Mortality rate and causes of death in women with self-reported musculoskeletal pain: Results from a 17-year follow-up study

2013 ◽  
Vol 4 (2) ◽  
pp. 86-92 ◽  
Author(s):  
Anne K. Nitter ◽  
Karin Ø. Forseth

AabstractIntroductionChronic musculoskeletal pain represents a significant health problem among adults in Norway. The prevalence of chronic pain is reported to be 35-53% in cross sectional studies of both genders. For many years, it has been a common opinion among medical doctors that chronic pain may indeed reduce a person’s quality of life, but not affect life expectancy. However, over the previous two decades, reports about mortality and cause of death in individuals with chronic pain have been published. So far, several studies conclude that there is an increased mortality in patients with chronic pain, but it is not clear what causes this. Increased occurrences of cardio-vascular death or cancer death have been reported in some studies, but not verified in other studies.Aims of the studyThe aims of this study were to estimate the mortality rate in females with different extent of pain, to identify potential risk factors for death and to investigate if the causes of death differ according to prior reported pain.MethodsThis is a prospective population-based study of all women between 20 and 50 years registered in Arendal, Norway, in 1989 (N = 2498 individuals). At follow-up in 2007, 2261 living females were retraced, 89 had died.All subjects received a questionnaire containing questions about chronic pain (pain ≥ 3 months duration in muscles, joints, back or the whole body) as well as 13 sub-questions about pain-modulating factors, non-specific health complaints and sleep problems, by mail in 1990, 1995 and 2007. Only subjects who answered the questionnaire in 1990 were included in the analyses. Of the deceased, 71 had answered the questionnaire in 1990.A multivariate model for cox regression analysis was used in order to clarify if chronic pain, sleep problems, feeling anxious, frightened or nervous and number of unspecific health were risk factors for death.The causes of death of 87 of the deceased individuals were obtained by linking the ID-number with the Norwegian Cause of Death Registry.ResultsThe ratio of deceased responders was 2% (14/870) among those with no pain versus 5% (57/1168) among those with chronic pain at baseline. When separating into chronic regional pain and chronic widespread pain, the mortality rate was respectively 4% and 8% in the different groups. Age adjusted hazard ratio for mortality rate in individuals with initially chronic pain was [HR 2.5 (CI 1.4–4.5)] compared to pain free individuals. In the multivariate analysis, having chronic pain [HR 2.1 (1.1–4.2)] and feeling anxious, frightened or nervous [HR 3.2 (1.8–5.6)] were associated with increased risk of death. There was no difference in death from cardiovascular disease or malignancies between the groups of pain free individuals vs. the group of individuals with chronic pain.ConclusionThe mortality rate was significantly higher for individuals with chronic pain compared to pain free individuals, adjusted for age. In addition, feeling anxious, frightened or nervous were risk factors for death. There was an increase in all-cause mortality.

2012 ◽  
Vol 3 (4) ◽  
pp. 210-217 ◽  
Author(s):  
Anne K. Nitter ◽  
Are H. Pripp ◽  
Karin Ø. Forseth

