Data on incidence of bleeding in patients with atrial fibrillation and advanced liver fibrosis on treatment with vitamin K or non-vitamin K antagonist oral anticoagulants

This article contains the data showing the different characteristics of atrial fibrillation (AF) patients treated with vitamin K (VKAs) or non-vitamin K antagonist oral anticoagulants (NOACs) screened for the presence of liver fibrosis (LF) and followed to record the occurrence of bleeding and cardiovascular events (CVEs). A detailed description of major and minor bleedings is provided according to anticoagulant treatment (VKAs vs. NOACs) and to the presence of LF. Data here reported also show a higher incidence rate of CVEs in VKA-treated patients, but not in those on NOACs. The data are supplemental to our original research article titled “Incidence of bleeding in patients with atrial fibrillation and advanced liver fibrosis on treatment with vitamin K or non-vitamin K antagonists oral anticoagulants” (Pastori et al., 2018) [1].

The relationship between liver fibrosis and bleeding events in Af patients on anticoagulants Experimental features Liver fibrosis defined by FIB-4 score 4 3.25.

Data source location
Multicenter study. Patients were recruited from Sapienza University of Rome, Rome, Italy; University Magna Graecia of Catanzaro, Catanzaro, Italy; University of Florence, Florence, Italy.

Data accessibility
The data are accessible within the article Related research article "Incidence of bleeding in patients with atrial fibrillation and advanced liver fibrosis on treatment with vitamin K or non-vitamin K antagonist oral anticoagulants" (Pastori et al., 2018 in press) [1] Value of the data Data presented here provide information about the characteristics of patients treated with VKAs or NOACs.
Data here presented provide a detailed description of bleeding events according to the presence of liver fibrosis.
These data for the subgroup analysis on the different risk of CVEs in patients treated with VKAs or NOACs.

Data
The data presented include clinical and biochemical characteristics of atrial fibrillation (AF) patients treated with vitamin K (VKAs) or non-vitamin K antagonist oral anticoagulants (NOACs) ( Table 1). Table 2 reports characteristics of patients experiencing or not a bleeding event.
A detailed description of major and minor bleedings according to anticoagulant treatment (VKAs vs. NOACs) is reported in Table 3. Table 4 reports major bleedings according to the presence of LF (defined by a FIB-4 score 4 3.25) in the all cohort.
Survival analysis showed that in VKA-treated patients with high FIB-4, a higher incidence of cardiovascular events (CVEs) compared to those with normal FIB-4 (2.1% vs. 9.8%, log-rank test p ¼ 0.005) was found (Fig. 1). In the NOAC group, a similar rate of CVEs was observed between the two groups (5.8% vs 3.0% in patients with and without high FIB-4, log-rank test, p ¼ 0.279, Fig. 2).

Experimental design, materials, and methods
We performed a post-hoc analysis of a prospective multicentre observational cohort study including 2330 AF patients treated with VKAs (n ¼ 1297) or NOACs (n ¼ 1033). All patients treated with VKAs (warfarin or acenocoumarol) were locally monitored in specialized anticoagulation clinics for INR determination and VKA prescription. None of the patients measured INRs at home (i.e. with point of care devices) and time in therapeutic range (TTR) was used to assess the quality of anticoagulation according to the linear interpolation method described by Rosendaal et al. [2]. NOACs were   [3]. Exclusion criteria were: prosthetic heart valves, cardiac revascularization in the previous year, severe cognitive impairment, chronic autoimmune systemic diseases, and active cancer. Patients treated with antiplatelet drugs alone were also excluded. At baseline, information about personal medical history and concomitant medications were collected, and HAS-BLED (the labile INR was 0 (0%) 1 (0.04%) Decrease of Hb Z 2 gr/dl (n) 0 (0%) 23 (1.0%) Cerebral/Subdural (n) 12 (9.3%) 108 (4.9%) scored 0 in NOAC users). and CHA 2 DS 2 -VASc scores were calculated. Cardiovascular risk factors, such as arterial hypertension [4], type 2 diabetes mellitus [5] and heart failure [6] were defined according to international guidelines. Patients underwent routine laboratory analyses including AST (U/l), ALT (U/l), haemoglobin (g/dl) and platelet count (× 10 9 /L).  The presence of significant LF was assessed non-invasively by FIB-4 in all patients; FIB-4 was calculated according Sterling et al. by the formula: age (years) × AST (U/L)/PLT (10 9 /L) × ALT (U/L) 1/2 . A value of FIB-4 4 3.25 was set as cut-off for LF [7]. FIB-4 has been validated in different settings of CLD, such viral and metabolic liver disease [8,9].

Study primary endpoint
Bleeding events were classified according to the International Society on Thrombosis and Hemostasis (ISTH) [10]. Major bleeding was defined as fatal bleeding, symptomatic bleeding in a critical area or organ, i.e. intracranial, intraspinal, intraocular, retroperitoneal, intra-articular, pericardial or intramuscular with compartment syndrome; bleeding causing a fall in haemoglobin level of 2 g/dl or more or leading to transfusion of two or more units of whole blood or red blood cells. All cases of clinically relevant bleeding events that were not classified as major were considered as minor.

Study secondary endpoint
The secondary endpoint was a composite of CVEs including fatal/non-fatal myocardial infarction (MI) or ischemic stroke, cardiac revascularization (stent placement or coronary artery bypass graft), cardiovascular death, transient ischemic attack (TIA) and systemic embolism. Diagnosis of MI was made according to the third universal definition [11]. The occurrence of ischemic stroke was determined on clinical manifestations and confirmed by computed tomography or magnetic resonance; TIA was defined according to the Classification of Cerebrovascular Diseases III [12]. If a patient died within 4 weeks of myocardial infarction or ischemic stroke, these events were recorded as fatal myocardial infarction or ischemic stroke, respectively. Systemic embolism was defined as an acute occlusion of a vessel of an extremity or organ, documented by imaging, surgery, or autopsy findings. Death was classified as cardiovascular unless an unequivocal non-cardiovascular cause of death was identified. Cardiovascular death included sudden death, progressive congestive HF, and procedurerelated death.

Statistical analysis
Categorical variables were reported as counts (percentages). The normal distribution of parameters was assessed by Kolmogorov-Smirnov test. Continuous variables were expressed as mean 7 standard deviation, or median and interquartile range. Independence of categorical variables was tested with the χ 2 test. Student t test for unpaired samples was used to compare means.
The cumulative incidence of bleedings and CVEs were estimated using a Kaplan-Meier productlimit estimator. Survival curves were formally compared using the log-rank test. Cox proportional hazards analyses were used to calculate the adjusted relative hazard ratio (HR) by each clinical variable. Due to a significant difference in the length of follow-up, a separate survival analysis was performed according to the use of VKAs or NOACs, respectively. Covariates used as candidates for multivariable models included: low TTR ( o 70%, only for VKA patients), age, sex, current cigarette smoking, arterial hypertension, diabetes, high FIB-4 ( 4 3.25), previous cardiac events, previous cardiovascular events, heart failure, haemoglobin, antiplatelet drugs and statins. The final multivariable model was chosen through forward stepwise selection.
Statistical significance was set at a p value o 0.05. All tests were two-tailed and analyses were performed using computer software packages (SPSS-18.0, SPSS Inc.).

Transparency document. Supplementary material
Transparency document associated with this article can be found in the online version at http://dx. doi.org/10.1016/j.dib.2018.01.109.