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In the published article, the title was published incorrectly as COVID-19.

In individuals with chronic obstructive pulmonary disease (COPD), skeletal muscle wasting and changes in muscle fiber composition limit the muscle strength with consequences on daily physical activities. In the present study we aimed to investigate about the interconnection among upper limb strength, body composition and health related quality of life (HRQoL) in patients with COPD to verify the impact of muscle mass loss on HRQoL. Twenty-six consecutive patients (69.2% male; age: 69.7±7.29 years) with COPD were included. Patients underwent pulmonary function tests. Body composition was evaluated through Bioelectrical Impedance Analysis (BIA); handgrip test was used for measure upper limb strength. St George’s Respiratory Questionnaire (SGRQ) was used to evaluate patients’ HRQoL. Upper limb muscle strength was negatively correlated with SGRQ (Pearson=-0.571; p=0.002) in particular with activity and impact domains (Pearson=-0.668; p

Klara Komici,1 Dino F Vitale,2 Dario Leosco,1 Angela Mancini,1 Graziamaria Corbi,3 Leonardo Bencivenga,1 Alessandro Mezzani,4 Bruno Trimarco,5 Carmine Morisco,5 Nicola Ferrara,1,2 Giuseppe Rengo1,2 1Division of Geriatrics, Department of Translational Medical Sciences, University of Naples Federico II, Naples, Italy; 2Cardiac Rehabilitation Division, Salvatore Maugeri Foundation, IRCCS, Scientific Institute of Telese Terme (BN), Telese Terme, Italy; 3Department of Medicine and Health Sciences, University of Molise Campobasso, Campobasso, Italy; 4Cardiac Rehabilitation Division, Salvatore Maugeri Foundation, IRCCS, Scientific Institute of Veruno, Veruno, Italy; 5Division of Cardiology, Department of Advanced Biomedical Sciences, University of Naples Federico II, Naples, Italy Objectives: To assess pressure injury (PI) incidence among patients hospitalized for acute myocardial infarction (AMI) in an intensive coronary care unit (ICCU) and to detect the impact of specific risk factors on the development of PI in this clinical setting.Patients and methods: Prospective cohort study in ICCU setting. Patients admitted for AMI: patients mean age 67.5±11.5 years (n=165). Norton Scale, Mini Nutritional Assessment (MNA), demographic, clinical and biochemical data collected at the time of ICCU admission have been tested in a logistic model to assess the odds ratios (ORs) of PI risk development. The jackknifed area under the receiver operating characteristic curve (AUC) and the decision curve analysis have been employed to assess the additive predictive value of a factor.Results: Twenty-seven (16.3%) patients developed PIs. An increased PI risk was associated with advanced age (OR =2.5 every 10-year increase; 95% CI =1.1–5.7), while probability of PI development was reduced in patients with higher left ventricular ejection fraction (LVEF) (OR =0.4 every 5% increase; 95% CI =0.24–0.66), MNA score (OR =0.65 every unit change; 95% CI =0.44–0.95) and Norton Scale score (OR =0.7 every unit change; 95% CI =0.57–0.88). The AUC and the decision curve analysis showed that LVEF inclusion improved the discrimination power and the clinical net benefit of the final model.Conclusion: Age, LVEF, Norton Scale and MNA scores have a strong and independent clinical value as predictors of in-hospital PI development in patients with AMI. This finding has the potential to improve the clinical management of patients admitted in ICCU. Keywords: pressure injury, Mini Nutritional Assessment, Norton Scale, acute myocardial systolic dysfunction

Since 1907, when it was first described, Alzheimer’s disease (AD) has been one of the most studied diseases, in order to clarify its complex pathogenesis. Since AD will become increasingly widespread in the next decades, resulting in enormous health care costs. Since current treatments do not alter the course of the disease, acting temporarily on symptoms, it is essential to identify factors involved in the pathogenesis of disease. Among these, the β-adrenergic receptor (β-ARs) system might play a crucial role. The central noradrenergic system undergoes substantial changes in the course of AD and β-ARs have been implicated both in the formation of amyloid in brain and in amyloid-induced neurotoxicity. Furthermore, it has been shown that GRK2, a G protein-coupled receptor kinase which regulates receptor desensitization and downregolation, has been implicated in neuronal dysfunction caused by amyloid deposition. Finally, GRK2 levels in circulating lymphocytes, which correlate with cognitive impairment, may be used as a biomarker to monitor cognitive decline and response to therapy.

