Mokuo Matsuhisa

Idiopathic sustained left ventricular tachycardia: clinical and electrophysiologic characteristics.

Electrophysiologic studies were performed in 16 patients 11 to 45 years old (mean 33 years) with idiopathic sustained (lasting more than 5 min) ventricular tachycardia (VT) originating from the left ventricle. Endocardial mapping during VT showed that the earliest site of activation was at the apical inferior portion of the left ventricle in 14 patients whose QRS morphology during VT showed a right bundle branch block pattern and left-axis deviation, but at the apical anterosuperior portion of the left ventricle in two patients whose QRS morphology during VT showed a right bundle branch block and right-axis deviation. Single programmed ventricular stimulation induced VT in 13 patients, and rapid ventricular pacing induced VT in the remaining three patients. Rapid ventricular pacing terminated VT in all patients. The relationship between the coupling interval and the echo interval was inverse in all eight patients with a wide VT inducible zone. Entrainment was recognized in three of six patients. The initiation of VT by constant pacing depended on the number of pacing beats but not the duration of pacing in all four patients tested. Intravenous verapamil terminated the VT in 13 of 14 patients. Long-term oral verapamil was also effective in all five patients who required long-term oral therapy for their symptoms associated with VT. In conclusion (1) idiopathic left ventricular tachycardia has unique electrocardiographic, electrophysiologic, and electropharmacological properties, (2) the electrophysiologic characteristics suggest that the mechanism is reentry, and (3) verapamil is effective in both the short- and long-term treatment of VT.

Early afterdepolarizations induced by isoproterenol in patients with congenital long QT syndrome.

Background Several recent experimental and clinical studies have shown that early afterde-polarizations (EADs) are important in the genesis of QTU prolongation and ventricular tachyarrhythmias (VTs) in patients with long QT syndrome. On the other hand, sympathetic stimulation is well known to contribute to the genesis of QTU prolongation and VTs in patients with congenital long QT syndrome. The present study was performed to examine the influence of isoproterenol on the genesis of EADs and on the action potential durations and QTU intervals in patients with congenital long QT syndrome. Methods and Results We recorded monophasic action potentials (MAPs) with a contact electrode during right atrial pacing at a constant cycle length of 500 msec before and after continuous isoproterenol infusion (1 μg/min). MAPs were obtained from the right and left ventricular endocardium in six patients with congenital long QT syndrome (LQT group, 18 recording sites) and in eight control patients (control group, 19 recording sites). Although no EADs were recorded from either group during the control state, MAP duration at 90% repolarization (MAPD90) was significantly longer in the LQT group (n = 18) than in the control group (n = 19) (275 ± 36 versus 231 ± 22 msec;p < 0.0005). Isoproterenol induced EADs in four of the six LQT patients (five of 18 recording sites) but not in the eight control patients (zero of 19 recording sites). The appearance of EADs in the LQT group was associated with an increased amplitude of the late component of the TU complex, and the corrected QT (QTj) interval was prolonged by isoproterenol from 543 ± 53 to 600 ± 30 msec12 (n = 6; p < 0.05). Isoproterenol also prolonged the MAPD90 from 275 ± 36 to 304 ± 50 msec in the LQT group (n = 18; p< 0.005), whereas it shortened the MAPD90 from 231 ± 22 to 224 ± 25 msec in the control group (n = 19; p< 0.05). Moreover, isoproterenol increased the dispersion of MAPD90 (difference between the longest MAPD90 and the shortest MAPD90 in each patient) from 30 ± 5 to 62 ± 35 msec in the LQT group (n = 6; p=0.08), whereas it did not change the dispersion of MAPD90 in the control group (n = 8; 25 ± 14 versus 27 ± 14 msec). Conclusions. These results suggest that patients with congenital long QT syndrome have primary repolarization abnormalities and that EADs induced by isoproterenol play an important role in the exaggeration of these repolarization abnormalities.

Bradycardia-induced abnormal QT prolongation in patients with complete atrioventricular block with torsades de pointes

Fourteen patients with complete atrioventricular block with or without torsades de pointes (TdP) were included in this study. They were divided into 2 groups, 6 patients with TdP (TdP[+] group) and 8 patients without TdP (TdP[-] group). The patients were evaluated at 2 different periods, before (acute period) and after (chronic period) pacemaker implantation. In the acute period, the QRS and heart rate during the escape rhythm were not significantly different between the 2 groups; however, the QT and QTc intervals were significantly longer in the TdP(+) group than in the TdP(-) group: 753 +/- 57.5 vs 635 +/- 78.4 ms (p less than 0.01) and 585 +/- 44.8 vs 476 +/- 58.3 ms (p less than 0.01). In the chronic period (greater than 2 months after pacemaker implantation), we changed the pacemaker rate from 90 or 100 beats/min to 50 beats/min and examined the QT interval changes in relation to the heart rate. The QT interval in the TdP(+) group was significantly prolonged compared with the TdP(-) group when the pacing rate was decreased less than or equal to 60 beats/min: 551 +/- 40 vs 503 +/- 36 ms at 60 beats/min (p less than 0.05), and 700 +/- 46 vs 529 +/- 43 ms at 50 beats/min (p less than 0.001). Patients with complete atrioventricular block with TdP had a bradycardia-sensitive repolarization abnormality and this characteristic remained after pacemaker implantation. The critical heart rate that induced abnormal QT prolongation in the TdP(+) group was less than or equal to 60 beats/min.

