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Comparative Study
Journal Article
Severe mitral regurgitation is associated with increased copeptin levels in heart failure with reduced ejection fraction.
Kardiologia Polska 2017
BACKGROUND AND AIM: The objective of this study was to assess the potential role of mitral regurgitation (MR) in the release of copeptin in heart failure patients with reduced ejection fraction (HFrEF).
METHODS: The study included 63 patients of whom 33 had functional mild MR (Group 1) and 30 had functional severe MR (Group 2). The functional class of both groups was New York Heart Association (NYHA) Class III. Blood samples for the determination of plasma copeptin and B-type natriuretic peptide (BNP) levels were obtained on the same day with the echo-cardiographic examination. Standard echocardiographic studies were performed.
RESULTS: Copeptin and BNP levels showed a substantial agreement in the whole study group (Kappa level: 0.607, p < 0.0001). Also, copeptin and BNP showed a strong correlation and were both increased and significantly higher in Group 2 than in Group 1 (p < 0.001 and p < 0.05, respectively). Left ventricular global longitudinal strain and left ventricular ejection fraction values were similar in both groups. The study population were divided into two subgroups on the basis of copeptin median level (6.4 ng/mL), and the prevalence of severe MR was significantly higher in the above-median-copeptin subgroup. A linear regression analysis showed that the presence of severe MR was the only independent predictor of high circulating plasma copeptin level (OR 7.5, 95% CI 2.8-12.1; p = 0.002).
CONCLUSIONS: Severe MR is an independent predictor of elevated plasma copeptin level in HFREF irrespective of systolic function.
METHODS: The study included 63 patients of whom 33 had functional mild MR (Group 1) and 30 had functional severe MR (Group 2). The functional class of both groups was New York Heart Association (NYHA) Class III. Blood samples for the determination of plasma copeptin and B-type natriuretic peptide (BNP) levels were obtained on the same day with the echo-cardiographic examination. Standard echocardiographic studies were performed.
RESULTS: Copeptin and BNP levels showed a substantial agreement in the whole study group (Kappa level: 0.607, p < 0.0001). Also, copeptin and BNP showed a strong correlation and were both increased and significantly higher in Group 2 than in Group 1 (p < 0.001 and p < 0.05, respectively). Left ventricular global longitudinal strain and left ventricular ejection fraction values were similar in both groups. The study population were divided into two subgroups on the basis of copeptin median level (6.4 ng/mL), and the prevalence of severe MR was significantly higher in the above-median-copeptin subgroup. A linear regression analysis showed that the presence of severe MR was the only independent predictor of high circulating plasma copeptin level (OR 7.5, 95% CI 2.8-12.1; p = 0.002).
CONCLUSIONS: Severe MR is an independent predictor of elevated plasma copeptin level in HFREF irrespective of systolic function.
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