Abstract WP415: Cigarette Smoking as Risk Factor for Hematoma Expansion in Primary Intracerebral Hemorrhage: Analysis From a Randomized Clinical Trial

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Shahram Majidi ◽  
Lydia Foster ◽  
Christopher P Kellner ◽  
Jose I Suarez ◽  
Adnan I Qureshi ◽  
...  

Background: Cigarette smoking is a well-known risk factor for ischemic and hemorrhagic stroke. We evaluated the impact of smoking status on hematoma expansion and clinical outcome in patients with primary intracerebral hemorrhage (ICH). Methods: This is a post hoc exploratory analysis of Antihypertensive Treatment at Acute Cerebral Hemorrhage(ATACH)-2 trial. Patients with ICH were randomized into intensive blood pressure lowering(SBP: <139 mmHg) versus Baseline characteristics were compared based on smoking status. Analysis of outcome measures was adjusted for covariates included in the ATACH-2 primary analysis or those associated with smoking status. Results: Of total of 914 patients in the trial with known smoking status, 439 (48%) patients were ever-smokers (264 current smokers and 175 former smokers). Current and former smokers were younger and more likely to be male. There was no difference in the baseline Glasgow Coma Scale(GCS) score and initial hematoma size based on smoking status. Ever-smokers had higher rate of thalamic hemorrhage (42% vs 34%) and intraventricular hemorrhage (29% vs 23%); this rate was highest among former smokers (49% and 35%, respectively). Ever-smokers had higher rate of hematoma expansion in 24 hour [adjusted RR (95% CI): 1.46; (1.05 -2.03)] compared to non-smokers after adjusting for confounding factors. There was no significant difference in the rate of death and disability at 90 days between the two groups [adjusted RR; (95% CI): 1.18; (0.93 -1.50)]. Conclusions: Our analysis demonstrates cigarette smoking as an independent predictor for hematoma expansion. There was no significant difference in death and disability based on smoking status.

2016 ◽  
Vol 4 (4) ◽  
pp. 636-640 ◽  
Author(s):  
Gordana Kamceva ◽  
Zorica Arsova-Sarafinovska ◽  
Tatjana Ruskovska ◽  
Milka Zdravkovska ◽  
Lidija Kamceva-Panova ◽  
...  

AIM: To determine whether cigarette smoking, as a risk factor for CAD, affects oxidative stress.MATERIAL AND METHODS: The study included patients with CAD divided according to smoking status and number of cigarettes smoked during a whole day. In all subjects were examined biological markers of oxidative stress (concentration of oxidants and activity of antioxidant enzymes).RESULTS: The study included 300 patients with CAD, with an average age of 62.97 ± 11.18 years, with a predominance of males. Of the total, 34.0% were active smokers, and 43.0% were non-smokers. The number of the most active smokers smoked cigarettes 1-20/day. In terms of concentration of oxidants (MDA and HP) it has not proved a significant difference between smokers versus non-smokers. Over the activity of antioxidant enzymes (SOD, CAT and GPX) statistically significant difference was found in the activity of GPX and among active smokers with CAD and non-smokers with CAD (p = 0.039).CONCLUSION:Smoking as a risk factor for CAD is closely associated with increased oxidative stress and the number of cigarettes smoked plays an important role in increasing the level of oxidative damage and reduced antioxidant defence.AIM: To determine whether cigarette smoking, as a risk factor for CAD, affects (anti)oxidant status.MATERIAL AND METHODS: The study included patients with CAD, divided according to their smoking status and the number of cigarettes smoked during a day. Biological markers of oxidative stress (concentration of oxidants and activity of antioxidant enzymes) were measured in all subjects.RESULTS: The study included 300 patients with CAD, (average age of 63 ± 11 years), predominantly males. Of the total, 34.0% were active smokers, 23.0% were former smokers, and 43.0% were non-smokers. Most of the active smokers smoked 1-20 cigarettes/day. In terms of concentration of oxidants (MDA and HP) there was not a significant difference between smokers versus non-smokers. As for the activity of antioxidant enzymes (SOD, CAT and GPX), a statistically significant difference was found in the activity of GPX among the active smokers with CAD and the non-smokers with CAD (p = 0.039). CONCLUSION: Smoking as a risk factor for CAD is closely associated with increased oxidative stress, and the number of cigarettes smoked plays an important role in increasing the level of oxidative damage and reducing antioxidant defence.


