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BACKGROUND@#The association between free triiodothyronine (FT3) and long-term prognosis in dilated cardiomyopathy (DCM) patients has not been evaluated. The purpose of this study was to determine whether the level of FT3 could provide prognostic value in patients with DCM.@*METHODS@#Data of consecutive patients diagnosed with DCM were collected from October 2009 to December 2014. FT3 was measured by fluoroimmunoassay. Other biochemical markers, such as free thyroxin (FT4), thyroid-stimulating hormone, red blood cell, hemoglobin, blood urea nitrogen, and serum creatinine, were tested at the same time. Follow-up was performed every 3 months. The primary endpoint was all-cause mortality. Pearson analysis was used to evaluate the correlation of FT3 and other lab metrics with DCM patients' prognosis. The association of long-term mortality in DCM and FT3 was compared using Cox hazards model.@*RESULTS@#Data of 176 patients diagnosed with DCM were collected. Of them, 24 patients missed FT3 values and six patients were lost to follow-up. Altogether, data of 146 patients were analyzed. During the median follow-up time of 79.9 (53.5-159.6) months, nine patients lost, 61 patients died (non-survival group), and 85 patients survived (survival group). FT3 was significantly lower in non-survival group than that in survival group (3.65 ± 0.83 pmol/L vs. 4.36 ± 1.91 pmol/L; P = 0.003). FT3 also showed a significantly positive correlation with red blood cell and hemoglobin, negatively correlated with age, blood urea nitrogen and serum creatinine (P < 0.05), respectively. Patients in the group of lower FT3 levels (FT3 ≤3.49 pmol/L) suffered from a higher risk of all-cause mortality (P for log-rank = 0.001). In multivariate Cox regression analysis, FT3 level was significantly associated with all-cause mortality (hazard ratio: 0.70, 95% confidence interval 0.52-0.95, P for trend = 0.021).@*CONCLUSION@#Low levels of FT3 were associated with increased all-cause mortality in patients with DCM.
RESUMEN
BACKGROUND: Factor V (FV) Leiden mutation-related activated protein C resistance (APCR) is one of the common inherited risk factors for venous thromboembolism (VTE) in caucasian population. Although APCR could be identified in some of the Chinese healthy people and patients with VTE, it was not related to FV Leiden mutation. In 2008, we have identified a novel FV mutation (FV E666D) in exon 13 in a hereditary APCR family. And we presumed that the novel mutation might be a genetic defect of APCR in the Chinese population. The aim of our study was to evaluate the prevalence of FV E666D mutation and its correlation with APCR in the Chinese population in a larger series. METHODS: From June 2009 to January 2011, 163 consecutive patients who underwent thrombophilia tests in our hospital were recruited. The clinical data were retrospectively reviewed. Thrombophilia tests included APCR, anticoagulant proteins, and antiphospholipid antibodies. Factor V E666D mutation was detected. RESULT: Of the 163 patients, 6 (3.7%) were identified as APCR positive, 2.9% for patients without thrombosis and 5.1% for patients with thrombosis or thrombosis history. Factor V E666D mutation was not detectable in all the 163 patients including 6 APCR-positive patients. CONCLUSIONS: The prevalence of APCR either in the nonthrombotic patients or in the patients with thrombosis was lower than that reported in other Chinese studies. Our study couldn't provide illustration whether FV E666D mutation is correlated with APCR in the Chinese population.