Background. The pandemic of Novel Coronavirus Disease 2019 (COVID-19) is challenging, given the large number of hospitalized patients. Cardiovascular co-morbidities are linked to a higher mortality risk. Thus, patients with Congenital Heart Disease (CHD) might represent a high-risk population. Nevertheless, no data about them are available, yet. Hence, we conducted a nationwide survey to assess clinical characteristics and outcomes in patients with congenital heart disease affected by COVID-19. Methods and Results. This is a multi-centre, observational, nationwide survey, involving high-volume Italian CHD centres. COVID-19 diagnosis was defined as either “clinically suspected” or “confirmed”, where a severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) test had been performed and was positive. Cardiovascular comorbidities were observed among adult patients—atrial fibrillation (seven; 9%), hypertension (five; 7%), obesity (seven; 9%) and diabetes (one; 1%)—but were absent among children. Cardiovascular complications were mainly observed in the “confirmed” COVID-19+ group, consisting of heart failure (9%), palpitations/arrhythmias (3%), stroke/TIA (3%) and pulmonary hypertension (3%). Cardiovascular symptoms such as chest pain (1%), myocardial injury (1%) and pericardial effusion (1%) were also recorded. On the contrary, CHD patients from the clinically suspected COVID-19 group presented no severe symptoms or complications. Conclusions. Despite previous reports pointing to a higher case-fatality rate among patients with cardiovascular co-morbidities, we observed a mild COVID-19 clinical course in our cohort of CHD patients. Although these results should be confirmed in larger cohorts to investigate the underlying mechanisms, the findings of low cardiovascular complications rates and no deaths are reassuring for CHD patients.

COronavirus Infectious Disease which started in 2019 (COVID-19) usually presents with the signs and symptoms of pneumonia. However, a growing number of recent reports highlight the fact that the infection may be by far more than only a respiratory disease. There is evidence of an increased thromboembolic risk in COVID-19 patients, with a variety of manifestations in terms of ischemic stroke, deep vein thrombosis, acute pulmonary embolism, acute myocardial infarction, systemic arterial

Severe acute respiratory syndrome coronavirus 2 (SARS- CoV-2), previously named “2019 novel coronavirus” (2019-nCoV) is an emerging disease and a major public health issue. At the moment, little is known, except that its spread is on a steady upward trend. That is the reason why it was declared pandemic since March 11th, 2020. Respiratory symptoms dominate the clinical manifestations of the virus, but in a few patients also other organs are involved, such as their heart. This review article provides an overview of the existing literature regarding imaging of heart injury during COVID-19 acute infection and follow-up.

Background Exercise is the cornerstone of rehabilitation programmes for individuals with cardiovascular disease (IwCVD). Although conventional cardiovascular rehabilitation (CCVR) programmes have significant advantages, non-conventional activities such as Nordic walking (NW) may offer additional health benefits. Our aim was to appraise research evidence on the effects of Nordic walking for individuals with cardiovascular disease. Design Systematic review and meta-analysis. Methods A literature search of clinical databases (PubMed, MEDLINE, Scopus, Web of Science, Cochrane) was conducted to identify any randomized controlled trials, including: (i) individuals with cardiovascular disease, (ii) analyses of the main outcomes arising from Nordic walking (NW) programmes. Data from the common outcomes were extracted and pooled in the meta-analysis. Standardized mean differences (SMDs) were calculated and pooled by random effects models. Results Fifteen randomized controlled trials were included and eight trials entered this meta-analysis. Studies focused on coronary artery disease, peripheral arterial disease, heart failure and stroke. In coronary artery disease, significant differences between NW+CCVR and CCVR were found in exercise capacity (SMD: 0.49; p = 0.03) and dynamic balance (SMD: 0.55; p = 0.01) favouring NW+CCVR. In peripheral artery disease, larger changes in exercise duration (SMD: 0.93; p < 0.0001) and oxygen uptake (SMD: 0.64; p = 0.002) were observed following NW compared with controls. In heart failure, no significant differences were found between NW and CCVR or usual care for peak VO and functional mobility. In post-stroke survivors, functional mobility was significantly higher following treadmill programmes with poles rather than without (SMD: 0.80; p = 0.03). Conclusions These data portray NW as a feasible and promising activity for individuals with cardiovascular disease. Further studies are necessary to verify whether NW may be incorporated within CCVR for individuals with cardiovascular disease.

