Kazuo Moroe

Efficacy of procainamide on ventricular tachycardia: Relation to prolongation of refractoriness and slowing of conduction

The effect of procainamide on intraventricular conduction and refractoriness, and the prevention of induction of ventricular tachycardia (VT) were studied in 29 patients who had remote myocardial infarction and inducible sustained monomorphic VT. AFter intravenous administration of 15 mg/kg procainamide, induction of VT was suppressed in seven (24%) patients (responders), while in 22 (76%) VT was still inducible (nonresponders). The percent change in paced QRS duration at a cycle length (CL) of 400 msec produced by procainamide was significantly less in responders than in nonresponders: 29.8 +/- 3.9% versus 38.9 +/- 10.8% (p = 0.0020). The percent change in the right ventricular effective refractory period (ERP) at CLs of 600 and 400 msec was significantly greater in responders than in nonresponders: 14.6 +/- 6.9% versus 7.9 +/- 7.3% (p = 0.0414) for ERP at a CL of 600 msec and 15.1 +/- 7.0% versus 8.0 +/- 7.4% (p = 0.0386) for ERP at a CL of 400 msec. Stepwise discriminant analysis showed that greater percent increase in ERP at a CL of 400 msec and lesser percent increase in paced QRS duration at a CL of 400 msec were significantly independent markers for the responders. These findings suggest that lesser slowing of conduction and greater prolongation of refractoriness by procainamide tend to abolish reentry within the reentrant circuit. Greater slowing of conduction and lesser prolongation of refractoriness tend to stabilize a reentrant circuit, and promote the continued induction of VT.

Arrhythmogenic effects of graded coronary blood flow reductions superimposed on prior myocardial infarction in dogs.

BackgroundWe studied arrhythmogenesis and its underlying pathophysiology during graded reductions of coronary blood flow, superimposed on prior myocardial infarction to test the hypothesis that spontaneous ventricular fibrillation and induced ventricular tachycardia are dependent on different patterns of coronary flow reduction in hearts with prior myocardial infarction. Methods and ResultsIn 10 sham-operated dogs (control group) and 24 dogs with 3-week-old experimental apical myocardial infarction, the left circumflex coronary artery was constricted to produce four grades of flow reduction: 25%, 50%1, 75%, and 100%. Among the sham-operated control animals, only one of 10 (10%) developed spontaneous ventricular fibrillation and only two of nine (22%) were inducible into sustained ventricular tachycardia during 100% circumflex coronary artery flow reduction. No spontaneous ventricular fibrillation or inducible ventricular tachycardia occurred with lesser grades (25%, 50%, or 75%) of flow reduction among the control animals. In the myocardial infarction group, five of 24 dogs (21%) were inducible before flow reduction. However, 50% flow reduction in the myocardial infarction group resulted in inducibility of ventricular tachycardia in 12 of 24 dogs (50%); nine of 16 (56%) during 75% flow reduction; and six of 11 (55%) with 100% flow reduction. In addition, none of the dogs in the myocardial infarction group developed spontaneous ventricular fibrillation during 25% or 50% flow reduction, whereas six of 22 (27%) developed ventricular fibrillation during 75% flow reduction and 10 of 21 (48%) during 100% flow reduction. In dogs with spontaneous ventricular fibrillation during flow reduction, the total myocardial mass of the ischemic “risk” zone and infarcted zone was significantly greater than in those without spontaneous ventricular fibrillation (68 ± 5% versus 56 ± 6% [p < 0.011). There was no difference in the total myocardial mass of the ischemic risk zone and infarcted zone between dogs with and without inducible ventricular tachycardia during flow reduction. ConclusionsIn canine model of subacute myocardial infarction, superimposed ischemia increased the likelihood of inducible sustained ventricular tachycardia with lesser grades of coronary flow reduction compared with that necessary to allow spontaneous ventricular fibrillation. The underlying pathophysiology appears to differ between spontaneous ventricular fibrillation and electrically induced sustained ventricular tachycardia. (Circulation 1991;84:368–377)

Sudden cardiac arrest recorded during Holter monitoring: Prevalence, antecedent electrical events, and outcomes

