Objective:To understand the role of ANP mRNA transcription regulation in gpl30-mediated cardiomyocyte hypertrophy,and the involved mitogen-aetivated protein kinase kinase(MEK)-extracellular signal-regulated kinase(ERK...Objective:To understand the role of ANP mRNA transcription regulation in gpl30-mediated cardiomyocyte hypertrophy,and the involved mitogen-aetivated protein kinase kinase(MEK)-extracellular signal-regulated kinase(ERK,also called p42/p44 MAPK)signaling pathway.Methods:isolated neonatal ventricular myocytes were treated with different concentrations of CT-1(10^(-9),10^(-8)and 10^(-7)mol/L).MTT was used to analyze the viability and RT-PCR was used to detect ANP mRNA levels in eardiomyocyte.To inhibit p42/p44 MAPK activity in hypertrophic cardiomyoeytes,the cells were pretreated with a specific MEKI inhibitor.Results:CT-1significantly induced ANP mRNA expression and the viability of canliomyocytes in a doseand time-dependent manner.Furthermore,blocking p42/p44 MAPK activity by the special MEk1 inhibitor uprcgulatcd the ANP mKNA.Conclusions:p42/p44 MAPK have an important role in suppressing ANP mRNA transcription and cell activity in gpl30-mediated hypertrophic ventricular myocytes.展开更多
PRKAG2 cardiac syndrome(PS)is a rare inherited disease due to PRKAG2 gene mutation and characterized by Wolff-Parkinson-White syndrome(WPWs),conduction system lesions and myocardial hypertrophy.It can also lead to ser...PRKAG2 cardiac syndrome(PS)is a rare inherited disease due to PRKAG2 gene mutation and characterized by Wolff-Parkinson-White syndrome(WPWs),conduction system lesions and myocardial hypertrophy.It can also lead to serious consequences,such as sudden death.But the genetic and clinical heterogeneity makes the early diagnosis of PS difficult.Here we studied a family with familial hypertrophic cardiomyopathy and other diverse manifestations.Gene analysis identified a missense mutation(Arg302Gln)in the five affected subjects of the family.The electrocardiograph performance of the five was composed of sinus bradycardia(SB),WPWs,right bundle branch block(RBBB),atrioventricular block(AVB),left bundle branch block(LBBB),supraventricular tachycardia(SVT)and atrial premature beat(APB).Among them,the youngest one began to show paroxysmal palpitation at the age of nine and was confirmed to have WPWs at 17 years old;two members progressed over time to serious conduction damage,and the proband received a pacemaker at the age of 27 due to AVB.Besides,according to cardiac magnetic resonance and echocardiography,the youngest one showed symmetric hypertrophy;three older members showed asymmetric myocardial hypertrophy characterized with a diffuse pattern of middle-anterior-lateral-inferior wall hypertrophy and especially interventricular septal hypertrophy;all five affected patients showed atrial enlargement regardless of myocardial hypertrophy at an earlier stage.In conclusion,the conduction system disorder,familial atrial enlargement and symmetric cardiac hypertrophy may occur in the early stage of PRKAG2 R302Q mutation.展开更多
目的本研究旨在探讨左心室肥厚伴或不伴劳损对合并高血压阵发性心房颤动（房颤）患者射频消融术后复发的影响。方法连续入选2007年1月至2014年5月于北京安贞医院第一次接受导管射频消融术的280例抗心律失常药物治疗无效或不能耐受并同...目的本研究旨在探讨左心室肥厚伴或不伴劳损对合并高血压阵发性心房颤动（房颤）患者射频消融术后复发的影响。方法连续入选2007年1月至2014年5月于北京安贞医院第一次接受导管射频消融术的280例抗心律失常药物治疗无效或不能耐受并同意手术治疗的合并高血压的症状性阵发性房颤患者。根据患者术前窦性心律心电图，依据左心室肥厚Romhilt-Estes评分系统及是否伴有ST-T劳损性改变，将患者共分为3组[1组（正常组，140例）；2组（左心室肥厚不伴劳损组，114例）；3组（左心室肥厚伴劳损组，26例）]，手术方式均为三维电解剖标测系统指导下行左心房重建及环肺静脉电隔离术，术后由随访人员定期随访患者主诉、心电图、24 h动态心电图、超声心动图等。结果截至2017年1月，平均手术1.19±0.46次，中位随访42（四分位数24~66）个月，169例维持窦性心律，104例复发，失访7例；1组患者窦性心律维持率明显高于2组及3组患者，分别为74.3%（1组）、48.2%（2组）、38.5%（3组），差异有统计学意义（P〈0.001）。单因素回归分析中，血栓栓塞评分（CHA2DS2-VASc积分），心电图异常包括左心室肥厚及左心室肥厚伴劳损，左心房内径以及脑钠肽是患者复发的危险因素；在多因素分析中，仅有心电图异常包括左心室肥厚及左心室肥厚伴劳损是合并高血压阵发性房颤患者射频消融术后复发的独立危险因素（HR=2.103，95% CI 1.231~3.590；HR=2.621，95% CI 1.238~5.550）。结论心电图异常左心室肥厚伴或不伴劳损是合并高血压阵发性房颤患者射频消融术后复发的独立危险因素。展开更多
