Background Thrombocytopenia is the most common non-criteria hematological feature in patients with antiphospholipid syndrome (APS). This condition is more common in patients with catastrophic APS (CAPS). Objectives To evaluate the prevalence of thrombocytopenia in a large series of high-risk patients with APS, and to assess the behavior of the platelet count during CAPS. Methods/Patients This was a cross-sectional study in which we analyzed the platelet counts of a homogeneous group of high-risk APS patients (triple-positive). Six of these patients developed a catastrophic phase of the disease, and the platelet count was recorded before the acute phase, during the acute phase, and at recovery. Results The mean platelet count in 119 high-risk triple-positive patients was 210 × 10 L . With a cut-off value for thrombocytopenia of 100 × 10 L , the prevalence of thrombocytopenia was 6% (seven patients). No difference between primary APS and secondary APS was found. In patients who suffered from CAPS, a significant decrease from the basal count (212 ± 51 × 10 L ) to that at the time of diagnosis (60 ± 33 × 10 L ) was observed. The platelet count became normal again at the time of complete remission (220 ± 57 × 10 L ). A decrease in platelet count always preceded the full clinical picture. Conclusions This study shows that, in high-risk APS patients, the prevalence of thrombocytopenia is low. A decrease in platelet count was observed in all of the patients who developed the catastrophic form of the disease. A decrease in platelet count in high-risk APS patients should be considered a warning signal for disease progression to CAPS.

Despite extensive research, the pathogenesis of antiphospholipid syndrome (APS) remains obscure in many aspects. However, it is widely accepted that thrombosis is the result of a hypercoagulable state caused by antibodies directed against β2-glycoprotein I (β2-GPI), a protein whose physiological role is unknown. Although underestimated, platelets may be involved in APS and its thrombotic manifestations, especially arterial, in several ways. Thrombocytopenia is the most relevant non-criteria manifestation of APS, possibly caused by direct binding of anti-β2-GPI antibodies or anti-β2-GPI-β2-GPI complexes. On the other hand, platelets may have a key role in APS-related thrombosis due to the presence of multiple receptors that can interact with anti-β2-GPI antibodies (especially apolipoprotein E receptor 2' (apoER2') and glycoprotein Ibα (GPIbα)) with consequent release of different procoagulant mediators such as thromboxane B2, platelet factor 4 (PF4), and platelet factor 4 variant (CXCL4L1). The aim of this review is to put together evidence on the possible role of platelets in APS and to stimulate further research on the issue.

Background Transthoracic echocardiography (TTE) is the first cardiac imaging modality generally requested for diagnosis of suspected infective endocarditis (IE), while transesophageal echocardiography (TEE) can be performed as initial or supplemental test. Although IE is a relatively rare disease characterized by high mortality, the number of daily in-hospital TTE and TEE requests to diagnose this disease is high, probably because of inappropriate prescriptions. Objective The principal aim of this study was to assess the clinical appropriateness of TTE and TEE requests for suspected IE. Methods Electronical data relative to TTE and TEE examinations performed for suspected IE between September 2013 and July 2022 at our center were extracted and retrospectively analyzed. All TTE and TEE requests were defined as appropriate according to the criteria indicated by the 2017 international guidelines on appropriateness for cardiac imaging in valvular heart disease. Results After exclusion of repeated ultrasound examinations, a total of 2249 first requests of echocardiographic examinations for suspected IE were analyzed (patients’ age 64±18 years, 61% males). TEE examinations were 447 (20%). Diagnosis of IE was made in 293/2249 (13%) cases. During the 10-year observation period, 33.1% of the TTE requests was appropriate and 12.2% of the appropriate examinations was positive for IE. Percentages of prescriptive appropriateness and diagnostic TTEs did not change significantly before and after publication of the 2017 international guidelines: in fact, appropriate TTE requests were 31.6% before and 35.3% after (P=0.579), and positive TTEs were 12.1% before and 12.4% after (P=0.948). Regarding TEEs, during the 10-year observation period 51.2% of the 447 examinations was appropriate and 35.8% of these evaluations was positive for IE. As for TTE, percentages did not vary significantly before and after publication of the 2017 international guidelines: appropriate TEE requests were 52.2% before and 50% after (P=0.756), and positive TEEs were 35.9% before and 35.6% after (P=0.965). Conclusions The majority of echocardiography requests for diagnosis of IE at our center during a 10-year observation period was inappropriate, especially TTE requests. No significant impact of the 2017 international guidelines on appropriateness for cardiac imaging in valvular heart disease was observed. A corrective strategy could be based on several actions: periodic monitoring of prescriptive appropriateness, dissemination of knowledge about published guidelines and development of in-hospital operative protocols shared among all physicians involved in TTE and TEE prescription.

