Yiyi Huang

Sun Yat-Sen University of Medical Sciences, Shengcheng, Guangdong, China

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Publications (3)21.33 Total impact

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    ABSTRACT: Background: The second-generation cryoballoon (CB-2G) is a promising technique to treat atrial fibrillation (AF). It's necessary to summarize and analyze the available data on 1-year clinical outcome of pulmonary vein isolation (PVI) with CB-2G. Methods: PubMed and the Web of Science were searched in May 2015. Studies that reported the 1-year clinical success rates after PVI using CB-2G were included. The 1-year clinical success rates were pooled using the random-effect model. Complication rates and acute success rates were also analyzed. Subgroup analyses were conducted based on AF type and ablation strategy. Results: Fifteen studies involving 2363 AF patients met the inclusion criteria. The overall clinical success rate of PVI using CB-2G was 81%. 82% of paroxysmal AF patients and 70% of persistent AF patients were in stable sinus rhythm 1 year after the procedure. The clinical success rates of the "no-bonus" strategy were 81% in all patients, 82% in paroxysmal AF patients and 73% in persistent AF patients. The corresponding success rates of the "bonus" strategy were 81%, 83% and 63%. Acute success rate was high. The overall rates of phrenic nerve palsy (PNP) and other procedure-related complication were 5.8% and 1.5%, respectively. Compared with "bonus" strategy, there was a trend of fewer PNPs in "no-bonus" strategy (4.6% vs. 6.5%). Conclusions: CB-2G is highly effective in the treatment of both paroxysmal AF and persistent AF. The "no-bonus" strategy is as effective as the "bonus" strategy in terms of 1-year clinical outcome. This article is protected by copyright. All rights reserved.
    Pacing and Clinical Electrophysiology 11/2015; DOI:10.1111/pace.12787 · 1.13 Impact Factor
  • Yue Zhou · Xin He · Yili Chen · Yiyi Huang · Lingling Wu · Jiangui He ·
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    ABSTRACT: Diabetes mellitus is a prominent risk factor for cardiovascular diseases. Diabetic cardiomyopathy is an important complication of the heart independent of hypertension and coronary artery disease and is accompanied by cardiac hypertrophy. Cardiac hypertrophy easily leads to heart failure, which is a leading cause of morbidity and mortality. Glucagon-like peptide 1 (GLP-1) is an incretin hormone, which has various beneficial roles in the cardiovascular system, and exendin-4 is a highly potent glucagon-like peptide 1 receptor agonist. However, the role of GLP-1 in cardiac hypertrophy remains unknown. Our study revealed that exendin-4 treatment ameliorated phenylephrine (PE)-induced cardiac hypertrophy, which presented as decreased cardiac hypertrophic markers (ANP, BNP, and β-MHC) and cell surface area. This condition was significantly reversed upon treatment with the GLP-1 receptor antagonist exendin9-39. We also discovered that Erk1/2 and AMPK signaling pathways were involved in this process. Furthermore, our data demonstrate that the AMPK inhibitor compound C inhibited the anti-hypertrophic effect of exendin-4, which is associated with the mTOR/p70S6K/4-EBP1 signaling pathway. Finally, exendin-4 enhanced the anti-hypertrophic effect of rapamycin. In summary, our study disclosed that exedin-4 inhibits cardiac hypertrophy by upregulating GLP-1 receptor expression and activating the AMPK/mTOR signaling pathway.
    Biochemical and Biophysical Research Communications 10/2015; DOI:10.1016/j.bbrc.2015.09.179 · 2.30 Impact Factor
  • Yue Zhou · Xin He · Yiyi Huang · Yili Chen · Jiangui He ·

    Journal of the American College of Cardiology 10/2015; 66(16):C30. DOI:10.1016/j.jacc.2015.06.1142 · 16.50 Impact Factor
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    ABSTRACT: Although short-term B-type natriuretic peptide (BNP) treatment has been shown to be effective for decompensated congestive heart failure, little is known about the effects of long-term BNP treatment in ventricular remodeling and heart failure in response to myocardial infarction. The aim of the present study was to investigate the effects of long-term BNP treatment on ventricular remodeling and heart failure after myocardial infarction in rats. Myocardial infarction was induced by ligating the left anterior descending coronary artery. The surviving rats were randomly divided into four groups: 1) vehicle-treated myocardial infarction group ('vehicle-treated group'), 2) rats treated with low-dose BNP ('low BNP group'), 3) rats treated with high-dose BNP ('high BNP group'), 4) sham-operated group. Eight weeks after the operation, rats were sacrificed. Compared with the sham-operated group, the vehicle-treated group had significantly higher collagen deposition and angiotensin II levels (P<0.01) and a significantly lower cardiac function (P<0.05). Both BNP-treated groups had significant improvement of these indexes compared with the vehicle-treated group (P<0.01). The high BNP group had significantly less collagen deposition and better cardiac function than the untreated and low BNP groups. Moreover, the mRNA and protein expression of TGFbeta1 and Smad2 in the vehicle-treated group was significantly higher than in the sham-operated group (P<0.01). Both BNP-treated groups had a suppression of TGFbeta1 and Smad2 expression (P<0.01). In conclusion, long-term treatment with BNP prevents ventricular remodeling and deterioration of cardiac function in a dose-dependent fashion, a process that may be associated with the inhibition of TGFbeta1/ Smad2 signaling.
    European journal of pharmacology 12/2008; 602(1):132-7. DOI:10.1016/j.ejphar.2008.10.064 · 2.53 Impact Factor