{"title":"血管加压素浓度与慢性心力衰竭严重程度的相关性:终末期和失代偿性心力衰竭患者的特征","authors":"E. S. Trofimov, A. S. Poskrebysheva, N. Shostak","doi":"10.17650/1818-8338-2018-12-1-36-42","DOIUrl":null,"url":null,"abstract":"Objective: to evaluate vasopressin (VP) concentration in patients with varying severity of chronic heart failure (CHF), intensity of clinical symptoms, and decreased level of left ventricular ejection fraction (LVEF). Materials and methods. In total, 120 patients (44 males, 76 females) with CHF of varying genesis (mean age 72.12 ± 10.18 years) and 30 clinically healthy individuals (18 males, 12 females) as a control group (mean age 33.4 ± 6.23 years) were examined. All patients underwent comprehensive clinical and instrumental examination in accordance with the standards for patients with CHF. The VP level was determined using ELISA. Statistical analysis was performed using the IBM SPSS Statistics v. 23 software.Results. The patients with CHF had significantly higher blood VP levels compared to the control group (72.91 ± 53.9 pg/ml versus 6.6 ± 3.2 pg/ml respectively; p <0.01). At the same time, patients with stage III CHF had significantly lower VP levels than patients with stages IIВ and IIА (35.61 ± 21.53 pg/ml versus 71.67 ± 48.31 pg/ml and 86.73 ± 59.78 pg/ml respectively; p<0.01). A similar picture was observed for the functional classes (FC). For instance, for CHF FC II and III, the VP level was 91.93 ± 67.13 pg/ml and 77.95 ± 54.01 pg/ml respectively, while for FC IV it decreased to 50.49 ± 28.18 pg/ml (p <0.01). The VP concentration in patients who subsequently perished was significantly lower than in patients who survived (48.79 ± 26.30 pg/ml versus 79.72 ± 57.73 pg/ml; p = 0.012). Moreover, in patients with LVEF <50 %, the VP level was significantly lower than in patients with LVEF >50 % (59.43 ± 42.51 pg/ml versus 86.43 ± 62.46 pg/ml respectively; p <0.05).Conclusion. The observed significant differences in VP in patients with stage III and IV CFH can indicate depletion of neurohumoral mediators in this patient category. However, a correlation between the VP level and the level of LVEF decrease can indicate a significant difference in the role of VP in CHF pathogenesis in patients with preserved and decreased LVEF. This observation requires further research.","PeriodicalId":82998,"journal":{"name":"The Clinician","volume":" ","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2018-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"CORRELATION BETWEEN VAS OPRESSIN CONCENTRATION AND CHRONIC HEART FAILURE SEVE RITY: CHARAC TERISTICS OF PA TIENTS WITH TERMINAL AND DECOMPE NSA TED HEART FAILURE\",\"authors\":\"E. S. Trofimov, A. S. Poskrebysheva, N. Shostak\",\"doi\":\"10.17650/1818-8338-2018-12-1-36-42\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Objective: to evaluate vasopressin (VP) concentration in patients with varying severity of chronic heart failure (CHF), intensity of clinical symptoms, and decreased level of left ventricular ejection fraction (LVEF). Materials and methods. In total, 120 patients (44 males, 76 females) with CHF of varying genesis (mean age 72.12 ± 10.18 years) and 30 clinically healthy individuals (18 males, 12 females) as a control group (mean age 33.4 ± 6.23 years) were examined. All patients underwent comprehensive clinical and instrumental examination in accordance with the standards for patients with CHF. The VP level was determined using ELISA. Statistical analysis was performed using the IBM SPSS Statistics v. 23 software.Results. The patients with CHF had significantly higher blood VP levels compared to the control group (72.91 ± 53.9 pg/ml versus 6.6 ± 3.2 pg/ml respectively; p <0.01). At the same time, patients with stage III CHF had significantly lower VP levels than patients with stages IIВ and IIА (35.61 ± 21.53 pg/ml versus 71.67 ± 48.31 pg/ml and 86.73 ± 59.78 pg/ml respectively; p<0.01). A similar picture was observed for the functional classes (FC). For instance, for CHF FC II and III, the VP level was 91.93 ± 67.13 pg/ml and 77.95 ± 54.01 pg/ml respectively, while for FC IV it decreased to 50.49 ± 28.18 pg/ml (p <0.01). The VP concentration in patients who subsequently perished was significantly lower than in patients who survived (48.79 ± 26.30 pg/ml versus 79.72 ± 57.73 pg/ml; p = 0.012). Moreover, in patients with LVEF <50 %, the VP level was significantly lower than in patients with LVEF >50 % (59.43 ± 42.51 pg/ml versus 86.43 ± 62.46 pg/ml respectively; p <0.05).Conclusion. The observed significant differences in VP in patients with stage III and IV CFH can indicate depletion of neurohumoral mediators in this patient category. However, a correlation between the VP level and the level of LVEF decrease can indicate a significant difference in the role of VP in CHF pathogenesis in patients with preserved and decreased LVEF. This observation requires further research.\",\"PeriodicalId\":82998,\"journal\":{\"name\":\"The Clinician\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2018-07-18\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"The Clinician\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.17650/1818-8338-2018-12-1-36-42\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"The Clinician","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.17650/1818-8338-2018-12-1-36-42","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
CORRELATION BETWEEN VAS OPRESSIN CONCENTRATION AND CHRONIC HEART FAILURE SEVE RITY: CHARAC TERISTICS OF PA TIENTS WITH TERMINAL AND DECOMPE NSA TED HEART FAILURE
Objective: to evaluate vasopressin (VP) concentration in patients with varying severity of chronic heart failure (CHF), intensity of clinical symptoms, and decreased level of left ventricular ejection fraction (LVEF). Materials and methods. In total, 120 patients (44 males, 76 females) with CHF of varying genesis (mean age 72.12 ± 10.18 years) and 30 clinically healthy individuals (18 males, 12 females) as a control group (mean age 33.4 ± 6.23 years) were examined. All patients underwent comprehensive clinical and instrumental examination in accordance with the standards for patients with CHF. The VP level was determined using ELISA. Statistical analysis was performed using the IBM SPSS Statistics v. 23 software.Results. The patients with CHF had significantly higher blood VP levels compared to the control group (72.91 ± 53.9 pg/ml versus 6.6 ± 3.2 pg/ml respectively; p <0.01). At the same time, patients with stage III CHF had significantly lower VP levels than patients with stages IIВ and IIА (35.61 ± 21.53 pg/ml versus 71.67 ± 48.31 pg/ml and 86.73 ± 59.78 pg/ml respectively; p<0.01). A similar picture was observed for the functional classes (FC). For instance, for CHF FC II and III, the VP level was 91.93 ± 67.13 pg/ml and 77.95 ± 54.01 pg/ml respectively, while for FC IV it decreased to 50.49 ± 28.18 pg/ml (p <0.01). The VP concentration in patients who subsequently perished was significantly lower than in patients who survived (48.79 ± 26.30 pg/ml versus 79.72 ± 57.73 pg/ml; p = 0.012). Moreover, in patients with LVEF <50 %, the VP level was significantly lower than in patients with LVEF >50 % (59.43 ± 42.51 pg/ml versus 86.43 ± 62.46 pg/ml respectively; p <0.05).Conclusion. The observed significant differences in VP in patients with stage III and IV CFH can indicate depletion of neurohumoral mediators in this patient category. However, a correlation between the VP level and the level of LVEF decrease can indicate a significant difference in the role of VP in CHF pathogenesis in patients with preserved and decreased LVEF. This observation requires further research.