P5341Predictive factors of atherosclerotic cardiovascular diseases events in HIV-HVC co-infected patients: results from hepavih ANRS co13 cohort

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
F Boccara ◽  
B K Tan ◽  
M Chalouni ◽  
D Salmon Ceron ◽  
A Cinaud ◽  
...  

Abstract Introduction Several studies highlighted an increased risk of cardiovascular disease (CVD) in HIV-HCV co-infected patients without clearly identifying specific virologic factors associated with atherosclerotic CVD (ASCVD) events. Purpose Hence, we analyzed data collection from the French nationwide ANRS CO13 HEPAVIH cohort to determine the incidence of ASCVD events in HIV-HCV co-infected patients and the predictive factors associated with its occurrence. Methods The French multicenter nationwide ANRS CO13 HEPAVIH clinic-based cohort collected prospective clinical and biological data from HIV-HCV co-infected patients followed-up in 28 different university hospitals between December 2005 to November 2016. Participants with at least one year of follow-up were included. Primary outcome was the occurrence of major ASCVD events (cardiovascular death, acute coronary syndrome, coronary revascularization and stroke). Secondary outcomes were total ASCVD events including major ASCVD events and minor ASCVD events (peripheral arterial disease [PAD]). Incidence rates were estimated using Aalen-Johansen method and factors associated with ASCVD identified with Cox proportional hazards models. Results A total of 1213 patients were included: median age 45.4 years [42.1–49.0], 70.3% men, current smoking 70.2%, overweight 19.5%, liver cirrhosis 18.9%, chronic alcohol consumption 7.8%, diabetes mellitus (5.9%), personal history of CVD 2.7%, and statins use 4.1%. After a median follow-up of 5.1 years [3.9–7.0], 44 participants experienced at least one ASCVD event (26 major ASCVD event, and 20 a minor event). Incidences for total, major and minor ASCVD events were of 6.98 [5.19; 9.38], 4.01 [2.78; 6.00], and 3.17 [2.05; 4.92] per 1000 person-years, respectively. Personal history of CVD (Hazard Ratio (HR)=13.94 [4.25–45.66]), high total cholesterol (HR=1.63 [1.24–2.15]), low HDL cholesterol (HR=0.08 [0.02–0.34]) and undetectable HIV viral load (HR=0.41 [0.18–0.96]) were identified as independent factors associated with major ASCVD events while cirrhosis status, liver fibrosis and HCV sustained viral response were not. Cumulative incidence of CV events Conclusion HIV-HCV co-infected patients experience a high incidence of ASCVD events both coronary and peripheral artery diseases. Traditional CV risk factors are the main determinants of ASCVD whereas undetectable HIV viral load seems to be protective. Management of cholesterol abnormalities and controlling viral load are essential to modify this high cardiovascular risk. Acknowledgement/Funding Agence Natoinale de Recherche sur le SIDA et les Hépatites virales

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Anita Mesic ◽  
Alexander Spina ◽  
Htay Thet Mar ◽  
Phone Thit ◽  
Tom Decroo ◽  
...  

Abstract Background Progress toward the global target for 95% virological suppression among those on antiretroviral treatment (ART) is still suboptimal. We describe the viral load (VL) cascade, the incidence of virological failure and associated risk factors among people living with HIV receiving first-line ART in an HIV cohort in Myanmar treated by the Médecins Sans Frontières in collaboration with the Ministry of Health and Sports Myanmar. Methods We conducted a retrospective cohort study, including adult patients with at least one HIV viral load test result and having received of at least 6 months’ standard first-line ART. The incidence rate of virological failure (HIV viral load ≥ 1000 copies/mL) was calculated. Multivariable Cox’s regression was performed to identify risk factors for virological failure. Results We included 25,260 patients with a median age of 33.1 years (interquartile range, IQR 28.0–39.1) and a median observation time of 5.4 years (IQR 3.7–7.9). Virological failure was documented in 3,579 (14.2%) participants, resulting in an overall incidence rate for failure of 2.5 per 100 person-years of follow-up. Among those who had a follow-up viral load result, 1,258 (57.1%) had confirmed virological failure, of which 836 (66.5%) were switched to second-line treatment. An increased hazard for failure was associated with age ≤ 19 years (adjusted hazard ratio, aHR 1.51; 95% confidence intervals, CI 1.20–1.89; p < 0.001), baseline tuberculosis (aHR 1.39; 95% CI 1.14–1.49; p < 0.001), a history of low-level viremia (aHR 1.60; 95% CI 1.42–1.81; p < 0.001), or a history of loss-to-follow-up (aHR 1.24; 95% CI 1.41–1.52; p = 0.041) and being on the same regimen (aHR 1.37; 95% CI 1.07–1.76; p < 0.001). Cumulative appointment delay was not significantly associated with failure after controlling for covariates. Conclusions VL monitoring is an important tool to improve programme outcomes, however limited coverage of VL testing and acting on test results hampers its full potential. In our cohort children and adolescents, PLHIV with history of loss-to-follow-up or those with low-viremia are at the highest risk of virological failure and might require more frequent virological monitoring than is currently recommended.


