Atherosclerosis is the primary process that underlies cardiovascular disease. The connection between LDL cholesterol and the formation of atherosclerotic plaques is established by solid evidence. PCSK9 inhibitors have proven to be a valuable and practical resource for lowering the LDL cholesterol of many patients in recent years. Their inhibitory effect on atherosclerosis progression seems to be driven not just by lipid metabolism modification but also by LDL-independent mechanisms. We review the effect of PCSK9 inhibitors on various mechanisms involving platelet activation, inflammation, endothelial dysfunction, and the resultant clot formation. The main effectors of PCSK9 activation of platelets are CD36 receptors, lipoprotein(a), oxidised LDL particles, tissue factor, and factor VIII. Many more molecules are under investigation, and this area of research is growing rapidly.

The coronavirus SARS-CoV2 disease (COVID-19) is connected with significant morbidity and mortality (3.4%), disorders in hemostasis, including coagulopathy, activation of platelets, vascular injury, and changes in fibrinolysis, which may be responsible for an increased risk of thromboembolism. Many studies demonstrated relatively high rates of venous and arterial thrombosis related to COVID-19. The incidence of arterial thrombosis in severe/critically ill intensive care unit–admitted COVID-19 patients appears to be around 1%. There are several ways for the activation of platelets and coagulation that may lead to the formation of thrombi, so it is challenging to make a decision about optimal antithrombotic strategy in patients with COVID-19. This article reviews the current knowledge about the role of antiplatelet therapy in patients with COVID-19.

Novel P2Y12 ADP receptor blockers (ADPRB) should be preferred in dual-antiplatelet therapy in patients with acute coronary syndrome. Nevertheless, there are still patients who do not respond optimally to novel ADP receptor blocker therapy, and this nonoptimal response (so-called “high on-treatment platelet reactivity” or “resistance”) could be connected with increased risk of adverse ischemic events, such as myocardial re-infarction, target lesion failure and stent thrombosis. In addition, several risk factors have been proposed as factors associated with the phenomenon of inadequate response on novel ADPRB. These include obesity, multivessel coronary artery disease, high pre-treatment platelet reactivity and impaired metabolic status for prasugrel, as well as elderly, concomitant therapy with beta-blockers, morphine and platelet count for ticagrelor. There is no literature report describing nonoptimal therapeutic response on cangrelor, and cangrelor therapy seems to be a possible approach for overcoming HTPR on prasugrel and ticagrelor. However, the optimal therapeutic management of “resistance” on novel ADPRB is not clear and this issue requires further research. This narrative review article discusses the phenomenon of high on-treatment platelet reactivity on novel ADPRB, its importance in clinical practice and approaches for its therapeutic overcoming.

Background: Impaired endothelial function has been associated with vascular complications in type 2 diabetes (T2D), but its role in T2D-related heart failure (HF) remains indeterminate. The aim of this study was to assess selected markers of endothelial function in T2D patients with acute decompensated HF. Methods: A pilot prospective study on patients with acute decompensated HF requiring in-hospital admission was carried out. The vascular endothelial growth factor (VEGF), intercellular adhesion molecule 1 (ICAM-1), and vascular cell adhesion molecule 1 (VCAM-1) were assessed at admission and after decongestion. Subsequently, differences in these markers between T2D and non-diabetic (ND) patients were studied. Results: In total, 39 patients (21 with T2D and 18 ND patients) were enrolled. Twenty-eight patients presented with preserved ejection fraction (EF), and 11 presented with reduced EF. Looking at the VEGF levels in T2D patients, on admission, a median of 233.0 pg/mL (1.7–598 pg/mL) was found compared to 106.0 pg/mL (1.7–888 pg/mL) in ND individuals; the differences reached statistical significance (p = 0.04). There were no significant differences in VEGF levels after decongestion, and in VCAM-1 (2237 ± 1195 vs. 2699 ± 1093 ng/mL, p = 0.37) and ICAM-1 (596 ± 268 vs. 638 ± 437 ng/mL, p = 0.79) levels between T2D and ND patients upon admission and after decongestion. The value of EF (preserved or reduced) affected the VEGF levels upon admission. Conclusions: This study identified significantly higher VEGF levels upon admission due to acute decompensated HF in T2D patients.

Background/Objectives: Cardiovascular diseases are the most prevalent comorbidities in patients with acromegaly (APs). Acromegalic cardiomyopathy is the leading cause of mortality in APs. This study aimed to assess changes in morphology and function of the left heart in naïve APs 12 months after the beginning of acromegaly treatment and to explore the effects of disease activity and body composition parameters on changes in the left heart. Methods: This prospective study involved 34 APs and 34 healthy controls (CON) matched for age, gender, and BMI. DXA and 2D echocardiography were performed at diagnosis and 12 months after the beginning of the treatment. Results: In APs, the prevalence of left ventricular (LV) hypertrophy was 70%. LV mass index (LVMI) was greater in APs compared to CON (124 vs. 86 ± g/m², p < 0.001), but with no difference in size and systolic function of the LV. APs presented with increased left atrium volume (LAVI) and with diastolic dysfunction of the LV. Twelve months after the beginning of acromegaly treatment, IGF-1 levels decreased significantly (p < 0.001), and biochemical control of disease was achieved in 73.52% of APs. We found that in all APs, LAVI and LVMI decreased (all p < 0.05), and diastolic function of the LV improved without changes in systolic function. In multiple analyses, the changes in body surface area (β = −0.444, p < 0.001) and in lean body mass (β = −0.298, p = 0.027) were independent predictors of reverse remodelling of LVMI after the treatment. Conclusions: This study confirmed remodelling reversal of the left heart structure, followed by an improvement in diastolic function in naïve APs 12 months after the beginning of acromegaly treatment.

Background: It was repeatedly demonstrated that patients with severe COVID-19 pneumonia, as well as patients with type 2 diabetes (T2D) have higher risk of thromboembolic complications. Rotational thromboelastometry (ROTEM®) is a viscoelastic hemostatic assay which allows complex assessment of hemostasis in whole blood. The aim of this study was to compare changes in hemostasis measured by ROTEM® in diabetic and nondiabetic patients with mild COVID-19 pneumonia. Methods: We performed a pilot, prospective, observational study and enrolled 33 consecutive patients (14 with T2D and 19 nondiabetic ones) admitted to regular ward with mild COVID-19 pneumonia. The control group consisted from 11 healthy, nondiabetic blood donors. Blood samples were tested with ROTEM® using INTEM® and EXTEM® reagents. Results: We detected significant differences in EXTEM® clotting time (CT), clot formation time (CFT), and maximum clot firmness (MCF) comparing patients with mild COVID-19 pneumonia and healthy donors. However, there were no significant differences in EXTEM®, INTEM®, and HEPTEM® parameters (CT, CFT, and MCF) according to diabetes status. Conclusions: Our study demonstrated hypercoagulation in patients with mild COVID-19 pneumonia. T2D did not affected ROTEM® parameters in patients with mild COVID-19 pneumonia.