 25-75% of patients.

The majority of the imaging techniques in cardiology could be applied in rheumatic diseases (RDs), such as echocardiography, single-photon emission computed tomography (SPECT), radionuclide ventriculography, angiography, cardiovascular MRI and CT. Inflammatory pericardial involvement is the most common cardiac manifestation in various forms of RD. Echocardiography is the gold standard for diagnosis of pericardial abnormalities, demonstrating location and amount of pericardial effusion. Cardiac MRI and CT can be used to assess the features of pericardial effusions and pericardial structures. In patients with valvular heart disease in RD, transoesophageal echocardiography is a superior method and offers reliable information about valve morphology, the severity of the disease and left ventricular (LV) function. In addition, cardiac MRI is a valuable tool for the evaluation of valvular stenosis and regurgitation severity. Myocardial involvement in RD is demonstrated by abnormalities in LV size and function, indicating myocardial inflammation. In these patients Doppler echocardiography and myocardial tissue imaging can provide essential diagnostic information. Both LV angiography and cardiac MRI can provide reliable information on LV size, function and mass. In patients with coronary disease associated with RD, LV ejection fraction and ventricular wall motion can be assessed by echocardiography, radionuclide ventriculography, gated SPECT and MRI. Three-dimensional (3D) echocardiography is considered superior to 2D echocardiographic techniques. Stress echocardiography is the most used method for detection of myocardial ischaemia. The only accurate visualization of the coronary arteries is by selective coronary arteriography, which remains the gold standard. Although new non-invasive techniques have been developed, including CT and MRI angiography, some limitations apply.

This study evaluated the diagnostic significance of a magnetic resonance imaging (MRI) based scoring model for identification of arrhythmogenic right ventricular cardiomyopathy (ARVC) in patients with MRI evidence of RV abnormalities. Fifty-three patients with RV myocardial abnormalities on MRI were divided into a group with ARVC 1 (n=17) and a group with other RV arrhythmias (n=37). Decision tree learning (DTL) and linear classification (based on a modified ARVC scoring model of major and minor criteria) were used to identify and assess MRI criterion information value, and to induce ARVC diagnostic rules. All major ARVC criteria were more frequent in the ARVC group. Among minor criteria regional RV hypokinesia, mild segmental RV dilatation, and prominent trabeculae were more frequent in the ARVC group while mild global RV dilatation was more frequent in the non-ARVC group. RV aneurysm achieved highest importance in ARVC diagnosis (predictive accuracy 76.8%). Better diagnostic accuracy (sensitivity 93.3%, specificity 89.5%) was achieved when the MRI score for the major and minor criteria reached threshold value of four: two major criteria, or one major and two minor, or four minor criteria. Combinations between major and minor criteria contributed to a statistically valid model for ARVC diagnosis.

Introduction: Autonomic regulation of cardiovascular functions in congestive heart failure is characterised by enhanced sympathetic and diminished parasympathetic activity. The long term predominance of sympathetic tone is a significant factor in arrhythmogenesis, sudden cardiac death, and progressive pump failure. Heart rate variability (HRV) is a noninvasive method for estimating the sympatho vagal balance in cardiovascular control., Aim: The aim of this study was to analyse the influence of heart failure severity on HRV., Method: HRV was estimated through the spectral analysis of short term ECG (Cardiovit AT 60, Schiller, CH) in 63 patients (78% male, mean age 56.9 +/- 10.9 years) and 14 healthy volunteers (57.1% male, mean age 53.1 +/- 8.2 years). The following spectral components were measured: VLF (very low frequency), LF (low frequency), HF (high frequency), and total power (Tot Power)., Results: All spectral componentswere statistically, significantly lower in patients with heart failure in comparison to healthy controls (VLF: 159.89 +/- 147.02 vs. 285.50 +/- 202.77 ms2; p = 0.023, LF: 161.48 +/- 204.01 vs. 474.57 +/- 362.93 ms2; p < 0.001, HF: 88.58 +/- 102.47 vs. 362.71+/- 318.28 ms2; p < 0.001), as well as total power (Tot Power: 723.39 +/- 644.52 vs. 1807.29 +/- 1204.74 ms2; p < 0.001). A significant, negative correlation between HRV parameters and NYHA class was detected in heart failure patients (VLF: r = -0.391; p = 0.002, LF: r = -0.401; p = 0.001, and Tot Power r = -0.372; p = 0.003). Ejection fraction proved to be in significant, positive correlation to VLF (r = 0.541; p = 0.002), LF (r = 0.531; p = 0.003), HF (r = 0.418; p = 0.020), and Tot Power (r = 0.457; p = 0.013)., Conclusion: Significant HRV reduction is a precursor to incipient heart failure (NYHA I). In heart failure progression, total power as well as the power of all spectral components is progressively reduced. LF and Tot Power are the most prominent parameters for discriminating between the different stages of heart failure. These results could promote HRV as an important decision-making tool in heart failure treatment as well as in monitoring the results of that treatment.

