AV reentrant and idiopathic ventricular double tachycardias: complicated interactions between two tachycardias.
(1/1980)
An electrophysiological study was performed in a 61 year old man with Wolff- Parkinson-White (WPW) syndrome. At baseline, neither ventricular nor supraventricular tachycardias could be induced. During isoprenaline infusion, ventricular tachycardia originating from the right ventricular outflow tract (RVOT) with a cycle length of 280 ms was induced and subsequently atrioventricular reentrant tachycardia (AVRT) with a cycle length of 300 ms using an accessory pathway in the left free wall appeared. During these tachycardias, AVRT was entrained by ventricular tachycardia. The earliest ventricular activation site during the ventricular tachycardia was determined to be the RVOT site and a radiofrequency current at 30 W successfully ablated the ventricular tachycardia at this site. The left free wall accessory pathway was also successfully ablated during right ventricular pacing. The coexistence of WPW syndrome and cathecolamine sensitive ventricular tachycardia originating from the RVOT has rarely been reported. Furthermore, the tachycardias were triggered by previous tachycardias. (+info)
Tachycardia induced tachycardia: case report of right ventricular outflow tract tachycardia and AV nodal reentrant tachycardia.
(2/1980)
Tachycardia induced tachycardia, or so called double tachycardia, is rare. A 34 year old woman is described who had a history of syncope, frequent extrasystoles, and episodes of non-sustained ventricular tachycardia, perceived as palpitation, without syncope. At electrophysiological study, during infusion of isoprenaline, an episode of non-sustained ventricular tachycardia arising from the right ventricular outflow tract initiated sustained atrioventricular nodal reentrant tachycardia, thought to be the cause of the patient's syncope. Ablation of the right ventricular outflow tract focus abolished the ventricular ectopy; the slow AV nodal pathway was also ablated. The patient no longer has either syncope or palpitation. (+info)
ECG diagnosis of native heart ventricular tachycardia in a heterotopic heart transplant recipient.
(3/1980)
A case is reported of haemodynamic collapse in a 51 year old male heterotopic heart transplant recipient caused by native heart ventricular tachycardia. An accurate diagnosis was made by selective right and left sided electrocardiography. Synchronised electrical cardioversion of the native heart (200 J) resulted in restoration of sinus rhythm with prompt relief of symptoms and amelioration of the clinical situation. (+info)
New-onset sustained ventricular tachycardia after cardiac surgery.
(4/1980)
BACKGROUND: The de novo occurrence of sustained ventricular tachycardia (VT) after CABG has been described, but the incidence, mortality rate, long-term follow-up, and mechanism are not well defined. METHODS AND RESULTS: This prospective study enrolled consecutive patients undergoing CABG at a single institution. Patients were followed up for the development of sustained VT, and a detailed analysis of clinical, angiographic, and surgical variables associated with the occurrence of VT was performed. A total of 382 patients participated, and 12 patients (3.1%) experienced >/=1 episode of sustained VT 4.1+/-4.8 days after CABG. In 11 of 12 patients, no postoperative complication explained the VT; 1 patient had a perioperative myocardial infarction. The in-hospital mortality rate was 25%. Patients with VT were more likely to have prior myocardial infarction (92% versus 50%, P<0.01), severe congestive heart failure (56% versus 21%, P<0.01), and ejection fraction <0.40 (70% versus 29%, P<0.01). When all 3 factors were present, the risk of VT was 30%, a 14-fold increase. Patients with VT had more noncollateralized totally occluded vessels on angiogram (1.4+/-0.97 versus 0.54+/-0.7, P<0.01), a bypass graft across a noncollateralized occluded vessel (1.50+/-1.0 versus 0.42+/-0.62, P<0.01), and a bypass graft across a noncollateralized occluded vessel to an infarct zone (1.50+/-1.0 versus 0.17+/-0.38, P<0.01). By multivariate analysis, the number of bypass grafts across a noncollateralized occluded vessel to an infarct zone was the only independent factor predicting VT. CONCLUSIONS: The first presentation of sustained monomorphic VT in the recovery period after CABG is uncommon, but the incidence is high in specific clinical subsets. Placement of a bypass graft across a noncollateralized total occlusion in a vessel supplying an infarct zone was strongly and independently associated with the development of VT. (+info)
Differential effects of a segment of slow conduction on reentrant ventricular tachycardia in the rabbit heart.
(5/1980)
BACKGROUND: The purpose of this study was to compare differential effects of a segment of slow conduction during ventricular tachycardia (VT) due to depression of the action potential and electrical uncoupling. METHODS AND RESULTS: In 33 Langendorff-perfused rabbit hearts, a ring of anisotropic left ventricular subepicardium was created by a cryoprocedure. Reentrant VT was produced by incremental pacing. Slow conduction in a segment of the ring was created by selective perfusion of the LAD with 10 mmol/L potassium or 0.75 mmol/L heptanol. As a result, VT cycle length increased from 193+/-34 to 235+/-37 ms (potassium) and 227+/-42 ms (heptanol). Reset curves were made by applying premature stimuli proximal to the area of depressed conduction. In a ring of uniform anisotropic tissue, the reset curve was almost completely flat. Electrical uncoupling of part of the ring (nonuniform anisotropy) resulted in a mixed reset curve. In both substrates, early premature beats failed to terminate VT. Depression of part of the ring by increasing K+ resulted in a completely sloped reset curve, indicating a gap of partial excitability. Under these conditions, in 19 of 24 hearts, premature beats terminated VT by conduction block in the high K+ area. CONCLUSIONS: The nature of the area of slow conduction determines the type of reset response and the ability to terminate VT. (+info)
Clinical application of an integrated 3-phase mapping technique for localization of the site of origin of idiopathic ventricular tachycardia.
