SUMMARY OBJECTIVE: The aim of our study was to determine the role of serum glucose–potassium ratio in predicting inhospital mortality in coronary care unit patients. METHODS: This study used data from the MORtality in CORonary Care Units in Turkey study, a national, observational, multicenter study that included all patients admitted to coronary care units between September 1, 2022, and September 30, 2022. Statistical analyses assessed the independent predictors of mortality. Two models were created. Model 1 included age, history of heart failure, chronic kidney disease, hypertension, diabetes mellitus, and coronary artery disease. Model 2 included glucose–potassium ratio in addition to these variables. Multivariate regression and receiver operating characteristic analysis were performed to compare Model 1 and Model 2 to identify if the glucose–potassium ratio is an independent predictor of inhospital mortality. RESULTS: In a study of 3,157 patients, the mortality rate was 4.3% (n=137). Age (p=0.002), female gender (p=0.004), mean blood pressure (p<0.001), serum creatinine (p<0.001), C-reactive protein (p=0.002), white blood cell (p=0.002), and glucose–potassium ratio (p<0.001) were identified as independent predictors of mortality through multivariate regression analysis. The receiver operating characteristic analysis indicated that Model 2 had a statistically higher area under the curve than Model 1 (area under the curve 0.842 vs area under the curve 0.835; p<0.001). A statistically significant correlation was found between the inhospital mortality and glucose–potassium ratio (OR 1.015, 95%CI 1.006–1.024, p<0.001). CONCLUSION: Our study showed that the glucose–potassium ratio may be a significant predictor of inhospital mortality in coronary care unit patients. OBJECTIVE glucosepotassium glucose potassium METHODS national observational 2022 30 created age failure disease hypertension mellitus variables RESULTS 3157 3 157 3,15 43 4 4.3 n=137. n137 n n=137 . 137 (n=137) p=0.002, p0002 p p=0.002 , 0 002 (p=0.002) p=0.004, p0004 p=0.004 004 (p=0.004) p<0.001, p0001 p<0.001 001 Creactive C reactive (p<0.001 0842 842 0.84 0.835 0835 835 p<0.001. p<0.001) OR 1015 015 1.015 95CI CI 95 10061024 006 024 1.006–1.024 CONCLUSION 202 315 15 3,1 4. n13 n=13 13 (n=137 p000 p=0.00 00 (p=0.002 (p=0.004 p<0.00 (p<0.00 084 84 0.8 0.83 083 83 101 01 1.01 9 1006102 02 1.006–1.02 20 31 3, n1 n=1 (n=13 p00 p=0.0 (p=0.00 p<0.0 (p<0.0 08 8 0. 10 1.0 100610 1.006–1.0 n= (n=1 p0 p=0. (p=0.0 p<0. (p<0. 1. 10061 1.006–1. (n= p=0 (p=0. p<0 (p<0 1006 1.006–1 (n p= (p=0 p< (p< 100 1.006– (p= (p 1.006 1.00

Abstract Objective: Mitral valve prolapse (MVP) is the most common cause of mitral regurgitation in developed countries. The role of inflammation in the pathogenesis of MVP is still not clear. In this study, we aimed to investigate how inflammatory markers such as monocyte/high-density lipoprotein ratio (MHR), lymphocyte/monocyte ratio (LMR), neutrophil/lymphocyte ratio (NLR), and platelet/neutrophil ratio (PLR) are affected in MVP patients. Methods: In this retrospective study, we included 461 patients with MVP and 459 normal echocardiographic patients, matched with gender and age. Inflammatory markers and all variables were compared between the two groups. Results: There were no statistically significant differences in age, sex, or body mass index between the two groups. Neutrophil counts (4,960 [3,900-6,780]. 4,200 [3,800-5,600], p < 0.001), NLR (2.488 [1.72-4.51], 1.857 [1.49-2.38], p < 0.001), MHR (14.9 [11.9-18.6], 12.2 [9.4-17.3], p = 0.003), PLR (122.4 [85-171], 104.4 [85-130], p < 0.001), and CRP (0.71 ± 0.50, 0.67 ± 0.33 p < 0.001) were significantly higher, and LMR (3.75 [2.75-5.09], 4.06 [3.12-4.83] p = 0.016) was significantly lower in the MVP group than the control group, respectively. In logistic regression analysis, NLR (odds ratio [OR]: 1.058 [1.047-1.072]; p < 0.001), LMR (OR: 1.560 [1.211-2.522]; p = 0.027), and PLR (OR: 1.015 [1.012-1.019]; p = 0.003) were found to be independent predictors for MVP presence. Conclusions: These parameters can be used as a simple, low-cost, practical tool to detect inflammation in MVP.

Resumen Objetivo: El prolapso de la válvula mitral (MVP) es la causa más común de insuficiencia mitral en los países desarrollados. El papel de la inflamación en la patogenia del MVP aún no está claro. En este estudio, nuestro objetivo fue investigar cómo los marcadores inflamatorios como la proporción monocitos/HDL (MHR), la proporción linfocitos/monocitos (LMR), la proporción neutrófilos/linfocitos (NLR) y la proporción plaquetas/neutrófilos (PLR) se ven afectados en pacientes con MVP. Métodos: En este estudio retrospectivo, incluimos a 461 pacientes con PVM y 459 pacientes ecocardiográficos normales, emparejados por sexo y edad. Se compararon los marcadores inflamatorios y todas las variables entre los dos grupos. Resultados: No hubo diferencias estadísticamente significativas en edad, sexo o índice de masa corporal entre los dos grupos. El recuento de neutrófilos (4,960 [3,900-6,780], 4,200 [3,800-5,600], p < 0.001), NLR (2.488 [1.72-4.51], 1,857 [1.49-2.38], p < 0.001), MHR (14.9 [11.9-18.6]), (12.2 [9.4-17.3], p = 0.003), PLR (122.4 [85-171], 104.4 [85-130], p < 0.001) y PCR (0.71 ± 0.50, 0.67 ± 0.33 p < 0.001) fueron significativamente mayores y LMR (3.75 [2.75-5.09], 4.06 [3.12-4.83] p = 0.016) fue significativamente menor en el grupo MVP que en el grupo de control, respectivamente. En el análisis de regresión logística; NLR (OR: 1.058 [1.047-1.072]; p < 0.001), LMR (OR: 1.560 [1.211-2.522]; p = 0.027) y PLR (OR: 1.015 [1.012-1.019]; p = 0.003) se encontraron como predictores independientes para la presencia de MVP. Conclusiones: Estos parámetros pueden utilizarse como una herramienta sencilla, práctica y de bajo costo para detectar la inflamación en el PVM.