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Background Serotonin reuptake inhibitor (SRI) antidepressants are implicated in increasing the risk of bleeding among users; however, the comparative increase in bleeding risk with concurrent antithrombotic therapy (anticoagulant or antiplatelet) remains unclear. As such, we performed a systematic review and meta-analysis of all available evidence to evaluate the effects of SRI and the risk of bleeding complications among patients receiving antithrombotic therapy. Methods We searched Medline, Embase, PubMed, PsycINFO, Cochrane Library, Web of Science, Scopus, CINAHL, and grey literature (Google Scholar and preprint reports) up to 26 November, 2020, with no language restrictions (updated on 31 July 2021). The primary outcome of interest was major bleeding. Secondary outcomes included intracranial haemorrhage, gastrointestinal bleeding, and any bleeding events. We used a random-effects model meta-analysis to estimate the odds ratios (ORs) and 95% confidence intervals (CIs). Results We did not identify any randomised studies but found 32 non-randomized studies (cohort or case–control) with 1,848,285 patients that fulfilled the study selection criteria and were included in the meta-analysis. Among individuals receiving anticoagulants (13 studies), SRI users experienced a statistically higher risk of major bleeding compared to non-SRI users: pooled OR was 1.39 (95% CI, 1.23–1.58; p

Background Hypertension is characterised by a high prevalence, low awareness and poor control among rheumatoid arthritis (RA) patients. Correct blood pressure (BP) measurement is highly important in these subjects. The “unattended” BP measurement aims to reduce the “white-coat effect,” a phenomenon associated with cardiovascular risk. Data on “unattended” BP measurement in RA and its impact on hypertensive organ damage are very limited. Methods BP was measured in the same patient both traditionally (“attended” BP) and by the “unattended” protocol (3 automated office BP measurements, at 1-min intervals, after 5 min of rest, with patient left alone) by a randomised cross-over design. Patients underwent clinical examination, 12-lead electrocardiography and trans-thoracic echocardiography to evaluate cardiac damage. Results Sixty-two RA patients (mean age 67 ± 9 years, 87% women) were enrolled. Hypertension was diagnosed in 79% and 66% of patients according to ACC/AHA and ESC/ESH criteria, respectively. Concordance correlation coefficients between the two techniques were 0.55 (95%, CI 0.38–0.68) for systolic BP and 0.73 (95%, CI 0.60–0.82) for diastolic BP. “Unattended” (121.7/68.6 mmHg) was lower than “attended” BP (130.5/72.8 mmHg) for systolic and diastolic BP (both p

Atherosclerosis is one of the leading causes of mortality and morbidity worldwide. Chemokines and their receptors are implicated in the pathogenesis of atherosclerosis. CXCL12 is a member of the chemokine family exerting a myriad role in atherosclerosis through its classical CXCR4 and atypical ACKR3 (CXCR7) receptors. The modulatory and regulatory functional spectrum of CXCL12/CXCR4/ACKR3 axis in atherosclerosis spans from proatherogenic, prothrombotic and proinflammatory to atheroprotective, plaque stabilizer and dyslipidemia rectifier. This diverse continuum is executed in a wide range of biological units including endothelial cells (ECs), progenitor cells, macrophages, monocytes, platelets, lymphocytes, neutrophils and vascular smooth muscle cells (VSMCs) through complex heterogeneous and homogenous coupling of CXCR4 and ACKR3 receptors, employing different downstream signalling pathways, which often cross-talk among themselves and with other signalling interactomes. Hence, a better understanding of this structural and functional heterogeneity and complex phenomenon involving CXCL12/CXCR4/ACKR3 axis in atherosclerosis would not only help in formulation of novel therapeutics, but also in elucidation of the CXCL12 ligand and its receptors, as possible diagnostic and prognostic biomarkers.Key messagesThe role of CXCL12 per se is proatherogenic in atherosclerosis development and progression.The CXCL12 receptors, CXCR4 and ACKR3 perform both proatherogenic and athero-protective functions in various cell typesDue to functional heterogeneity and cross talk of CXCR4 and ACKR3 at receptor level and downstream pathways, regional boosting with specific temporal and spatial modulators of CXCL12, CXCR4 and ACKR3 need to be explored.

