The patient database at the First Department of Internal Medicine in Martin, the Central Slovak Institute for Cardiac and Vascular Diseases in Banska Bystrica, and the National Slovak Institute of Cardiovascular Diseases in Bratislava was searched to identify patients with benign tumors of the heart seen during the 5-year period between 2011 and 2016. Forty-one patients with primary cardiac myxomas were identified and their medical records were reviewed for details pertaining to presenting symptoms, staging modalities, treatment approaches, and outcomes. Most of the studied patients were diagnosed with echocardiography (n = 35, 85%). The occurrence of the tumor was higher in the female population (n = 25, 61%). The most common presenting symptoms were dyspnoea (n = 17, 42%), chest pain (n = 3, 7%), or pain and paraesthesia of the limbs (n = 2, 5%). Acute embolic event due to embolization of tumor fragments resulted in cerebral stroke (n = 5, 12%). All patients were treated by resection. Only one comorbid patient died due to multiple-organ dysfunction syndrome two weeks after the resection. The most common postoperative complication was bleeding (n = 2, 5%) and infection (n = 2, 5%). The early diagnosis and appropriate treatment are often curative, with very low risk of recurrence. Postoperative survival is high.

Background Natriuretic peptides are routinely quantified to diagnose heart failure (HF). Their concentrations are also elevated in atrial fibrillation (AF). To clarify their value in predicting future cardiovascular events, we measured natriuretic peptides in unselected patients with cardiovascular conditions and related their concentrations to AF and HF status and outcomes. Methods and Results Consecutive patients with cardiovascular conditions presenting to a large teaching hospital underwent clinical assessment, 7‐day ECG monitoring, and echocardiography to diagnose AF and HF. NT‐proBNP (N‐terminal pro‐B‐type natriuretic peptide) was centrally quantified. Based on a literature review, four NT‐proBNP groups were defined (<300, 300–999, 1000–1999, and ≥2000 pg/mL). Clinical characteristics and NT‐proBNP concentrations were related to HF hospitalization or cardiovascular death. Follow‐up data were available in 1616 of 1621 patients (99.7%) and analysis performed at 2.5 years (median age, 70 [interquartile range, 60–78] years; 40% women). HF hospitalization or cardiovascular death increased from 36 of 488 (3.2/100 person‐years) in patients with neither AF nor HF, to 55 of 354 (7.1/100 person‐years) in patients with AF only, 92 of 369 (12.1/100 person‐years) in patients with HF only, and 128 of 405 (17.7/100 person‐years) in patients with AF plus HF ( P <0.001). Higher NT‐proBNP concentrations predicted the outcome in patients with AF only (C‐statistic, 0.82; 95% CI, 0.77–0.86; P <0.001) and in other phenotype groups (C‐statistic in AF plus HF, 0.66; [95% CI, 0.61–0.70]; P <0.001). Conclusions Elevated NT‐proBNP concentrations predict future HF events in patients with AF irrespective of the presence of HF, encouraging routine quantification of NT‐proBNP in the assessment of patients with AF.

The thrombin-induced platelet aggregation is reduced in non-valvular AF patients receiving dabigatran after a week-long therapy.

Rivaroxaban and apixaban are direct oral anticoagulants whose target specificity is to activate factor X (FXa). It is still not fully understood how xabans impact platelet function. This single-center observational study aimed to assess in vitro platelet function in patients with atrial fibrillation receiving rivaroxaban or apixaban. It examined quantification of platelet aggregation assessed by light transmission aggregometry in thirty-four patients treated with apixaban or rivaroxaban. The thrombin-induced platelet aggregation was significantly lower 2 h after taking selected xabans compared to baseline value (69.55 ± 32.15% vs. 44.79 ± 34.97.9%; p < 0.0001). This effect was only observed in patients who received rivaroxaban or apixaban for more than 1 week. The thrombin-induced platelet aggregation is reduced in cardiovascular patients receiving rivaroxaban or apixaban. This reduction is likely to depend on the duration of the treatment. Duration of treatment should be considered in future studies focusing on DOACs and platelet aggregation.