Genetic testing for potentially heritable cardiomyopathies has advanced from basic scientific discovery to clinical application. Nowadays, genetic diagnostic tests for cardiomyopathies are clinically available. As a consequence is fundamental the understanding of the clinical utility, in terms of diagnosis and prognosis, of genetic test results. In addition, the genetic counselling, regarding risks, benefits and options, is recommended for all patients and their relatives. However the relation between genotype and phenotype remains often unclear, and there is frequently a variance of uncertain significance. Consequently, the genetic test should always be approached as one component of a comprehensive cardio-genetic evaluation. This review aims to explore when genetic tests are indicated in patients with dilated and hypertrophic cardiomyopathy.

The elderly may represent a specific cluster of high-risk patients for developing COVID-19 with rapidly progressive clinical deterioration. Indeed, in older individuals, immunosenescence and comorbid disorders are more likely to promote viral-induced cytokine storm resulting in life-threatening respiratory failure and multisystemic involvement. Early diagnosis and individualized therapeutic management should be developed for elderly subjects based on personal medical history and polypharmacotherapy. Our review examines the pathogenesis and clinical implications of ageing in COVID-19 patients; finally, we discuss the evidence and controversies in the management in the long-stay residential care homes and aspects of end-of-life care for elderly patients with COVID-19.

Lung cancer (LC) and chronic obstructive pulmonary disease (COPD) represent leading causes of morbidity and mortality worldwide. Common risk factors lead to an increased inflammatory response, enhances oxidative stress, and changes in lung microenvironment contributing to fine-tuned interaction between these respiratory disorders. Despite evidence that COPD represents a main risk factor for LC, assessment of LC risk features among COPD patients is not routinely considered in the clinical practice. In LC patients concurrent COPD may impact on clinical scenario influencing the response to treatment. Better understanding LC and COPD coexistence may impact on clinical scenario influencing therapeutic approach. In this review, we describe the basis of this network and how the complex interplay between these respiratory disorders affects the clinical decision-making process.

Background: Frailty has been associated with increased mortality among hepatobiliary pancreatic (HBP) cancer patients. Nevertheless, estimates of frailty prevalence in HBP cancers and the precise average effect regarding mortality remains uncertain. The present systematic review and meta-analysis aimed to quantify: (1) the prevalence of frailty in patients with liver and pancreatic cancers and (2) the impact of frailty on mortality in patients affected by liver and pancreatic cancers. Methods: MEDLINE/PubMed database search was conducted from inception until 1 November 2021, the pooled prevalence and relative risk (RR) estimate were calculated. Results: A total of 34,276 patients were identified and the weighted prevalence of frailty was 39%; (95% [C.I.] 23–56; I2 = 99.9%, p < 0.0001). Frailty was significantly associated with increased mortality RR 1.98 (95% [C.I.] 1.49–2.63; I2 = 75.9%, p = 0.006). Conclusions: Frailty prevalence is common among HBP cancer patients and exerts a significant negative impact on survival. These findings are characterized by significant heterogeneity and caution is warranted on their interpretation. However, stratification of patients with HBP cancer by frailty status may provide prognostic information and may inform priorities for decision-making strategy.

Rheumatoid Arthritis (RA) is a chronic autoimmune inflammatory disease characterized by the swelling of multiple joints, pain and stiffness, and accelerated atherosclerosis. Sustained immune response and chronic inflammation, which characterize RA, may induce endothelial activation, damage and dysfunction. An equilibrium between endothelial damage and repair, together with the preservation of endothelial integrity, is of crucial importance for the homeostasis of endothelium. Endothelial Progenitor Cells (EPCs) represent a heterogenous cell population, characterized by the ability to differentiate into mature endothelial cells (ECs), which contribute to vascular homeostasis, neovascularization and endothelial repair. A modification of the number and function of EPCs has been described in numerous chronic inflammatory and auto-immune conditions; however, reports that focus on the number and functions of EPCs in RA are characterized by conflicting results, and discrepancies exist among different studies. In the present review, the authors describe EPCs’ role and response to RA-related endothelial modification, with the aim of illustrating current evidence regarding the level of EPCs and their function in this disease, to summarize EPCs’ role as a biomarker in cardiovascular comorbidities related to RA, and finally, to discuss the modulation of EPCs secondary to RA therapy.