Background and aim: Since the relation between Helicobacter pylori (H. pylori) and atherosclerosis has been evidenced, we aimed to analyze whether there is a relationship between the patient's H. pylori infection and age, gender, BMI, blood lipids, and carotid plaque formation. Methods: 810 patients from January 2016 to December 2019 were enrolled in this study, and divided the subjects into H. pylori (+) group and H. pylori (-) group based on the results of UBT. To analyze whether H. pylori infection is related to gender, age, BMI, blood lipids, and neck vascular plaque formation. Results: The single-factor analysis showed that the BMI ≥ 25kg/m2, triglycerides >1.7 mmol/l, the formation of cervical plaques were significantly higher in patients infected with H. pylori in compared to normal cases. Also, multi-variant logistic regression analysis showed that H. pylori infection affects the BMI ≥ 25kg/m2 and triglycerides >1.7 mmol/l to induce vascular plaque. Also, we showed that patients with H. pylori infection are 1.424 times higher than the non-infected group to have triglycerides more elevated than 1.7mmol/l. Conclusion: In this study, we conclude that H. pylori infection is an independent risk factor for higher BMI (>25), triglyceride (>1.7 mmol/l), and neck vascular plaque formation. The multi-variant analysis showed that patients with H. pylori infection are prone to have higher BMI, triglycerides, and neck vascular plaque formation over 1.4-times higher in non-infected individuals.KEY MESSAGESH. pylori infection is an independent risk factor for higher BMI, triglyceride, and neck vascular plaque formation.H. pylori can accelerate vascular plaque formation through increasing BMI and triglyceride.

Objective Ventricular arrhythmias (VAs) are a common complication of chronic ischaemic heart failure (CIHF). The purpose of this study is to investigate the efficacy of pinocembrin in a rat model of VAs induced by CIHF and further examine the possible mechanism. Methods Rats were subjected to ligation of left anterior descending coronary artery to mimic CIHF and then received pinocembrin treatment daily for 2 months. The vivo electrophysiology were performed to determine the effect of pinocembrin on ventricular electrical activity. The expression of Cav1.2, Kv4.2, and NGF was determined by Western blot. The structural change of ventricle was tested by the Echocardiography, Masson staining, and HE staining. The effect of pinocembrin on sympathetic nerve-related markers was detected by the immunostaining and the ELISA was used to test for biomarkers associated with heart failure. Results Pinocembrin increased the expression of ion channel protein Cav1.2 and Kv4.3, ameliorated the shortening of action potential duration (APD) and reduced the incidence and duration of ventricular fibrillation (VF). Pinocembrin also reduced the expression of nerve growth factor (NGF) and improved the autonomic nerve remodelling. In addition, pinocembrin reduced the area of infarct area and myocardial fibrosis, accompanied by increasing the expression of connexin protein 43 (CX43). Conclusion We demonstrate that pinocembrin reduces cardiac nerve remodelling and protects against Vas induced by CIHF. The findings suggest that pinocembrin can be a promising candidate for the treatment of VAs.

Atrial fibrillation (AF) is one of the main cardiac arrhythmias associated with higher risk of cardiovascular morbidity and mortality. AF can cause adverse symptoms and reduced quality of life. One of the strategies for the management of AF is rate control, which can modulate ventricle rate, alleviate adverse associated symptoms and improve the quality of life. As primary management of AF through rate control or rhythm is a topic under debate, the purpose of this review is to explore the rationale for the rate control approach in managing AF by considering the guidelines, recommendations and determinants for the choice of rate control drugs, including beta blockers, digoxin and non- dihydropyridine calcium channel blockers for patients with AF and other comorbidities and atrioventricular nodal ablation and pacing. Despite the limitations of rate control treatment, which may not be effective in preventing disease progression or in reducing symptoms in highly symptomatic patients, it is widely used for almost all patients with atrial fibrillation. Although rate control is one of the first line management of all patient with atrial fibrillation, several issues remain debateable.