BACKGROUND Causative arrhythmias of sudden cardiac arrest (SCA) are changing in this age of improved coronary care. OBJECTIVE The purpose of this study was to examine the frequency of terminal arrhythmias and the electrical events prior to SCA. METHODS We analyzed 24-hour Holter recordings of 132 patients enrolled from 41 institutions who either died (n = 88) or had an aborted death (n = 44). The Holter recordings were obtained for diagnosing and evaluating diseases and arrhythmias in those without any episodes suggestive of SCA. RESULTS In 97 patients (73%), SCA was associated with ventricular tachyarrhythmias and in 35 (27%) with bradyarrhythmias. The bradyarrhythmia-related SCA patients were older than those with a tachyarrhythmia-related SCA (70 ± 13 years vs. 58 ± 19 years, P < .001). The most common arrhythmia for a tachyarrhythmia-related SCA was ventricular tachycardia degenerating to ventricular fibrillation (45%). The bradyarrhythmia-related SCA was caused by asystole (74%) or AV block (26%). Spontaneous conversion was observed in 37 patients (38%) with ventricular tachyarrhythmias. Of those, 62% of the patients experienced symptoms including syncope, chest pain, or convulsion. Multivariate logistic analysis revealed that independent predictors of mortality for tachyarrhythmia-related SCAs were advanced age (odds ratio 1.04, 95% confidence interval 1.02-1.08) and ST elevation within the hour before SCA (odds ratio 3.54, 95% confidence interval 1.07-13.5). In contrast, the presence of preceding torsades de pointes was associated with spontaneous conversion (odds ratio 0.20, 95% confidence interval 0.05-0.66). CONCLUSION The most frequent cause of SCA remains ventricular tachyarrhythmias. Advanced age and ST elevation before SCA are risk factors for mortality in tachyarrhythmia-related SCAs.

Wavelength index: a predictor of the response to disopyramide in paroxysmal lone atrial fibrillation.

We investigated whether the new parameter wavelength index could predict the response to chronic disopyramide therapy in patients with paroxysmal atrial fibrillation (AF). Twenty-seven patients with AF underwent electrophysiologic studies and the wavelength index was determined before and after intravenous administration of disopyramide. Then all patients were treated with oral disopyramide for 6 months. In 17 patients, AF was eliminated (group A), while it persisted in another 10 patients (group B). The ratio of the wavelength index before and after intravenous disopyramide was higher in group A than in group B. Thus, the wavelength index proved useful for predicting the response of AF to disopyramide.

Effects of Verapamil on Electrophysiological Properties in Paroxysmal Atrial Fibrillation

Verapamil is used to control ventricular response during atrial fibrillation (AF). Limited data is available on the effects of verapamil on atrial vuinerability in human AF. The effects of intravenous verapamil (0.15 mg/kg) on electrophysiological properties of the atrium were investigated in 12 patients with documented paroxysmal AF by electrophysiological studies. Sinus cycle length, sinus node recovery time, and the effective refractory period of the right atrium were not significantly affected by verapamil. The intraatrial conduction delay zone was significantly increased (33 ± 20 msec before verapamil versus 50 ± 22 msec after verapamil, P < 0.01, and the maximal intraatrial conduction delay was also significantly prolonged by verapamil, both to the His bundle region (30 ±12 msec before verapamil versus 42 ± 15 msec after verapamil. P < 0.01) and to the coronary sinus (40 ± 15 msec before verapamil versus 53 ± 17 msec after verapamil, P < 0.01). The fragmented atrial activity zone was significantly increased (15 ± 14 msec before verapamil versus 25 ± 22 msec after verapamil, P < 0.02), and the percentile fragmented atrial activity was also significantiy increased by verapami] (149 ± 18 msec before verapamil versus 174 ± 44 msec after verapamil, P < 0.05). The repetitive atriaJ firing zone remained unchanged. Sustained AF spontaneousiy occurred in only one patient after the administration of verapamil. Thus, verapamil may modulate the abnormal atrial electrophysiology in paroxysmal AF, and wouid favor production of atrial reentry.

Observations on the Initiation of Sustained Ventricular Tachycardia by Programmed Stimulation

We analyzed the initiation of sustained monomorphic ventricular tachycardia (VT) by programmed ventricular stimulation (PVS) in 50 consecutive patients who had clinical VT or aborted sudden cardiac death with remote myocardial infarction. In 25 of 50 patients, the first induced QRS complex of VT was morphologically identical to the succeeding QRS complexes of VT (type I). In 25 other patients, the first VT beat had a different morphology (type II). Type I had a significantly longer VT cycle length than type II (333 ± 65 msec and 293 ± 66 msec, P = 0.036). Type II VT initiation required more aggressive stimulation protocol than type I (type I: type II; number of extrastimulus required for induction 2.5 ± 0.9 : 3.0 ± 0.6, P = 0.026; shortest extrastimuli coupling interval 244 ± 28 msec : 220 ± 23 msec, P = 0.002). The interval between the last extrastimulus and the onset of the first VT beat was 408 ± 88 msec in type I and 336 ± 75 msec in type II (P= 0.004). Furthermore, there was good correlation between the VT cycle length and the interval from last extrastimulus to the onset of nonpaced beat in type I but not in type II. We conclude; (1) in type I VT initiation, when compared to type II, the induced sustained VT had slower rates and required less extrastimuli and longer coupling interval of extraslimulus for induction; (2) in type I, initiation of VT suggests establishment of a reentrant circuit with the first nonpaced beat; (3) in type I, shortening of refractoriness is more important than the conduction delay in establishing sustained VT; and (4) in type II, the mechanisms of initiation of VT are heterogeneous.

