ABSTRACT
Objective: To summarize the clinical characteristics of heart failure patients with recovered ejection fraction (HFrecEF) and identify variables capable of predicting left ventricular ejection fraction (LVEF) recovery. Methods: This case control study included patients with heart failure, who admitted to Department of Cardiology of Beijing Hospital from January 1, 2009 to December 31, 2017. The patients were divided into 3 groups based on the baseline LVEF and changes of LVEF: heart failure with reduced ejection fraction (HFrEF, baseline LVEF≤40%, follow-up LVEF≤40% or follow-up LVEF>40% but LVEF increase<10% from baseline), HFrecEF(baseline LVEF≤40%, follow-up LVEF>40% and increase≥10% from baseline), and heart failure with preserved ejection fraction (HFpEF, baseline LVEF>40%). Clinical data were collected and endpoint events (all-cause death, cardiovascular death and sudden death) were recorded. The Log-rank test was used to evaluate the differences of terminal events in different groups, and Kaplan-Meier survival analysis was performed. Logistic regression equation was used to identify prognostic factors of HFrecEF. Results: A total of 310 patients with heart failure were included. There were 91(29.4%) HFrEF patients, 38(12.3%) HFrecEF patients and 181(58.4%) HFpEF patients. Compared with HFrEF patients and HFpEF patients, HFrecEF patients were featured by younger age, more likely to be female, higher systolic blood pressure, diastolic blood pressure and resting heart rate (all P<0.05). Dilated cardiomyopathies were more common, while old myocardial infarctions were less common in HFrecEF (both P<0.05). During a median follow-up of 36.7(18.0, 63.9) months, Kaplan-Meier survival analysis found that HFrecEF patients had the lowest all-cause mortality (Log-rank P=0.047, HFrecEF vs. HFpEF P=0.017, HFrecEF vs. HFrEF P=0.016, and HFpEF vs. HFrEF P=0.782).The cardiovascular mortality ranged from low to high was in HFrecEF patients, HFpEF patients, and HFrEF patients (Log-rank P<0.001, HFrecEF vs. HFpEF P=0.029, HFrecEF vs. HFrEF P<0.001, HFrEF vs. HFpEF P=0.005). Sudden death rate was similar among the three groups (Log-rank P=0.520). Logistic regression analysis showed that left ventricular end-diastolic diameter (LVEDD)≤55 mm (OR=5.922, 95%CI 1.685-20.812, P=0.006), higher diastolic blood pressure (OR=1.058, 95%CI 1.017-1.100, P=0.005), faster resting heart rate (OR=1.042, 95%CI 1.006-1.080, P=0.024), absence of old myocardial infarction (OR=5.343, 95%CI 1.731-16.488, P=0.004) were independent prognostic factors of LVEF recovery after clinical treatment. Conclusions: Patients with HFrecEF are associated with a better prognosis as compared to patients with HFrEF and HFpEF. LVEDD≤55 mm, higher diastolic blood pressure, faster heart rate,and absence of old myocardial infarction are independent prognostic factors of LVEF recovery after clinical treatment.
Subject(s)
Female , Humans , Male , Case-Control Studies , Heart Failure , Prognosis , Stroke Volume , Ventricular Dysfunction, Left , Ventricular Function, LeftABSTRACT
<p><b>OBJECTIVE</b>To investigate the effects of Cyclin A1 on the proliferation of SKM-1 cells and its underlying role in myelodysplastic syndrome (MDS).</p><p><b>METHODS</b>Cyclin A1 was knocked down with its small interfering RNA (siRNA). The efficiency of siRNA transfection was measured by Western blot and RT-PCR. Then the proliferation of SKM-1 cells and the expression of CDK2,RUNX1 and SRSF2 with and without knockdown of Cyclin A1 recorded and analysed respectively.</p><p><b>RESULTS</b>Cyclin A1 was knocked down by siRNA after transfected for 48 h. The kncokdown of Cyclin A1 inhibited the proliferation of SKM-1 cells and down-regulated the expression of CDK2, RUNX1 and SRSF2, and these effects were at least partially mediated through RUNX1 and SRSF2 signaling pathway.</p><p><b>CONCLUSION</b>Cyclin A1 plays an important role in the proliferation of SKM-1 cells. These findings provide new insights into the pathogenesis of MDS, and it may be a potential target in the treatment of MDS.</p>