Introduction Non-ischaemic heart disease (NIHD) is the underlying pathology in∼20% of all sudden cardiac deaths (SCDs). Heavy drinking is known to be associated with SCD due to ischaemic heart disease, but studies on association of recent alcohol consumption and SCD in patients with NIHD are scarce. We evaluated the blood alcohol levels of autopsy verified non-ischaemic SCD victims. Methods Study population was derived from the Finnish Genetic Study of Arrhythmic Events (Fingesture) (n = 5869, mean age 65 ± 12, 79% males). All deaths occurred in Northern Finland during 1998–2017. All victims underwent a medico-legal autopsy. Subjects of SCD due to ischaemic heart disease were excluded. Results A total of 1301 (mean age 57 ± 12, 78% males) victims of SCD due to NIHD were included in the study. The blood ethanol level was elevated in 543 (42%) subjects, out of which the blood alcohol level was ≥0.10%in 339 (62%) subjects and ≥0.15%in 252 (46%) subjects. Male SCD victims had alcohol in blood more frequently compared to females (45% versus 31%, p

Heart failure with preserved ejection fraction (HFpEF) might soon become the most prevalent type of acute heart failure. Still, despite more than 30 years of research on HFpEF, not only do we lack specific treatment, but also a generally accepted definition of HFpEF. Since 2016, several definitions and algorithms have been proposed for diagnosing both diastolic dysfunction and overt HFpEF. However, all of them focus exclusively on chronic (and not acute) HFpEF. Recent studies showed that acute HFpEF may be overdiagnosed in patients presenting with acute dyspnoea. The aim of our article was to address two questions: (1) why there is a need for specific diagnostic criteria for acute HFpEF, and (2) what such definition of acute HFpEF should encompass.KEY MESSAGES:Several scores and algorithms have been proposed for diagnosing chronic heart failure with preserved ejection fraction (HFpEF), however, so far, there is no definition of acute HFpEF.Acute HFpEF seems to be overdiagnosed in patients presenting with acute dyspnoea.Definition of acute HFpEF should comprise both (1) features of chronic HFpEF and (2) markers of increased left ventricular filling pressures and/or of pulmonary congestion.

Aims: To evaluate risk factors for major adverse cardiac event (MACE) after the first acute coronary syndrome (ACS) and to examine the prevalence of risk factors in post-ACS patients. Methods: We used Finnish population-based myocardial infarction register, FINAMI, data from years 1993–2011 to identify survivors of first ACS (n = 12686), who were then followed up for recurrent events and all-cause mortality for three years. Finnish FINRISK risk factor surveys were used to determine the prevalence of risk factors (smoking, hyperlipidaemia, diabetes and blood pressure) in post-ACS patients (n = 199). Results: Of the first ACS survivors, 48.4% had MACE within three years of their primary event, 17.0% were fatal. Diabetes (p = 4.4 × 10−7), heart failure (HF) during the first ACS attack hospitalization (p = 6.8 × 10−15), higher Charlson index (p = 1.56 × 10−19) and older age (p = .026) were associated with elevated risk for MACE in the three-year follow-up, and revascularization (p = .0036) was associated with reduced risk. Risk factor analyses showed that 23% of ACS survivors continued smoking and cholesterol levels were still high (>5mmol/l) in 24% although 86% of the patients were taking lipid lowering medication. Conclusion: Diabetes, higher Charlson index and HF are the most important risk factors of MACE after the first ACS. Cardiovascular risk factor levels were still high among survivors of first ACS.