A rapid and reliable assessment of the dabigatran effect is desirable in dabigatran treated patients with uncontrolled bleeding or before acute surgery. The aim of this study was to study the anticoagulant effects of dabigatran in patients with atrial fibrillation (AF) as assessed by the whole blood assays ROTEM, and how data from these methods correlate to plasma dabigatran concentrations measured by Hemoclot. ROTEM was performed with ROTEM Gamma (Pentapharm GmbH, Munich, Germany). The assays used in our study were Ex-tem and In-tem assay. Plasma dabigatran concentrations were determined by hemoclot thrombin inhibitor assay (Hyphen BioMed, France) at trough and post-dose in 27 patients on dabigatran 150 mg BID. Median plasma dabigatran concentrations at trough were 74 ng/mL (11.2–250) and post-dose (2 h after ingestion) 120 ng/mL (31–282). The ROTEM clotting time (CT) and maximum clot firmnes (MCF) correlated strongly with dabigatran concentrations when activated with the reagents Ex-tem (p < 0.0001) and In-tem (p < 0.0001). In summary, in our study, we have found that the ROTEM variable CT and MCF, when activated with triggers Ex-tem and In-tem, has a strong and highly significant correlation with the plasma dabigatran concentration in a real-life population of AF-patients and could thereby be an alternative to estimate dabigatran concentration in emergency situations. However, additional studies are needed to further validate these findings.

No abstract

The availability of direct oral anticoagulants has caused a paradigm shift in the management of thrombosis. Rivaroxaban and apixaban are 2 direct oral anticoagulants whose target specificity is activated factor X (FXa). However, it is still not fully understood if and how xabans impact platelet function. This observational study aimed to assess the in vitro platelet function in patients with atrial fibrillation receiving xabans. This was a single-center study quantifying platelet aggregation in 41 patients treated with apixaban or rivaroxaban by light transmission aggregometry. The thrombin receptor activating peptide (TRAP)-induced platelet aggregation was significantly lower 2 hours after taking rivaroxaban or apixaban compared to baseline value (56.15% [8.53%] vs 29.51% [12.9%]; P = .000). Moreover, concomitant use of angiotensin-converting enzyme blockers, proton pump inhibitors, and statins reduces the efficiency of xabans. The TRAP-induced platelet aggregation was reduced in patients with cardiovascular disease 2 hours after receiving xabans.

The availability of direct oral anticoagulants has caused a paradigm shift in thrombosis management. The direct thrombin inhibitor dabigatran seems to obstruct tenase complex by inhibiting thrombin generated in the initial phase and feed back to the amplification phase of cell-based coagulation reactions. However, it is still not fully understood if and how dabigatran impact platelet function. This observational study aimed to assess in vitro platelet function in patients with atrial fibrillation receiving dabigatran. Platelet aggregability was tested with platelet-rich plasma using platelet aggregometry (PACKS-4 aggregometer). Blood samples were stimulated with thrombin receptor agonist peptide (TRAP; 32 mmol/L). Results: A total of 28 patients with nonvalvular atrial fibrillation were enrolled. The mean age was 71.57 (9.75) years (range: 50-87 years), 16 patients were women, and the mean CHA 2 DS 2 VASc score was 3.93 (1.41). All patients began treatment with dabigatran as initial anticoagulant treatment. The minimum term use of dabigatran was 18 days. Dabigatran doses were 110 mg (57.14%) or 150 mg (42.86%) twice daily. The TRAPinduced platelet aggregation was significantly lower 2 hours after taking dabigatran compared to baseline value (79.39 [13.38] vs 90.14 [10.5]). Conclusion: The TRAP-induced platelet aggregation was reduced in cardiovascular patients 2 hours after receiving dabigatran. Our findings could have some important clinical implications because platelet aggregation and coagulation cascade are affected at the same time.