2020 ◽  
pp. 107110072097126
Author(s):  
Jack Allport ◽  
Jayasree Ramaskandhan ◽  
Malik S. Siddique

Background: Nonunion rates in hind or midfoot arthrodesis have been reported as high as 41%. The most notable and readily modifiable risk factor that has been identified is smoking. In 2018, 14.4% of the UK population were active smokers. We examined the effect of smoking status on union rates for a large cohort of patients undergoing hind- or midfoot arthrodesis. Methods: In total, 381 consecutive primary joint arthrodeses were identified from a single surgeon’s logbook (analysis performed on a per joint basis, with a triple fusion reported as 3 separate joints). Patients were divided based on self-reported smoking status. Primary outcome was clinical union. Delayed union, infection, and the need for ultrasound bone stimulation were secondary outcomes. Results: Smoking prevalence was 14.0%, and 32.2% were ex-smokers. Groups were comparable for sex, diabetes, and body mass index. Smokers were younger and had fewer comorbidities. Nonunion rates were higher in smokers (relative risk, 5.81; 95% CI, 2.54-13.29; P < .001) with no statistically significant difference between ex-smokers and nonsmokers. Smokers had higher rates of infection ( P = .05) and bone stimulator use ( P < .001). Among smokers, there was a trend toward slower union with heavier smoking ( P = .004). Conclusion: This large retrospective cohort study confirmed previous evidence that smoking has a considerable negative effect on union in arthrodesis. The 5.81 relative risk in a modifiable risk factor is extremely high. Arthrodesis surgery should be undertaken with extreme caution in smokers. Our study shows that after cessation of smoking, the risk returns to normal, but we were unable to quantify the time frame. Level of Evidence: Level III, retrospective cohort study.


2021 ◽  
Vol 104 (Suppl. 1) ◽  
pp. S64-S69

Background: Hypercholesterolemia is a risk factor for developing coronary artery disease. Lifestyle modification including an intake of healthy food as well as medication have approved effect in lowering serum cholesterol. Objective: The primary objective of the present study was to determine the impact of a gamma-oryzanol-enriched rice bran oil, a product of Thailand, on serum cholesterol level. Materials and Methods: A total of in 54 hypercholesterolemic patients were divided into two groups; RBOh (20,000 ppm of gammaoryzanol, n = 27), and RBOn (5,000 ppm gamma-oryzanol, n = 27). The assigned RBO (15 ml) was intake each day for 8 weeks. Fasting serum lipids were measured at baseline and at the 4th and 8th weeks of the intervention. All patients were advised about lifestyle modifications. Results: When compared to the baseline, subjects received RBOh showed a significant difference in 2 parameters including a reduction of cholesterol level at 8th weeks (p-value = 0.0101), and decrease in LDL-C level at the end of 8th weeks (p-value = 0.0013). In the group treated with RBOn, a significant increase in HDL-C level at the end of 8th weeks (p-value = 0.0303) without any effect on total cholesterol or LDL was observed. No sign of toxic effect on liver or renal functions was seen in both treatment groups. Conclusion: RBO with gamma-oryzanol-enriched could decrease cholesterol and LDL-C level in hypercholesterolemic patients. Therefore, gamma-oryzanol-enriched RBO is a functional food that may reduce cardiovascular disease risk factor. Keywords: Hypercholesterolemia, Rice bran oil, Gamma-oryzanol, Oryza sativa


2018 ◽  
Vol 46 (3-4) ◽  
pp. 116-122
Author(s):  
Yoshitaka Yamaguchi ◽  
Masatoshi Koga ◽  
Shoichiro Sato ◽  
Hiroshi Yamagami ◽  
Kenichi Todo ◽  
...  

