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The aim of our study was to assess the lung sequelae and clinical consequences 3 and 6 months after hospitalization for COVID-19 pneumonia in older patients. An observational study was conducted on 55 patients aged 65 years and older. Activities of daily living (ADL) and clinical frailty scale (CFS) were assessed at baseline and after 3 months. Both quantitative assessment at chest high-resolution computed tomography (CT) and semi-quantitative severity score (CTSS) were performed at baseline and after 3 and 6 months. Mean age: 82.3 ± 7.1 years. Male prevalence: 56.4%. After 6 months, ground-glass opacities (GGO) were still detectable in 22% of subjects, while consolidations were no longer appreciable. During follow-up, CTSS reached an overall median score of zero after 6 months. Fibrotic-like changes were found in 40% of subjects with an overall median score of 0 (0–5) points, being more prevalent in males. Patients reporting worsening ADL and CFS were 10.9% and 45.5%, respectively. They were associated with the burden of comorbidities, especially history of heart failure and chronic obstructive pulmonary disease at baseline. Amnesic disorders, exertional dyspnea, and fatigue were the most relevant symptoms reported. No association emerged between persistent or new-onset symptoms and evidence of fibrotic-like changes. The typical chest CT abnormalities of the COVID-19 pneumonia acute phase resolved in most of our older patients. Mild fibrotic-like changes persisted in less than half of the patients, especially males, without significantly affecting the functional status and frailty condition, which instead were more likely associated with pre-existing comorbidities.

Since the publication of the RECOVERY trial, the use of glucocorticoid drugs (GC) has spread for the treatment of severe COVID-19 worldwide. However, the benefit of dexamethasone was largest in patients who received mechanical ventilation or supplemental oxygen therapy, while no benefit was found among patients without hypoxemia. In addition, a positive outcome was found in patients who received dexamethasone after several days of symptoms, while possible harm could exist if administered early. The right time interval for GC administration is still a matter of debate. Previous studies showed that an early GC use during the first phase of the disease, when viral replication peaks, may negatively affect the innate immune response through several mechanisms, such as the inhibition of pro-inflammatory and antiviral cytokine production and signaling pathway, including type I interferon, that is fundamental to counteract the virus and that was found to be impaired in several patients with life-threatening COVID-19. The GC misuse can lead to a more severe disease even in patients who do not have the established risk factors, such as obesity and cardiovascular diseases. In our focused review, we describe the role of immune response in viral infections, especially SARS-CoV-2, and discuss the potential harms of GC misuse in COVID-19. Supplementary Information The online version contains supplementary material available at 10.1007/s11739-021-02860-3.

To reduce intensive care unit overcrowding and optimize resources, elderly patients affected by suspected infection with declining clinical conditions could be managed in internal medicine departments with stepdown beds. However, commonly used prognostic scores, as Sequential Organ Failure Assessment (SOFA) or quick SOFA (qSOFA) have never been studied in this specific setting. The aim of this study was to evaluate the role and the accuracy of SOFA and qSOFA as prognostic scores in a population of elderly patients with suspected infection admitted to stepdown beds of two internal medicine departments. Elderly patients admitted from the emergency department in the stepdown beds of two different internal medicine departments for suspected infection were assessed with SOFA and qSOFA scores at the admission. All patients were treated according to current guidelines. Age, sex, comorbidities, Charlson comorbidity index, SOFA and qSOFA were assessed. In-hospital death and length of hospital admission were also recorded. 390 subjects were enrolled. In-hospital death occurred in 144 (36.9%) patients; we observed that both SOFA (HR 1.189; 95% CI 1.128–1.253; p

