目的通过比较冷冻球囊与射频消融术对心房颤动(简称房颤)患者心肌损伤程度的差异,探讨其对术后房颤急性期复发率的影响。方法 45例房颤患者按照消融术式的不同分为两组:射频组(n=20)与冷冻组(n=25)。于术前、术后6~12h内及术后3~5d内对...目的通过比较冷冻球囊与射频消融术对心房颤动(简称房颤)患者心肌损伤程度的差异,探讨其对术后房颤急性期复发率的影响。方法 45例房颤患者按照消融术式的不同分为两组:射频组(n=20)与冷冻组(n=25)。于术前、术后6~12h内及术后3~5d内对患者抽血检测肌钙蛋白I(cTnI)水平,并在术后3~5d内行24h动态心电图检查。结果 (1)与术前相比,射频组与冷冻组两组术后6~12h内cTnI水平均显著升高[1.59(0.82,1.95)μg/L vs 0.01(0.01,0.01)μg/L]vs[7.16(4.23,9.31)μg/L vs 0.01(0.01,0.01)μg/L,P均<0.001];射频组与冷冻组术后3~5d内较术后6~12h内cTnI水平明显下降[(0.09(0.03,0.29)μg/L vs 1.59(0.82,1.95)μg/L]vs[0.45(0.13,0.86)μg/L vs 7.16(4.23,9.31)μg/L,P均<0.001];(2)与射频组相比,冷冻组术后6~12h内、术后3~5d内cTnI水平明显升高(P<0.01),而术前两组间cTnI水平无明显差别;(3)术后急性期冷冻组与射频组房颤复发率无差别(32%vs 25%,P=0.607)。结论冷冻球囊消融术对房颤患者心肌损伤程度大于射频消融术,但对房颤急性期复发率无影响。展开更多
Background Studies have shown that B-blockers can improve cardiac performance in heart failure （HF） by reversing protein kinase A （PKA）-mediated sarcoplasmic reticulum （SR） Ca^2＋ leak. However, it is being stro...Background Studies have shown that B-blockers can improve cardiac performance in heart failure （HF） by reversing protein kinase A （PKA）-mediated sarcoplasmic reticulum （SR） Ca^2＋ leak. However, it is being strongly questioned as to whether the PKA-mediated ryanodine receptor （RyR2） hyper-phosphorylation is a critical regulator of SR Ca^2＋ leak. In this study, we used a rabbit HF model to investigate whether β-blockers affect SR Ca^2＋ leak by other potential mechanisms.展开更多
文摘目的通过比较冷冻球囊与射频消融术对心房颤动(简称房颤)患者心肌损伤程度的差异,探讨其对术后房颤急性期复发率的影响。方法 45例房颤患者按照消融术式的不同分为两组:射频组(n=20)与冷冻组(n=25)。于术前、术后6~12h内及术后3~5d内对患者抽血检测肌钙蛋白I(cTnI)水平,并在术后3~5d内行24h动态心电图检查。结果 (1)与术前相比,射频组与冷冻组两组术后6~12h内cTnI水平均显著升高[1.59(0.82,1.95)μg/L vs 0.01(0.01,0.01)μg/L]vs[7.16(4.23,9.31)μg/L vs 0.01(0.01,0.01)μg/L,P均<0.001];射频组与冷冻组术后3~5d内较术后6~12h内cTnI水平明显下降[(0.09(0.03,0.29)μg/L vs 1.59(0.82,1.95)μg/L]vs[0.45(0.13,0.86)μg/L vs 7.16(4.23,9.31)μg/L,P均<0.001];(2)与射频组相比,冷冻组术后6~12h内、术后3~5d内cTnI水平明显升高(P<0.01),而术前两组间cTnI水平无明显差别;(3)术后急性期冷冻组与射频组房颤复发率无差别(32%vs 25%,P=0.607)。结论冷冻球囊消融术对房颤患者心肌损伤程度大于射频消融术,但对房颤急性期复发率无影响。
基金This work was supported in part by grants from the Jiangsu Province ＂135 Project＂ Key Laboratory Fund （No. SK200205） in China and the National Natural Science Foundation of China （No. 30800460）.
文摘Background Studies have shown that B-blockers can improve cardiac performance in heart failure （HF） by reversing protein kinase A （PKA）-mediated sarcoplasmic reticulum （SR） Ca^2＋ leak. However, it is being strongly questioned as to whether the PKA-mediated ryanodine receptor （RyR2） hyper-phosphorylation is a critical regulator of SR Ca^2＋ leak. In this study, we used a rabbit HF model to investigate whether β-blockers affect SR Ca^2＋ leak by other potential mechanisms.