(6/1980)
BACKGROUND: Radiofrequency (RF) catheter ablation provides curative treatment for idiopathic ventricular tachycardia (VT). METHODS AND RESULTS: Nineteen consecutive patients with an idiopathic VT underwent RF catheter ablation. An integrated 3-phase mapping approach was used, consisting of the successive application of online 62-lead body surface QRS integral mapping, directed regional paced body surface QRS integral mapping, and local activation sequence mapping. Mapping phase 1 was localization of the segment of VT origin by comparing the VT QRS integral map with a database of mean paced QRS integral maps. Mapping phase 2 was body surface pace mapping during sinus rhythm in the segment localized in phase 1 until the site at which the paced QRS integral map matched the VT QRS integral map was identified (ie, VT exit site). Mapping phase 3 was local activation sequence mapping at the circumscribed area identified in phase 2 to identify the site with the earliest local endocardial activation (ie, site of VT origin). This site became the ablation target. Ten VTs were ablated in the right ventricular outflow tract, 2 at the basal LV septum, and 7 at the midapical posterior left ventricle. A high long-term ablation success (mean follow-up duration, 14+/-9 months) was achieved in 17 of the 19 patients (89%) with a low number of RF pulses (mean, 3.3+/-2.2 pulses per patient). CONCLUSIONS: This prospective study shows that integrated 3-phase mapping for localization of the site of origin of idiopathic VT offers efficient and accurate localization of the target site for RF catheter ablation. (+info)
Cardiac involvement in proximal myotonic myopathy.
(7/1980)
Proximal myotonic myopathy (PROMM) is a recently described autosomal dominantly inherited disorder resulting in proximal muscles weakness, myotonia, and cataracts. A few patients with cardiac involvement (sinus bradycardia, supraventricular bigeminy, conduction abnormalities) have been reported. The cases of three relatives with PROMM (weakness of neck flexors and proximal extremity muscles, calf hypertrophy, myotonia, cataracts) are reported: a 54 year old man, his 73 year old mother, and 66 year old aunt. All three presented with conduction abnormalities and one had repeated, life threatening, sustained monomorphic ventricular tachycardia. This illustrates that severe cardiac involvement may occur in PROMM. (+info)
Mechanisms of altered excitation-contraction coupling in canine tachycardia-induced heart failure, I: experimental studies.
(8/1980)
Pacing-induced heart failure in the dog recapitulates many of the electrophysiological and hemodynamic abnormalities of the human disease; however, the mechanisms underlying altered Ca2+ handling have not been investigated in this model. We now show that left ventricular midmyocardial myocytes isolated from dogs subjected to 3 to 4 weeks of rapid pacing have prolonged action potentials and Ca2+ transients with reduced peaks, but durations approximately 3-fold longer than controls. To discriminate between action potential effects on Ca2+ kinetics and direct changes in Ca2+ regulatory processes, voltage-clamp steps were used to examine the time constant for cytosolic Ca2+ removal (tauCa). tauCa was prolonged by just 35% in myocytes from failing hearts after fixed voltage steps in physiological solutions (tauCa control, 216+/-25 ms, n=17; tauCa failing, 292+/-23 ms, n=22; P<0.05), but this difference was markedly accentuated when Na+/Ca2+ exchange was eliminated (tauCa control, 282+/-30 ms, n=13; tauCa failing, 576+/-83 ms, n=11; P<0. 005). Impaired sarcoplasmic reticular (SR) Ca2+ uptake and a greater dependence on Na+/Ca2+ exchange for cytosolic Ca2+ removal was confirmed by inhibiting SR Ca2+ ATPase with cyclopiazonic acid, which slowed Ca2+ removal more in control than in failing myocytes. beta-Adrenergic stimulation of SR Ca2+ uptake in cells from failing hearts sufficed only to accelerate tauCa to the range of unstimulated controls. Protein levels of SERCA2a, phospholamban, and Na+/Ca2+ exchanger revealed a pattern of changes qualitatively similar to the functional measurements; SERCA2a and phospholamban were both reduced in failing hearts by 28%, and Na+/Ca2+ exchange protein was increased 104% relative to controls. Thus, SR Ca2+ uptake is markedly downregulated in failing hearts, but this defect is partially compensated by enhanced Na+/Ca2+ exchange. The alterations are similar to those reported in human heart failure, which reinforces the utility of the pacing-induced dog model as a surrogate for the human disease. (+info)