Tao Tian

Beijing Fuwai Hospital, Peping, Beijing, China

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Publications (10)21.63 Total impact

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    ABSTRACT: Liddle's syndrome, an autosomal dominant form of monogenic hypertension, is characterized by salt-sensitive hypertension with early penetrance, hypokalemia, metabolic alkalosis, suppression of plasma rennin activity and aldosterone secretion, and a clear-cut response to epithelial sodium channel (ENaC) blockers but not spironolactone therapy. Our understanding of ENaCs and Na+transport defects has expanded greatly over the past two decades and provides detailed insight into the molecular basis of Liddle's syndrome. In this review, we offer an overview of recent advances in understanding the molecular genetics of Liddle's syndrome, involving mutation analysis, molecular mechanisms and genetic testing. The ENaC in the distal nephron is composed of α, β and γ subunits that share similar structures. Mutations associated with Liddle's syndrome are positioned in either β or γ subunits and disturb or truncate a conserved proline-rich sequence (i.e., PY motif), leading to constitutive activation of the ENaC. Genetic testing has made it possible to make accurate diagnoses and develop tailored therapies for mutation carriers.
    Clinica Chimica Acta. 05/2014; 436.
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    ABSTRACT: Left ventricular non-compaction (LVNC) is genetically heterogeneous. It has been previously shown that LVNC is associated with defects in TAZ, DNTA, LDB3, YWHAE, MIB1, PRDM16, and sarcomeric genes. This study was aimed to investigate sarcomeric gene mutations in a Chinese population with LVNC. From 2004 to 2010, 57 unrelated Chinese patients with LVNC were recruited at Fuwai Hospital, Beijing, China. Detailed clinical evaluation was performed on the probands and available family members. DNA samples isolated from the peripheral blood of the index cases were screened for 10 sarcomeric genes, including MYH7, MYBPC3, MYL2, MYL3, MYH6, TNNC1, TNNT2, TNNI3, TPM1, and ACTC1. Seven heterozygous mutations (6 missense and 1 deletion) were identified in 7 (12 %) of the patients. These mutations were distributed among 4 genes, 4 in MYH7, and 1 each in ACTC1, TNNT2, and TPM1. Six of the mutations were novel and another one was reported previously. All mutations affected conserved amino acid residues and were predicted to alter the structure of the proteins by in silico analysis. No significant difference was observed between mutation-positive and mutation-negative patients with respect to clinical characteristics at baseline and mortality during follow-up. In conclusion, our study indicates that sarcomeric gene mutations are uncommon causes of LVNC in Chinese patients and genetic background of the disease may be divergent among the different races.
    Heart and Vessels 04/2014; · 2.13 Impact Factor
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    ABSTRACT: Objective This study was undertaken to evaluate the efficacy of intramyocardial bone marrow cell (BMC) transplant therapy for ischemic heart disease (IHD). Methods The PubMed, Embase, and Cochrane Library databases through October 2013 were searched for randomized clinical trials (RCTs) of intramyocardial BMCs to treat IHD. The primary endpoint was change in left ventricular ejection fraction (LVEF). Secondary endpoints were changes in left ventricular end-systolic volume (LVESV) and left ventricular end-diastolic volume (LVEDV). Weighted mean differences for the changes were estimated with a random-effects model. Results Eleven RCTs with 492 participants were included. Intramyocardial BMC transplantation increased LVEF (4.91%; 95% confidence interval [CI] 2.84%–6.99%; P < 0.00001), reduced LVESV (10.66 mL; 95% CI, −18.92 mL to −2.41 mL; P = 0.01), and showed a trend toward decreased LVEDV (−7.82 mL; 95% CI, −16.36 mL–0.71 mL; P = 0.07). Patients suitable for revascularization with coronary artery bypass grafting had greater improvement in LVEF (7.60%; 95% CI, 4.74%–10.46%, P < 0.00001) than those unsuitable for revascularization (3.76%; 95% CI, 2.20%–5.32%; P < 0.00001). LVEDV reduction was also more significant in revascularizable IHD (−16.51 mL; 95% CI, −22.05 mL to −10.07 mL; P < 0.00001) than non-revascularizable IHD (−0.89 mL; 95% CI, −8.44 mL–6.66 mL; P = 0.82). Conclusion Intramyocardial BMC injection contributes to improvement in left ventricular dysfunction and reduction in left ventricular volume. Patients with revascularizable IHD may benefit more from this therapy.