AbstractIntroductionChronic musculoskeletal pain represents a significant health problem among adults in Norway. The prevalence of chronic pain can be up to 50% in both genders. However, the prevalence of chronic widespread pain is significantly higher in females than in males. Chronic widespread pain is seen as the end of a continuum of pain. There is rather sparse knowledge about the incidence of pain in initially pain free individuals and the course of self-reported pain over time. Moreover, little is known about risk factors for incidence of chronic pain or prognostic factors for the course of self-reported pain. We believe that such knowledge may contribute to develop strategies for treatment at an early stadium of the pain condition and thereby reduce the prevalence of chronic pain included chronic widespread pain.Aims of the studyThe aims of this study were threefold: (1) to calculate the incidence of self-reported musculoskeletal pain in a female cohort, (2) to describe the course of pain and (3) to investigate whether or not health complaints and sleep problems are predictive factors for onset of pain or prognostic factors for the course of pain.MethodsThis is a prospective population-based study of all women between 20 and 50 years who were registered in Arendal, Norway, in 1989 (N = 2498 individuals). A questionnaire about chronic pain (pain >3 months duration in muscles, joints, back or the whole body), modulating factors for pain, sleep problems and seven non-specific health complaints was mailed to all traceable women, in 1990 (N =2498), 1995 (n = 2435) and 2007 (n = 2261). Of these, 1338 responded on all three occasions. Outcome measures were presence and extent of chronic pain.ResultsThe prevalence of chronic pain was 57% in 1990 and 61% in 2007. From 1990 to 2007, 53% of the subjects changed pain category. The incidence of chronic pain in initially pain free individuals during follow-up was 44%, whereas the recovery rate was 25%. Impaired sleep quality predicted onset of chronic pain. There was a linear association between the number of health complaints and the incidence of chronic pain in initially pain free individuals. Equivalent results were found for persistence of pain and worsening of pain.ConclusionThe prevalence of chronic pain was rather stable throughout the follow-up period, but the prevalence of chronic widespread pain increased. Individual changes in pain extent occurred frequently. The presence of sleep disturbances and number of health complaints predicted onset, persistence and worsening of pain.ImplicationsSleep problems must be thoroughly addressed as a possible risk factor for onset or worsening of pain. Elimination of sleep problems in an early phase is an interesting approach in treating chronic pain. More research is needed to illuminate the possible pathogenetic relations between pain, non-specific health complaints, sleep problems and also depression.


CJEM ◽  
2020 ◽  
Vol 22 (S1) ◽  
pp. S100-S100
Author(s):  
J. French ◽  
C. Somayaji ◽  
D. Dutton ◽  
S. Benjamin ◽  
P. Atkinson

Introduction: The New Brunswick Trauma Registry is a database of injury admissions from eight hospitals throughout the province. Data tracks individuals in-hospital. By linking this information with vital statistics, we are able to observe outcomes post-discharge and can model health outcomes for participants. We want to know how outcomes for trauma patients compare with the general population post discharge. Methods: Using data from 2014-15, we followed over 2100 trauma registry observations for one year and tracked mortality rate per 1,000 people by age-group. We also compared the outcomes of this group to all Discharge Abstract Database (DAD) entries in the province (circa. 7500 total). We tracked mortality in-hospital, at six months, and one year after discharge. We truncated age into groups aged 40-64, 65-84, and 85 or older. Results: In-hospital mortality among those in the trauma registry is approximately 20 per 1,000 people for those age 40-64, 50 per 1,000 people for those aged 65-84, and 150 per 1,000 people aged 85 or older. For the oldest age group this is in line with the expected population mortality rate, for the younger two groups these estimates are approximately 2-4 times higher than expected mortality. The mortality at six-month follow-up for both of the younger groups remains higher than expected. At one-year follow-up, the mortality for the 65-84 age group returns to the expected population baseline, but is higher for those age 40-64. Causes of death for those who die in hospital are injury for nearly 50% of observations. After discharge, neoplasms and heart disease are the most common causes of death. Trends from the DAD are similar, with lower mortality overall. Of note, cardiac causes of death account for nearly as many deaths in the 6 months after the injury in the 40 -64 age group as the injury itself. Conclusion: Mortality rates remain high upon discharge for up to a year later for some age groups. Causes of death are not injury-related. Some evidence suggests that the injury could have been related to the eventual cause of death (e.g., dementia), but questions remain about the possibility for trauma-mitigating care increasing the risk of mortality from comorbidities. For example, cardiac death, which is largely preventable, is a significant cause of death in the 40-64 age group after discharge. Including an assessment of Framingham risk factors as part of the patients rehabilitation prescription may reduce mortality.


Blood ◽  
2020 ◽  
Vol 136 (Supplement 1) ◽  
pp. 37-38
Author(s):  
Monica Else ◽  
Stuart J Blakemore ◽  
Jonathan C Strefford ◽  
Daniel Catovsky

