Atherosclerotic cardiovascular diseases (ASCVD) are the major cause of mortality worldwide. Despite the continuous progress in ASCVD therapy, the residual risk persists beyond the management of traditional risk factors. Several infections including Helicobacter pylori infection, periodontal disease, and viral infections are associated with the increased risk of ASCVD, both directly by damage to the heart muscle and vasculature, and indirectly by triggering a systemic proinflammatory state. Hence, beyond the optimal management of the traditional ASCVD risk factors, infections should be considered as an important non-classical risk factor to enable early diagnosis and appropriate treatment. Here, we summarized the currently available evidence regarding the role of inflammation in ASCVD and the association between the particular infections and pathogens (Helicobacter pylori, periodontal disease, pneumonia, Cytomegalovirus, Human immunodeficiency virus, Herpes simplex virus, and severe acute respiratory syndrome coronavirus 2) on the development and progression of ASCVD. We also speculated about the potential therapeutic implications of the anti-inflammatory and anti-infective drugs on ASCVD outcomes, including drugs routinely administered in patients with ASCVD (statins, P2Y12 receptor inhibitors, and angiotensin-converting enzyme inhibitors/angiotensin receptor blockers) and novel strategies aiming at residual risk reduction (colchicine, anti-cytokine drugs, and methotrexate). Considering the emerging association between infections and ASCVD, it is crucial to determine the possible advantages of infection prevention and treatment in patients with ASCVD.

Background: Stroke is the second main cause of mortality and the third leading cause of mortality and permanent disability combined. Many potential biomarkers have been described to contribute to the diagnosis, prognosis of outcomes, and risk stratification after stroke. Copeptin is an inactive peptide that is produced in an equimolar ratio to arginine vasopressin (AVP) in response to the activation of the endogenous stress system. Methods: The present study isa systematic review and meta-analysis to assess plasma copeptin concentrations, diagnostic and prognostic values for risk stratification after acute ischemic stroke and transient ischemic attack. Results: Mean copeptin level in stroke vs. non-stroke groups varied and amounted to 19.8 ± 17.4 vs. 9.7 ± 6.6 pmol/L, respectively (mean differences [MD]: 12.75; 95% confidence interval [CI]: 5.00 to 20.49; p < 0.001), in good vs. poor outcome 12.0 ± 3.6 vs. 29.4 ± 14.5 (MD: −8.13; 95% CI: −8.37 to −7.88; p < 0.001) and in survive vs. non-survive stroke patients: 13.4 ± 3.2 vs. 33.0 ± 12.3, respectively (MD: −13.43; 95% CI: −17.82 to −9.05; p < 0.001). Conclusions: The above systematic review and meta-analysis suggests that monitoring the copeptin levels may help predict the long-term prognosis of ischemic stroke efficiently. Determining the copeptin level may help individualize the management of ischemic stroke patients, keep stroke risk lower, reduce post-stroke complications, including patient death, and minimize healthcare costs. Background: Stroke is the second main cause of mortality and the third leading cause of mortality and permanent disability combined. Many potential biomarkers have been described to contribute to the diagnosis, prognosis of outcomes, and risk stratification after stroke. Copeptin is an inactive peptide that is produced in an equimolar ratio to arginine vasopressin (AVP) in response to the activation of the endogenous stress system. Methods: The present study isa systematic review and meta-analysis to assess plasma copeptin concentrations, diagnostic and prognostic values for risk stratification after acute ischemic stroke and transient ischemic attack. Results: Mean copeptin level in stroke vs. non-stroke groups varied and amounted to 19.8 ± 17.4 vs. 9.7 ± 6.6 pmol/L, respectively (mean differences [MD]: 12.75; 95% confidence interval [CI]: 5.00 to 20.49; p < 0.001), in good vs. poor outcome 12.0 ± 3.6 vs. 29.4 ± 14.5 (MD: −8.13; 95% CI: −8.37 to −7.88; p < 0.001) and in survive vs. non-survive stroke patients: 13.4 ± 3.2 vs. 33.0 ± 12.3, respectively (MD: −13.43; 95% CI: −17.82 to −9.05; p < 0.001). Conclusions: The above systematic review and meta-analysis suggests that monitoring the copeptin levels may help predict the long-term prognosis of ischemic stroke efficiently. Determining the copeptin level may help individualize the management of ischemic stroke patients, keep stroke risk lower, reduce post-stroke complications, including patient death, and minimize healthcare costs.