Background: Previous studies have revealed that hematoma growth mainly occurs during the first 6 h after the onset of spontaneous intracerebral hemorrhage (ICH). Early lowering of blood pressure (BP) may be beneficial for preventing hematoma growth. However, relationships between timing of BP lowering and hematoma growth in ICH remain unclear. We investigated associations between timing of BP lowering and hematoma growth for ICH. Methods: The Stroke Acute Management with Urgent Risk-factor Assessment and Improvement (SAMURAI)-ICH Study was a multicenter, prospective, observational study investigating the safety and feasibility of early (within 3 h from onset) reduction of systolic BP (SBP) to < 160 mm Hg with intravenous nicardipine for acute hypertension in cases of spontaneous ICH. The present study was a post hoc analysis of the SAMURAI-ICH study. We examined relationships between time from onset, imaging, and initiation of treatment to target SBP achievement and hematoma growth (absolute growth ≥6 mL) in ICH patients. Target SBP achievement was defined as the time at which SBP first became < 160 mm Hg. Results: Among 211 patients, hematoma growth was seen in 31 patients (14.7%). The time from imaging to target SBP and time from treatment to target SBP were significantly shorter in patients without hematoma growth than in those with (p = 0.043 and p = 0.032 respectively), whereas no significant difference was seen in time from onset to SBP < 160 mm Hg between groups (p = 0.177). Patients in the lower quartiles of time from imaging to target SBP and time from treatment to target SBP showed lower incidences of hematoma growth (p trend = 0.023 and 0.037 respectively). The lowest quartile of time from imaging to target SBP (< 38 min) was negatively associated with hematoma growth on multivariable logistic regression (OR 0.182; 95% CI 0.038–0.867; p = 0.032). Conclusions: Early achievement of target SBP < 160 mm Hg is associated with a lower risk of hematoma growth in ICH.


Stroke ◽  
2016 ◽  
Vol 47 (suppl_1) ◽  
Author(s):  
Daniel Vela-Duarte ◽  
Ramnath Santosh Ramanathan ◽  
Atif Zafar ◽  
Ather Taqui ◽  
Stacey Winners ◽  
...  

Introduction: The mobile stroke unit (MSTU) is an on-site pre-hospital treatment team that incorporates laboratory and CT scanner and reduces times to treatment for ischemic stroke thrombolysis. The impact of MSTU on treatment and outcomes of intracerebral hemorrhage (ICH) remains unknown. We report our initial experience with ICH encountered on MSTU. Hypothesis: ICH can be quickly identified using MSTU. Hypertension and coagulopathy are common in ICH evaluated on MSTU. Methods: We identified ICH cases from the prospectively collected database encounters. Demographics, clinical features, MSTU imaging and repeat imaging characteristics were reviewed. Initial and follow-up hematoma volume was calculated by the ABC/2 method. Results: Of 295 encounters on MSTU from July 2014 to July 2015, 20 (6.7%) had intracranial hemorrhage, which comprised of 17 intracerebral, 1 subarachnoid and 2 subdural hemorrhages. Median time to CT diagnosis of ICH from emergency medical dispatch was 31 minutes (interquartile range (IQR) 28-36) and that from last known well was 118 minutes (IQR 39-301). Of the 17 ICH patients, 15 (88%) were hypertensive, with a mean systolic blood pressure of 178.1 and diastolic 91.0 mm Hg. Five (29.4%) individuals were found with INR>1.4, 1 of whom received 4-factor prothrombin complex concentrate. Median NIH Stroke Scale was 11 (IQR 7.5-14.5), and median hematoma volume was 10.7 cc (IQR 4.3-30.8). One patient had significant hematoma expansion as defined by >6 cc or 33% relative volume increase. Conclusions: Over 5% of the cases evaluated in the unit presented with ICH, most of whom were hypertensive and had small hematoma volume. MSTU enables early diagnosis of ICH after activation of emergency system, can provide early treatment, and appropriate triage.