Author(s):  
Boun Kim Tan ◽  
Mathieu Chalouni ◽  
Dominique Salmon Ceron ◽  
Alexandre Cinaud ◽  
Laure Esterle ◽  
...  

Abstract Background An increased risk of cardiovascular disease (CVD) was reported in patients coinfected with human immunodeficiency virus (HIV) and hepatitis C virus (HCV), without identifying factors associated with atherosclerotic CVD (ASCVD) events. Methods HIV–HCV coinfected patients were enrolled in the ANRS CO13 HEPAVIH nationwide cohort. Primary outcome was total ASCVD events. Secondary outcomes were coronary and/or cerebral ASCVD events, and peripheral artery disease (PAD) ASCVD events. Incidences were estimated using the Aalen-Johansen method. Factors associated with ASCVD were identified using cause-specific Cox proportional hazards models. Results At baseline, median age of the study population (n=1213) was 45.4 (interquartile range [IQR] 42.1−49.0) years and 70.3% were men. After a median follow-up of 5.1 (IQR 3.9−7.0) years, the incidence was 6.98 (95% confidence interval [CI] 5.19−9.38) per 1000 person-years for total ASCVD events, 4.01 (2.78−6.00) for coronary and/or cerebral events, and 3.17 (2.05−4.92) for PAD ASCVD events. Aging (hazard ratio [HR] 1.06, 95% CI 1.01−1.12), prior CVD (HR 8.48, 95% CI 3.14−22.91), high total cholesterol (HR 1.43, 95% CI 1.11−1.83), high-density lipoprotein cholesterol (HR 0.22, 95% CI 0.08−0.63), statin use (HR 3.31, 95% CI 1.31−8.38), and high alcohol intake (HR 3.18, 95% CI 1.35−7.52) were independently associated with total ASCVD events, while undetectable baseline viral load (HR 0.41, 95%CI 0.18−0.96) with coronary and/or cerebral events. Conclusion HIV–HCV coinfected patients experienced a high incidence of ASCVD events. Some traditional cardiovascular risk factors were the main determinants of ASCVD. Controlling cholesterol abnormalities and maintaining undetectable HIV viral load are essential to control cardiovascular risk.


2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Jialun Zhou ◽  
Junko Tanuma ◽  
Romanee Chaiwarith ◽  
Christopher K. C. Lee ◽  
Matthew G. Law ◽  
...  

This study examined characteristics of HIV-infected patients in the TREAT Asia HIV Observational Database who were lost to follow-up (LTFU) from treatment and care. Time from last clinic visit to 31 March 2009 was analysed to determine the interval that best classified LTFU. Patients defined as LTFU were then categorised into permanently LTFU (never returned) and temporary LTFU (re-entered later), and these groups compared. A total of 3626 patients were included (71% male). No clinic visits for 180 days was the best-performing LTFU definition (sensitivity 90.6%, specificity 92.3%). During 7697 person-years of follow-up, 1648 episodes of LFTU were recorded (21.4 per 100-person-years). Patients LFTU were younger (P=0.002), had HIV viral load ≥500 copies/mL or missing (P=0.021), had shorter history of HIV infection (P=0.048), and received no, single- or double-antiretroviral therapy, or a triple-drug regimen containing a protease inhibitor (P<0.001). 48% of patients LTFU never returned. These patients were more likely to have low or missing haemoglobin (P<0.001), missing recent HIV viral load (P<0.001), negative hepatitis C test (P=0.025), and previous temporary LTFU episodes (P<0.001). Our analyses suggest that patients not seen at a clinic for 180 days are at high risk of permanent LTFU, and should be aggressively traced.


2019 ◽  
Vol 40 (44) ◽  
pp. 3641-3648 ◽  
Author(s):  
Bhupendar Tayal ◽  
Patricia Fruelund ◽  
Peter Sogaard ◽  
Sam Riahi ◽  
Christoffer Polcwiartek ◽  
...  