Background: Limited evidence exists regarding adverse modifications affecting cardiovascular and pulmonary function in physical active adults affected by COVID-19, especially in athletic populations. We aimed to describe the clinical presentation of COVID-19 in a cohort of competitive athletes, as well as spirometry and echocardiography findings and cardio-respiratory performance during exercise. Methods: Twenty-four competitive athletes with COVID-19 were recruited for this study after ending self-isolation and confirmation of negative laboratory results. All athletes underwent clinical evaluation, spirometry, echocardiography and cardiopulmonary exercise testing (CPET). These data were compared to a group of healthy control athletes. Results: Anosmia was the most frequent symptom present in 70.83% patients, followed by myalgia, fatigue and ageusia. The most frequent persisting symptoms were anosmia 11 (45.83%) and ageusia 8 (33.33%). Compared to controls, COVID-19 patients presented lower FEV1%: 97.5 (91.5–108) vs. 109 (106–116) p = 0.007. Peak Oxygen Uptake (VO2) in COVID-19 patients was 50.1 (47.7–51.65) vs. 49 (44.2–52.6) in controls (p = 0.618). Conclusions: Reduced exercise capacity was not identified and pulmonary and cardiovascular function are not impaired during early recovery phase in a population of physical active adults except FEV1 reduction.

Background: Sarcopenia is a progressive loss of skeletal muscle mass whose pathophysiology has been proposed to possibly involve mechanisms of altered inflammatory status and endocrine function. Adiponectin has been shown to modulate inflammatory status and muscle metabolism. However, the possible association between adiponectin levels and sarcopenia is poorly understood. In order to fill this gap, in the present manuscript we aimed to summarize the current evidence with a systematic review and a meta-analysis of studies reporting serum adiponectin levels in patients with sarcopenia compared to non-sarcopenic controls. Methods: An electronic search through Medline/PubMed, Cochrane Library and Science Direct was performed till 1 march 2020. From the included papers, meta-analysis of cross-sectional studies comparing serum levels of adiponectin between patients with sarcopenia and controls was performed. Results: Out of 1808 1370 initial studies, 5 7 studies were meta-analyzed. Sarcopenic participants had significantly higher levels of adiponectin Hedges's g with 95% CI 0.85 (0.64-1.07) p < 0.001, I2 98.98% than controls. Hedges's g with 95% Confidence Interval (CI) : 1.20 (0.19- 2.22), p = 0.02 than controls. Subgroup analysis, performed in Asian population and focused only on identification of the condition based on AWGS criteria, and DEXA evaluation, and reported higher adiponectin levels in sarcopenic population (1.34 (1.06-1.61), p < 0.001 and I2 99.43%, 0.71 (0.45-0.96), p < 0.001 and I2 99.08%, respectively). 2.1 (0.17-4.03), p = 0.03 and I2=98.98%. Meta-regression analysis revealed female gender to significantly influence the results as demonstrated by beta = 0.11 95% CI (0.01 0.22), p = 0.034. beta=0.14 95% CI (0.010-0.280), p=0.040. Conclusions: Our meta-analysis found evidence that sarcopenia is associated with higher adiponectin levels. However, caution is warranted on the interpretation of these findings and future longitudinal research is required to disentangle and better understand the topic.

Dietary phytochemicals are considered an innovative strategy that helps to reduce cardiovascular risk factors. Some phytochemicals have been shown to play a beneficial role in lipid metabolism, to improve endothelial function and to modify oxidative stress pathways in experimental and clinical models of cardiovascular impairment. Importantly, investigation on phytochemical effect on cardiac remodeling appears to be promising. Nowadays, drug therapy and implantation of devices have demonstrated to ameliorate survival. Of interest, sex-gender seems to influence the response to HF canonical therapies. In fact, starting by the evidence of the feminization of world population and the scarce efficacy and safety of the traditional drugs in women, the search of alternative therapeutic tools has become mandatory. The aim of this review is to summarize the possible role of dietary phytochemicals in HF therapy and the evidence of a different sex-gender-oriented response.

