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Approximately half a century has passed since the discovery of beta-blockers. Then, their prime therapeutic purpose was to treat angina and cardiac arrhythmias; nowadays, beta-blockers' usage and effectiveness are extended to treat other cardiovascular diseases, such as hypertension, congestive heart failure, and coronary artery disease. Safety concerns were raised about beta- blockers and their use for chronic obstructive pulmonary disease (COPD) patients with concurrent cardiovascular disease. After thorough research of the literature, this review summarizes the evidence proving that beta-blockers not only might be well tolerated in COPD patients, but they might also have a beneficial effect in this group of patients., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Obesity is a major risk factor for the development of chronic heart failure (CHF) and does not only pose diagnostic challenges, but also has prognostic implications for these patients. Paradoxically, obese patients with CHF have a better prognosis than thinner individuals. In recent years, it has been demonstrated that the adipose tissue, even in patients with HF, is not always detrimental, and that obesity may coexist with a phenotype of benign adiposity without systemic metabolic abnormalities. Experimental data have shown that natriuretic peptides (NPs), and in particular brain natriuretic peptide (BNP), play a major role in the communication of the heart with the adipose tissue. Body fat distribution and adipose tissue function show a large degree of heterogeneity among depots and may explain the complex relationship between NPs and body fat. NPs can affect both the quality and the behaviour of fatty tissue, promoting a healthy adipocyte phenotype, and can favourably affect body fat metabolism. In this article, we review the existing literature on the bidirectional effects of BNP and adipose tissue in HF and highlight the complexity of this relationship.

Introduction: Heart failure (HF) with reduced ejection fraction (HFrEF) remains a challenging problem due to its high mortality rate. The PARADIGM HF trial and a new class of drugs - angiotensin receptor-neprilysin inhibitors (ARNIs) - managed to change the current perception of HF treatment by reducing cardiovascular mortality and morbidity as well as HF hospitalizations compared with enalapril and have emerged as an evidence-based therapy for HFrEF. Another novelty in HF therapy is dapagliflozin, a sodium-glucose transporter-2 inhibitor (SGLT2i) which decreased the rates of cardiac death and worsening of HF in the DAPA-HF trial, when added in other guideline recommended therapy. A recent study evaluated the potency of dapagliflozin in terms of mortality and deterioration of HF, in patients taking sacubitril/valsartan and in patients who were naive. Material and methods: A prospective cohort study of 30 symptomatic HF patients with EF < 35% (aged 65 ±10 years) was conducted. Diabetic (2TDM) patients of NYHA status II-III, previously treated with ARNI, β-blocker, and mineralocorticoid receptor antagonists (MRA) were included. Dapagliflozin was added to their therapy. Results: Echocardiographic evaluation revealed improvement of both conventional tissue Doppler and diastolic strain parameters by dapagliflozin addition on HF therapy. Conclusions: Dapagliflozin impact on diastolic function may explain the symptom amelioration and the improvement of quality of life. And more specifically, the ratio of early diastolic transmitral flow velocity to global strain rate at the early filling phase of diastole (E/SRE)may be considered a reliable index of HF therapy responders. [ABSTRACT FROM AUTHOR]

Background: Atrial fibrillation (AF) constitutes a relatively infrequent pregnancy complication, which may be a therapeutic Gordian knot. Indeed, sparse data exist regarding the prevalence, prognosis, and management of AF during pregnancy. In general, AF occurs as a benign, self-limited arrhythmia, but occasionally may have severe hemodynamic consequences in pregnant patients suffering from heart failure, congenital heart disease, or other comorbidities. Extra-cardiac causes of AF should always be meticulously excluded.Review: Treatment decisions are difficult, since medications may cross the placental barrier and potentially affect fetal growth and organogenesis, or even result in fetal bradyarrhythmias. Treatment goals are not differentiated in comparison to those regarding AF occurring in the general population. Still, while maternal treatment is prioritized, issues regarding fetal health must deliberately be considered. Consequently, hemodynamic instability is to be promptly treated with synchronized electrical cardioversion. In contrast, in stable patients, pharmacologic cardioversion, under appropriate antithrombotic regimen, should be attempted. Selection of appropriate antithrombotic therapy, including novel oral anticoagulants, imposes further difficulties on therapeutic decision-making. Further clinical trials are warranted in order to assess the pathophysiology and prognosis of AF in pregnancy and ameliorate the evidence-based therapeutic strategy in this specific group of the population. [ABSTRACT FROM AUTHOR]