Kardiologia polska最新文献

Background: Renal dysfunction increases thromboembolic risk but is not consistently included in standard risk scores.

Aims: To compare the prevalence of left atrial thrombus (LAT) in atrial fibrillation (AF)/atrial flutter (AFl) patients based on renal function and oral anticoagulant (OAC) regimens.

Methods: Consecutive AF/AFl patients undergoing transesophageal echocardiography before cardioversion or ablation were included.

Results: Among 2790 patients with creatinine clearance (CrCl) data, 89% had CrCl ≥50 ml/min, 9.6% had CrCl 30-49 ml/min, and 1.5% had CrCl <30 ml/min. LAT prevalence was 6.7%, 16%, and 19%, respectively (P = 0.008). CrCl <50 ml/min was an independent predictor of LAT (odds ratio [OR], 1.81; 95% confidence interval [CI], 1.25-2.64). Of 2028 patients treated with non-vitamin K antagonist OACs (NOACs), 17% received reduced doses, with 56% of these reductions deemed inappropriate. LAT prevalence was higher with reduced NOAC doses (12%) compared to standard doses (4.6%; P <0.001). Patients with no indication for dose reduction but receiving reduced doses had a higher LAT risk (12% vs. 4.2%; P <0.001). Among those with an indication for reduced doses, LAT prevalence was similar (11%) regardless of dose appropriateness. There were no significant differences in LAT prevalence among different NOACs. Inappropriate NOAC dosing increased LAT risk (OR, 1.74; 95% CI, 1.11-2.73). Inappropriate dose reductions, especially with apixaban and rivaroxaban, were the main issue in inappropriate NOAC prescribing, likely influenced by age, bleeding risk, anemia, low CrCl, and antiplatelet use.

Conclusions: AF patients with CrCl <50 ml/min face a doubled LAT risk despite OAC therapy. Inappropriate NOAC dosing, particularly with apixaban and rivaroxaban, leads to double LAT risk.

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.

Background: Osmolarity is a key indicator of the balance between water and osmotically active molecules. It plays a crucial role in the diuretic response among patients with congestion in acute heart failure (AHF), and therefore, it may provide clinically meaningful information.

Aims: This study investigated the association between urine (pre- and post-diuretic) and serum osmolarity during early diuretic treatment and one-year outcomes in AHF patients.

Methods: It was single-center, prospective, observational study that included AHF. The patients were recruited between March 2021 and November 2023 and underwent one-year follow-up. Serum and urine osmolarity and their contributors (sodium, urea, glucose) were measured before loop diuretic exposure and 3 hours after infusion start. The main endpoints included: 1) all-cause mortality and 2) all-cause unplanned rehospitalizations.

Results: In a one-year follow-up, 59 (23%) patients died (26 [10%] during index hospitalization), and 95 (40%) were rehospitalized. Higher pre-diuretic urine osmolarity was independently associated with a lower probability for mortality (hazard ratio [HR], 0.95; 95% confidence interval [CI], 0.93-0.98; P <0.01) and rehospitalization (HR, 0.98; 95% CI, 0.95-0.99; P = 0.03). Pre-diuretic urine osmolarity was significantly lower in patients with an event during follow-up (359 [272-403] vs. 419 [332-509] mOsm/l; P <0.001 for mortality and 384 [303-463] vs. 430 [342-524] mOsm/l; P = 0.03 for rehospitalization). Moreover, the degree of urine osmolarity drop was lower in patients who died (32 [8-77] vs. 122 [50-208] mOsm/l; P <0.001) and significantly influenced death probability (0.93 [0.89-0.97]; P <0.01), while significance was not proven regarding rehospitalizations (0.98 [0.95-1.00]; P = 0.16). Serum and post-diuretic urine osmolarity had no prognostic significance.

Conclusions: Pre-diuretic urine osmolarity and the degree of its decrease (reflecting the potential for urine dilution) during early decongestion are associated with one-year outcomes in AHF.