Purpose Epicardial fat thickness is an interesting parameter of early atherosclerosis. We prospectively assessed whether weight loss following laparoscopic sleeve gastrectomy (LSG) leads to a significant reduction in the epicardial fat thickness (EFT) and the correlation between the decline in the epicardial fat thickness with other clinical parameters. Methods A prospective analysis of 98 cases that were scheduled to undergo LSG and followed up for 12 months was conducted. EFT was assessed using two-dimensional (2 D) echocardiography. Results A total of 98 cases and 70 controls were enrolled. EFT demonstrated a significant reduction at follow-up in the whole group (median 8.9 (1.95) versus 7.65 (1.67) mm, respectively). The degree of reduction was higher in the LSG cohort compared to control cohort 1.3 (0.4) versus 1 (0.4), respectively; p

Background Low triiodothyronine syndrome (LT3S), frequently seen in patients with acute myocardial infarction (AMI), has been regarded as a predictor of poor outcomes after AMI. However, little is known about the prognostic value of LT3S in euthyroid patients with myocardial infarction with nonobstructive coronary arteries (MINOCA). Methods A total of 1162 MINOCA patients were enrolled and divided into LT3S and no-LT3S groups. LT3S was defined as decreased free T3 (fT3

Aims Rhythm control using electrical cardioversion (CV) is a common treatment strategy for patients with symptomatic atrial fibrillation (AF). To guide clinical decision making, we sought to assess if electrocardiographic interatrial blocks could predict CV failure or AF recurrence as the phenomenon is strongly associated with atrial arrhythmias. Methods This study included 715 patients who underwent a CV for persistent AF lasting >48 h. P-wave duration and morphology were analyzed in post-procedure or the most recent sinus rhythm electrocardiograms and compared with rates of CV failure and AF recurrence within 30 days after CV as well as their combination (ineffective CV). Results CV was unsuccessful in 63 out of 715 patients (8.8%) and AF recurred in 209 out of 652 (29.2%) patients within 30 days after CV. Overall, 272 (38.0%) CVs turned out ineffective. Advanced interatrial block (AIAB) defined as P-wave duration ≥120 ms and biphasic morphology in inferior leads (II, III and aVF) was diagnosed in 72 (10.1%) cases. AIAB was an independent predictor for CV failure (OR 4.51, 95%CI 1.76–11.56, p = .002), AF recurrence (OR 2.93, 95%CI 1.43–5.99, p = .003) and ineffective CV (OR 3.87, 95%CI 2.04–7.36, p

The liver fat score (LFS) has been proposed to be a simple non-invasive marker of non-alcoholic fatty liver disease (NAFLD), which is highly prevalent in the general population. We tested its association with cardiovascular diseases (CVDs) and prognosis. 17,244 adult participants from the National Health and Nutrition Examination Survey 1999–2016 were included. LFS is calculated from variables including serum aspartate transaminase/alanine transaminase (AST/ALT) ratio, fasting serum aspartate transaminase (AST) level, fasting serum insulin level, presence of metabolic syndrome and diabetes mellitus. In cross-sectional analysis, logistic regression was used to examine the association of the LFS with coronary heart disease (CHD), myocardial infarction (MI), congestive heart failure (CHF), stroke and angina pectoris. Mortality during follow-up was analysed using Cox proportional hazard regression. LFS was associated with CHD (adjusted odds ratio [OR]: 1.09 per standard deviation [SD], 95% confidence interval [95% CI]: 1.03–1.15) (p = .003), CHF (1.11, 1.04–1.18) (p = .003) and angina pectoris (1.08, 1.02–1.13) (p = .005). LFS was not associated with MI or stroke, but was associated with increased all-cause and cardiovascular mortality with hazard ratios (HRs) of 1.10 (95% CI: 1.07–1.13) (p < .001) and 1.12 (95% CI: 1.06–1.17) (p < .001), respectively. NAFLD is usually asymptomatic, but this large study of a large general population shows that LFS is associated with CHD, CHF, angina pectoris, cardiovascular and all-cause mortality. Determining the LFS is worthwhile, as it identifies people with NAFLD, who may also be at increased cardiovascular risk.Key MessagesLiver fat score (LFS), a non-invasive marker of non-alcoholic fatty liver disease (NAFLD), is associated with coronary heart disease (CHD), congestive heart failure (CHF) and angina.LFS is also associated with increased cardiovascular and all-cause mortality.Determining the LFS is worthwhile as it identifies people with NAFLD as well as increased cardiovascular risk. Liver fat score (LFS), a non-invasive marker of non-alcoholic fatty liver disease (NAFLD), is associated with coronary heart disease (CHD), congestive heart failure (CHF) and angina. LFS is also associated with increased cardiovascular and all-cause mortality. Determining the LFS is worthwhile as it identifies people with NAFLD as well as increased cardiovascular risk.

