Objective: To study the pathological basis of right atrial fibrillation in rheumatic heart disease (RHD) patients with atrial fibrillation (AF). Methods: Twenty-nine patients with mitral valve replacement of RHD were ...Objective: To study the pathological basis of right atrial fibrillation in rheumatic heart disease (RHD) patients with atrial fibrillation (AF). Methods: Twenty-nine patients with mitral valve replacement of RHD were divided into AF group (n=13) and sinus rhythm group (SN group) (n=16). There was no significant statistical difference in clinical factors between the 2 groups. During the operation of valve replace-ment, the samples of right atrial appendages were taken and the qualitative and quantitative study were made by light microscopy and electron microscopy. Results: (1) Light microscope: The interstitial fibrosis and the arrangement of myocardium was more disordered in AF group than that in SN group. However, no statistic difference was found in interstitial fibrosis and cellar hypertrophy degree between the 2 groups. (2) Electron microscope: Mitochondrial crosta broke and dissolved obviously in AF group. The mitochondrial volume in AF group was smaller than that in SN group. Volume density, average area and average perimeter in AF group were less than that in SN group ; specific surface in AF group was bigger than that in SN group. There was significant difference of above factors between the 2 groups; but there was no significant difference of surface density and numerical density on area in the 2 groups. Volume density of myofibril in AF group and SN group were less than that in SN group. (3)Split of Intercalated disc(ID) gap was found in AF group, and there was marrowing and floccular substance in ID gap. Conclusion : There were significant differences in the pathological changes of right atrial myocardium between AF and SN with RHD, these changes may be the im-portant pathological basis for RA fibrillation of AF patients with RHD.展开更多
Objective To explore the characteristics of arrhythmogenic right ventricular cardiomyopathy (ARVC) Methods Seven patients with arrhythmogenic right ventricular cardiomyopathy and 34 members of three families were ...Objective To explore the characteristics of arrhythmogenic right ventricular cardiomyopathy (ARVC) Methods Seven patients with arrhythmogenic right ventricular cardiomyopathy and 34 members of three families were studied All patients and family members underwent history collection, clinical examination, electrocardiogram (ECG), two dimensional echocardiography (2 DE) and a signal averaging electrocardiogram Programmed ventricular stimulation was performed in five patients Results All patients and family members had normal morphologic characteristics and normal function of the left ventricular by 2 DE Fourteen persons had abnormal findings indicating ARVC Five had enlargement of the right ventricular with diffused hypocontractility, eight had thin and systolic bulging in the focal anterior wall with hypokinesia and one had bulging of the inferior wall Twenty five persons (seven patients and 18 family members) had abnormal findings in ECG Positive ventricular late potential was recorded in 13 persons (six patients) Two to three monomorphic ventricular tachycardia (VT) with left bundle branch block (LBBB) configurations were induced in five patients Ventricular fibrillation was induced in two patients during the electrophysiologic study (EPS) Five patients had very high pacing threshold and/or ineffective pacing in one or many regions of the right ventricle Two members of one family died suddenly One member was a dwarf with ARVC Spontaneous VT with a left bundle branch block (LBBB) configuration was recorded in five patients, polymorphic VT with extremely short coupling interval in one, and premature ventricular complexes with LBBB configuration in 12 (six patients) Conclusion Our familial study strongly suggests that ARVC may be a hereditary disease and it is helpful in the diagnosis and detection of ARVC The most common manifestations were abnormal structure and function of the right ventricle and abnormal ECG of repolarization and ventricular arrhythmia which originates from the right ventricle展开更多
The mechanism of idiopathic ventricular tachycardia originating from the right ventricular outflow tract (RVOT) is not clear. Many clinical reports have suggested a mechanism of triggered activity. However, there ar...The mechanism of idiopathic ventricular tachycardia originating from the right ventricular outflow tract (RVOT) is not clear. Many clinical reports have suggested a mechanism of triggered activity. However, there are few studies investigating this be- cause of the technical difficulties associated with examining this theory. The L-type calcium current (/Ca-L), an important in- ward current of the action potential (AP), plays an important role in arrhythmogenesis. The aim of this study was to explore differences in the APs of right ventricular (RV) and RVOT cardiomyocytes, and differences in electrophysiological character- istics of the ICa-L in these myocytes. Rabbit RVOT and RV myocytes were isolated and their AP and Ic,-L were investigated us- ing the patch-clamp technique. RVOT cardiomyocytes had a wider range of AP duration (APD) than RV cardiomyocytes, with some markedly prolonged APDs and markedly shortened APDs. The markedly shortened APDs in RVOT myocytes were abolished by treatment with 4-AP, an inhibitor of the transient outward potassium current, but the markedly prolonged APDs remained, with some myocytes with a long AP plateau not repolarizing to resting potential. In addition, early afterdepolariza- tion (EAD) and second plateau responses were seen in RVOT myocytes but not in RV myocytes. RVOT myocytes had a high- er current density for/Ca-L than RV myocytes (RVOT (13.16±0.87) pA pF-1, RV (8.59±1.97) pA pF-1; P〈0.05). The ICa-L and the prolonged APD were reduced, and the EAD and second plateau response disappeared, after treatment with nifedipine (10 μmol L^-1), which blocks the Ica-L. In conclusion, there was a wider range of APDs in RVOT myocytes than in RV myocytes, which is one of the basic factors involved in arrhythmogenesis. The higher current density for ICa-L is one of the factors causing prolongation of the APD in RVOT myocytes. The combination of EAD with prolonged APD may be one of the mechanisms of RVOT-VT generation.展开更多
