[Sustained ventricular tachycardia: induced polymorphism. Clinical and electrophysiological aspects; therapeutic implications].
By induced polymorphism (I.P.) we mean the electrical induction during endocavitary electrophysiologic study (E.E.S.) either of two or more morphologically distinct types of Sustained Ventricular Tachycardia (S.V.T.) (i.e. different bundle branch block patterns or with shifting of QRS by greater than or equal to 90 degrees) or of one type of sustained ventricular tachycardia other than the spontaneous one. Twenty-two patients with clinical sustained ventricular tachycardia, in whom at least one episode of sustained ventricular tachycardia was induced during endocavitary electrophysiologic study, were divided into 2 groups depending on the presence or not of induced polymorphism: Group I consisted of 13 patients with induced polymorphism; Group II consisted of 9 patients without induced polymorphism. All the patients of the Group I had chronic ischemic heart disease (C.I.H.D.); 12/13 previously had myocardial infarction. Only 1 patient of the Group II had chronic ischemic heart disease. Intraventricular conduction defect was present in 9 patients of the Group I and in 2 of the Group II. An overall of 26 sustained ventricular tachycardia episodes were induced in patients of the Group I: 9 with RBBB, 10 with LBBB and 7 with "bizarre" QRS morphology. Sustained ventricular tachycardia reinduction was attempted in 10 patients of the Group I after acute drug testing (Ajmaline, Propafenone, Amiodarone): sustained ventricular tachycardia was no longer inducible in 6, but in 3 of those 4 in whom it was, a marked increase in polymorphism was observed as compared to pre-test pattern. Of the 11 alive patients of Group I, 10 are on Amiodarone alone or in combination with other antiarrhythmic drugs. We conclude as follows: different morphological types of sustained ventricular tachycardia can be quite commonly induced during endocavitary electrophysiologic study; according to our cases induced polymorphism is observed only in patients with chronic ischemic heart disease; patients with induced polymorphism often have intraventricular conduction defect; induced polymorphism furtherly accounts for reentry as the mechanism of sustained ventricular tachycardia in patients with chronic ischemic heart disease; a prevalent morphology of the endocavitary electrophysiologic study induced sustained ventricular tachycardia in patients with chronic ischemic heart disease was not observed at least in our patients; Amiodarone is the drug of choice for the treatment of induced polymorphic sustained ventricular tachycardia patients.
D000328:Adult; D000368:Aged; D000404:Ajmaline / Q000627:therapeutic use; D000638:Amiodarone / Q000627:therapeutic use; D004558:Electric Stimulation; D004562:Electrocardiography; D004594:Electrophysiology; D005260:Female; D006327:Heart Block / Q000209:etiology; D006352:Heart Ventricles / Q000503:physiopathology; D006801:Humans; D008297:Male; D008875:Middle Aged; D011405:Propafenone; D011427:Propiophenones / Q000627:therapeutic use; D013610:Tachycardia / Q000188:drug therapy / Q000209:etiology* / Q000503:physiopathology
D011427:Propiophenones; D000404:Ajmaline; D011405:Propafenone; D000638:Amiodarone
Tachicardia ventricolare sostenuta: polimorfismo indotto. Aspetti clinici ed elettrofisiologici, implicazioni terapeutiche.