We report three cases of sustained monomorphic ventricular tachycardia(VT) in the setting of coronary artery disease,resistant to beta-blockers in two patients and to amiodarone in all,successfully terminated by low d...We report three cases of sustained monomorphic ventricular tachycardia(VT) in the setting of coronary artery disease,resistant to beta-blockers in two patients and to amiodarone in all,successfully terminated by low doses of intravenous(IV) epinephrine.VT was the first manifestation of coronary artery disease in one patient,whereas the other two patients had a previous history of myocardial infarction and were recipients of an implantable cardioverter-defibrillator(ICD).One of these two patients experienced an arrhythmic storm.All had hemodynamic instability at the time of epinephrine administration.A single slow administration of IV epinephrine(0.5 to 1 mg administered over 30 to 60 s) restored sinus rhythm after 30-90 s with only minor side effects.In the ICD patient with recurrent VT and several cardioversions due to transformation of VT to ventricular fibrillation,epinephrine injection led to the avoidance of further shocks.Although potentially harmful,low doses of IV epinephrine used alone or in combination with beta-blocker treatment and electrical cardioversion may be an alternative effective therapy for sustained monomorphic VT refractory to amiodarone.The role of epinephrine in the termination of VT should be studied further,especially in patients pre-treated with amiodarone in combination with beta-blockers.展开更多
“Arrhythmogenic right ventricular dysplasia” (ARVD), a heart muscle disorder characterized by the presence of fibro-fatty tissue and ventricular electrical vulnerability related to sudden death, was first described ...“Arrhythmogenic right ventricular dysplasia” (ARVD), a heart muscle disorder characterized by the presence of fibro-fatty tissue and ventricular electrical vulnerability related to sudden death, was first described in 1977 by a French team. Since then, other terms such as “arrhythmogenic right ventricular cardiomyopathy” (ARVC), “arrhythmogenic cardiomyopathy” (AC), “left-dominant arrhythmogenic cardiomyopathy” (LDAC), and “arrhythmogenic left ventricular dysplasia” (ALVD) have been introduced. These changes in nomenclature of the same disease entity are based on different explanations of pathomorphologic patterns. The dysplasia theory claims cardiac growth “maldevelopment” whereas the cardiomyopathy has been seen as an atrophy from acquired injury (myocyte death) and repair (fibrofatty replacement). The other area of divergent opinion is with regards to involvement of both ventricles rather than being an isolated right ventricular anomaly that may result in increased likelihood of diagnosing the concealed form manifesting with pre-dominant left ventricular arrhythmias. Multiple line of evidences support common disease path-ways: Presence of fibro-fatty and superimposed myocarditis, desmosome mutations and malfunc-tion. These compelling data regarding the heart growth, and pathological, clinical, phenotype/ genotype correlates have advanced our understanding of arrhythmogenic ventricular dysplasia/ cardiomyopathy and increased the diagnostic accuracy as well as providing an avenue for future development of new mechanism-based therapies.展开更多
文摘We report three cases of sustained monomorphic ventricular tachycardia(VT) in the setting of coronary artery disease,resistant to beta-blockers in two patients and to amiodarone in all,successfully terminated by low doses of intravenous(IV) epinephrine.VT was the first manifestation of coronary artery disease in one patient,whereas the other two patients had a previous history of myocardial infarction and were recipients of an implantable cardioverter-defibrillator(ICD).One of these two patients experienced an arrhythmic storm.All had hemodynamic instability at the time of epinephrine administration.A single slow administration of IV epinephrine(0.5 to 1 mg administered over 30 to 60 s) restored sinus rhythm after 30-90 s with only minor side effects.In the ICD patient with recurrent VT and several cardioversions due to transformation of VT to ventricular fibrillation,epinephrine injection led to the avoidance of further shocks.Although potentially harmful,low doses of IV epinephrine used alone or in combination with beta-blocker treatment and electrical cardioversion may be an alternative effective therapy for sustained monomorphic VT refractory to amiodarone.The role of epinephrine in the termination of VT should be studied further,especially in patients pre-treated with amiodarone in combination with beta-blockers.
文摘“Arrhythmogenic right ventricular dysplasia” (ARVD), a heart muscle disorder characterized by the presence of fibro-fatty tissue and ventricular electrical vulnerability related to sudden death, was first described in 1977 by a French team. Since then, other terms such as “arrhythmogenic right ventricular cardiomyopathy” (ARVC), “arrhythmogenic cardiomyopathy” (AC), “left-dominant arrhythmogenic cardiomyopathy” (LDAC), and “arrhythmogenic left ventricular dysplasia” (ALVD) have been introduced. These changes in nomenclature of the same disease entity are based on different explanations of pathomorphologic patterns. The dysplasia theory claims cardiac growth “maldevelopment” whereas the cardiomyopathy has been seen as an atrophy from acquired injury (myocyte death) and repair (fibrofatty replacement). The other area of divergent opinion is with regards to involvement of both ventricles rather than being an isolated right ventricular anomaly that may result in increased likelihood of diagnosing the concealed form manifesting with pre-dominant left ventricular arrhythmias. Multiple line of evidences support common disease path-ways: Presence of fibro-fatty and superimposed myocarditis, desmosome mutations and malfunc-tion. These compelling data regarding the heart growth, and pathological, clinical, phenotype/ genotype correlates have advanced our understanding of arrhythmogenic ventricular dysplasia/ cardiomyopathy and increased the diagnostic accuracy as well as providing an avenue for future development of new mechanism-based therapies.
