Aim:Myasthenia gravis(MG)is a neuromuscular transmission disorder caused by acetylcholine receptor autoantibodies.Cardiac autonomic dysfunctions were rarely reported in patients with MG.Functional cardiac abnormalitie...Aim:Myasthenia gravis(MG)is a neuromuscular transmission disorder caused by acetylcholine receptor autoantibodies.Cardiac autonomic dysfunctions were rarely reported in patients with MG.Functional cardiac abnormalities were variable and reported in patients at severe stages of the disease and with thymoma.We investigated cardiac functions in patients with MG using Ambulatory 24‑h electrocardiographic Holter‑Monitoring.Methods:This study included 20 patients with MG with a mean age of 28.45±8.89 years and duration of illness of 3.52±1.15 years.The standard Holter reports include data for heart‑rate,ventricular ectopies(VEs),supraventricular ectopies(SVEs),heart-rate variability(HRV),ST,QT,atrial fibrillation and T‑wave alternans.Results:VEs,SVEs and ST‑T changes were reported in 55%,40%and 20%of patients respectively.Compared with healthy subjects(n=20),HRV components including SDNN,SDANN,SDNN Index,RMS‑SD and pNN50(P=0.001 for all)were reduced in patients indicating sympathetic and parasympathetic autonomic dysfunctions.HRV abnormalities were reported in 30-60%of patients.No significant correlations were identified between SDNN,RMS‑SD,pNN50,and duration of illness.Conclusion:Depressed HRV may be an early manifestation of autonomic neuropathy in patients with MG even in milder stages of the disease.This information is useful in rating disease progression and the efficacy of therapeutic interventions.展开更多
Objective The exact biological mechanism whereby exposure to ambient ozone(O3)may contribute to clinical onset of cardiovascular events remains unclear.In this study,we aim to examine the impacts of O3 exposure on car...Objective The exact biological mechanism whereby exposure to ambient ozone(O3)may contribute to clinical onset of cardiovascular events remains unclear.In this study,we aim to examine the impacts of O3 exposure on cardiac arrhythmias and potential pathways involved through autonomic dysfunction and myocardial injury.Methods Seventy-three non-smoking healthy adults were followed with 4 repeated measurements of 24-hour ambulatory arrhythmias,heart rate variability,ST-segment deviation,and blood pressure(BP)in Beijing,China,2014‒2016.Generalized additive mixed models coupled with distributed lag nonlinear models were constructed to evaluate the associations and potential interlinks between O3 exposure and outcome measurements.Results During the study period,24-hour average concentrations of ambient O3 were 47.4µg/m3(ranging from 1.0 to 165.9µg/m3).Increased risks of premature ventricular contraction and ventricular tachycardia were associated with interquartile range increases in O3 exposure during the last 5 days before each participant's clinic visit,with relative risks of 2.14(95%confidence interval[CI]:1.95 to 2.32)and 5.47(95%CI:3.51 to 7.43),respectively.Mediation analyses further showed that sympathetic activation,parasympathetic inhibition,and elevated BP levels,as well as heightened risks of ST-segment depression could mediate up to 47.74%of the risks of arrhythmias attributable to O3 exposure.Conclusion Our results suggest that short-term exposure to ambient O3 could prompt the genesis of arrhythmias partially through worsening autonomic function and myocardial burden.展开更多
文摘Aim:Myasthenia gravis(MG)is a neuromuscular transmission disorder caused by acetylcholine receptor autoantibodies.Cardiac autonomic dysfunctions were rarely reported in patients with MG.Functional cardiac abnormalities were variable and reported in patients at severe stages of the disease and with thymoma.We investigated cardiac functions in patients with MG using Ambulatory 24‑h electrocardiographic Holter‑Monitoring.Methods:This study included 20 patients with MG with a mean age of 28.45±8.89 years and duration of illness of 3.52±1.15 years.The standard Holter reports include data for heart‑rate,ventricular ectopies(VEs),supraventricular ectopies(SVEs),heart-rate variability(HRV),ST,QT,atrial fibrillation and T‑wave alternans.Results:VEs,SVEs and ST‑T changes were reported in 55%,40%and 20%of patients respectively.Compared with healthy subjects(n=20),HRV components including SDNN,SDANN,SDNN Index,RMS‑SD and pNN50(P=0.001 for all)were reduced in patients indicating sympathetic and parasympathetic autonomic dysfunctions.HRV abnormalities were reported in 30-60%of patients.No significant correlations were identified between SDNN,RMS‑SD,pNN50,and duration of illness.Conclusion:Depressed HRV may be an early manifestation of autonomic neuropathy in patients with MG even in milder stages of the disease.This information is useful in rating disease progression and the efficacy of therapeutic interventions.
基金This work was supported by China Postdoctoral Science Foundation(2021M690249)Michigan Medicine-PKUHSC Joint Institute for Translational and Clinical Research(BMU20140467).
文摘Objective The exact biological mechanism whereby exposure to ambient ozone(O3)may contribute to clinical onset of cardiovascular events remains unclear.In this study,we aim to examine the impacts of O3 exposure on cardiac arrhythmias and potential pathways involved through autonomic dysfunction and myocardial injury.Methods Seventy-three non-smoking healthy adults were followed with 4 repeated measurements of 24-hour ambulatory arrhythmias,heart rate variability,ST-segment deviation,and blood pressure(BP)in Beijing,China,2014‒2016.Generalized additive mixed models coupled with distributed lag nonlinear models were constructed to evaluate the associations and potential interlinks between O3 exposure and outcome measurements.Results During the study period,24-hour average concentrations of ambient O3 were 47.4µg/m3(ranging from 1.0 to 165.9µg/m3).Increased risks of premature ventricular contraction and ventricular tachycardia were associated with interquartile range increases in O3 exposure during the last 5 days before each participant's clinic visit,with relative risks of 2.14(95%confidence interval[CI]:1.95 to 2.32)and 5.47(95%CI:3.51 to 7.43),respectively.Mediation analyses further showed that sympathetic activation,parasympathetic inhibition,and elevated BP levels,as well as heightened risks of ST-segment depression could mediate up to 47.74%of the risks of arrhythmias attributable to O3 exposure.Conclusion Our results suggest that short-term exposure to ambient O3 could prompt the genesis of arrhythmias partially through worsening autonomic function and myocardial burden.