AimsWe conducted a population-based cross-sectional study to assess the prevalence of both preclinical and clinical heart failure (HF) in the elderly. Methods and resultsA sample of 2001 subjects, 65-to 84-year-old residents in the Lazio Region (Italy), underwent physical examination, biochemistry/N-terminal pro brain natriuretic peptide (NT-proBNP) assessment, electrocardiography, and echocardiography. Systolic left ventricular dysfunction (LVD) was defined as left ventricular ejection fraction (LVEF) ,50%. Diastolic LVD was defined by a Doppler-derived multiparametric algorithm. The overall prevalence of HF was 6.7% [95% confidence interval (CI) 5.6 -7.9], mainly due to HF with preserved LVEF (HFpEF) (4.9%; 95% CI 4.0 -5.9), and did not differ by gender. A systolic asymptomatic LVD (ALVD) was detected more frequently in men (1.8%; 95% CI 1.0 -2.7) than in women (0.5%; 95% CI 0.1 -1.0; P ¼ 0.005), whereas the prevalence of diastolic ALVD was comparable between genders (men: 35.8%; 95% CI ¼ 32.7-38.9; women: 35.0%; 95% CI ¼ 31.9-38.2). The NT-proBNP levels and severity of LVD increased with age. Overall, 1623 subjects (81.1% of the entire studied population) had preclinical HF (Stage A: 22.2% and stage B: 59.1% respectively). A large number of subjects in stage B of HF showed risk factor levels not at target. ConclusionsIn a population-based study, the prevalence of preclinical HF in the elderly is high. The prevalence of clinical HF is mainly due to HFpEF and is similar between genders.--

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Gait speed is independently associated with death, hospitalization for HF, and all-cause hospitalization and improves risk stratification in older patients with HF evaluated using the Cardiac and Comorbid Conditions Heart Failure score. Assessment of frailty using gait speed is simple and should be part of the clinical evaluation process.

Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) commonly complicates with coagulopathy. A syndrome called Long-COVID-19 is emerging recently in COVID-19 survivors, characterized, in addition to the persistence of symptoms typical of the acute phase, by alterations in inflammatory and coagulation parameters due to endothelial damage. The related disseminated intravascular coagulation (DIC) can be associated with high death rates in COVID-19 patients. It is possible to find a prothrombotic state also in Long-COVID-19. Early administration of anticoagulants in COVID-19 was suggested in order to improve patient outcomes, although exact criteria for their application were not well-established. Low-molecular-weight heparin (LMWH) was commonly adopted for counteracting DIC and venous thromboembolism (VTE), due to its pharmacodynamics and anti-inflammatory properties. However, the efficacy of anticoagulant therapy for COVID-19-associated DIC is still a matter of debate. Thrombin and Factor Xa (FXa) are well-known components of the coagulation cascade. The FXa is known to strongly promote inflammation as the consequence of increased cytokine expression. Endothelial cells and mononuclear leucocytes release cytokines, growth factors, and adhesion molecules due to thrombin activation. On the other hand, cytokines can activate coagulation. The cross-talk between coagulation and inflammation is mediated via protease-activated receptors (PARs). These receptors might become potential targets to be considered for counteracting the clinical expressions of COVID-19. SARS-CoV-2 is effectively able to activate local and circulating coagulation factors, thus inducing the generation of disseminated coagula. LMWH may be considered as the new frontier in the treatment of COVID-19 and Long-COVID-19. Indeed, direct oral anticoagulants (DOACs) may be an alternative option for both early and later treatment of COVID-19 patients due to their ability to inhibit PARs. The aim of this report was to evaluate the role of anticoagulants—and DOACs in particular in COVID-19 and Long-COVID-19 patients. We report the case of a COVID-19 patient who, after administration of enoxaparin developed DIC secondary to virosis and positivity for platelet factor 4 (PF4) and a case of Long-COVID with high residual cardiovascular risk and persistence of blood chemistry of inflammation and procoagulative state.

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