A dysregulation of the renin-angiotensin system (RAS) has been involved in the genesis of lung injury and acute respiratory distress syndrome from different causes, including several viral infections. The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection of pneumocytes, the hallmark of the pandemic coronavirus disease 2019 (COVID-19) involving both alveolar interstitium and capillaries, is linked to angiotensin-converting enzyme 2 (ACE2) binding and its functional downregulation. ACE2 is a key enzyme for the balance between the two main arms of the RAS: the ACE/angiotensin (Ang) II/Ang II type 1 receptor axis (“classic RAS”) and the ACE2/Ang(1–7)/Mas receptor (MasR) axis (“anti-RAS”). The ACE2 downregulation, as a result of SARS-coronaviruses binding, enhances the classic RAS, leading to lung damage and inflammation with leaky pulmonary blood vessels and fibrosis, when the attenuation mediated by the anti-RAS arm is reduced. ACE inhibitors (ACE-I) and Ang II type 1 receptor blockers (ARB), effective in cardiovascular diseases, were found to prevent and counteract acute lung injury in several experimental models by restoring the balance between these two opposing arms. The evidence of RAS arm disequilibrium in COVID-19 and the hypothesis of a beneficial role of RAS modulation supported by preclinical and clinical studies are the focus of the present review. Preclinical and clinical studies on drugs balancing RAS arms might be the right way to counter COVID-19.

Age is traditionally considered a major cardiovascular (CV) risk factor, but its real weight in the absence of other modifiable risk factors is not clear. To compare the prevalence of subclinical carotid atherosclerosis, and its association with the main CV risk factors, between older adults and hypertensive adults. Cross-sectional study on 210 consecutive patients: 70 older adults (age ≥ 80 years), and 140 hypertensive adults having at least another CV risk factor. Patients had no history of peripheral artery disease or major CV events. Mean age was 54.2 ± 7.2 years in hypertensive adults and 88.5 ± 5.5 years in older adults with a female prevalence in the latter group. Dyslipidemia and smoking were more prevalent in hypertensive adults, while chronic kidney disease was more prevalent in older adults. Prevalence of carotid plaques did not differ between hypertensive adults and older adults (48.2% vs 55.6%, respectively, p = 0.311). Age ≥ 80 years was not associated with a higher risk of carotid plaques even after adjusting for other risk factors (p = 0.204). Hypertension and dyslipidemia were the risk factors more strongly associated with carotid plaques in older adults and hypertensive adults, respectively. When older adults with hypertension were excluded from the analysis, prevalence of carotid plaques was significantly higher in hypertensive adults (p = 0.042). Hypertension and dyslipidemia are the major determinant of atherosclerosis regardless of age in our study. Our findings support the concept that aging is not necessarily synonymous with atherosclerosis and highlight the key role played by superimposed CV risk factors on arterial ‘‘bad aging’’.

Herpesviridae reactivation such as cytomegalovirus (CMV) has been described in severe COVID-19 (COronaVIrusDisease-2019). This study aimed to understand if CMV reactivation in older COVID-19 patients is associated with increased inflammation and in-hospital mortality. In an observational single-center cohort study, 156 geriatric COVID-19 patients were screened for CMV reactivation by RT-PCR. Participants underwent a comprehensive clinical investigation that included medical history, functional evaluation, laboratory tests and cytokine assays (TNF-α, IFN-α, IL-6, IL-10) at hospital admission. In 19 (12.2%) of 156 COVID-19 patients, CMV reactivation was detected. Multivariate Cox regression models showed that in-hospital mortality significantly increased among CMV positive patients younger than 87 years (HR: 9.94, 95% CI: 1.66–59.50). Other factors associated with in-hospital mortality were C-reactive protein (HR: 1.17, 95% CI: 1.05–1.30), neutrophil count (HR: 1.20, 95% CI: 1.01–1.42) and clinical frailty scale (HR:1.54, 95% CI: 1.04–2.28). In patients older than 87 years, neutrophil count (HR: 1.13, 95% CI: 1.05–1.21) and age (HR: 1.15, 95% CI: 1.01–1.31) were independently associated with in-hospital mortality. CMV reactivation was also correlated with increased IFN-α and TNF-α serum levels, but not with IL-6 and IL-10 serum changes. In conclusion, CMV reactivation was an independent risk factor for in-hospital mortality in COVID-19 patients younger than 87 years old, but not in nonagenarians.