* These authors contributed equally Introduction Causes of death and, in particular, deaths due to infection have not been widely studied in randomised trials in chronic lymphocytic leukaemia (CLL). With long-term follow-up (median 13 years), we were able to examine the cause of death in 600/777 patients in the LRF CLL4 trial. Blood samples taken at randomization from 499 patients were available, allowing us to examine the relationship between deaths due to infection and a large panel of genes which are commonly mutated in CLL. Several gene mutations have been linked to earlier death in the LRF CLL4 trial, including mutations of TP53, NOTCH1, SF3B1, EGR2 and MAPK-ERK (Gonzalez et al, J Clin Oncol 2011; 29:2223-9; Oscier et al, Blood 2013; 121:468-75; Young et al, Leukemia 2017; 31:1547-54; Blakemore et al, Leukemia 2020; 34:1760-4). In this study we aimed to identify gene mutations which were specifically associated with death due to infection. Methods In LRF CLL4 patients were randomized between 1999-2004 to receive chlorambucil or fludarabine, with or without cyclophosphamide. Follow-up continued until September 2016. Causes of death were assessed centrally by the principal investigator. Results In the LRF CLL4 trial 614 of 777 patients (79%) died before the end of follow-up. The cause of death was known in 600 patients. Deaths tended to be multifactorial, but infection was a cause of death in 258 patients (43%). Fatal infections were pneumonia (67%), and/or sepsis (38%) and/or opportunistic infections such as aspergillus (11%). Patients who died of infection were more likely than those who died of other causes to have received more than one line of treatment and to have died in the winter months (Table 1). Mutations of BRAF, FBXW7, NRAS and XPO1 were significantly associated with death due to infection versus other deaths. However, with multiple hypothesis testing, NRAS was the only genetic mutation to survive a false discovery rate (FDR) q-value = 0.05 (odds ratio: 17, P = 0.0004). No other significant differences were found between patients who died of infection versus those whose death did not have an infectious cause. In particular, the rate of deaths due to infection was not influenced by other demographic or laboratory factors, nor by the randomised treatment, the response to treatment, or the size/experience of the CLL treatment centre. In multivariate analysis the factors most significantly associated with death from infection versus all other deaths were mutations of the BRAF, FBXW7, NRAS and XPO1 genes (Table 1). Of the 499 patients in the trial for whom gene mutation data were available, 73 (15%) carried one or more of the four gene mutations BRAF (6%), FBXW7 (2%), NRAS (2%) and XPO1 (6%) (Table 2). Only six of these 73 remained alive. Death was caused by infection in 46/67 assessable patients (69%) who had a mutation of one or more of these four genes versus only 129/333 patients (39%) without any of these mutations (odds ratio: 3.46 [95% C.I. 1.98-6.07] P<0.0001). In order to test the robustness of our results, the same analysis was repeated in the full trial, comparing the patients who died of infection with all the other trial patients, including those who remained alive. The presence of one or more of the four gene mutations BRAF, FBXW7, NRAS and XPO1 was the most significant predictor of death from infection in univariate analysis in this larger dataset (odds ratio: 3.92 [95% C.I. 2.34-6.59] P<0.0001). Patients who died of infection lost on average 2 years 4 months of life compared with the median overall survival of all the other trial patients (6 years 11 months, log-rank P<0.0001). Conclusion Patients in LRF CLL4 were at some risk of death due to infection, irrespective of their demographic characteristics, disease stage and treatment history. Nevertheless, those who had received more lines of treatment were particularly at risk, as were those who carried a BRAF, FBXW7, NRAS or XPO1 mutation. A meta-analysis of datasets from other trials could be important to assess the validity of the link between these gene mutations and deaths from infections in patients with CLL and possibly other leukaemias and lymphomas. Careful management of infection risk, together with prophylaxis against infection, may be important in patients who carry one or more of these mutations. Disclosures No relevant conflicts of interest to declare.


Lupus ◽  
2019 ◽  
Vol 28 (12) ◽  
pp. 1488-1494
Author(s):  
R F Ingvarsson ◽  
A J Landgren ◽  
A A Bengtsson ◽  
A Jönsen