    Atherosclerosis 04/2014; 233(2):485–492. · 3.71 Impact Factor
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    ABSTRACT: Objective High level of homocysteine induces injury of endothelial cells and predicts adverse cardiovascular events. The objective was to assess the effect of homocysteine-lowering therapy with folic acid on flow-mediated vasodilation in patients with coronary artery disease. Methods and results We conducted a meta-analysis of randomized controlled trials identified from PubMed, Embase, the Cochrane Library. Eight studies were included. Homocysteine-lowering therapy with folic acid in patients with coronary artery disease significantly improve FMD as compared with placebo using random-effect model (SMD = 1.65 with 95% CI 1.12–2.17, p < 0.001). Subgroup analysis of subjects revealed that lipid-lowering therapy, study duration, and Delphi criteria had no effects on FMD. Conclusion Our meta-analysis demonstrated that folic acid supplementation can significantly improve endothelial dysfunction as assessed by FMD in the brachial artery in patients with coronary heart disease.
    Atherosclerosis 01/2014; 235(1):31–35. · 3.71 Impact Factor
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    ABSTRACT: Sex plays an important role in the clinical expression and prognosis of various cardiovascular diseases. This study was designed to observe the effects of sex on hypertrophic cardiomyopathy (HCM).
    PLoS ONE 01/2014; 9(7):e102969. · 3.53 Impact Factor
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    ABSTRACT: The prognostic significance of myocardial bridging in hypertrophic cardiomyopathy (HCM) remains controversial. This investigation sought to evaluate the impact of myocardial bridging on prognosis of patients with HCM. A total of 298 adult patients (73% male, mean age, 53 ± 12 years) with HCM were retrospectively enrolled at Fuwai Hospital from 1999 to 2011. Myocardial bridging was evaluated by coronary angiography. Follow-up data were collected by telephone interviews and mailed questionnaires. Thirty-four (11%, 34/298) patients were determined with myocardial bridging and the middle of left anterior descending artery was the most frequently involved segment (77%, 26/34). Patients with myocardial bridging were younger than those without bridging (48 ± 9 versus 54 ± 12 years, P = 0.001). During the follow-up of 4.2 ± 2.3 years (range, 0.7-12.2 years), the presence of myocardial bridging was not evidently associated with increased risk for all-cause death (P = 0.54), cardiovascular death (P = 0.60), sudden cardiac death (P = 0.53) and deterioration of heart failure (P = 0.84). Myocardial bridging was a relatively common morphological component of HCM but not a predictor for adverse clinical outcomes.
    The American Journal of the Medical Sciences 11/2013; · 1.33 Impact Factor
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    ABSTRACT: Objectives: The clinical outcomes of hypertrophic cardiomyopathy (HCM) are largely unpredictable. This study aimed to investigate the relationship between atrial fibrillation (AF) and its prognostic implications in Chinese patients with HCM. Methods: From 1999 to 2011, 654 unrelated HCM patients were consecutively recruited at Fuwai Hospital. Medical history, including electrocardiographic and echocardiographic data, was analyzed. Results: AF was documented in 158 patients (24%). During follow-up of 4.2 ± 2.8 years, Kaplan-Meier analysis revealed that the presence of AF was associated with an increased risk for all-cause death (p = 0.001), cardiovascular death (p < 0.001), severe heart failure (p < 0.001) and ischemic stroke (p < 0.001). Multivariate analysis identified AF as an independent predictor of stroke-related death (HR 6.71, 95% CI 1.23-38.58, p = 0.03), advanced heart failure (HR 1.83, 95% CI 1.04-3.22, p = 0.04) and ischemic stroke (HR 9.98, 95% CI 4.06-24.53, p < 0.001). Furthermore, enlarged left atrial diameter was positively related to all-cause death (HR 1.09, 95% CI 1.05-1.13, p < 0.001), cardiovascular death (HR 1.08, 95% CI 1.04-1.20, p < 0.001) and development of advanced heart failure (HR 1.05, 95% CI 1.01-1.10, p = 0.01). Conclusions: AF predicts poor outcomes for patients with HCM. Left atrial dilation is also related to an adverse prognosis and provides additional prognostic information. © 2013 S. Karger AG, Basel.