基金supported by a grant from the National Natural Science Foundation of China(30260032.81000073 and 81160020)Key Program of Science and Technology of Hainan Province(061011 and ZDXM20100045)+2 种基金Education Department of Hainan Province(Hj2007113)Natural Science Foundation of Hainan Province(310043 and 811197)Key Project of Chinese Ministry of Education(212137) and HJHZ2013-06
文摘Objective:To understand the role of ANP mRNA transcription regulation in gpl30-mediated cardiomyocyte hypertrophy,and the involved mitogen-aetivated protein kinase kinase(MEK)-extracellular signal-regulated kinase(ERK,also called p42/p44 MAPK)signaling pathway.Methods:isolated neonatal ventricular myocytes were treated with different concentrations of CT-1(10^(-9),10^(-8)and 10^(-7)mol/L).MTT was used to analyze the viability and RT-PCR was used to detect ANP mRNA levels in eardiomyocyte.To inhibit p42/p44 MAPK activity in hypertrophic cardiomyoeytes,the cells were pretreated with a specific MEKI inhibitor.Results:CT-1significantly induced ANP mRNA expression and the viability of canliomyocytes in a doseand time-dependent manner.Furthermore,blocking p42/p44 MAPK activity by the special MEk1 inhibitor uprcgulatcd the ANP mKNA.Conclusions:p42/p44 MAPK have an important role in suppressing ANP mRNA transcription and cell activity in gpl30-mediated hypertrophic ventricular myocytes.
文摘PRKAG2 cardiac syndrome(PS)is a rare inherited disease due to PRKAG2 gene mutation and characterized by Wolff-Parkinson-White syndrome(WPWs),conduction system lesions and myocardial hypertrophy.It can also lead to serious consequences,such as sudden death.But the genetic and clinical heterogeneity makes the early diagnosis of PS difficult.Here we studied a family with familial hypertrophic cardiomyopathy and other diverse manifestations.Gene analysis identified a missense mutation(Arg302Gln)in the five affected subjects of the family.The electrocardiograph performance of the five was composed of sinus bradycardia(SB),WPWs,right bundle branch block(RBBB),atrioventricular block(AVB),left bundle branch block(LBBB),supraventricular tachycardia(SVT)and atrial premature beat(APB).Among them,the youngest one began to show paroxysmal palpitation at the age of nine and was confirmed to have WPWs at 17 years old;two members progressed over time to serious conduction damage,and the proband received a pacemaker at the age of 27 due to AVB.Besides,according to cardiac magnetic resonance and echocardiography,the youngest one showed symmetric hypertrophy;three older members showed asymmetric myocardial hypertrophy characterized with a diffuse pattern of middle-anterior-lateral-inferior wall hypertrophy and especially interventricular septal hypertrophy;all five affected patients showed atrial enlargement regardless of myocardial hypertrophy at an earlier stage.In conclusion,the conduction system disorder,familial atrial enlargement and symmetric cardiac hypertrophy may occur in the early stage of PRKAG2 R302Q mutation.
文摘目的本研究旨在探讨左心室肥厚伴或不伴劳损对合并高血压阵发性心房颤动（房颤）患者射频消融术后复发的影响。方法连续入选2007年1月至2014年5月于北京安贞医院第一次接受导管射频消融术的280例抗心律失常药物治疗无效或不能耐受并同意手术治疗的合并高血压的症状性阵发性房颤患者。根据患者术前窦性心律心电图，依据左心室肥厚Romhilt-Estes评分系统及是否伴有ST-T劳损性改变，将患者共分为3组[1组（正常组，140例）；2组（左心室肥厚不伴劳损组，114例）；3组（左心室肥厚伴劳损组，26例）]，手术方式均为三维电解剖标测系统指导下行左心房重建及环肺静脉电隔离术，术后由随访人员定期随访患者主诉、心电图、24 h动态心电图、超声心动图等。结果截至2017年1月，平均手术1.19±0.46次，中位随访42（四分位数24~66）个月，169例维持窦性心律，104例复发，失访7例；1组患者窦性心律维持率明显高于2组及3组患者，分别为74.3%（1组）、48.2%（2组）、38.5%（3组），差异有统计学意义（P〈0.001）。单因素回归分析中，血栓栓塞评分（CHA2DS2-VASc积分），心电图异常包括左心室肥厚及左心室肥厚伴劳损，左心房内径以及脑钠肽是患者复发的危险因素；在多因素分析中，仅有心电图异常包括左心室肥厚及左心室肥厚伴劳损是合并高血压阵发性房颤患者射频消融术后复发的独立危险因素（HR=2.103，95% CI 1.231~3.590；HR=2.621，95% CI 1.238~5.550）。结论心电图异常左心室肥厚伴或不伴劳损是合并高血压阵发性房颤患者射频消融术后复发的独立危险因素。