Objective To ascertain the mortality rate and causes of death in patients with systemic lupus erythematosus (SLE) within a defined region in southern Sweden during the time period 1981–2014 and determine whether these have changed over time. Methods In 1981, a prospective observation study of patients with SLE was initiated in southern Sweden. All incident SLE patients within a defined geographic area were identified using previously validated methods including diagnosis and immunology registers. Patients with a confirmed SLE diagnosis were then followed prospectively at the Department of Rheumatology in Lund. Clinical data was collected at regular visits. Patients were recruited from 1981 to 2006 and followed until 2014. The patient cohort was split into two groups based on the year of diagnosis to determine secular trends. Causes of death were retrieved from medical records and from the cause of death registry at The National Board of Health and Welfare in Sweden. Results In all, 175 patients were diagnosed with SLE during the study period. A total of 60 deaths occurred during a total of 3053 years of follow-up. In the first half of the study inclusion period 46 patients died, compared with 14 in the latter. The majority of patients (51.7%) died of cardiovascular disease. Infections caused 15% of the deaths and malignancy was the cause of death in 13.3% of patients. SLE was the main cause of death for 6.7% of the patients and a contributing factor for half of the patients. Standardized mortality ratio was increased in patients by a factor of 2.5 compared with the general population. Deaths occurred at an even rate throughout the whole observation period. No significant difference in standardized mortality ratio was observed between genders but was increased in older female patients. Furthermore, secular mortality trends were not identified. Conclusions In this long-term epidemiologic follow-up study of incident SLE, we report a substantially raised mortality rate amongst SLE patients compared with the general population. The mortality rates have not changed significantly during the observation period that spanned three decades. The main cause of death was cardiovascular disease and this finding was consistent over time.


2020 ◽  
Vol 4 (19) ◽  
pp. 4739-4747
Author(s):  
Ming Y. Lim ◽  
Dunlei Cheng ◽  
Michael Recht ◽  
Christine L. Kempton ◽  
Nigel S. Key

Abstract Although persons with nonsevere hemophilia A (NSHA) account for about one-half of the hemophilia A population, epidemiological data in this subset of individuals are scarce. We set out to describe the clinical characteristics of persons with NSHA with inhibitors, and to determine mortality rates, predictors of mortality, and primary causes of death in persons with NSHA in the United States over a 9-year period (2010-2018). We queried the American Thrombosis and Hemostasis Network dataset (ATHNdataset) for information on demographics, inhibitor status, and date and cause of death. A total of 6624 persons with NSHA (86.0% men; 14.0% women) were observed for an average of 8.5 years; total 56 119 person-years . The prevalence of inhibitors was 2.6% (n = 171), occurring at a median age of 13 years. At the end of follow-up, 136 persons died at a median age of 63 years; an age-adjusted mortality rate of 3.3 deaths per 1000 person-years. Three deaths occurred in inhibitor participants. Presence of inhibitors was not associated with increased mortality risk (hazard ratio [HR], 0.7, 95% confidence interval [CI], 0.2-2.3). Factors independently associated with increased risk of death (HR, 95% CI) were the following: age (10-year increase) (2.1, 2.0-2.4); male (2.6, 1.0-6.4); hepatitis C (2.2, 1.5-3.1); and HIV (3.6, 2.2-6.0). The most common primary cause of death was malignancy (n = 27, 20.0%). In persons with NSHA, the development of inhibitors occurred at an early age and was not associated with increased mortality.


Blood ◽  
2020 ◽  
Vol 136 (Supplement 1) ◽  
pp. 22-23
Author(s):  
Senthil Sukumar ◽  
Max Brodsky ◽  
Sarah Hussain ◽  
Spero Cataland ◽  
Shruti Chaturvedi