Abstract Aims The objective of the current study is to investigate the risk of heart failure (HF) after implantation of a pacemaker (PM) with a right ventricular pacing (RVP) lead in comparison to a matched cohort without a PM and factors associated with this risk. Methods and results All patients without a known history of HF who had a PM implanted with an RVP lead between 2000 and 2014 (n = 27 704) were identified using Danish nationwide registries. An age- and gender-matched control cohort (matched 1:5, n = 138 520) without PM and HF was identified to compare the risk. Outcome was the cumulative incidence of HF including fatal HF within the first 2 years of PM implantation, with all-cause mortality and myocardial infarction (MI) as competing risks. Due to violation of proportional hazards, the follow-up period was divided into three time-intervals: <30 days, 30–180 days, and >180 days–2 years. The cumulative incidence of HF including fatal HF was observed in 2937 (10.6%) PM patients. Risks for the three time-intervals were <30 days [hazard ratio (HR) 5.98, 95% CI 5.19–6.90], 30–180 days (HR 1.84, 95% CI 1.71–1.98), and >180 days (HR 1.11, 95% CI 1.04–1.17). Among patients with a PM device, factors associated with increased risk of HF were male sex (HR 1.33, 95% CI 1.24–1.43), presence of chronic kidney disease (CKD) (HR 1.64, 95% CI 1.29–2.09), and prior MI (1.77, 95% 1.50–2.09). Conclusions Pacemaker with an RVP lead is strongly associated with risk of HF specifically within the first 6 months. Patients with antecedent history of MI and CKD had substantially increased risk.


2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Leticia Ferraz Pamplona ◽  
Giovana Romano Rennó Costa ◽  
Bruno Michel e Silva ◽  
Gustavo De Araújo Pinto ◽  
Rodolfo Souza de Faria ◽  
...  

Introduction: The acquired immunodeficiency syndrome remains a health challenge in Brazil. Therapeutic failures, characterized by detectable viral load, must have their causes evaluated. Among the most relevant reasons is the lack of adherence to treatment. Objective: To evaluate factors associated with inadequate control of viral load in individuals with HIV in the CAP of Itajubá (MG). Methods: This is an observational, cross-sectional and documentary study with 261 medical records. The variables analyzed were gender, age, education, residence, sexual orientation, first and last test results of tests for viral load and CD4+ T lymphocytes, history of poor adherence, use of current antiretroviral therapy (ART), duration of ART use, depression and/or anxiety, use of illicit drugs, follow-up time at the CAP. Results: Of the patients, 90.42% had an undetectable viral load and 64.37% had a CD4+ T count ≥500 in the last available test. Some characteristics were related to detectable viral load in the last exam: history of poor adherence during treatment (p<0,0001), inconsistent use of ART (p<0,0001) and use of illicit drugs (p=0,0155). Anxiety and/or depression was not statistically significant (p=0,3321). Conclusion: History of poor adherence, inconsistent use of ART and use of illicit drugs were associated with an increased risk ok virological failure. The identification of groups at risk of poor adherence to treatment can support the development of intervention strategies in an early and transdisciplinary way to improve adherence and generate better results in the control of HIV infection.


2013 ◽  
Vol 31 (35) ◽  
pp. 4394-4399 ◽  
Author(s):  
Wen-Qing Li ◽  
Abrar A. Qureshi ◽  
Jing Ma ◽  
Alisa M. Goldstein ◽  
Edward L. Giovannucci ◽  
...  

Purpose Steroid hormones, particularly androgens, play a major role in prostatic carcinogenesis. Personal history of severe acne, a surrogate for higher androgen activity, has been associated with an increased risk of prostate cancer (PCa), and one recent study indicated that severe teenage acne was a novel risk factor for melanoma. These findings suggest a possible relationship between PCa and risk of melanoma. We prospectively evaluated this association among US men. Methods A total of 42,372 participants in the Health Professionals' Follow-Up Study (HPFS; 1986 to 2010) were included. Biennially self-reported PCa diagnosis was confirmed using pathology reports. Diagnosis of melanoma and nonmelanoma skin cancer (NMSC) was self-reported biennially, and diagnosis of melanoma was pathologically confirmed. We sought to confirm the association in 18,603 participants from the Physicians' Health Study (PHS; 1982 to 1998). Results We identified 539 melanomas in the HPFS. Personal history of PCa was associated with an increased risk of melanoma (multivariate-adjusted hazard ratio [HR], 1.83; 95% CI, 1.32 to 2.54). Although we also detected a marginally increased risk of NMSC associated with PCa (HR, 1.08; 95% CI, 0.995 to 1.16), the difference in the magnitude of the association between melanoma and NMSC was significant (P for heterogeneity = .002). We did not find an altered risk of melanoma associated with personal history of other cancers. The association between PCa and risk of incident melanoma was confirmed in the PHS (HR, 2.17; 95% CI, 1.12 to 4.21). Conclusion Personal history of PCa is associated with an increased risk of melanoma, which may not be entirely a result of greater medical scrutiny.