Hyperinsulinemia in Patients with Spastic Angina Pectoris

We evaluated the association between coronary spasm and hyperinsulinemia (high immunoreactive insulin, IRI) in patients with angina pectoris. The study cohort comprised 30 patients with spastic angina pectoris, 30 patients with angina pectoris showing fixed-obstructive coronary sclerosis and 30 control subjects who were matched for body mass index, age and sex. A 75-gram oral glucose test was performed, and blood sugar and IRI were serially measured concomitant with serum total cholesterol, triglyceride and HDL cholesterol. The IRI level at 60 min, the peak IRI during the test, sigma IRI and sigma IRI/sigma blood sugar were significantly higher in the patients than in the controls. Total cholesterol and LDL cholesterol levels were significantly increased in patients showing fixed-obstructive coronary sclerosis compared to controls.

Electrophysiological Properties in Paroxysmal Atrial Fibrillation Complicated with the Wolff-Parkinson-White Syndrome: Comparison with Paroxysmal Atrial Fibrillation Alone

Electrophysiological studies were performed in 26 patients with atrial fibrillation (AF). Thirteen patients had the Wolff-Parkinson-White (WPW) syndrome (group A), and another 13 patients did not have the WPW syndrome (group B). The right atrium effective refractory period was significantly shorter in group A than in group B. The wavelength index which was defined as the ratio of the refractory period to the conduction delay was significantly lower in group A than in group B. Accordingly, patients in group A had a greater tendency to produce atrial reentry than those in group B.

A Transarterial Approach of Electrical Ablation of Atrioventricular Junction in a Dog Model: Comparison of the Effects between High and Low Energy Shocks

To analyze the effective ness of a ctransarterial catheter technique for electrical ablation of the atrioventricular junction, 30 mongrel dogs were studied by means of synchronized electrical shock between the catheter adjacent to the noncoronary cusp and a metal plate behind the dogs back using a standard cardioversion unit. These dogs were classified into two groups according to the energy delivered. The high energy group received more than 100 joules (group A) and the low energy group received from 20 to 60 joules (group B). Complete atrioventricular block was induced by a single shock in all dogs. In group A, ventricular premature beats appeared in all dogs; ventricular fibrillation and ventricular tachycardia appeared immediately in half (6/12) after electrical ablation. No ventricular dysrhythmios occurred in group B. Temporary right ventricular pacing was also performed in 10 out of 12 dogs in group A after electrical ablation. In contrast only one dog required pacing in group B. The cycle length of the subsidiary pacemaker rhythm was essentially identical in both groups. The QRS duration of the subsidiary pacemaker rhythm in group A was significantly longer in group B (P < 0.01). The extent of myocardial damage induced by electrical ablation in group B was more localized than those in group A. However, the histological lesion representing the granulation tissue with necrosis and slight chronic inflammatory cell infiltration, was identical between both groups A and B. It was concluded that this technique of low energy electrical ablation of the atrioventricular junction adjacent to the noncoronary cusp via a transarterial approach was useful in producing an experimental model of chronic complete AV block.

Rapid Assessment of Rate and Antiarrhythmic Drug Effect on the Myocardium Using Asymmetric Biphasic Pulse Stimulation

An asymmetric biphasic pulse which stimulates the heart and neutralizes the poststimulation polarization at the electrode‐myocardial interface permitting the recording of the evoked endocardial response (EER) up to approximately 1 ms poststimulation with the same electrode used for stimulation is described. Using this mode of cardiac stimulation in 20 dogs the effects on the EER of increasing heart rate and antiarrhythmic drugs, procainamide (PA) and N‐acetylpro‐cainamide (NAPA), were studied. EERs were recorded during bipolar and unipolar pacing rates of 120, 150, and 200/min before and during a five step PA or NAPA infusion which resulted in progressively increasing PA and NAPA plasma concentrations (Cps), 1.7 — 32.5 mg/l for PA and 8.1 — 116.1 mg/l for NAPA.