A Novel Indicator of Myocardial Injury after Acute Myocardial Infarction: 'DPP-3'.

BACKGROUND: Dipeptidyl peptidase 3 (DPP-3) is an intracellular enzyme that causes hemodynamic instability and cardiac depression in several cases such as cardiogenic shock, sepsis and burns where DPP-3 is released into the blood due to cell death. Data on the effect of higher DPP-3 levels on acute coronary syndrome (ACS) patients are currently lacking. The aim of this study was to evaluate the effect of DPP-3 levels on ACS patients. METHODS: In this prospective study, we included ACS patients including STEMI and non-STEMI groups and a control group to compare various demographic, echocardiographic and laboratory parameters including DPP-3. DPP-3 levels were measured at 24th, 48th, and 72nd h from the onset of symptoms in ACS patients and then compared with left ventricle ejection fraction (LVEF) for the assessment of left ventricle systolic function. RESULTS: A total of 70 ACS patients (age 62.5 ± 11 years, 68.6% male) were recruited and 48 normal individuals were included as control group (age 61.1 ± 10 years, 66.7% male). It has been demonstrated that DPP-3 levels are significantly higher in the ACS group than the control group like troponin I levels. DPP-3 levels were found to be one of the independent predictors of LVEF similar to NT-proBNP and troponin I. CONCLUSIONS: This study suggests that DPP-3 could be an important indicator of myocardial depression predicting left ventricle systolic function in ACS.

The effect of ferric carboxymaltose treatment on the Tp-e interval and the Tp-e/QT and Tp-e/QTc ratios in heart failure patients with iron deficiency.

Aim    In heart failure (HF) patients with iron deficiency, cardiac electrical irregularity is a cause of arrhythmias. The aim of our study was to evaluate the effect of ferric carboxymaltose (FCM) treatment on T wave peak to end (Tp-e) interval and the Tp-e / QT and Tp-e / corrected QT (QTc) ratios that reflect the transmural dispersion of repolarization in HF patients with iron deficiency.Material and methods    Forty HF patients with iron deficiency that were treated with FCM were included in our single center, observational study. Repolarization parameters on electrocardiograms recorded before and 12 wks after FCM treatment were compared. Additionally, these parameters were compared with ventricular repolarization parameters of 40 healthy age and gender matched individuals and with another group of 40 HF patients without iron deficiency.Results    In the HF patients with iron deficiency, the Tp-e interval and the Tp-e / QT and Tp-e / QTc ratios before FCM treatment were 103.7±19.1 ms, 0.25± 0.04, 0.23±0.04, respectively. These values were higher compared to the healthy the group and HF group without iron deficiency (p<0.001). In the HF patients with iron deficiency, the Tp-e interval and the Tp-e / QT and Tp-e / QTc ratios after FCM treatment were lower compared to pre-treatment and similar to the HF patients without iron deficiency (89.4±18.6 ms, 0.22±0.04, 0.20±0.04, respectively; p<0.001).Conclusion    FCM treatment of HF patients with iron deficiency corrects prolonged Tp-e interval and high Tp-e / QT and Tp-e / QTc ratios, which are risk factors for ventricular arrhythmias.

Prognostic performance of copeptin among patients with acute decompensated heart failure.

BACKGROUND: In heart failure (HF), various biomarkers have been established for prognosis. However, little is known about the relevance of copeptin measurements to HF. This study aimed to explore the prognostic value of copeptin for predicting cardiovascular (CV) death or HF-related re-hospitalisation in patients with acute decompensated HF. MATERIALS AND METHODS: We prospectively enrolled 155 consecutive patients with acute signs and symptoms of HF. Plasma copeptin and N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels were measured at admission. Patients were monitored for 90 days regarding the composite endpoint of CV death or acute HF-related re-hospitalisation. RESULTS: Of the 155 patients enrolled, 40 reached the endpoint, and 115 were in a stable condition during follow-up. Patients who reached an adverse endpoint showed higher NT-proBNP and copeptin levels compared to patients in stable condition. Receiver operating characteristic curve analysis revealed that the area under curve of copeptin 0.844 (95% CI, 0.753-0.935) was superior to that of NT-proBNP 0.809 (95% CI, 0.729-0.890) for the prediction of adverse events within 90 days. Meanwhile, compared to the group with lower copeptin levels (<34 pmol/L), patients with higher copeptin levels (≥34 pmol/L) were at a 10.672-times higher risk of CV death or acute HF-related re-hospitalisation. Multivariate Cox proportional hazards regression analysis revealed that increased copeptin level was a significantly independent predictor of adverse events (risk ratio, 1.051; 95% CI, 1.020-1.083; p < 0.001). CONCLUSION: Copeptin was found to be a strong, novel marker for predicting CV death or HF-related re-hospitalisation in patients with acute decompensated HF.