Pathogenesis of atherosclerosis involves multiple mechanisms, including imbalanced lipid metabolism, disturbed equilibrium of the immune response, and chronic inflammation of the artery wall. Several reports have shown a relationship between the development of atherosclerosis and the presence of infectious diseases, widely occurring in the general population, often chronic and/or asymptomatic. Beyond Chlamydia pneumoniae, a large number of infectious agents have been linked with an increased risk of vascular disease, with variable strength of supporting data: Porphyromonas gingivalis, Helicobacter pylori, influenza A virus, herpes virus, hepatitis C virus, cytomegalovirus, and human immunodeficiency virus. Infections may contribute to atherosclerosis either via direct infection of vascular cells or via the indirect effects of cytokines or acute phase proteins induced by infection at “nonvascular” sites. More recently, investigators reported that the aggregate burden (“infectious burden”) of these chronic infections, rather than the effects of a single organism, might contribute to atherosclerosis and its thrombotic complications. However, the role of infection, as a proinflammatory cause of atherosclerosis, is still debated in the literature. This article will review available data suggesting a relationship between different infective pathogens and atherothrombosis, the hypothesized mechanisms, and the potential role for antimicrobial treatment.

Background: A high incidence of venous thromboembolism (VTE) is reported in hospitalized COVID-19 patients, in particular in patients admitted to the intensive care unit (ICU). In patients with respiratory tract infections, including influenza A (H1N1), many studies have demonstrated an increased incidence of thromboses, but evidence is lacking regarding the risk difference (RD) of the occurrence of VTE between COVID-19 and non-COVID-19 patients. Methods: In this systematic review with meta-analysis, we evaluated the RD of the occurrence of VTE, pulmonary embolism (PE), and deep venous thrombosis (DVT) between COVID-19 and other pulmonary infection cohorts, in particular H1N1, and in an ICU setting. We searched for all studies comparing COVID-19 vs. non-COVID-19 regarding VTE, PE, and DVT. Results: The systematic review included 12 studies and 1,013,495 patients. The RD for VTE in COVID-19 compared to non-COVID-19 patients was 0.06 (95% CI 0.11–0.25, p = 0.011, I² = 97%), and 0.16 in ICU (95% CI 0.045–0.27, p = 0.006, I² = 80%). The RD for PE between COVID-19 and non-COVID-19 patients was 0.03 (95% CI, 0.006–0.045, p = 0.01, I² = 89%). The RD for PE between COVID-19 and non-COVID-19 patients was 0.021 in retrospective studies (95% CI 0.00–0.04, p = 0.048, I² = 92%) and 0.11 in ICU studies (95% CI 0.06–0.16, p < 0.001, I² = 0%). Conclusions: The growing awareness and understanding of a massive inflammatory response combined with a hypercoagulable state that predisposes patients to thrombosis in COVID-19, in particular in the ICU, may contribute to a more appropriate strategy of prevention and earlier detection of the thrombotic events.

Antiphospholipid syndrome (APS) is an autoimmune disorder characterized by the presence of antiphospholipid antibodies, vascular thrombosis (venous, arterial, or small vessels), and/or pregnancy morbidity. Diagnosis of APS is based on the presence of at least one clinical criterion (thrombotic events or pregnancy morbidity) and at least one of the laboratory criteria (persistently medium/high titer immunoglobulin G [IgG]/immunoglobulin M [IgM] anticardiolipin antibodies, and/or medium/high titer IgG/IgM anti-β2-glycoprotein I antibodies, and/or a positive lupus anticoagulant test), confirmed after repetition at least 12 weeks apart. The clinical spectrum of APS encompasses additional (extracriteria) clinical manifestations, including cardiac diseases. Heart involvement may become evident as a consequence of direct (autoimmune-mediated) or indirect (thrombosis) mechanisms, and include valve heart disease (vegetations and/or thickening associated with functional abnormalities) and intracardiac thrombosis, coronary, and vascular accelerated atherosclerosis, along with ischemic heart disease. APS can also cause pulmonary arterial hypertension, left ventricular dysfunction, and heart failure. This review describes the major cardiac manifestations of APS and illustrates the role of cardiac imaging for diagnosing subclinical and overt heart involvement and addressing management of these patients. The possible role of therapeutic strategies in cardiac manifestations of APS is also discussed.

Summary. Aging itself is a risk factor for venous thromboembolism, and the prevalence in the elderly of additional risk factors (e.g. cancer, orthopedic surgery, immobility) increase its intrinsic risk. Many in the medical community are reluctant to prescribe anticoagulation (for primary and secondary prevention of venous thromboembolism) to their geriatric patients for the fear that bleeding complications may outweigh the benefits. A thorough analysis of the data support the concept that the under‐use of heparin in primary prevention in the elderly is more related to medical beliefs than to facts. The risk of bleeding due to oral anticoagulants (secondary prevention) is greatly reduced by keeping the International Normalized Ratio (INR) values within therapeutic ranges and carefully avoiding conditions/drugs that may interfere with such treatment. The oral direct thrombin inhibitor ximelagatran has been studied for primary (hip and knee replacement surgery) and for secondary prophylaxis of venous thromboembolism, and for acute venous thromboembolism treatment. The selective factor Xa inhibitor fondaparinux has been approved for primary prophylaxis of venous thromboembolism in hip and knee replacement surgery and in hip fracture surgery. Studies on the latter drugs, where most of the patients were > 65 years of age, further show that the fear of bleeding complications due to anticoagulation in the elderly is largely unjustified.