Exercise is a major challenge for cardiovascular apparatus since it recruits chronotropic, inotropic, pre-load, and afterload reserves. Regular physical training induces several physiological adaptations leading to an increase in both cardiac volume and mass. It appears that several genderrelated physiological and morphological differences exist in the cardiovascular adjustments and adaptations to dynamic exercise in humans. In this respect, gender may be important in determining these adjustments and adaptations to dynamic exercise due to genetic, endocrine, and body composition differences between sexes. Females seem to have a reduced vasoconstriction and a lower vascular resistance in comparison to males, especially after exercise. Significant differences exist also in the cardiovascular adaptations to physical training, with trained women showing smaller cardiac volume and wall thickness compared with male athletes. In this review, we summarize these differences.

A large number of adults worldwide suffer from essential hypertension, and because blood pressures (BPs) tend to remain within the same percentiles throughout life, it has been postulated that hypertensive pressures can be tracked from childhood to adulthood. Thus, children with higher BPs are more likely to become hypertensive adults. These "pre-hypertensive" subjects can be identified by measuring arterial BP at a young age, and compared with age, gender and height-specific references. The majority of studies report that 1 to 5% of children and adolescents are hypertensive, defined as a BP > 95(th) percentile, with higher prevalence rates reported for some isolated geographic areas. However, the actual prevalence of hypertension in children and adolescents remains to be fully elucidated. In addition to these young "pre-hypertensive" subjects, there are also children and adolescents with a normal-high BP (90(th)-95(th) percentile). Early intervention may help prevent the development of essential hypertension as they age. An initial attempt should be made to lower their BP by non-pharmacologic measures, such as weight reduction, aerobic physical exercise, and lowered sodium intake. A pharmacological treatment is usually needed should these measures fail to lower BP. The majority of antihypertensive drugs are not formulated for pediatric patients, and have thus not been investigated in great detail. The purpose of this review is to provide an update concerning juvenile hypertension, and highlight recent developments in epidemiology, diagnostic methods, and relevant therapies.

ACE2 receptor has a broad expression pattern in the cellular membrane and provides a protective action against the development of cardiovascular diseases. Recently, this enzyme has become of extreme interest during the pandemic infection of COVID-19 (coronavirus disease 2019). This virus invades alveolar epithelium and cardiomyocytes using ACE2 as a transmembrane receptor. ACE2 is a counter-regulatory peptide that degrades Ang II into Ang 1–7, thereby attenuating the biological effects of the AT1 receptor. The binding between the spike protein of COVID-19 and the enzyme is crucial for the virus to enter the target cells, but whether an increase in ACE2 activity could facilitate the infection is not yet demonstrated. However, this aspect has raised many concerns about the use of ACE inhibitors or ARBs in infected patients or patients at risk of infection. It appears that cellular infection leads to a reduction in ACE2 expression and an increase in the activity of the Ang II--AT1 axis, which leads to the release of pro-inflammatory cytokines, ARDS, myocarditis, and hypercoagulability with the possibility of exacerbation of acute coronary syndrome, induction of pulmonary embolism, or appearance of disseminated intravascular coagulation. Therefore, ACE inhibitors or angiotensin receptor blocker drugs should be continued in infected patients, as their discontinuation can increase Ang II activity and induce injury to the lungs or cardiovascular system.

Currently, the world is coping with the COVID-19 pandemic with a few vaccines. So far, the European Medicine Agency has approved four of them. However, following widespread vaccination with the recombinant adenoviral vector-based Oxford-AstraZeneca vaccine, available only in the United Kingdom and Europe, many concerns have emerged, especially the report of several cases of the otherwise rare cerebral sinus vein thrombosis and splanchnic vein thrombosis. The onset of thrombosis particularly at these unusual sites, about 5-14 days after vaccination, along with thrombocytopenia and other specific blood test abnormalities, are the main features of the vaccine side effects. The acronym vaccine-induced prothrombotic immune thrombocytopenia (VIPIT) has been coined to name this new condition, with the aim of highlighting the difference from the classic heparin-induced thrombocytopenia (HIT). VIPIT seems to primarily affect young to middle-aged women. For this reason, the vaccine administration has been stopped or limited in a few European countries. Coagulopathy induced by the Oxford-AstraZeneca vaccine (and probably by Janssen/Johnson & Johnson vaccine as well in the USA) is likely related to the use of recombinant vector DNA adenovirus, as experimentally proven in animal models. Conversely, Pfizer and Moderna vaccines use mRNA vectors. All vaccine-induced thrombotic events should be treated with a nonheparin anticoagulant. As the condition has some similarities with HIT, patients should not receive any heparin or platelet transfusion, as these treatments may potentially worsen the clinical course. Aspirin has limited rational use in this setting and is not currently recommended. Intravenous immunoglobulins may represent another potential treatment, but, most importantly, clinicians need to be aware of this new unusual postvaccination syndrome.