Circulation ◽  
2021 ◽  
Vol 143 (Suppl_1) ◽  
Author(s):  
Douglas Levy ◽  
Sydney L Goldberg ◽  
Emily P Hyle ◽  
Krishna P Reddy

Background: The AHA’s 2030 Impact Goals seek to increase population health-adjusted life expectancy (LE) by 2y. Tobacco is a top contributor to all-cause mortality and cardiovascular disease (CVD). We estimated the potential contribution of improved tobacco control to achieve the 2030 Impact Goals in the US. Methods: We used the validated STOP microsimulation model with NHIS estimates of age- and sex-stratified mortality and CVD incidence to project changes in LE, as well as 10y, 20y, and lifetime CVD cumulative incidence, if cigarette smoking declined among the current US population. We assessed the impact of preventing initiation (current v never smokers) or increasing cessation (current v former smokers) at different ages. To examine the maximum impact of population-wide cessation, we projected changes in population LE and CVD incidence if smoking prevalence among those ≥20yo went immediately to 0%. Results: Preventing smoking initiation increases LE by 10.2y (men [M]) and 9.1y (women [W]) and reduces lifetime CVD incidence by 16.8% (M) and 26.2% (W) compared to lifetime smoking. Even cessation at age 60 extends LE by 3.7y (M) and 2.5y (W) and reduces 10y CVD incidence by 39.1% (M) and 59.4% (W) (Table). Total elimination of cigarette smoking in the 2020 US population aged ≥20y (e.g. by outlawing cigarettes) would increase the cohort LE by 0.4 (M) and 0.2 (W) years and reduce 20y CVD incidence by 6.0% (M) and 7.0% (W). Conclusion: Preventing smoking initiation offers the greatest benefit, but cessation at any age substantially improves LE and reduces CVD risk. The modest potential contribution of tobacco elimination to achieving the 2030 Impact Goals is due to already low smoking prevalence: <14% (projected) in 2020.


Author(s):  
Adriana Pérez ◽  
Elena Penedo ◽  
Meagan A. Bluestein ◽  
Baojiang Chen ◽  
Cheryl L. Perry ◽  
...  

This study examined the recalled age of initiation of seven different tobacco products (TPs) and explored potential influences of sex, race/ethnicity, and cigarette-smoking status on tobacco use initiation among adults 26–34 years old using the PATH study. Methods: Secondary analyses were conducted in the adult restricted PATH wave 1 (2013–2014) dataset. Weighted statistics are reported using the balanced repeated replication method and Fay’s correction to account for PATH’s complex study design. Distributions and histograms of the recalled age of initiation of seven different TPs (cigarettes, cigarillos, traditional cigars, filtered cigars, hookah, smokeless tobacco, and e-cigarettes) are reported, as well as the impact of sex and race/ethnicity using Cox proportional hazard models. The impact of cigarette-smoking status on the recalled age of initiation of each tobacco product other than cigarettes was explored. Results: The highest modes of the recalled age of initiation of cigarette use were at 14–15 and 15–16 years old. The distributions of the recalled age of initiation of cigarillos, traditional cigars, filtered cigars, hookah, and smokeless tobacco occurred later, with the highest modes at 15–16 and 17–18 years old. The distribution of the recalled age of initiation of e-cigarettes had a different shape than the other TPs, with the highest mode reported at 27–28 years old. Conclusion: Due to the ever-changing tobacco marketplace, understanding when contemporary adults aged 26–34 years recall initiating TP use is important and will inform prevention researchers.


Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 4211-4211
Author(s):  
Sarah A Bennett ◽  
Lara N Roberts ◽  
Rosie Rogers ◽  
Lynda Bonner ◽  
Raj K Patel ◽  
...  

