Aortic valve stenosis (AS) is a common heart valve disease in the elderly population, and its pathogenesis remains an interesting area of research. The degeneration of the aortic valve leaflets gradually progresses to valve sclerosis. The advanced phase is marked by the presence of extracellular fibrosis and calcification. Turbulent, accelerated blood flow generated by the stenotic valve causes excessive damage to the aortic wall. Elevated shear stress due to AS leads to the degradation of high-molecular weight multimers of von Willebrand factor, which may involve bleeding in the mucosal tissues. Conversely, elevated shear stress has been associated with the release of thrombin and the activation of platelets, even in individuals with acquired von Willebrand syndrome. Moreover, turbulent blood flow in the aorta may activate the endothelium and promote platelet adhesion and activation on the aortic valve surface. Platelets release a wide range of mediators, including lysophosphatidic acid, which have pro-osteogenic effects in AS. All of these interactions result in blood coagulation, fibrinolysis, and the hemostatic process. This review summarizes the current knowledge on high shear stress-induced hemostatic disorders, the influence of AS on platelets and antiplatelet therapy.

Background/Objectives: Angiotensin receptor–neprilysin inhibitor (ARNI) has a well-established advantage over angiotensin-converting enzyme inhibitor or angiotensin receptor blocker (ACEI/ARB) therapy in patients (pts) with heart failure with reduced ejection fraction (HFrEF), but in pts after acute myocardial infarction (AMI) with left ventricular (LV) systolic dysfunction, the advantage of ARNI has not been clearly proven. The efficacy of ARNI is compared with that of ACEI/ARB therapy in patients with their first AMI in terms of improvement of post-infarction LV systolic function. Methods: The study was conducted as a retrospective one-center cross-sectional analysis. Overall, 1473 pts (990 M, median age 71 [64; 77]) with AMI (their first AMI, complete coronary revascularization, no prior coronary revascularization or history of HF) hospitalized in 2022–2024 were enrolled in a retrospective cross-sectional analysis. The study population was categorized into pts receiving ARNI and ACEI/ARB. Then, based on the ARNI subgroup, matching that included age, sex, and LV ejection fraction (LVEF) was performed by using the 1:1 nearest neighbor method without returning. Finally, two groups (ARNI vs. ACEI/ARB) of 30 pts were obtained and analyzed at baseline and at a 6-week follow-up. The improvement of post-infarction LV systolic function was obtained in terms of LVEF, ΔLVEF, and relative ΔLVEF values (ΔLVEF/baseline LVEF). Results: The comparison of baseline characteristics revealed borderline lower initial LVEF (30 vs. 36%, p = 0.076) and a higher frequency of SGLT-2 inhibitor use (70% vs. 36.7%, p = 0.01) in the ARNI subgroup. At the 6-week follow-up, in both subgroups, a significant improvement in the median LVEF values was achieved—from a median LVEF value of 30% (27.3; 38) to 37% (30; 43; p = 0.0008) in the ARNI subgroup and from a median LVEF value of 36% (33; 39) to 45% (42; 52; p < 0.0001) in the ACEI/ARB subgroup. The median ΔLVEF in the ACEI/ARB subgroup was higher [10% (6; 12)] than in the ARNI subgroup [6% (2; 10.25), p = 0.018]. Similarly, the median relative ΔLVEF was higher in the ACEI/ARB subgroup [30% (15.4; 40)] than in the ARNI group [17.5% (7; 31.9), p = 0.047]. The vast majority of patients, particularly in the ARNI group (99.7%), were treated with the lowest available dose of the drug. Conclusions: Our current experience in ARNI therapy after AMI is promising; however, it is limited to a small group of patients with severe impairment of LV systolic function. Regardless of the significant improvement in the baseline LVEF observed in patients receiving both ACEI/ARB and ARNI at the 6-week follow-up, the absolute and relative increases in the LVEF were higher in subjects treated with ACEI/ARB. However, the clinical benefits of ARNI therapy may emerge more gradually, and its advantages could become more apparent over a longer follow-up period. The clinical efficacy of early use of ARNI in the setting of AMI needs further evaluation.

Amyloidoza jest rzadką chorobą charakteryzującą się nieprawidłowym gromadzeniem się białka amyloidowego w tkankach. Amyloidozę można podzielić na dwa główne podtypy: amyloidozę transtyretynową (ATTR-CA) i amyloidozę łańcuchów lekkich immunoglobulin (AL-CA). Nagromadzenie białka amyloidu w mięśniu sercowym może doprowadzić do zaburzeń przewodzenia, kardiomiopatii restrykcyjnej i w konsekwencji niewydolności serca. Objawy mogą obejmować spadek tolerancji wysiłku, duszność, obrzęki oraz omdlenia. Rozpoznanie opiera się na badaniach laboratoryjnych, obrazowych oraz biopsji. Leczenie koncentruje się głównie na spowolnieniu postępu choroby oraz leczeniu objawowym.