(1) Background: Pulmonary embolism (PE) is the third most frequent acute cardiovascular condition worldwide. PE response teams (PERTs) have been created to facilitate treatment implementation in PE patients. Here, we report on the 5-year experience of PERT operating in Warsaw, Poland, with regard to the characteristics and outcomes of the consulted patients. (2) Methods: Patients diagnosed with PE between September 2017 and December 2021 were included in the study. Clinical and treatment data were obtained from medical records. Patient outcomes were assessed in-hospital, at a 1- and 12-month follow-up. (3) Results: There were 235 PERT activations. The risk of early mortality was low in 51 patients (21.8%), intermediate–low in 83 (35.3%), intermediate–high in 80 (34.0%) and high in 21 (8.9%) patients. Anticoagulation alone was the most frequently administered treatment in all patient subgroups (altogether 84.7%). Systemic thrombolysis (47.6%) and interventional therapy (52%) were the prevailing treatment options in high-risk patients. The in-hospital mortality was 6.4%. The adverse events during 1-year follow-up included five deaths, two recurrent VTE and two minor bleeding events. (4) Conclusions: Our initial 5-year experience showed that the activity of the local PERT facilitated patient-tailored decision making and the access to advanced therapies, with subsequent low overall mortality and treatment complication rates, confirming the benefits of PERT implementation.

Introduction and objective: In COVID-19, the rapid prediction of the severity of a patient’s condition using modern biomarkers can accelerate the implementation of appropriate therapy, and thus improve the patient’s prognosis. Material and methods: A meta-analysis was conducted of data...

The SARS-CoV-2 (COVID-19) pandemic is a major issue that necessitates the use of cutting-edge disease prediction models. The aim of the study was to assess the existing evidence regarding association between Krebs von den Lungen-6 levels and COVID-19 severity. A literature search was performed on Web of Science, PubMed, Scopus and Cochrane Central Register of Controlled Trials databases from 1 January 2020 up to 2 August 2022. The electronic database search was supplemented by searching Google Scholar. In addition, reference lists of relative articles were also reviewed. KL-6 levels among COVID-19 positive vs. negative patients varied and amounted to 443.37 ± 249.33 vs. 205.73 ± 86.8 U/mL (MD = 275.33; 95%CI: 144.57 to 406.09; p < 0.001). The KL-6 level was 402.82 ± 261.16 U/mL in the severe group and was statistically significantly higher than in the non-severe group (297.38 ± 90.46 U/mL; MD = 192.45; 95%CI: 118.19 to 266.72; p < 0.001). The KL-6 level in the mild group was 272.28 ± 95.42 U/mL, compared to 268.04 ± 55.04 U/mL in the moderate COVID-19 group (MD = −12.58; 95%CI: −21.59 to −3.57; p = 0.006). Our meta-analysis indicates a significant association between increased KL-6 levels and SARS-CoV-2 infection. Moreover, KL-6 levels are significantly higher in patients with a more severe course of COVID-19, indicating that KL-6 may be a useful predictor to identify patients at risk for severe COVID-19.

Chronic thromboembolic pulmonary hypertension (CTEPH) is a rare condition caused by thromboembolic occlusions of the pulmonary arteries and characterised by elevated pulmonary pressure, vascular remodelling and right ventricular overload, which can be effectively treated with balloon pulmonary angioplasty (BPA). The study aimed to evaluate whether elevated pulmonary arterial wedge pressure (PAWP), associated with left ventricular dysfunction, influences the effectiveness and safety of BPA treatment. Does elevated PAWP affect the effectiveness and safety of BPA in patients with CTEPH? A retrospective analysis was conducted on 170 patients with CTEPH treated with BPA. Patients were classified into two groups: with normal PAWP and with elevated PAWP. Hemodynamic parameters, exercise capacity, treatment outcomes and safety profiles were compared between the groups. Multivariate analysis of overall survival was also performed. Elevated PAWP was present in 13.5% of patients. The elevated PAWP group was older, had a higher body mass index (BMI), elevated baseline troponin levels, and a greater burden of comorbidities, including diabetes, atrial fibrillation, deep vein thrombosis, and chronic kidney disease, than patients with normal PAWP. After treatment, patients with elevated PAWP exhibited significantly smaller reduction in mean pulmonary artery pressure (mPAP) (p=0.026), lower improvement in pulmonary arterial compliance (PAC) (p=0.002) and 6-minute walk distance (p=0.011) compared to those with normal PAWP. There were no significant differences in overall survival or adverse event rates observed between the two groups. Elevated PAWP, likely reflecting coexisting left heart dysfunction, was associated with reduced hemodynamic and functional benefits from BPA in CTEPH patients. Nevertheless, it did not compromise procedural safety or long-term survival, suggesting that BPA remains a viable option in this subgroup, albeit with more modest clinical gains.