Liyuan Han1, Chongke Zhong2, Xiaoqing Bu3, Tan Xu3, Aili Wang3, Yanbo Peng4, Tian Xu5, Jinchao Wang6, Hao Peng3, Qunwei Li7, Zhong Ju8, Deqing Geng9, Yonghong Zhang10, Jiang He11. 1. Department of Epidemiology, School of Public Health and Jiangsu Key Laboratory of Preventive and Translational Medicine for Geriatric Diseases, Medical College of Soochow University, Suzhou, Jiangsu, China; Department of Preventive Medicine, Zhejiang Provincial Key Laboratory of Pathophysiology, School of Medicine, Ningbo University, Ningbo, China; Department of Epidemiology, Tulane University School of Public Health and Tropical Medicine, New Orleans, LA, USA. 2. Department of Epidemiology, School of Public Health and Jiangsu Key Laboratory of Preventive and Translational Medicine for Geriatric Diseases, Medical College of Soochow University, Suzhou, Jiangsu, China; Department of Epidemiology, Tulane University School of Public Health and Tropical Medicine, New Orleans, LA, USA. 3. Department of Epidemiology, School of Public Health and Jiangsu Key Laboratory of Preventive and Translational Medicine for Geriatric Diseases, Medical College of Soochow University, Suzhou, Jiangsu, China. 4. Department of Neurology, Affiliated Hospital of North China University of Science and Technology, Tangshan, Hebei, China. 5. Department of Epidemiology, School of Public Health and Jiangsu Key Laboratory of Preventive and Translational Medicine for Geriatric Diseases, Medical College of Soochow University, Suzhou, Jiangsu, China; Department of Neurology, Affiliated Hospital of Nantong University, Nantong, Jiangsu, China. 6. Department of Neurology, Yutian County Hospital, Tangshan, Hebei, China. 7. Department of Epidemiology, School of Public Health, Taishan Medical College, Taian, Shandong, China. 8. Department of Neurology, Kerqin District First People's Hospital of Tongliao City, Tongliao, Inner Mongolia, China. 9. Department of Neurology, Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu, China. 10. Department of Epidemiology, School of Public Health and Jiangsu Key Laboratory of Preventive and Translational Medicine for Geriatric Diseases, Medical College of Soochow University, Suzhou, Jiangsu, China; Department of Epidemiology, Tulane University School of Public Health and Tropical Medicine, New Orleans, LA, USA. Electronic address: yhzhang@suda.edu.cn. 11. Department of Epidemiology, School of Public Health and Jiangsu Key Laboratory of Preventive and Translational Medicine for Geriatric Diseases, Medical College of Soochow University, Suzhou, Jiangsu, China; Department of Epidemiology, Tulane University School of Public Health and Tropical Medicine, New Orleans, LA, USA. Electronic address: jhe@tulane.edu.
Abstract
BACKGROUND AND AIMS: We performed a prospective investigation of the longer-term prognostic value of lipoprotein-associated phospholipase A2 (Lp-PLA2) mass for all-cause mortality and vascular events within one year after acute ischemic stroke. METHODS: We examined the Lp-PLA2 mass among 3401 participants enrolled in the China Antihypertensive Trial in Acute Ischemic Stroke. The primary outcome was all-cause mortality. Cox proportional hazard ratios (HRs) and 95% confidence intervals (95% CIs) were constructed to assess the independent associations between the baseline Lp-PLA2 mass and the outcomes after adjustment for variables in models 1, 2, and 3 [further adjusted for low-density lipoprotein cholesterol (LDL-C)]. RESULTS: Overall, 3278 patients completed the follow-up, during which, 188 all-cause death events occurred. The Kaplan-Meier survival curve showed that the cumulative incidence rate of all-cause mortality increased across quartiles of Lp-PLA2 mass (log-rank p = 0.018). Compared with the lowest quartile of Lp-PLA2, the HRs (95% CIs) for the highest quartile of Lp-PLA2 were 1.89 (1.22-2.91), 2.16 (1.31-3.55), and 2.17 (1.32-3.58) for all-cause mortality after adjusting for the covariables in models 1, 2, and 3, respectively. In addition, patients in the highest quartile of Lp-PLA2 mass coupled with higher LDL-C had significantly highest risk of all-cause mortality (HR, 1.81; 95% CI, 1.05 to 3.11; p = 0.032). CONCLUSIONS: The elevated Lp-PLA2 mass was associated with all cause-death independently of other risk factors within one year after acute ischemic stroke.
BACKGROUND AND AIMS: We performed a prospective investigation of the longer-term prognostic value of lipoprotein-associated phospholipase A2 (Lp-PLA2) mass for all-cause mortality and vascular events within one year after acute ischemic stroke. METHODS: We examined the Lp-PLA2 mass among 3401 participants enrolled in the China Antihypertensive Trial in Acute Ischemic Stroke. The primary outcome was all-cause mortality. Cox proportional hazard ratios (HRs) and 95% confidence intervals (95% CIs) were constructed to assess the independent associations between the baseline Lp-PLA2 mass and the outcomes after adjustment for variables in models 1, 2, and 3 [further adjusted for low-density lipoprotein cholesterol (LDL-C)]. RESULTS: Overall, 3278 patients completed the follow-up, during which, 188 all-cause death events occurred. The Kaplan-Meier survival curve showed that the cumulative incidence rate of all-cause mortality increased across quartiles of Lp-PLA2 mass (log-rank p = 0.018). Compared with the lowest quartile of Lp-PLA2, the HRs (95% CIs) for the highest quartile of Lp-PLA2 were 1.89 (1.22-2.91), 2.16 (1.31-3.55), and 2.17 (1.32-3.58) for all-cause mortality after adjusting for the covariables in models 1, 2, and 3, respectively. In addition, patients in the highest quartile of Lp-PLA2 mass coupled with higher LDL-C had significantly highest risk of all-cause mortality (HR, 1.81; 95% CI, 1.05 to 3.11; p = 0.032). CONCLUSIONS: The elevated Lp-PLA2 mass was associated with all cause-death independently of other risk factors within one year after acute ischemic stroke.