Kardiologia polska最新文献

Platelet-fibrin clot generation at the site of vascular injury in coronary arteries is a primary pathophysiologic event that leads to vascular occlusion and the subsequent clinical manifestations of acute coronary syndrome (ACS). Therefore, a strategy to optimally inhibit both platelet and coagulation pathways simultaneously - known as dual pathway inhibition (DPI) - has been proposed. In this strategy, when bleeding risk is acceptable, patients suffering from ACS are often treated with potent parenteral antiplatelet and anticoagulant therapies to facilitate efficient reperfusion and prevent reocclusion of coronary arteries. With the development of safer direct oral anticoagulants in recent years, a DPI strategy has been explored for the long-term management of patients with a history of ACS. It has been hypothesized that FXIa and FXIIa are essential for the amplification of thrombin generation beyond the initial burst of thrombin generated by tissue factor, and for the growth and stabilization of pathological clot, but not for normal hemostasis. In this scenario, potential oral agents include FXa (rivaroxaban, apixaban, edoxaban), FXIa (asundexian and milvexian), and FXIIa inhibitors. However, trials of full-dose FXa inhibitors added to an antiplatelet agent were associated with an unacceptable risk of bleeding. In patients with recent ACS, very low dose (2.5 mg bid) was associated with a significant reduction in efficacy endpoints compared to dual antiplatelet therapy and lower bleeding compared to 5 mg bid rivaroxaban dose. In patients with chronic atherosclerotic vascular disease, very low dose rivaroxaban plus aspirin compared to aspirin alone was associated with favorable net clinical benefits. Understanding the relative contributions of platelet and coagulation pathways to clot formation in an individual patient is likely critical to achieve a balance between anti-ischemic effects and bleeding risk. In this line, we discuss the importance of objectively measuring thrombogenicity and its potential role in personalizing DPI strategies in patients with ACS.

Background: We present the first multicenter, non-interventional, longitudinal observational study of patients diagnosed with cardiac transthyretin amyloidosis (ATTR-CA) in Poland.

Aims: The aim of this study was to describe the clinical characteristics, survival rates, and treatment outcomes of patients with ATTR-CA in Poland, and to identify potential markers linked to an increased risk of disease progression.

Methods: Between 2017 and 2025, consecutive patients with confirmed ATTR-CA were evaluated at 4 cardiology centers. Assessments included blood tests, standard 12-lead electrocardiography, and transthoracic echocardiography. The primary endpoint was defined as death or heart transplantation.

Results: ATTR-CA was confirmed in 115 patients, including 21 (18.2%) with hereditary disease. The median follow-up was 24 (12-41) months for the entire cohort and 25 (14.2-46.7) months for surviving patients (n = 78). The primary endpoint occurred in 37 (32.2%) patients. In multivariable analysis, the ratio of the transmitral early peak velocity (E) estimated by pulsed wave Doppler over the early mitral annulus velocity (e'), body mass index, and levels of high-sensitivity cardiac troponin T and N-terminal pro-B-type natriuretic peptide were independent predictors of the primary endpoint. Tafamidis was received by 81 (70.4%) patients and was associated with significantly lower risk of the primary endpoint (P = 0.005), stroke, or transient ischemic attack (P = 0.047), and a markedly longer median survival (84 months [95% confidence interval, 68-116] vs. 14 months [95% confidence interval, 7-36]; log-rank P <0.0001). In tafamidis-treated patients, N-terminal pro-B-type natriuretic peptide and high-sensitivity cardiac troponin T levels remained stable at 6 and 12 months of follow-up, in contrast to untreated patients, who showed an increase in these biomarkers.

Conclusions: This study provides the first multicenter data on ATTR-CA in Poland. Our findings enhance understanding of the disease course and treatment effects, underline the importance of disease-modifying therapy in improving outcomes, provide valuable real-world data on tafamidis treatment, and indicate directions for further research.