Abstract Abstract 4211 Platelet size is thought to reflect reactivity; Mean platelet volume (MPV) was recently reported as a possible predictor for VTE, but it is not clear whether ethnic origin impacts on this risk factor. King's serves an ethnically diverse community and to assess whether MPV is a predictor of VTE in our population, we conducted a retrospective analysis of consecutive patients referred to our DVT service between January 2007 and October 2009. Patients with a confirmed first lower limb DVT (provoked n=153, unprovoked n=110) were included as subjects and controls (n=151) were derived from consecutive patients referred with objective exclusion of a DVT and no previous history of VTE, active cancer or surgery in the previous 6 weeks. All patients had a full blood count at presentation analysed on an automated analyser (using optical light scatter for MPV) within 4 hours of collection. There was no difference in mean age (54.7 vs 54.8), smoking status or ethnic group (51% vs 52.3% white, 38.4% vs 33.8% black and 10.6% vs 13.9% other) between subjects and controls respectively. Males accounted for 47.5% of subjects and 27.2% of controls. DVTs were unprovoked in 41.8% with 13.7% associated with surgery, 7.6% cancer, 10.6% pregnancy or hormone therapy. The remainder (25.1%) were secondary to cast, trauma, immobilisation or travel. Mean MPV was significantly higher in subjects than controls (8.17 vs 7.79, p=0.001) with a more marked difference in those with unprovoked DVT compared with controls (8.28 vs 7.79, p<0.001). The platelet count was lower in the DVT group (median, range 270, 21–812 vs 293, 31–642 p=0.027), with a more marked difference in those with unprovoked DVT (median, range 250, 21–584 vs 293, 31–642 p<0.001). Relative risk associated with MPV > 9.18 (90th centile) was 1.26 (95% CI 1.08– 4.76, p=0.01) and increased to 1.59 (1.18-2.1, p=0.008) in those with unprovoked DVT. Relative risk associated with platelet count <210 (10th centile) was 1.21 (1.02-1.43, p=0.06) and increased with unprovoked DVT to 1.70 (1.3-2.2, p=0.002). An inverse correlation between MPV and platelet count was confirmed (-0.305, p<0.001). Logistic regression was undertaken to investigate effect of MPV, platelet count, age and smoking status. MPV was the only significant risk factor for DVT with odds ratio 1.39 (1.14-1.68). For unprovoked DVT, both MPV and platelet count contributed to risk with odds ratio of 1.36 (1.06-1.74, p=0.015) and 0.997 (0.994-1.0, p=0.037) respectively. Further analysis was undertaken to compare MPV in white (provoked 84, unprovoked 50, controls 79) and black (provoked 55, unprovoked 46, controls 51) subgroups. There was no difference in mean age between white and black subjects or controls. Interestingly, in the black subgroup 73.9% of males had an unprovoked DVT compared with 26.1% of females. This gender difference was not seen in the white subgroup (unprovoked 37.9% males, 36.8% females) and was not explained by the presence of pregnancy or hormone use (18 vs 18.4% black vs white females). There was no significant difference in MPV or platelet count between white and black subjects or white and black controls. There remained a significant difference between white subjects and white controls mean MPV (8.1 vs 7.7, p=0.014) accentuated in the unprovoked subgroup (8.3 vs7.7, P=0.007); median platelet count was only significantly lower for unprovoked DVT compared to controls (251.5, 21–509 vs 285, 31–687, p=0.02). MPV was also significantly higher in black subjects compared to controls (8.3 vs 7.8, p=0.011), and platelet count was significantly lower (256, 129–811 vs 293, 138–642 p=0.032). MPV was no different between unprovoked DVTs and controls, however the effect of platelet count was accentuated (244.5, 167–584 vs 293, 138–642 p<.001). Logistic regression confirmed male gender as the only predictive factor for unprovoked VTE in the black subgroup (OR 5.8, 95% CI 2.36–14, p<0.001); neither MPV nor platelet count contributed to DVT risk. Limitations include the retrospective nature of the study, number of subjects, unavailable body mass indices and the discrepant gender distribution between controls and subjects. In summary, MPV is a risk factor for DVT in both white and black populations, though this link appears to hold true for unprovoked DVT in white populations only. Disclosures: No relevant conflicts of interest to declare.


2012 ◽  
Vol 30 (15_suppl) ◽  
pp. 7588-7588
Author(s):  
Mohit Butaney ◽  
Jennifer Porter ◽  
Neal Ian Lindeman ◽  
Pasi A. Janne ◽  
Michael S. Rabin ◽  
...  