Introduction: Patients suffering from chronic ischaemic cardiomyopathy and left ventricular ejection fraction (LVEF) lower than 30% represent a difficult and controversial population for surgical treatment., Objective: The aim of this study was to evaluate the effects of surgical treatment on the early and long-term outcome of these patients., Method: The patient population comprised 50 patients with LVEF < 30% (78% male, mean age: 58.3 years, range: 42-75 years) who underwent surgical myocardial revascularisation during the period 1995-2000. Patients with left ventricular aneurysms or mitral valve insufficiency were excluded from the study. The following echocardiography parameters were evaluated as possible prognostic indicators: LVEF, fraction of shortening (FS), left ventricular systolic and diastolic diameters (LVEDD, LVESD) and volumes (LVEDV, LVESV), as well as their indexed values (LVESVI)., Results: Fifteen patients (30%) died during the follow-up, 2/50 intraoperatively (4%). The presence of diabetes mellitus, previous myocardial infarction, main left coronary artery disease, and three-vessel disease, correlated significantly with the surgical outcomes. The patient's age, family history, smoking habits, hypertension, hyperlipidaemia, history of stroke, peripheral vascular disease, and renal failure, did not correlate with the mortality rate. A comparison of preoperative echocardiography parameters between survivors and non-survivors revealed significantly divergent LVEF, LVEDD, LVESD, LVEDV, LVESV, and LVESVI values. Preoperative LVESVI offered the highest predictive value (R = 0.595)., Conclusion: Diabetes mellitus, history of myocardial infarction, stenosis of the main branch, and three-vessel disease, significantly affected the perioperative and long-term outcome of surgical revascularisation in patients with ischaemic cardiomyopathy and LVEF < 30%. In survivors, LVEF, FS, and systolic and diastolic echocardiography parameters, as well as their indexed values, significantly improved after surgical revascularisation. LVESVI provided the highest predictive value for mortality.

Bacterial pericarditis occurs by direct infection during trauma, thoracic surgery, or catheter drainage, by spread from an intrathoracic, myocardial, or subdiaphragmatic focus, and by hematogenous dissemination. The frequent causes are Staphylococcus and Streptococcus (rheumatic pancarditis), Haemophilus, and M. tuberculosis. In AIDS pericarditis, the incidence of bacterial infection is much higher than in the general population, with a high proportion of Mycobacterium avium-intracellulare infection. Purulent pericarditis is the most serious manifestation of bacterial pericarditis, characterized by gross pus in the pericardium or microscopically purulent effusion. It is an acute, fulminant illness with fever in virtually all patients. Chest pain is uncommon. Purulent pericarditis is always fatal if untreated. The mortality rate in treated patients is 40%, and death is mostly due to cardiac tamponade, systemic toxicity, cardiac decompensation, and constriction. Tuberculous infection may present as acute pericarditis, cardiac tamponade, silent (often large) relapsing pericardial effusion, effusive-constrictive pericarditis, toxic symptoms with persistent fever, and acute, subacute, or chronic constriction. The mortality in untreated patients approaches 85%. Urgent pericardial drainage, combined with intravenous antibacterial therapy (e.g. vancomycin 1g twice daily, ceftriaxone 1-2g twice daily, and ciprofloxacin 400 mg/day) is mandatory in purulent pericarditis. Irrigation with urokinase or streptokinase, using large catheters, may liquify the purulent exudate, but open surgical drainage is preferable. The initial treatment of tuberculous pericarditis should include isoniazid 300 mg/day, rifampin 600 mg/day, pyrazinamide 15-30 mg/kg/day, and ethambutol 15-25 mg/kg/day. Prednisone 1-2 mg/kg/day is given for 5-7 days and progressively reduced to discontinuation in 6-8 weeks. Drug sensitivity testing is essential. Pericardiectomy is reserved for recurrent effusions or continued elevation of central venous pressure after 4-6 weeks of antituberculous and corticosteroid therapy.