Aim of the present study was to assess the impact of gender on the relationship between long-term mortality and clinical frailty. In an observational, longitudinal study on 10-year mortality, we examined 1284 subjects. The Frailty Staging System was used to assess frailty. The Cox model was employed to assess variables independently associated with survival using a backward stepwise algorithm. To investigate the possible interactions between gender and the selected variables, an extension of the multivariable fractional polynomial algorithm was adopted. Women were more likely to be older, have a higher disability, present with more comorbidities, consume more drugs, be frail and have a higher rate of survival at the follow-up than were men. At the Cox multivariate analysis only age (HR 2.26), female gender (HR 0.43), and number of drugs (HR 1.57) were significant and independent factors associated with all-cause mortality. In the survival analyses, only frailty (vs no frailty) showed significant interaction with gender (p

Heart failure (HF) represents the end-stage condition of several structural and functional cardiovascular diseases, characterized by reduced myocardial pump function and increased pressure load. The dysregulation of neurohormonal systems, especially the hyperactivity of the cardiac adrenergic nervous system (ANS), constitutes a hallmark of HF and exerts a pivotal role in its progression. Indeed, it negatively affects patients’ prognosis, being associated with high morbidity and mortality rates, with a tremendous burden on global healthcare systems. To date, all the techniques proposed to assess the cardiac sympathetic nervous system are burdened by intrinsic limits that hinder their implementation in clinical practice. Several biomarkers related to ANS activity, which may potentially support the clinical management of such a complex syndrome, are slow to be implemented in the routine practice for several limitations due to their assessment and clinical impact. Lymphocyte G-protein-coupled Receptor Kinase 2 (GRK2) levels reflect myocardial β-adrenergic receptor function in HF and have been shown to add independent prognostic information related to ANS overdrive. In the present manuscript, we provide an overview of the techniques currently available to evaluate cardiac ANS in HF and future perspectives in this field of relevant scientific and clinical interest.

Ischemic heart disease is currently a major cause of mortality and morbidity worldwide. Nevertheless, the actual therapeutic scenario does not target myocardial cell regeneration and consequently, the progression toward the late stage of chronic heart failure is common. Endothelial progenitor cells (EPCs) are bone marrow-derived stem cells that contribute to the homeostasis of the endothelial wall in acute and chronic ischemic disease. Calcium modulation and other molecular pathways (NOTCH, VEGFR, and CXCR4) contribute to EPC proliferation and differentiation. The present review provides a summary of EPC biology with a particular focus on the regulatory pathways of EPCs and describes promising applications for cardiovascular cell therapy.

Background. Several dietary phytochemicals potentially regulate the equilibrium between oxidant and antioxidant species. The aim of this study was to evaluate the effects of Lippia citriodora, Raphanus sativus, and Solanum lycopersicum on blood parameters, oxidative/antioxidant status, and SIRT1 activity in the rabbit’s heart and liver. Methods. Twenty rabbits were divided into 4 groups of 5 animals each. The control group (CN) received a feed without any additives. One intervention group received a supplement containing verbascoside (VB), another Raphanus sativus extract (RAP), and lastly lycopene (LYC). Oxidant-antioxidant parameters and SIRT1 activity were measured in plasma and in the heart and liver, respectively. Results. The treatment with VB, RAP, and LYC resulted in a marked improvement in the blood lipid and glycaemic profile in respect to CN. VB was the most effective, but all three plant extracts induced a significant reduction in oxidant parameters as well as an increase in antioxidant tissue activity and vitamin A and E levels. SIRT1 activity was significantly increased in both VB and LYC compared to CN, but the increased levels in the VB group were far the highest. The multivariate analysis suggests that the benefits of VB, particularly the antiglycaemic and antioxidant effects, might be mediated by increasing SIRT1 activity.