(1) Background: Emerging data regarding patients recovered from COVID-19 are reported in the literature, but cardiac sequelae have not yet been clarified. To quickly detect any cardiac involvement at follow-up, the aims of the research were to identify: elements at admission predisposing subclinical myocardial injury at follow up; the relationship between subclinical myocardial injury and multiparametric evaluation at follow-up; and subclinical myocardial injury longitudinal evolution. (2) Methods and Results: A total of 229 consecutive patients hospitalised for moderate to severe COVID-19 pneumonia were initially enrolled, of which 225 were available for follow-up. All patients underwent a first follow-up visit, which included a clinical evaluation, a laboratory test, echocardiography, a six-minute walking test (6MWT), and a pulmonary functional test. Of the 225 patients, 43 (19%) underwent a second follow-up visit. The median time to the first follow-up after discharge was 5 months, and the median time to the second follow-up after discharge was 12 months. Left ventricular global longitudinal strain (LVGLS) and right ventricular free wall strain (RVFWS) were reduced in 36% (n = 81) and 7.2% (n = 16) of the patients, respectively, at first the follow-up visit. LVGLS impairment showed correlations with patients of male gender (p 0.008, OR 2.32 (95% CI 1.24–4.42)), the presence of at least one cardiovascular risk factor (p < 0.001, OR 6.44 (95% CI 3.07–14.9)), and final oxygen saturation (p 0.002, OR 0.99 (95% CI 0.98–1)) for the 6MWTs. Subclinical myocardial dysfunction had not significantly improved at the 12-month follow-ups. (3) Conclusions: in patients recovered from COVID-19 pneumonia, left ventricular subclinical myocardial injury was related to cardiovascular risk factors and appeared stable during follow-up.

Post-acute COVID-19 is characterized by the persistence of dyspnea, but the pathophysiology is unclear. We evaluated the prevalence of dyspnea during follow-up and factors at admission and follow-up associated with dyspnea persistence. After five months from discharge, 225 consecutive patients hospitalized for moderate to severe COVID-19 pneumonia were assessed clinically and by laboratory tests, echocardiography, six-minute walking test (6MWT), and pulmonary function tests. Fifty-one patients reported persistent dyspnea. C-reactive protein (p = 0.025, OR 1.01 (95% CI 1.00–1.02)) at admission, longer duration of hospitalization (p = 0.005, OR 1.05 (95% CI 1.01–1.10)) and higher body mass index (p = 0.001, OR 1.15 (95% CI 1.06–1.28)) were independent predictors of dyspnea. Absolute drop in SpO2 at 6MWT (p = 0.001, OR 1.37 (95% CI 1.13–1.69)), right ventricular (RV) global longitudinal strain (p = 0.016, OR 1.12 (95% CI 1.02–1.25)) and RV global longitudinal strain/systolic pulmonary artery pressure ratio (p = 0.034, OR 0.14 (95% CI 0.02–0.86)) were independently associated with post-acute COVID-19 dyspnea. In conclusion, dyspnea is present in many patients during follow-up after hospitalization for COVID-19 pneumonia. While higher body mass index, C-reactive protein at admission, and duration of hospitalization are predictors of persistent dyspnea, desaturation at 6MWT, and echocardiographic RV dysfunction are associated with this symptom during the follow-up period.