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Recent evidence shows that a range of persistent or new symptoms can manifest after 4-12 weeks in a subset of patients who have recovered from acute SARS-CoV-2 infection, and this condition has been coined long COVID by COVID-19 survivors among social support groups. Long COVID can affect the whole spectrum of people with COVID-19, from those with very mild acute disease to the most severe forms. Like the acute form, long COVID has multisystemic aspects. Patients can manifest with a very heterogeneous multitude of symptoms, including fatigue, post-exertional malaise, dyspnea, cognitive impairment, sleep disturbances, anxiety and depression, muscle pain, brain fog, anosmia/dysgeusia, headache, and limitation of functional capacity, which impact their quality of life. Because of the extreme clinical heterogeneity, and also due to the lack of a shared, specific definition, it is very difficult to know the real prevalence and incidence of this condition. Risk factors for developing long COVID would be female sex, initial severity, and comorbidities. Globally, with the re-emergence of new waves, the population of people infected with SARS-CoV-2 continues to expand rapidly, necessitating a more thorough understanding of potential sequelae of COVID-19. This review summarizes up to date definitions and epidemiological aspects of long COVID.

Background A large amount of information on genotypic and phenotypic expressions has become available since the first clinical observations of cardiac manifestations secondary to lamin A/C gene mutations. Aims We aim to describe one of the longest longitudinal follow-ups reported so far (>22 years), concerning a whole family affected by a missense lamin A/C mutation (Arg60Gly), which manifested as an overlapping phenotype with cardiac and extracardiac involvement over time. Methods Starting from the family history, two generations of that family were prospectively observed, from 1997 until 2020. At baseline, four individuals with dilated cardiomyopathy and cardiac conduction defects showed the same mutation. This was also found in three young individuals, phenotypically unaffected at baseline assessment. Results The prolonged clinical and laboratory evaluation has shown the evolution of an overlapping phenotype in which cardiac alterations have been associated with lipodystrophy and neurological manifestations. In the first observed generation, the prognosis was negatively affected by the progression of heart failure and lipodystrophy, whereas in the second generation the first phenotypic manifestations became evident after the 2nd decade. Cardiac magnetic resonance played a relevant role in the early detection of cardiac alteration. Right bundle branch block was another sign of initial phenotypical expression. Conclusion In lamin A/C gene mutation carriers, a strict, multidisciplinary follow-up allows the opportunity to monitor the progress of the disease and to intervene precociously with the best available treatments.

In this study we investigated whether the metabolomic analysis could identify a specific fingerprint of coronary blood collected during primary PCI in STEMI patients. Fifteen samples was subjected to metabolomic analysis. Subsequently, the study population was divided into two groups according to the peripheral blood neutrophil-to-lymphocyte ratio (NLR), a marker of the systemic inflammatory response. Regression analysis was then applied separately to the two NLR groups. A partial least square (PLS) regression identified the most significant involved metabolites and the PLS-class analysis revealed a significant correlation between the metabolic profile and the total ischemic time only in patients with an NLR > 5.77.

Several studies have evidenced high prevalence of myocardial systolic and diastolic dysfunction among patients with systemic sclerosis (SSc). Exercise echocardiography has shown a diagnostic and prognostic role in identifying early left ventricular (LV) dysfunction in several myocardial pathological settings. The aim of our study was to evaluate early signs of LV impairment under exercise and their correlation to patient’s exercise tolerance. Forty-five patients (age 60.4 ± 10.3 years) with SSc and 20 age and sex comparable controls were enrolled in the study. All patients underwent clinical evaluation, 2D echocardiography associated with Tissue Doppler and speckle tracking to evaluate LV deformation indexes, and an exercise echocardiography to evaluate left ventricle contractile reserve (LVCR) and exercise pulmonary pressures. Finally, a 6-minute walking test (6MWT) to evaluate exercise tolerance was also performed. Compared to controls, SSc patients showed an impaired diastolic function (E/E′ 10.9 ± 3.7 vs 8.36 ± 2.01; p