Introduction Little is known about the relationship between arterial stiffness and cardiovascular target organ damage (TOD) in the general population. The aim was to analyse the relationship between different measurements of arterial stiffness and TOD, in a general Spanish population without a history of cardiovascular event. Materials and methods Transversal descriptive study. Through stratified random sampling, a total of 501 individuals were included. Carotid-femoral pulse wave velocity (cf-PWV) was measured using a SphygmoCor System®, the cardio-ankle vascular index (CAVI) was determined with aVasera VS-1500® and brachial-ankle pulse wave velocity (ba-PWV)was calculated through a validated equation. Results The average age was 55.84 ± 14.26.The percentage of vascular TOD, left ventricular hypertrophy (LVH) and renal TOD was higher in men (p

Background Oscillometric pulse wave velocity (o-PWV) represents an attractive, non invasive and non operator-dependent method to estimate arterial stiffness. Tonometric carotid-femoral measurements (cf-PWV),are considered the gold-standard for non-invasive aortic stiffness assessment. To date, no studies in the general population comparing the two methods have been performed. Methods and Results 1162 subjects were analysed. O-PWV and cf-PWV showed a mean difference of −0.31 m/sec(p ≤ 0.001). No significant differences between cf-PWV and o-PWVs were observed in patients without cardiovascular risk factors. The Bland and Altman analysis showed a moderate agreement between 24 h-o-PWV and cf-PWV (mean difference −0.99, LoA 4.23 to −6.22m/s). O-PWVs underestimate and overestimate arterial stiffness under and over 50 years respectively(p ≤ 0.001). Systolic blood pressure (SBP) and age differently impact cf-PWV and in office o-PWV variability (r2 0.35 and 0.88 respectively). In younger subjects a strong relationship between o-PWV and SBP reducing as age increases was found. Analysing the impact of age, an opposite trend was noticed. Conclusions Oscillometric PWV estimates provide reliable values in the general population. An o-PWV tendency to underestimate arterial stiffness in younger subjects and in subjects with diseases known to increase arterial stiffness and to overestimate it with increasing age was found, even if scarcely relevant in clinical perspective. Overall the present findings underline an acceptable and satisfactory agreement between oscillometric and tonometric methods for the PWV assessment.KEY MESSAGESOscillometric and tonometric PWV estimates showed a good and satisfactory agreement in the general population, above all in subjects without cardiovascular risk factors or a documented vascular damage.In comparison with tonometric values, oscillometric PWV estimates showed, however, the tendency to underestimate arterial stiffness in younger subjects and to overestimate it with increasing age, while diverging when diseases known to increase arterial stiffness are present.The magnitude of differences in PWV estimates between tonometric and oscillometric methods found in the general population appears most likely not to be significant in everyday clinical practice.