2021 ◽  
Vol 11 (3) ◽  
pp. 178
Author(s):  
Noah R. Delapaz ◽  
William K. Hor ◽  
Michael Gilbert ◽  
Andrew D. La ◽  
Feiran Liang ◽  
...  

Post-traumatic stress disorder (PTSD) is a prevalent mental disorder marked by psychological and behavioral changes. Currently, there is no consensus of preferred antipsychotics to be used for the treatment of PTSD. We aim to discover whether certain antipsychotics have decreased suicide risk in the PTSD population, as these patients may be at higher risk. A total of 38,807 patients were identified with a diagnosis of PTSD through the ICD9 or ICD10 codes from January 2004 to October 2019. An emulation of randomized clinical trials was conducted to compare the outcomes of suicide-related events (SREs) among PTSD patients who ever used one of eight individual antipsychotics after the diagnosis of PTSD. Exclusion criteria included patients with a history of SREs and a previous history of antipsychotic use within one year before enrollment. Eligible individuals were assigned to a treatment group according to the antipsychotic initiated and followed until stopping current treatment, switching to another same class of drugs, death, or loss to follow up. The primary outcome was to identify the frequency of SREs associated with each antipsychotic. SREs were defined as ideation, attempts, and death by suicide. Pooled logistic regression methods with the Firth option were conducted to compare two drugs for their outcomes using SAS version 9.4 (SAS Institute, Cary, NC, USA). The results were adjusted for baseline characteristics and post-baseline, time-varying confounders. A total of 5294 patients were eligible for enrollment with an average follow up of 7.86 months. A total of 157 SREs were recorded throughout this study. Lurasidone showed a statistically significant decrease in SREs when compared head to head to almost all the other antipsychotics: aripiprazole, haloperidol, olanzapine, quetiapine, risperidone, and ziprasidone (p < 0.0001 and false discovery rate-adjusted p value < 0.0004). In addition, olanzapine was associated with higher SREs than quetiapine and risperidone, and ziprasidone was associated with higher SREs than risperidone. The results of this study suggest that certain antipsychotics may put individuals within the PTSD population at an increased risk of SREs, and that careful consideration may need to be taken when prescribed.


Author(s):  
Shinwan Kany ◽  
Johannes Brachmann ◽  
Thorsten Lewalter ◽  
Ibrahim Akin ◽  
Horst Sievert ◽  
...  

Abstract Background Non-paroxysmal (NPAF) forms of atrial fibrillation (AF) have been reported to be associated with an increased risk for systemic embolism or death. Methods Comparison of procedural details and long-term outcomes in patients (pts) with paroxysmal AF (PAF) against controls with NPAF in the prospective, multicentre observational registry of patients undergoing LAAC (LAARGE). Results A total of 638 pts (PAF 274 pts, NPAF 364 pts) were enrolled. In both groups, a history of PVI was rare (4.0% vs 1.6%, p = 0.066). The total CHA2DS2-VASc score was lower in the PAF group (4.4 ± 1.5 vs 4.6 ± 1.5, p = 0.033), while HAS-BLED score (3.8 ± 1.1 vs 3.9 ± 1.1, p = 0.40) was comparable. The rate of successful implantation was equally high (97.4% vs 97.8%, p = 0.77). In the three-month echo follow-up, LA thrombi (2.1% vs 7.3%, p = 0.12) and peridevice leak > 5 mm (0.0% vs 7.1%, p = 0.53) were numerically higher in the NPAF group. Overall, in-hospital complications occurred in 15.0% of the PAF cohort and 10.7% of the NPAF cohort (p = 0.12). In the one-year follow-up, unadjusted mortality (8.4% vs 14.0%, p = 0.039) and combined outcome of death, stroke and systemic embolism (8.8% vs 15.1%, p = 0.022) were significantly higher in the NPAF cohort. After adjusting for CHA2DS2-VASc and previous bleeding, NPAF was associated with increased death/stroke/systemic embolism (HR 1.67, 95% CI 1.02–2.72, p = 0.041). Conclusion Atrial fibrillation type did not impair periprocedural safety or in-hospital MACE patients undergoing LAAC. However, after one year, NPAF was associated with higher mortality. Graphic abstract


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
J Martinez Milla ◽  
C Garcia-Talavera ◽  
B Arroyo ◽  
A Camblor ◽  
A Garcia-Ropero ◽  
...  