7588 Background: KRAS is one of the most commonly mutated oncogenes in non-small cell lung cancer (NSCLC). While the impact of EGFR mutations and EML4-alk translocations has been well-described, there is limited information about the impact of these somatic mutations on response to chemotherapy. Methods: We retrospectively reviewed the demographics and clinical outcomes of patients with KRAS mutations and compared these to patients who were KRAS wild-type (WT). Eligible pts received 1st-line IV chemo for stage IV NSCLC at DFCI and had known information about both KRAS and EGFR status. Since the biology and impact of EGFR mutations on response to chemo is well-described, we excluded such pts from the analysis. The primary endpoint was progression-free survival (PFS) with first-line chemo; secondary endpoints included radiographic response rate (RR) and overall survival (OS). Results: Between 2/05 and 8/11, there were 63 eligible KRAS pts and 97 eligible WT pts. The groups were similar in age (median 65yrs in both groups), % female (K 62, WT 54) race (K 89% white/6% black, 5% other; WT 86% white,/6% black/8% other), histology (K 90%adeno/8% NSCLC NOS; WT 86% adeno/9%NSCLC NOS), and % of pts receiving 1/2/3 agents in 1st line (K 11/56/33; WT 18/53/30). KRAS pts were less likely to be never or light smokers (4% vs 33% for WT). Nonsmokers were more likely to harbor KRAS transition rather than transversion mutations (3 transition, 1 transversion), while the converse held for smokers (51 transversions, 8 transitions). Median PFS was similar for KRAS vs WT (K .65 vs WT 4.8 months, p=0.81). RR (29% for both groups), disease control rates (K 73% vs WT 78%), and median OS (K 13.5 vs WT 12.1 months, p=.525) were also similar. Outcomes of KRAS pts to 2nd line chemotherapy (PFS 2.2, OS 8.6) are similar to those seen for WT patients in this setting. There was no significant difference in outcomes based on gender, smoking status, drug received (pemetrexed-based vs taxane based), or specific KRAS genotype. Conclusions: Pts with KRAS mutations experience similar outcomes to standard chemotherapy as those who are wild-type for EGFR and KRAS. Going forward, these data can serve as a reference for control arms of KRAS-specific randomized trials.


2015 ◽  
Vol 33 (3_suppl) ◽  
pp. 110-110 ◽  
Author(s):  
George D. Demetri ◽  
Peter Reichardt ◽  
Yoon-Koo Kang ◽  
Jean-Yves Blay ◽  
Heikki Joensuu ◽  
...  

110 Background: The GRID study showed that regorafenib improves progression-free survival compared with placebo in patients with advanced GIST after failure of at least imatinib and sunitinib (HR 0.27; 1-sided p<0.0001; Demetri 2013). At the time of the primary analysis, no significant difference in the secondary endpoint of overall survival (OS) was observed (HR 0.77; p=0.199), but this result may have been confounded by the high rate of crossover to regorafenib (85%) of placebo patients at progression. We conducted exploratory analyses of updated OS data to assess the effect of correcting for this protocol-planned crossover. Methods: The data cut-off for this updated OS analysis was 31 January 2014 (2 years after the primary analysis). OS was corrected using two randomization-based methods: rank preserving structural failure time (RPSFT) and iterative parameter estimation (IPE); both methods are considered as best choice among all correction analytics. Hazard ratios and 95% CI were derived using the Cox model. Results: A total of 139 deaths had occurred at the time of data cut-off: 91 events (68.4% of patients) in the regorafenib group and 48 (72.7%) in the placebo group. A total of 22 patients remained on regorafenib treatment (median duration 2.1 years, range 0.9–2.4). The updated hazard ratio for OS favored regorafenib (0.85, 95% CI: 0.60 - 1.21; p=0.18). Median OS was estimated as 17.4 months in both groups, with crossover from placebo. The corrected HRs for OS are less than the uncorrected HR (Table). Conclusions: The updated analysis of OS in the GRID trial is consistent with the primary analysis. An exploratory analysis correcting for the impact of cross-over on OS suggests a survival benefit for regorafenib in GIST. Clinical trial information: NCT01271712. [Table: see text]


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