    Cardiology 10/2013; 126(4):258-264. · 1.52 Impact Factor
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    ABSTRACT: This study was undertaken to evaluate the clinical course of isolated left ventricular noncompaction (ILVNC) and to identify the predictors for adverse outcomes in an adult cohort with ILVNC. Between March 2003 and April 2012, 106 adult patients diagnosed with ILVNC at Fuwai Hospital were included in this study. The medical history, electrocardiograms, and echocardiograms of these patients were retrospectively analyzed by chart review. Of these patients, 64 (60 %) were in New York Heart Association (NYHA) functional class III/IV and 84 (79 %) had systolic dysfunction (left ventricular ejection fraction (LVEF) <50 %). During a follow-up of 2.9 ± 2.1 years, 28 (26 %) patients died or underwent heart transplantation. The annual incidence of death or transplantation was 9.1 %. The determinants of death or heart transplantation included NYHA functional class III/IV (hazard ratio (HR) 4.52; 95 % confidence interval (CI) 1.57-13.04; P = 0.005), decreased left ventricular ejection fraction (HR 0.94; 95 % CI 0.90-0.97; P = 0.001), dilated left ventricular end-diastolic diameter (HR, 1.06; 95 % CI, 1.02-1.09; P = 0.001), increased left atrial diameter (HR 1.08; 95 % CI 1.03-1.14; P = 0.001), reduced systolic blood pressure (HR 0.96; 95 % CI 0.94-0.99; P = 0.003), the presence of pulmonary hypertension (HR 3.50; 95 % CI 1.63-7.51; P = 0.001), and right bundle branch block (HR 7.79; 95 % CI 2.56-23.76; P < 0.001). In conclusion, this study demonstrates that ILVNC is related to a high incidence of death or heart transplantation. Advanced heart failure, a dilated left heart with systolic dysfunction, reduced systolic blood pressure, pulmonary hypertension, and right bundle branch block predict adverse outcomes of ILVNC.
    Heart and Vessels 10/2013; · 2.13 Impact Factor
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    ABSTRACT: Background: Hypertrophic cardiomyopathy (HCM), which is characterized by unexplained and asymmetric left ventricular hypertrophy in the absence of other cardiac or systemic diseases, is an inherited cardiovascular disease and presents rising penetrance with aging. Objective: The purpose of this review is to offer an outline of recent progress in the molecular genetics of HCM and to discuss characteristics of elderly HCM patients. Methods: Studies were analyzed which included disease genes related to HCM, relationships between genotype and phenotype, potential pathogenesis of HCM, and the features of elderly patients with HCM. Results: HCM is caused by mutations in genes encoding myofilament proteins of the sarcomere, Z-disc proteins, Ca(2+)-handling proteins, and other proteins related to the sarcomere. Phenotypic manifestations of HCM are not just determined by these genes; modifying genes and epigenetic factors also contribute to the complexity of the HCM phenotype. The potential pathogenesis of HCM involves dominant negative function, an imbalance of myocardial energetic metabolism, and haploinsufficiency. Late-onset HCM presents its own features in the distribution of causal genes. Mutations in MYBPC3 may be the most common cause of delayed expression of HCM, and the sarcomere gene screen is most likely to be negative in elderly HCM patients. Conclusions: Despite progress in the identification of genetic causes and pathogenesis of HCM, there are still some questions that need to be better understood. It remains a great challenge to identify the cause of 50% of HCM cases in patients without an identified mutation. The application of a new genetic study technology may completely uncover the genetic background of these cases. In addition, the influences of causal mutations on the function and signaling of cardiocytes are expected to be elucidated further.
    Gerontology 01/2013; · 2.68 Impact Factor
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    ABSTRACT: Liddle's syndrome is a rare autosomal-dominant monogenic form of salt-sensitive hypertension. This study aimed to screen the gene mutation in β and γ subunits of the epithelial sodium channel (ENaC) of a Chinese family with Liddle's syndrome, an autosomal dominant form of hypertension. DNA samples from the proband with early-onset, treatment-resistant hypertension and suppressed plasma renin activity were initially screened for mutations in the C-terminal exons of the ENaC β or γ subunit genes, using amplification by polymerase chain reaction and direct DNA sequencing. We also screened the C-terminus of SCNN1B and SCNN1G in family members, and screened for the mutation in 150 controls. Genetic analysis of the β ENaC gene revealed a missense mutation of CCC to TCC at codon 616 in the proband, her mother and her grandmother. One hundred and fifty randomly selected controls had not the mutation, indicating that this is not a common genetic polymorphism. There was no mutation of the γ ENaC gene in any of the individuals examined. Through direct DNA sequencing analysis, we established the diagnosis of Liddle's syndrome for the proband and her families, and provided tailored therapies to this abnormality. These results provide further evidence that Pro616Ser is a critical amino acid that has a key role in the inhibition of sodium channel activity.
    Chinese medical journal 04/2012; 125(8):1401-4. · 0.90 Impact Factor