Introduction: Immune thrombotic thrombocytopenic purpura (iTTP) is a potentially lethal thrombotic microangiopathy; however, prompt therapy with plasma exchange and immunosuppression leads to survival in over 90% of patients. Though TTP survivors were previously thought to return to baseline levels of health, recent reports suggest that TTP survivors have high rates of adverse health sequelae including hypertension, stroke, cognitive impairment, and poor quality of life as well as higher mortality rates compared with an age, race, and sex matched controls population. We conducted this multi-center cohort study to evaluate long term mortality and causes of death in patients that survived their first TTP episode. Methods: All available patients in The Ohio State University and Johns Hopkins Hospital Thrombotic Microangiopathy (TMA) registries were reviewed. Patients with confirmed iTTP based on ADAMTS13 activity <10% during an acute episode were included for analysis. A total of 238 patients met inclusion criteria, with 38 experiencing death during follow up. We evaluated primary and secondary cause of death where applicable. We also collected data on patient demographics, details of TTP history, and comorbidities including hypertension, diabetes, obesity, heart failure, hyperlipidemia, autoimmune conditions, chronic kidney disease, smoking, etc. Mortality was compared with an age, sex and race standardized US population using indirect standardization methods. A multivariable cox regression analysis was used to evaluate risk factors for reduced survival. Results: A total of 222 patients were enrolled in the Ohio State University and Johns Hopkins TTP registries between 2003 and 2020, of which 70.3% were female, and median age at enrollment was 42 (IQR [interquartile range] 29, 55) years. There were 38 deaths over a median follow up of 4 (IQR 0, 11) years (and a total of 1318 patient years of follow up). Characteristics of the study cohort are summarized in Table 1. Of the 38 patients that died, 9 died during their first episode of TTP and 29 died after surviving the first TTP episode. Median age at death among those that survived the first TTP episode was 49 (IQR 39, 65) years. Among survivors of acute TTP, cardiovascular disease was the leading primary cause of death (27.6%) followed by relapsed TTP (27.6%), malignancy (20.7%), infection (13.8%), and other/unknown causes (10.3%) (Table 2). Cardiovascular disease was the primary or secondary cause of death in 31% (9 of 29) patients. Cardiovascular causes of death included myocardial infarction, arrhythmia, decompensated heart failure, stroke, and hypertensive emergency. The median age of death from any cardiovascular cause (primary or secondary) was 49 years. Among TTP survivors, male sex [HR 4.39 (95% CI 1.83-10.52, P=0.001), age [HR 1.03 (95% CI 1.01-1.06), P=0.039] and number of TTP episodes [HR 1.12 (96% CI 1.05-1.21), P=0.001] were risk factors for mortality in a Cox regression model also adjusted for hypertension [HR 0.60 (95% CI 0.26-1.37), P=0.228], CKD [HR 1.38 (95% CI 0.61-3.13, P=0.436] and SLE [HR 1.26 (95% CI 1.04-1.21), P=0.771]. The mortality rate in TTP survivors was significantly higher than the expected mortality rate from an age and sex standardized reference US population (2228.3 per 100,000 person years versus 1273.8 per 100,000 person years, P = 0.007) (Figure 1). The median age at death was also lower in TTP survivors compared with the general population (49 versus 78.7 years). Conclusions: TTP survivors have two-fold higher mortality rate than expected rates from a reference US population, adjusted for age, sex and race. Cardiovascular disease is a leading cause of death in patients that survive their first episode of TTP. This may be due to higher rates of cardiovascular risk factors such as hypertension in TTP survivors. Reduced ADAMTS13 activity is a risk factor for all cause and cardiovascular death in the general population (Sonneveld et al.Arterioscler Thromb Vasc Biol. 2016) and may contribute to cardiovascular death in TTP survivors. Our results highlight the need to screen and aggressively manage cardiovascular risk factors in TTP survivors, and for prospective studies examining the vascular sequelae of TTP. Disclosures Cataland: Ablynx/Sanofi: Consultancy, Research Funding; Alexion: Consultancy, Research Funding. Chaturvedi:Alexion: Honoraria, Membership on an entity's Board of Directors or advisory committees; Sanofi: Honoraria, Membership on an entity's Board of Directors or advisory committees.


2001 ◽  
Vol 126 (1) ◽  
pp. 89-96 ◽  
Author(s):  
S. GJERULDSEN ◽  
M. ABDELNOOR ◽  
S. OPJORDSMOEN ◽  
B. MYRVANG

A cohort of 214 drug addicts with serum hepatitis and a cohort of 193 hepatitis patients without drug addiction were examined in respect of death rates, causes of death and a number of risk factors for reduced survival. The death rate was significantly higher among the drug addicts than among non-addicts. The annual mortality rate was 1·5% in the drug addict group and 0·7% in the non-addict group. The highest relative risk of death was 860 for female drug addicts in age group 15–24 compared to females of the same age in the general population. The most prevalent cause of death in the drug addict group was drug overdose (53%), whereas in the other group 66% died from various somatic diseases. Hepatitis or complications of viral hepatitis played no role as cause of death among the drug addicts, and infections as a whole were also responsible for very few deaths. For male drug addicts, imprisonment before admission and leaving hospital without the doctors' permission were risk factors for early death.