Background: In the last decades aging of population is becoming even more prevalent, with consequent increasing requirement in health assistance and services. Physical and social environments can affect health directly, or through barriers or incentives conditioning opportunities, decisions and behavior. Moreover, the relationship with environment varies according to several personal characteristics including family background, sex and ethnicity. The impact of these factors is often skewed by these characteristics, leading to inequalities in health. In virtually all countries, the older population is predominantly female. The prevalence and incidence of Cardiovascular Diseases (CVD) are reported to be lower in women than in men, increasing with age in both genders, but at advanced ages women outnumber men. Gender-differences in the contribution of various pathophysiological processes, combined with suboptimal recognition of female specificities, may explain sex-differences in presentation and outcomes of CVD and also partially explain the differences in cardiovascular drug therapy related to gender, where other behavioral and cultural factors can be involved. Purpose: Starting by the conflicting data in literature, the aim of this article is to summarize the gender differences available on the use of the main cardiovascular drugs, and the possible explanation for these disparities. Conclusion: Up to date, data on gender differences in cardiovascular therapy are still controversial, and overall no established factors have been identified to discriminate the different approach in the choice of cardiovascular drugs by gender. Then further more structured and bigger trials should be performed to target these issues, and to better clarify the underlining involved mechanisms.

Background: Cardiovascular diseases are the leading causes of mortality and hospitalizations especially in elderly patients, whose therapeutic management is particularly challenging due to the lack of specific recommendations, particularly in old patients with multiple comorbidities and disability. The ageing process is highly heterogeneous with several possible phenotypes ranging from healthy ageing to frailty. While in healthy old individuals, cardiovascular diseases can be treated following suggestions derived from international guidelines, treatment of pre-frail and frail elderly patients is extremely complicated and very frequently recommended standard treatments in these patients cannot be applied. Objective: In the present review, we will discuss the management and treatment of cardiovascular diseases in the elderly. Methods: This review was based on searches of the PubMed database using the following terms: “elderly”, “aging”, “frailty”, “heart failure”, “hypertension”, “atrial fibrillation”, “stroke prevention”, “guidelines”, “therapy”, “management”. Results: we have summarized the current therapies for elderly patients with cardiovascular disease, focusing our attention on heart failure, hypertension and atrial fibrillation that are very common and often coexisting diseases in the elderly. Conclusion: new studies involving frail elderly patients are needed in order to provide evidence-based treatment strategies and to allow more personalized medical approaches.

Background Short-term changes of neurohormones can give important prognostic information in heart failure (HF) patients. In this study, we evaluate whether changes in plasma Norepinephrine (NE) and serum N-terminal pro-brain natriuretic peptide (NT-proBNP) after exercise training predict cardiac mortality in HF patients. Methods and results We enrolled 221 HF patients (mean age 72.5 ± 10.2 year) followed-up for a mean period of 27.64 ± 10.7 months. All pts underwent a 3-month exercise training. Before training, clinical examination, echocardiography, peak VO2 determination, and blood draw for NT-proBNP and NE measurements were performed. Primary end-point was cardiac related mortality. Eighty-six-nine percent of patients were in NYHA class III, mean left ventricular ejection fraction (LVEF) was 32.5 ± 10.4%, and mean peak VO2 was 12.36 ± 1.45 ml/kg/min. At baseline, mean NT-proBNP was 2111.4 ± 1145.6 pg/ml and mean NE was 641.8 ± 215.3 pg/ml. One hundred-one subjects died for cardiac causes. Training was associated with a significant increase of peak VO2 and LVEF, whereas NE, NT-proBNP, and heart rate decreased. Multiple Cox proportional hazards regression analysis was performed using delta% values (post vs pre-training) of LVEF, heart rate, NE, and NT-proBNP along with baseline covariates, revealing delta value of NE as the strongest predictor of cardiac mortality. Noteworthy, training reduced NT-proBNP in both survivor and non-survivor patients, while a lack of reduction of NE was observed in non survivors. Conclusions In our HF population, short-term changes of NE after exercise training independently predicted long-term cardiac mortality.