Aims The objective was to evaluate the clinical characteristics, management and two-year outcomes of patients with newly diagnosed non-valvular atrial fibrillation at risk for stroke in Nordic countries. Methods We examined the baseline characteristics, antithrombotic treatment, and two-year clinical outcomes of patients from four Nordic countries. Results A total of 52,080 patients were enrolled in the GARFIELD-AF. Out of 29,908 European patients, 2,396 were recruited from Nordic countries. The use of oral anticoagulants, alone or in combination with antiplatelet (AP), was higher in Nordic patients in all CHA2DS2-VASc categories: 0–1 (72.8% vs 60.3%), 2–3 (78.7% vs 72.9%) and ≥4 (79.2% vs 74.1%). In Nordic patients, NOAC ± AP was more frequently prescribed (32.0% vs 27.7%) and AP monotherapy was less often prescribed (10.4% vs 18.2%) when compared with Non-Nordic European patients. The rates (per 100 patient years) of all-cause mortality and non-haemorrhagic stroke/systemic embolism (SE) were similar in Nordic and Non-Nordic European patients [3.63 (3.11–4.23) vs 4.08 (3.91–4.26), p value = .147] and [0.98 (0.73–1.32) vs 1.02 (0.93–1.11), p value = .819], while major bleeding was significantly higher [1.66 (1.32–2.09) vs 1.01 (0.93–1.10), p value

Purpose The aim of this study is to investigate the prevention and treatment patterns of deep vein thrombosis (DVT) in critically ill patients and to explore the risk factors for DVT in people from Zhejiang Province, China. Materials and methods This study prospectively enrolled patients admitted in intensive care units (ICUs) of 54 hospitals from 09/16/2019 to 01/16/2020. The risk of developing DVT and subsequent prophylaxis was evaluated. The primary outcome was DVT occurrence during ICU hospitalisation. Univariate and multivariate logistic regression were performed to determine the risk factors for DVT. Results A total of 940 patients were included in the study. Among 847 patients who received prophylaxis, 635 (75.0%) patients received physical prophylaxis and 199 (23.5%) patients received drug prophylaxis. Fifty-eight (6.2%) patients were diagnosed with DVT after admission to the ICU, and 36 patients were treated with anticoagulants (all patients received low molecular weight heparin [LMWH]). D-dimer levels (OR = 1.256, 95% CI: 1.132–1.990), basic prophylaxis (OR = 0.092, 95% CI: 0.016–0.536), and physical prophylaxis (OR = 0.159, 95% CI: 0.038–0.674) were independently associated with DVT in ICU patients. The short-term survival was similar between DVT and non-DVT patients. Conclusions DVT prophylaxis is widely performed in ICU patients. Prophylaxis is an independent protective factor for DVT occurrence. The most common treatment of DVT patients is LMWH, although it might increase the rate of bleeding.Key messagesThis is the only multicenter and prospective study of DVT in ICUs in China.d-dimer levels were independently associated with DVT in ICU patients.Prophylaxis was an independent protective factor for DVT occurrence in ICU.

Introduction Type II diabetes mellitus (DM) is a proinflammatory process and a known risk factor for major adverse cardiac events (MACE). The same inflammatory markers may be present in prediabetes (pDM); however, the relationship between pDM by HbA1c and MACE is not well studied. We sought to see if pDM increases one’s risk for MACE. Methods We retrospectively studied patients at Beaumont Health, Michigan between 2006 and 2020. We divided patients into groups (G1–G5) based on haemoglobin A1c (HbA1c) trends over the study period as follows: G1: pDM patients who remained pDM; G2: pDM who progressed into DM; G3: pDM who normalized their HbA1c; G4: patients who maintained a normal HbA1c; and G5: patients with HbA1c persistently in the DM range. We compared MACE between the groups by univariate and multivariate regression analyses. Results A total of 119,271 patients were included in the study (G1: N = 13,520, G2: N = 6314, G3: N = 1585, G4: N = 15,018, G5: N = 82,834). Pairwise comparison revealed a statistically significant increase in the odds of MACE in all groups compared to those with normal HbA1c values (G4; p