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
P Milani ◽  
G Cavenaghi ◽  
L Obici ◽  
R Mussinelli ◽  
C Klersy ◽  
...  

Abstract Background Skeletal scintigraphy with bone tracers is a key tool for cardiac ATTR diagnosis. However its prognostic value has not been systematically assessed. Purpose We evaluated the prognostic relevance of a quantitative method to assess regional 99mTc-DPD uptake by SPECT in the heart of ATTRwt patients. Methods All ATTRwt patients (n=229) undergoing clinical assessment and bone scintigraphy at our center (from 2012 to 2019) were enrolled. Theyreceived approximately 700 MBq of 99mTc-DPD. Planar whole body acquisition 10' after the injection followed by cardiac SPECT after 3 hours were performed. SPECT data were reconstructed into 64x64 matrices with an ordered-subset expectation maximization algorithm. For each wall region and for the apex, a circular region of interest (ROI, 20 pixels) was manually drawn and a value equating to the number of counts contained in the ROI was obtained. Partial correlation of ln-transformed ROI and biomarkers was retrieved from a multivariable regression model, while controlling for each cardiac wall region. Multivariable Cox regression was used to assess the prognostic role of lnROI while adjusting for wall region, NT-proBNP, cTnI and eGFR. Hazard ratios and 95% confidence intervals (HR, 95% CI) were computed. The Harrell's c statistic was reported for model discrimination. The interaction of biomarker and regional wall on survival was assessed; also, to account for intra-subject correlation of measures, within subject robust standard errors were computed. Results Median follow-up was 21 months (IQR 11, 40) and 39 (17%) patients died. Median age was 76 years (IQR, 72–80), NT-proBNP 2944 ng/L (IQR, 1815–5319), cTnI 0.095 ng/L (IQR, 0.062–0.144) and eGFR 62 mL/min (IQR, 51–77). ROI did not correlate with any of NT-proBNP, eGFR, age, cTnI or mLVWT (R<1% in all cases). All analyses were adjusted for cardiac wall. At the multivariable Cox regression (Harrell's c=0.75), there was a linear increase in the risk of death associated with lnROI (HR 2.14, P=0.014), which was independent of cardiac wall region, NTproBNP, cTnI and eGFR. Only cTnI maintained a significant prognostic value. The association of lnROI and mortality was not modified by the site of measurement test for interaction with cardiac wall p=0.818). At the predefined subgroup analysis, the risk of death was similar for all walls; we computed the optimal cut-off for 12 months survival at the apex (a region usually lately involved) to 4193 (AUC: 0.68, sensitivity 80%, specificity 68%). At the multivariable Cox regression (Harrell's c 0.76), apex ROI>4193 was an independent predictor of death (HR 3.60, 95% CI 1.45–8.93, p=0.006) and outperformed all the biomarkers tested. Conclusions Quantitative assessment of ROI uptake at cardiac SPECT is a powerful predictor of survival in ATTRwt patients, independent of and outperforming the other known prognostic factors. This observation warrants validation with prolonged follow-up and in independent patient series. Funding Acknowledgement Type of funding source: None


2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Runzhen Chen ◽  
Chen Liu ◽  
Peng Zhou ◽  
Yu Tan ◽  
Zhaoxue Sheng ◽  
...  

