Ya-Wen Lu1, Shu-Fen Lu2, Ruey-Hsing Chou3, Po-Shan Wu4, Yu-Chen Ku5, Chin-Sung Kuo6, Chun-Chin Chang7, Yi-Lin Tsai1, Cheng-Hsueh Wu8, Po-Hsun Huang9. 1. Division of Cardiology, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan; Cardiovascular Research Center, National Yang-Ming University, Taipei, Taiwan. 2. Department of Nursing, Taipei Veterans General Hospital, Taipei, Taiwan; School of Nursing, National Yang-Ming University, Taipei, Taiwan. 3. Division of Cardiology, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan; Cardiovascular Research Center, National Yang-Ming University, Taipei, Taiwan; Department of Critical Care Medicine, Taipei Veterans General Hospital, Taipei, Taiwan; Institute of Clinical Medicine, National Yang-Ming University, Taipei, Taiwan. Electronic address: thanatosrs@gmail.com. 4. Division of Clinical Nutrition, Department of Dietetics and Nutrition, Taipei Veterans General Hospital, Taipei, Taiwan. 5. Department of Nursing, Taipei Veterans General Hospital, Taipei, Taiwan. 6. Cardiovascular Research Center, National Yang-Ming University, Taipei, Taiwan; Institute of Clinical Medicine, National Yang-Ming University, Taipei, Taiwan; Division of Endocrinology and Metabolism, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan. 7. Division of Cardiology, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan; Cardiovascular Research Center, National Yang-Ming University, Taipei, Taiwan; Institute of Clinical Medicine, National Yang-Ming University, Taipei, Taiwan. 8. Division of Cardiology, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan; Department of Critical Care Medicine, Taipei Veterans General Hospital, Taipei, Taiwan. 9. Division of Cardiology, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan; Cardiovascular Research Center, National Yang-Ming University, Taipei, Taiwan; Department of Critical Care Medicine, Taipei Veterans General Hospital, Taipei, Taiwan; Institute of Clinical Medicine, National Yang-Ming University, Taipei, Taiwan. Electronic address: huangbsvgh@gmail.com.
Abstract
BACKGROUND & AIMS: Aggressive lipid reduction is recommended for patients with AMI, but reverse epidemiology, the lipid paradox, has been reported in several clinical studies. The cause of lipid paradox remains uncertain, and nutrition is one possible explanation. In this single-center retrospective study, we investigated the relationships between baseline LDL concentrations and clinical outcomes in patients with AMI, stratified by different nutritional status. METHODS: Totally 409 patients were enrolled for analysis. The Nutritional Risk Index (NRI) was used to estimate the risk of malnutrition. Subjects were grouped into tertiles according to their NRIs. Clinical outcomes were compared among patients with varying NRIs and LDL levels. RESULTS: Patients in the lowest NRI tertile had increased incidences of in-hospital mortality, cardiogenic shock, decompensated heart failure, renal failure, and sepsis. This tertile was also associated with increased long-term mortality during the follow-up period of 832 ± 744 days. Mortality was increased among patients with baseline LDL concentrations ≤70 mg/dL in the lowest NRI tertile (log rank test, p = 0.0257), but not in the high or median tertiles. Moreover, baseline LDL level ≤70 mg/dL was an independent risk factor of all-cause mortality (adjusted hazard ratio = 1.73; 95% confidence interval, 1.01-2.94; p = 0.045) in the lowest NRI tertile. CONCLUSIONS: Lipid paradox was observed in the high-risk of malnutrition population among patients with AMI. Aggressive lipid-lowering therapy is still recommended for patients with AMI and fair nutritional status. However, when treating patients at high risk of malnutrition, the improvement of nutritional status may be more beneficial than strict LDL control.
BACKGROUND & AIMS: Aggressive lipid reduction is recommended for patients with AMI, but reverse epidemiology, the lipid paradox, has been reported in several clinical studies. The cause of lipid paradox remains uncertain, and nutrition is one possible explanation. In this single-center retrospective study, we investigated the relationships between baseline LDL concentrations and clinical outcomes in patients with AMI, stratified by different nutritional status. METHODS: Totally 409 patients were enrolled for analysis. The Nutritional Risk Index (NRI) was used to estimate the risk of malnutrition. Subjects were grouped into tertiles according to their NRIs. Clinical outcomes were compared among patients with varying NRIs and LDL levels. RESULTS:Patients in the lowest NRI tertile had increased incidences of in-hospital mortality, cardiogenic shock, decompensated heart failure, renal failure, and sepsis. This tertile was also associated with increased long-term mortality during the follow-up period of 832 ± 744 days. Mortality was increased among patients with baseline LDL concentrations ≤70 mg/dL in the lowest NRI tertile (log rank test, p = 0.0257), but not in the high or median tertiles. Moreover, baseline LDL level ≤70 mg/dL was an independent risk factor of all-cause mortality (adjusted hazard ratio = 1.73; 95% confidence interval, 1.01-2.94; p = 0.045) in the lowest NRI tertile. CONCLUSIONS:Lipid paradox was observed in the high-risk of malnutrition population among patients with AMI. Aggressive lipid-lowering therapy is still recommended for patients with AMI and fair nutritional status. However, when treating patients at high risk of malnutrition, the improvement of nutritional status may be more beneficial than strict LDL control.
Authors: Stephen Ellison; Jawan W Abdulrahim; Lydia Coulter Kwee; Nathan A Bihlmeyer; Neha Pagidipati; Robert McGarrah; James R Bain; William E Kraus; Svati H Shah Journal: Sci Rep Date: 2020-12-07 Impact factor: 4.379