文摘Objective: To study the pathological basis of right atrial fibrillation in rheumatic heart disease (RHD) patients with atrial fibrillation (AF). Methods: Twenty-nine patients with mitral valve replacement of RHD were divided into AF group (n=13) and sinus rhythm group (SN group) (n=16). There was no significant statistical difference in clinical factors between the 2 groups. During the operation of valve replace-ment, the samples of right atrial appendages were taken and the qualitative and quantitative study were made by light microscopy and electron microscopy. Results: (1) Light microscope: The interstitial fibrosis and the arrangement of myocardium was more disordered in AF group than that in SN group. However, no statistic difference was found in interstitial fibrosis and cellar hypertrophy degree between the 2 groups. (2) Electron microscope: Mitochondrial crosta broke and dissolved obviously in AF group. The mitochondrial volume in AF group was smaller than that in SN group. Volume density, average area and average perimeter in AF group were less than that in SN group ; specific surface in AF group was bigger than that in SN group. There was significant difference of above factors between the 2 groups; but there was no significant difference of surface density and numerical density on area in the 2 groups. Volume density of myofibril in AF group and SN group were less than that in SN group. (3)Split of Intercalated disc(ID) gap was found in AF group, and there was marrowing and floccular substance in ID gap. Conclusion : There were significant differences in the pathological changes of right atrial myocardium between AF and SN with RHD, these changes may be the im-portant pathological basis for RA fibrillation of AF patients with RHD.
文摘Objective To explore the characteristics of arrhythmogenic right ventricular cardiomyopathy (ARVC) Methods Seven patients with arrhythmogenic right ventricular cardiomyopathy and 34 members of three families were studied All patients and family members underwent history collection, clinical examination, electrocardiogram (ECG), two dimensional echocardiography (2 DE) and a signal averaging electrocardiogram Programmed ventricular stimulation was performed in five patients Results All patients and family members had normal morphologic characteristics and normal function of the left ventricular by 2 DE Fourteen persons had abnormal findings indicating ARVC Five had enlargement of the right ventricular with diffused hypocontractility, eight had thin and systolic bulging in the focal anterior wall with hypokinesia and one had bulging of the inferior wall Twenty five persons (seven patients and 18 family members) had abnormal findings in ECG Positive ventricular late potential was recorded in 13 persons (six patients) Two to three monomorphic ventricular tachycardia (VT) with left bundle branch block (LBBB) configurations were induced in five patients Ventricular fibrillation was induced in two patients during the electrophysiologic study (EPS) Five patients had very high pacing threshold and/or ineffective pacing in one or many regions of the right ventricle Two members of one family died suddenly One member was a dwarf with ARVC Spontaneous VT with a left bundle branch block (LBBB) configuration was recorded in five patients, polymorphic VT with extremely short coupling interval in one, and premature ventricular complexes with LBBB configuration in 12 (six patients) Conclusion Our familial study strongly suggests that ARVC may be a hereditary disease and it is helpful in the diagnosis and detection of ARVC The most common manifestations were abnormal structure and function of the right ventricle and abnormal ECG of repolarization and ventricular arrhythmia which originates from the right ventricle
文摘The mechanism of idiopathic ventricular tachycardia originating from the right ventricular outflow tract (RVOT) is not clear. Many clinical reports have suggested a mechanism of triggered activity. However, there are few studies investigating this be- cause of the technical difficulties associated with examining this theory. The L-type calcium current (/Ca-L), an important in- ward current of the action potential (AP), plays an important role in arrhythmogenesis. The aim of this study was to explore differences in the APs of right ventricular (RV) and RVOT cardiomyocytes, and differences in electrophysiological character- istics of the ICa-L in these myocytes. Rabbit RVOT and RV myocytes were isolated and their AP and Ic,-L were investigated us- ing the patch-clamp technique. RVOT cardiomyocytes had a wider range of AP duration (APD) than RV cardiomyocytes, with some markedly prolonged APDs and markedly shortened APDs. The markedly shortened APDs in RVOT myocytes were abolished by treatment with 4-AP, an inhibitor of the transient outward potassium current, but the markedly prolonged APDs remained, with some myocytes with a long AP plateau not repolarizing to resting potential. In addition, early afterdepolariza- tion (EAD) and second plateau responses were seen in RVOT myocytes but not in RV myocytes. RVOT myocytes had a high- er current density for/Ca-L than RV myocytes (RVOT (13.16±0.87) pA pF-1, RV (8.59±1.97) pA pF-1; P〈0.05). The ICa-L and the prolonged APD were reduced, and the EAD and second plateau response disappeared, after treatment with nifedipine (10 μmol L^-1), which blocks the Ica-L. In conclusion, there was a wider range of APDs in RVOT myocytes than in RV myocytes, which is one of the basic factors involved in arrhythmogenesis. The higher current density for ICa-L is one of the factors causing prolongation of the APD in RVOT myocytes. The combination of EAD with prolonged APD may be one of the mechanisms of RVOT-VT generation.