Cardiac natriuretic peptides (NPs), atrial NP (ANP) and B-type NP (BNP) are true hormones produced and released by cardiomyocytes, exerting several systemic effects. Together with C-type NP (CNP), mainly expressed by endothelial cells, they also exert several paracrine and autocrine activities on the heart itself, contributing to cardiovascular (CV) health. In addition to their natriuretic, vasorelaxant, metabolic and antiproliferative systemic properties, NPs prevent cardiac hypertrophy, fibrosis, arrhythmias and cardiomyopathies, counteracting the development and progression of heart failure (HF). Moreover, recent studies revealed that a protein structurally similar to NPs mainly produced by skeletal muscles and osteoblasts called musclin/osteocrin is able to interact with the NPs clearance receptor, attenuating cardiac dysfunction and myocardial fibrosis and promoting heart protection during pathological overload. This narrative review is focused on the direct activities of this molecule family on the heart, reporting both experimental and human studies that are clinically relevant for physicians.

Aims Sodium-glucose co-transporter-2 inhibitors (SGLT2i) have been proven to lead to relevant cardiovascular benefits, regardless of glycemic control function. SGLT2i have on the one hand led to reduction in cardiovascular events such as heart failure and on the other hand to renal protection. Blood pressure reduction and kidney function play a central role in these outcomes. This focused review describes the main mechanisms and clinical aspects of SGLT2i. Data synthesis These drugs act on the proximal renal tubule and behave as diuretics with a “hybrid” mechanism, as they can favour both natriuresis and enhanced diuresis due to an osmotic effect dependent on glycosuria, resulting in blood pressure decrease. The exclusive peculiarity of these “diuretics”, which distinguishes them from loop and thiazide diuretics, lies also in the activation of the tubule-glomerular feedback. Conclusions This mechanism, resulting in modulation of arterioles’ tone and renin secretion, contributes to the favorable outcomes, suggesting a wider use of SGLT2i in internal medicine, nephrology and cardiology.

Since the first months of the coronavirus disease 2019 (COVID-19) pandemic, several specific physiologic traits, such as male sex and older age, or health conditions, such as overweight/obesity, arterial hypertension, metabolic syndrome, and type 2 diabetes mellitus, have been found to be highly prevalent and associated with increased risk of adverse outcomes in hospitalized patients. All these cardiovascular morbidities are widespread in the population and often coexist, thus identifying a common patient phenotype, characterized by a hyper-activation of the “classic” renin-angiotensin system (RAS) and mediated by the binding of angiotensin II (Ang II) to the type 1-receptor. At the same time, the RAS imbalance was proved to be crucial in the genesis of lung injury after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, where angiotensin-converting-enzyme-2 (ACE2) is not only the receptor for SARS-CoV-2, but its down-regulation through internalization and shedding, caused by the virus binding, leads to a further dysregulation of RAS by reducing angiotensin 1-7 (Ang 1-7) production. This focused narrative review will discuss the main available evidence on the role played by cardiovascular and metabolic conditions in severe COVID-19, providing a possible pathophysiological link based on the disequilibrium between the two opposite arms of RAS.

OBJECTIVE Statin therapy was associated with lower blood pressure (BP) in some but not all studies. We evaluated the association between statin therapy and ambulatory BP in a large hypertensive population using 'propensity score matching'. METHODS Retrospective observational study on 1827 consecutive essential hypertensive patients evaluated with 24-h ambulatory BP monitoring. Antihypertensive treatment intensity (ATI) was calculated to compare different drug associations. We used a propensity score matching to compare two equally-sized cohorts of patients with similar characteristics according to statin therapy. Matching was performed on log-transformed propensity score in a 1 : 1 fashion with a caliper of 0.1, in order to account for the different baseline characteristics between statin and no-statin group. RESULTS Mean age: 58.1 ± 13.8 years; male sex: 55%. Patients on statin therapy: 402 (22%). These patients showed lower 24-h BP (-2.8/-7.1 mmHg), daytime (-3.3/-7.6 mmHg) and night-time BP (-2.5/-6.0 mmHg, all P