Purposes There is increasing concern regarding cardiovascular risk in non-alcoholic fatty liver disease (NAFLD) patients with liver fibrosis. This study aims: (1) to assess the association between NAFLD and liver fibrosis status and the development of carotid plaque (CP), and (2) to identify CP risk factors among general population with different baseline NAFLD and liver fibrosis status. Methods This retrospective cohort study included 14,288 adult participants who went for regular health check-ups between 2014 and 2019, in one hospital in Zhejiang, China. NAFLD was diagnosed by abdominal ultrasound and the NAFLD fibrosis score (NFS) was calculated to reflect the extent of liver fibrosis. Cox proportional hazards analyses were applied to assess the risk of CP development across groups with different baseline NAFLD and NFS status. Results NAFLD participants with high NFS had higher risk of CP compared to non-NAFLD participants (adjusted hazard ratio 1.68, 95% confidence interval [CI] 1.43–1.96, p

Background: Exosomes-encapsulated microRNAs (miRNAs) have been established to be implicated in the pathogenesis of different diseases. Nevertheless, circulating exosomal miRNAs of thromboangiitis obliterans (TAO) remains poorly understood. This study aimed to explore the effects of exosomal miRNAs associated with TAO on human vascular smooth muscle cells (HVSMCs). Methods: The exosomes were isolated from the plasma of TAO patients and normal controls and then were sent for small RNA sequencing. Differentially expressed miRNAs (DE-miRNAs) were identified by bioinformatics analysis and were confirmed by RT-qPCR. After that, PKH67 staining was used to label exosomes and co-cultured with HVSMCs. Cell viability and apoptosis were, respectively, tested by CCK-8 assay and flow cytometry. Finally, dual-luciferase reporter assay was used to confirm the downstream targets of miR-223-5p. Results: A total of 39 DE-miRNAs were identified between TAO patients and normal controls, of which, miR-223-5p was one of the most significantly up-regulated miRNAs. TAO plasma-derived exosomes or miR-223-5p mimics inhibited cell viability of HVSMCs and promoted cell apoptosis. The pro-apoptotic effect of TAO plasma-derived exosomes was alleviated by miR-223-5p inhibitor. Additionally, the expressions of VCAM1 and IGF1R were down-regulated by exosomes and miR-223-5p mimics, and were abrogated by miR-223-5p inhibitor. Dual-luciferase report showed that VCAM1 was the target of miR-223-5p. Conclusions: Our findings imply that circulating exosomal miR-223-5p may play an essential role in the pathogenesis of TAO, and provide a basis for miR-6515-5p/VCAM1 as novel therapeutic targets and pathways for TAO treatment.

Background We carried out this study to demonstrate the effects of outcome sensitivity, participant exclusions, and covariate manipulations on results of the epidemiological analysis of coronary heart disease (CHD) and its behaviour-related risk factors. Material and methods Our study population consisted of 1592 54-year-old men, who participated in the Kuopio Ischaemic Heart Disease Risk Factor (KIHD) Study. We used the Cox proportional-hazards model to predict the hazard of CHD and applied different sets of outcomes concerning outcome sensitivity and data preprocessing procedures regarding participant exclusions and covariate manipulations. Results The mean follow-up time was 23 years, and 730 men received the CHD diagnosis. Cox regressions based on data with no participant exclusions most often discovered statistically significant associations. Loose inclusion criteria for study participants with any CVD during the follow-up and strict exclusion criteria for participants with no CVD were best in discovering the associations between risk factors and CHD. Outcome sensitivity affected the associations, whereas the covariate type, continuous or categorical, did not. Conclusions This study suggests that excluding study participants who are not disease-free at baseline is probably unnecessary for epidemiological analyses. Epidemiological research reports should present results based on no data exclusions together with results based on reasoned exclusions.