Background: Heart failure (HF) patients show high morbidity and mortality rate with increased risk of malignant arrhythmia and thromboembolism. Anticoagulation reduces embolic event and death rates in HF patients with atrial fibrillation, but if antithrombotic therapy is beneficial in patients with HF in sinus rhythm is still debated. Methodology and Principal Findings: We conducted a systematic review of prospective, randomized controlled trials (RCTs) to assess the efficacy and safety of oral anticoagulant therapies (OATs) compared to antiplatelet treatment in HF patients in sinus rhythm. MEDLINE, Web of Science, CENTRAL and Scopus databases were searched up to May 2012. Four RCTs were identified and a total of 3663 patients were included in the meta-analysis. Patients with both ischemic and non-ischemic HF were included. There was no significant difference in mortality (odds ratio (OR) 1.01, 95% confidence interval (CI) 0.86 to 1.19) between OATs group and antiplatelet drug group. OATs have reduced ischemic stroke risk (OR 0.49, 95% CI 0.32 to 0.74), but have increased major bleeding risk (OR 2.01, 95% CI 1.40 to 2.88) compared to antiplatelet treatment. Conclusion: In HF patients in sinus rhythm OATs do not show a better risk-benefit profile compared to antiplatelet treatment in cardioembolism prevention. Warfarin and aspirin seem to be similar in reducing mortality. Warfarin reduces the incidence of ischemic stroke, but increases major bleedings. Thus, it is possible to speculate that aspirin prescription be indicated in patients with high risk of bleeding, whereas warfarin could be preferred in patients with high thromboembolic risk. © 2013 Rengo et al.

Background— Impaired angiogenesis in the post-myocardial infarction heart contributes to the progression to heart failure. The inhibition of vascular endothelial growth factor (VEGF) signaling has been shown to be crucial for the transition from compensatory hypertrophy to cardiac failure. Importantly, β-adrenergic receptor blocker therapy has been also shown to improve myocardial perfusion by enhancing neoangiogenesis in the failing heart. Methods and Results— Eight weeks from surgically induced myocardial infarction, heart failure rats were randomized to receive bisoprolol (B) or vehicle. At the end of a 10-week treatment period, echocardiography revealed reduced cardiac diameters and improved cardiac function in B-treated compared with vehicle-treated rats. Moreover, B treatment was associated with increased cardiac angiogenesis and in vivo coronary perfusion and reduced cardiac fibrosis. Importantly, 2 weeks after B treatment was started, increased cardiac VEGF expression and Akt and endothelial NO synthase activation were observed by comparing B-treated with drug-untreated failing hearts. To test whether the proangiogenic effects of B act via activation of VEGF pathway, rats were intravenously injected with adenoviral vector encoding a decoy VEGF receptor (Ad-Flk) or a control adenovirus (Ad-C), at the start of the treatment with B. After 10 weeks, histological analysis revealed reduced capillary and coronary perfusion in B-treated plus Ad-Flk rats compared with B-treated plus Ad-C rats. Moreover, VEGF inhibition counteracted the positive effects of B on cardiac function and remodeling. Conclusions— β-Blockade promotes cardiac angiogenesis in heart failure via activation of VEGF signaling pathway. β-Blocker–induced enhancement of cardiac angiogenesis is essential for the favorable effects of this therapy on cardiac function and remodeling.

Alzheimer's disease (AD) is a devastating form of dementia that imposes a severe burden on health systems and society. Although several aspects of AD pathogenesis have been elucidated over the last few decades, many questions still need to be addressed. In fact, currently available medications only provide symptomatic improvement in patients with AD without affecting disease progression. The β-adrenergic receptor (β-AR) system can be considered a possible target that deserves further exploration in AD. The central noradrenergic system undergoes substantial changes in the course of AD and β-ARs have been implicated not only in amyloid formation in AD brain but also in amyloid-induced neurotoxicity. Moreover, clinical evidence suggests a protective role of β-AR blockers on AD onset. In addition to that, post-receptor components of β-AR signaling seem to have a role in AD pathogenesis. In particular, the G protein coupled receptor kinase 2, responsible for β-AR desensitization and downregulation, mediates amyloid-induced β-AR dysfunction in neurons, and its levels in circulating lymphocytes of AD patients are increased and inversely correlated with patient's cognitive status. Therefore, there is an urgent need to gain further insight on the role of the adrenergic system components in AD pathogenesis in order to translate preclinical and clinical knowledge to more efficacious prognostic and therapeutic strategies.