Sarkoidoza serca (cardiac sarcoidosis – CS) jest rzadkim i trudnym do zdiagnozowania schorzeniem prowadzącym do zaburzeń przewodzenia, rytmu i nagłej śmierci sercowej. Rozpoznanie CS jest niezwykle trudne, ponieważ we wczesnych stadiach może nie dawać objawów i często imituje inne stany. Narzędziami diagnostycznymi wykorzystywanymi w diagnostyce CS są: echokardiografia, rezonans magnetyczny, pozytonowa tomografia emisyjna oraz biopsja zmienionej tkanki. Leczenie polega na zastosowaniu leków hamujących układ odpornościowy. Niektóre zaburzenia rytmu serca i przewodzenia związane z CS mogą mieć charakter odwracalny, jednak częściej wymagają one zabezpieczenia urządzeniami takimi jak rozruszniki serca czy defibrylatory. Konieczne są dalsze badania w celu opracowania skuteczniejszych strategii diagnostycznych dla poprawy wykrywania i leczenia tego stanu.

We aimed to evaluate the rate and risk factors of in-hospital mortality in patients undergoing coronary angiography/angioplasty with IABP use as support. We included 214 patients (mean age: 67.5 ± 7.5 years, M/F: 143/71) with an IABP used as the periprocedural support between 2012 and 2020. The main indications for an IABP were cardiogenic shock (143 pts; 66.8%: 55 survivors (51.9%)/88 non-survivors (81.5%); p < 0.001) and infarction with an initial significant impairment of ventricular function (34 pts; 15.9%: 21 (19.8%)/13 (12%); p = 0.12). In-hospital death was the endpoint of this study. In-hospital death occurred in 108 (50.5%, M/F: 69.4%/30.6%) patients. The mean hospitalization time was 7 days (2–13); deaths occurred more frequently on the first day after the procedure (1 (1–3 days) vs. 3 (1–8), p < 0.001); and the mean hospitalization time was 2 days (1–6) for non-survivors vs. 11 days (7–17) for survivors (p < 0.001). Regarding the patients who did not survive, they were older (69 vs. 66.5, p = 0.043), their LVEF was lower (0–15%: 15 (13.9%) vs. 12 (11.3%); 16–40%: 73 (67.6%) vs. 65 (61.3%); >40%: 14 (13%) vs. 29 (27.4%); p = 0.007), and hyperlipidemia was less common (30 (27.8%) vs. 55 (51.9%) pts, p = 0.001) than in those who survived. The IABP is still a method for cardiac support; however, mortality limits its use.

Background/Objectives: Angiotensin receptor-neprilysin inhibitor (AR-NI) has a well-established advantage over angiotensin converting enzyme inhibitor or angiotensin receptor blocker (ACEI/ARB) therapy in patients (pts) with heart failure with reduced ejection fraction (HFrEF), but in pts after acute myocardial infarction (AMI) with left ventricular (LV) systolic dysfunction the advantage of ARNI has not been clearly proven. To com-pare of the efficacy of ARNI versus ACEI/ARB therapy in patients with the first AMI in terms of improvement of post-infarction LV systolic function. Methods: Overall 1473 pts (990M, median age 71 [64;77]) with AMI (the first AMI, complete coronary revascularization, no prior: coronary revas-cularization, history of HF) hospitalized in 2022-2024 were enrolled into retrospective cross-sectional analysis. The study population was catego-rized into pts receiving ARNI and ACEI/ARB. Then based on ARNI subgroup included age, sex, and LV ejection fraction (LVEF) matching was performed by using the 1:1 nearest neighbour method without returning. Finally two groups (ARNI vs ACEI/ARB) of 30 pts were obtained and an-alysed at baseline and in 6-week follow-up. The improvement of post-infarction LV systolic function was obtained as LVEF value, ΔLVEF and relative ΔLVEF (ΔLVEF / baseline LVEF). Results: The comparison of baseline characteristics revealed borderline lower initial LVEF (30 vs 36%, p=0.076) and higher frequency of of SGLT-2 inhibitors use (70% vs 36.7%, p=0.01) in the ARNI subgroup. In 6-week follow-up in both subgroups a significant improvement in the median LVEF values was achieved: from median LVEF value 30% (27.3; 38) up to 37% (30; 43; p=0.0008) in ARNI and from median LVEF value 36% (33; 39) up to 45% (42; 52; p<0.0001) in ACEI/ARB subgroup. Median ΔLVEF in the ACEI/ARB subgroup was higher [10% (6; 12)] than in the ARNI subgroup [6% (2; 10.25), p=0.018]. Similarly median relative ΔLVEF was higher in the ACEI/ARB subgroup [30% (15.4; 40)] than in the ARNI group [17.5% (7; 31.9), p=0.047]. Conclusions: Our current experience in ARNI therapy after AMI is promising, however, it is limited to a small group of patients with severe impairment of LV systolic function. Regardless of significant improvement of baseline LVEF observed in patients receiving both ACEI/ARB and ARNI in 6 week follow-up the value of absolute and relative LVEF increase were higher in subjects treated with ACEI/ARB. The clinical efficacy of early use of ARNI in the setting of AMI needs further evaluation.