Introduction We evaluated the prevalence and control of dyslipidemia in a wide sample of patients referred to our ESH “Hypertension Excellence Centre” for high blood pressure (BP). Furthermore, we evaluated the role of adiposity on the serum lipid profile. Methods Observational study on 1219 consecutive outpatients with valid ambulatory BP monitoring (ABPM) referred for high BP. Patients with body mass index (BMI) ≥ 25 kg/m2 were defined as overweight/obese (OW/OB). Dyslipidemia and the control rates of low-density lipoprotein cholesterol (LDLc) were defined according to the 2016 ESC/EAS Guidelines. Results Mean age: 56.5 ± 13.7 years. Male prevalence: 55.6%. OW/OB patients were 70.2%. The prevalence of dyslipidemia was 91.1%. Lipid-lowering drugs were taken by 23.1% of patients. Patients with controlled LDLc comprised 28.5%, while BP was controlled in 41.6% of patients. Only 12.4% of patients had both 24-h BP and LDLc controlled at the same time. The higher the cardiovascular (CV) risk was, the lower was the rate of LDLc control (p

Proprotein convertase subtilisin/kexin type 9 (PCSK9) binds to and degrades the low-density lipoprotein receptor (LDLR), contributing to hypercholesterolemia. Adipose tissue plays a role in lipoprotein metabolism, but there are almost no data about PCSK9 and LDLR regulation in human adipocytes. We studied PCSK9 and LDLR regulation by insulin, atrial natriuretic peptide (ANP, a potent lipolytic agonist that antagonizes insulin), and LDL in visceral adipose tissue (VAT) and in human cultured adipocytes. PCSK9 was expressed in VAT and its expression was positively correlated with body mass index (BMI). Both intracellular mature and secreted PCSK9 were abundant in cultured human adipocytes. Insulin induced PCSK9, LDLR, and sterol-regulatory element-binding protein-1c (SREBP-1c) and -2 expression (SREBP-2). ANP reduced insulin-induced PCSK9, especially in the context of a medium simulating hyperglycemia. Human LDL induced both mature and secreted PCSK9 and reduced LDLR. ANP indirectly blocked the LDLR degradation, reducing the positive effect of LDL on PCSK9. In conclusion, PCSK9 is expressed in human adipocytes. When the expression of PCSK9 is induced, LDLR is reduced through the PCSK9-mediated degradation. On the contrary, when the induction of PCSK9 by insulin and LDL is partially blocked by ANP, the LDLR degradation is reduced. This suggests that NPs could be able to control LDLR levels, preventing PCSK9 overexpression.

Age is one of the main risk factor for the presence of obstructive sleep apnea (OSA). This syndrome is associated with hypertension, cardiovascular disease, cognitive impairment and metabolic abnormalities, such as type 2 diabetes. Continuous positive airway pressure (CPAP) represents the gold standard therapy, but its benefit is still to be determined in very elderly. We report the blood pressure and metabolic changes in a very elderly obese with severe OSA after 3-month CPAP therapy. We have evaluated a very elderly obese male affected by severe symptomatic OSA, poor controlled nocturnal hypertension and insulin resistance. After 3-month CPAP therapy, without any changes in drug therapy, we observed a normalization of circadian blood pressure (BP) pattern, an improved insulin sensitivity, together with a reduced resting energy expenditure, despite no significant change in weight. This case report shows the benefits of OSA treatment with CPAP, not only on BP profile, but also on metabolic parameters in a very elderly, a particular type of patient in which scientific evidence is still scant. Further studies are needed to better investigate the relationship between OSA, CPAP therapy and energy expenditure not only in adults but also in elderly patients.

Background A significant proportion of individuals clinically diagnosed with familial hypercholesterolemia (FH), but without any disease-causing mutation, are likely to have polygenic hypercholesterolemia. We evaluated the distribution of a polygenic risk score, consisting of 12 low-density lipoprotein cholesterol (LDL-C)-raising variants (polygenic LDL-C risk score), in subjects with a clinical diagnosis of FH. Methods and Results Within the Lipid Transport Disorders Italian Genetic Network (LIPIGEN) study, 875 patients who were FH-mutation positive (women, 54.75%; mean age, 42.47±15.00 years) and 644 patients who were FH-mutation negative (women, 54.21%; mean age, 49.73±13.54 years) were evaluated. Patients who were FH-mutation negative had lower mean levels of pretreatment LDL-C than patients who were FH-mutation positive (217.14±55.49 versus 270.52±68.59 mg/dL, P