Background Conflicting data suggest that statins could cause chronic liver disease in certain group of patients, while improving prognosis in those with chronic viral hepatitis (CVH). Purpose To quantify the potential protective role of statins on some main liver-related health outcomes in clinical studies on CVH patients. Data Sources: The search strategy was explored by a medical librarian using bibliographic databases, from January 2015 to April 2020. Data synthesis: The results showed no significant difference in the risk of mortality between statin users and non-users in the overall analysis. However, the risk of mortality significantly reduced by 39% in statin users who were followed for more than three years. Moreover, the risk of HCC, fibrosis, and cirrhosis in those on statins decreased by 53%, 45% and 41%, respectively. Although ALT and AST reduced slightly following statin therapy, this reduction was not statistically significant. Limitations A significant heterogeneity among studies was observed, resulting from differences in clinical characteristics between statin users and non-users, study designs, population samples, diseases stage, comorbidities, and confounding covariates. Conclusion Not only long-term treatment with statins seems to be safe in patients affected by hepatitis, but also it significantly improves their prognosis.

Aim: This study examines epidemiological trends of acute myocardial infarction (AMI) in Germany from 2004–2015 across different age groups, using data of the population-based KORA myocardial infarction registry. Methods: Annual age-standardised, age-group- and sex-specific mortality and event rates (incident and recurrent) per 100,000 population as well as 28-day case fatality were calculated from all registered cases of AMI and coronary heart disease deaths in 25–74-year-olds from 2004–2015 and 75–84-year-olds from 2009–2015. Average annual percentage changes (AAPC) were calculated by joinpoint regression. Results: Mortality rates declined considerably among the elderly (75–84 years), in men by –6.0% annually, due to declines of case fatality by –3.0% and incidence rate by 3.4% and in women by –10.0%, driven by declines in incidence (–9.1%) and recurrence rate (–4.9%). Significant mortality declines also occurred in males, 65–74 years of age (AAPC –3.8%). Among the age groups 25–54 years and 55–64 years, there was no substantial decline in mortality, event rates or case fatality except for a decline of incidence rate in 55–64-year-old men (AAPC –1.8%). Conclusion: Inhomogeneous AMI trends across age-groups indicate progress in prevention and treatment for the population >64 years, while among

To study the long-term outcome differences between acute myocardial infarction (MI) and stable coronary artery disease (CAD) patients treated with coronary artery bypass grafting (CABG). We studied retrospectively patients with MI (n = 1882) or stable CAD (n = 13117) treated with isolated CABG between 2004 and 2014. Inverse propensity probability weight adjustment for baseline features was used. Median follow-up was 7.9 years. In-hospital mortality (8.6% vs. 1.6%; OR 5.94; p < .0001) and re-sternotomy (5.5% vs. 2.7%; OR 2.07; p < .0001) were more common in MI patients compared to stable CAD patients. Hospital surviving MI patients had higher all-cause mortality (28.2% vs. 22.2%; HR 1.37; p = .002) and MACE rate (34.4% vs. 27.4%; HR 1.22; CI 1.00–1.50; p = .049) at 10-year follow-up. Cardiovascular mortality (15.9% vs. 12.7%; HR 1.36; p = .017) and rate of new myocardial infarction (12.0% vs. 9.8%; HR 1.40; p = .034) were also higher in MI patients during follow-up. In follow-up of stabilized first-year survivors, the difference in all-cause (26.5% vs. 20.7%; HR 1.40; p = .003) and cardiovascular (14.2% vs. 11.4%; HR 1.37; p = .027) mortality continued to increase between MI and stable CAD patients. MI patients have poorer short- and long-term outcomes compared to stable CAD patients after CABG and risk difference continues to increase with time.Key MessagesPatients with myocardial infarction have poorer short- and long-term outcomes compared to stable coronary artery disease patients after coronary artery bypass grafting (CABG).Higher risk of death continues also in stabilized first-year myocardial infarct survivors.The importance of efficient secondary prevention and follow-up highlights in post-myocardial infarct population after CABG. Patients with myocardial infarction have poorer short- and long-term outcomes compared to stable coronary artery disease patients after coronary artery bypass grafting (CABG). Higher risk of death continues also in stabilized first-year myocardial infarct survivors. The importance of efficient secondary prevention and follow-up highlights in post-myocardial infarct population after CABG.