Abstract Background Associations between D-dimer and outcomes of patients with acute coronary syndromes (ACS) remain controversial. This study aimed to investigate the prognostic value of D-dimer in ACS patients treated by percutaneous coronary intervention (PCI). Methods In this observational study, 3972 consecutive patients with ACS treated by PCI were retrospectively recruited. The X-tile program was used to determine the optimal D-dimer thresholds for risk stratifications. Cox regression with multiple adjustments was used for outcome analysis. Restricted cubic spline (RCS) analysis was performed to assess the dose-response association between D-dimer and outcomes. The C-index was calculated to evaluate the additional prognostic value of D-dimer when added to clinical risk factors and commonly used clinical risk scores, with internal validations using bootstrapping methods. The primary outcome was all-cause death. Results During a median follow-up of 720 days, 225 deaths occurred. Based on the thresholds generated by X-tile, ACS-PCI patients with median (420–1150 ng/mL, hazard ratio [HR]: 1.58, 95 % confidence interval [CI]: 1.14–2.20, P = 0.007) and high (≥ 1150 ng/mL, HR: 1.98, 95 % CI: 1.36–2.89, P < 0.001) levels of D-dimer showed substantially higher risk of death compared to those with low D-dimer (< 420 ng/mL). RCS analysis depicted a constant relation between D-dimer and various outcomes. The addition of D-dimer levels significantly improved risk predictions for all-cause death when combined with the fully adjusted models (C-index: 0.853 vs. 0.845, P difference = 0.021), the GRACE score (C-index: 0.826 vs. 0.814, P difference = 0.027), and the TIMI score (C-index: 0.804 vs. 0.776, P difference < 0.001). The predicted mortality at the median follow-up (two years) was 1.7 %, 5.2 %, and 10.9 % for patients with low, median, and high D-dimer, respectively, which was well matched with the observed mortality (low D-dimer group: 1.2 %, median D-dimer group: 5.2 %, and high D-dimer group: 12.6 %). Conclusions For ACS patients treated by PCI, D-dimer level was an independent predictor for adverse outcomes, and provided additional prognostic value when combined with clinical risk factors and risk scores. Risk stratifications based on D-dimer was plausible to differentiate ACS-PCI patients with higher risk of death.


2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 1224.3-1225
Author(s):  
J. Nossent ◽  
D. Preen ◽  
W. Raymond ◽  
H. Keen ◽  
C. Inderjeeth

Background:IgA vasculitis is generally considered to be a self-limiting condition, but this is at odds with the increased mortality observed in adult patients with IgA vasculitis (1).Objectives:With sparse data on prognostic factors in IgAV, we investigated whether pre-existing conditions are risk factors for mortality in adult IgAV patients.Methods:Observational population-based cohort study using state-wide linked longitudinal health data for adults with IgAV (n=267) and matched controls (n=1080) between 1980-2015. Charlson comorbidity index (CCI) and serious infections (SI) were recorded over an extensive lookback period prior to diagnosis. Date and causes of death were extracted from the WA Death Registry. Mortality rate (deaths/1000 person-years) ratios (MRR) and time dependent survival analysis assessed the risk of death. Age and gender specific mortality rate data were obtained from the Australian Bureau of Statistics.Results:During 9.9 (±9.8) years lookback IgAV patients accrued higher CCI scores (2.60 vs1.50 p<0.001) and had higher risk of SI (OR 8.4, p<0.001), not fully explained by CCI scores. During 19 years follow-up, the risk of death in IgAV patients (n=137) was higher than in controls (n=397) (MRR 2.06, CI 1.70-2.50, p<0.01) and the general population (SMRR 5.64, CI 4.25, 7.53, p<0.001). Survival in IgAV was reduced at five (72.7 vs. 89.7 %) and twenty years (45.2% vs. 65.6 %) (both p<0.05). CCI (HR1.88, CI:1.25 - 2.73, p=0.001), renal failure (HR 1.48, CI: 1.04 - 2.22, p=0.03) and prior SI (HR 1.48, CI:1.01 – 2.16, p=0.04) were independent risk factors. Death from infections (5.8 vs 1.8%, p=0.02) was significantly more frequent in IgAV patients.Conclusion:Premorbid accrual of comorbidity is increased and predicts premature death in IgAV patients. However, comorbidity does not fully explain the increased risk of serious infections prior to diagnosis or the increased mortality due to infections in IgAV.References:[1]Villatoro-Villar M, Crowson CS, Warrington KJ, Makol A, Ytterberg SR, Koster MJ. Clinical Characteristics of Biopsy-Proven IgA Vasculitis in Children and Adults: A Retrospective Cohort Study. Mayo Clin Proc. 2019;94(9):1769-80.Acknowledgements:The authors would like to acknowledge the support of the Arthritis Foundation of WA and acknowledge the Western Australian Data Linkage Branch, the Western Australian Department of Health, and the data custodians of, the Hospital and Morbidity Data Collection, the Emergency Department Data Collection the WA Cancer Register and the WA Death Register for their assistance with the study.Disclosure of Interests:None declared


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