Abstract Introduction Cardiac resynchronization therapy with defrilator (CRT-D) has been shown to reduce mortality in HFrEF. The width and morphology of the QRS are essential when deciding on the implantation of these devices. QRS fragmentation (fQRS) has been shown to be a good predictor of cardiovascular events in certain patients, but its role in patients with CRT-D has not been studied. The aim of this study is to determine whether the presence of a fQRS at the time of CRT-D implantation can predict clinical events. Methods All patients who underwent CRT-D implantation from 2010 to 2017 were included. Patients' ECG were evaluated at the time of implantation, and the incidence of clinical events during follow-up was also assessed. fQRS was defined as the presence of an RSR' pattern with a notch in the R wave or in the ascending or descending branch of the S wave in two continuous leads on the ECG. Results We studied 131 patients (mean age 73 years, 76.5% male). The mean follow-up period was 37±26 months. No difference in baseline characteristics was found (Table 1); the proportion of fQRS was 48.9%. 25 patients (19.1%) had hospital admissions secondary to cardiovascular causes (heart failure, arrhythmic events, acute coronary syndrome, and death from other causes). We performed a multivariate logistic regression analysis aiming at an association between the presence of fQRS and the increased risk of hospital admissions due to cardiovascular causes OR 2.92 (95% CI: 1.04–8.21, P=0.04). Conclusion The presence of a fQRS at the time of implantation of a CRT-D is an independent predictor of hospital admissions due to cardiovascular causes. Therefore this could be a useful marker to identify the population at high risk of cardiovascular events, for this we consider necessary to conduct future studies and thus assess the value of the fQRS for the selection of patients requiring closer monitoring thus avoiding further hospital admissions. Funding Acknowledgement Type of funding source: None


2021 ◽  
Vol 9 (1) ◽  
pp. e001948
Author(s):  
Marion Denos ◽  
Xiao-Mei Mai ◽  
Bjørn Olav Åsvold ◽  
Elin Pettersen Sørgjerd ◽  
Yue Chen ◽  
...  

IntroductionWe sought to investigate the relationship between serum 25-hydroxyvitamin D (25(OH)D) level and the risk of type 2 diabetes mellitus (T2DM) in adults who participated in the Trøndelag Health Study (HUNT), and the possible effect modification by family history and genetic predisposition.Research design and methodsThis prospective study included 3574 diabetes-free adults at baseline who participated in the HUNT2 (1995–1997) and HUNT3 (2006–2008) surveys. Serum 25(OH)D levels were determined at baseline and classified as <50 and ≥50 nmol/L. Family history of diabetes was defined as self-reported diabetes among parents and siblings. A Polygenic Risk Score (PRS) for T2DM based on 166 single-nucleotide polymorphisms was generated. Incident T2DM was defined by self-report and/or non-fasting glucose levels greater than 11 mmol/L and serum glutamic acid decarboxylase antibody level of <0.08 antibody index at the follow-up. Multivariable logistic regression models were applied to calculate adjusted ORs with 95% CIs. Effect modification by family history or PRS was assessed by likelihood ratio test (LRT).ResultsOver 11 years of follow-up, 92 (2.6%) participants developed T2DM. A higher risk of incident T2DM was observed in participants with serum 25(OH)D level of<50 nmol/L compared with those of ≥50 nmol/L (OR 1.72, 95% CI 1.03 to 2.86). Level of 25(OH)D<50 nmol/L was associated with an increased risk of T2DM in adults without family history of diabetes (OR 3.87, 95% CI 1.62 to 9.24) but not in those with a family history (OR 0.72, 95% CI 0.32 to 1.62, p value for LRT=0.003). There was no effect modification by PRS (p value for LRT>0.23).ConclusionSerum 25(OH)D<50 nmol/L was associated with an increased risk of T2DM in Norwegian adults. The inverse association was modified by family history of diabetes but not by genetic predisposition to T2DM.


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