Relation between the widening of the fragmented atrial activity zone and atrial fibrillation

Fragmented electrical activity is often recorded by a local atrial electrogram in response to atrial extrastimuli. To assess the relation between fragmented activity and the spontaneous occurrence of atrial fibrillation or flutter (AFF), the fragmented activity zone was measured in 57 patients. The electrograms of the high right atrium, low right atrium and left atrium (through the coronary sinus) were recorded simultaneously during high right atrial stimulation. The fragmented activity zone was defined as the S1-S2 interval (S1 = stimulus of a basic beat, S2 = stimulus of a premature beat) during which a significant fragmented activity was recorded by a high right atrial electrogram after S2. Fifteen patients had neither sinoatrial disease nor atrial arrhythmias (Group I, controls), 16 had sick sinus syndrome (SSS) with a history of paroxysmal AFF (Group II), 14 had SSS without a history of paroxysmal AFF (Group III), and 12 had idiopathic paroxysmal AFF (Group IV). The fragmented activity zone was significantly wider in Group II (112 +/- 26 ms [mean +/- standard deviation], p less than 0.001), Group III (77 +/- 38 ms, p less than 0.001) and Group IV (86 +/- 19 ms, p less than 0.001) than in Group I (31 +/- 25 ms). Patients in Group II had a wider fragmented activity zone than those in Group III (p less than 0.01). Thus, the widening of the fragmented atrial activity zone is characteristic of AFF and may be a good index of a tendency to develop spontaneous AFF.

The role of initial minimum potentials on body surface maps in predicting the site of accessory pathways in patients with Wolff-Parkinson-White syndrome.

Forty-one patients (23 men and 18 women, ages 20 to 66 years) with Wolff-Parkinson-White syndrome were studied with isopotential body surface maps during sinus rhythm to find the most reliable index for predicting the sites of single accessory pathways. The sites predicted by surface maps were compared with those confirmed by multicatheter electrophysiologic study or in the course of surgical operation. Location of the initial minimum by a time criterion, 40 msec after onset of the QRS complex, was not reliable enough for prediction in patients with the small delta wave on their electrocardiograms, because ventricular activation via the normal conduction pathway significantly influenced the location of the minimum. Location of the minimum by an amplitude criterion, -0.15 mV or slightly deeper, was influenced minimally by fusion of ventricular activation, the patients body size, or age and corresponded well to the site of the accessory pathway in 36 of 41 patients. Those minima appeared on circumscribed areas of the map in accordance with the anatomic subdivisions of the atrioventricular ring. Thus location of the minimum by the amplitude criterion was an excellent index for predicting the site of the accessory pathway, regardless of the degree of ventricular fusion. These amplitude-based map features suggest that nonstandard electrocardiograms recorded from selected positions on the body surface can be used as accurate predictors of the sites of accessory pathways.

Pulmonary regurgitation studied with the ultrasonic pulsed Doppler technique.

Sixty patients with pulmonary regurgitation were studied by the pulsed Doppler technique combined with two-dimensional and M-mode echocardiography. Patients with pulmonary regurgitation had abnormal Doppler signals just below the pulmonic valve in the right ventricular outflow tract in diastole on the two-dimensional image. These signals were considered to indicate the regurgitant flow. There are two patterns of pulmonary regurgitant Doppler signals. In pulmonary hypertension, the maximal component of instantaneous flow velocity is sustained at about the same signal strength throughout diastole, but when the pulmonary arterial pressure is normal, the velocity slows down gradually from early diastole to end-diastole. Pulmonary regurgitation was detected by phonocardiography in about half the patients. In the remaining half, pulmonary regurgitant murmur could not be differentiated from aortic regurgitant murmur or was masked by coexistent aortic regurgitation or patent ductus arteriosus, whereas the Doppler technique indicated pulmonary regurgitation.

Significance of atrial fibrillation as a precursor of embolism

all levels of ST elevation had inducible ventricular tachycardia. This retrospective analysis of patients who had had an anterior wall acute myocardial infarction failed to demonstrate by clinical electrophysiologic testing any distinguishing characteristics of patients with persistence of ST elevation for at least 2 weeks. Patients were equally vulnerable to programmed stimulation irrespective of the presence or magnitude of this finding. The patients studied were highly selected. In 27 of the 36, sudden death or sustained ventricular tachycardia led to the study. Thus, individuals with anterior wall infarction without such rhythm disturbances are underrepresented. Nevertheless, it is unlikely that absence of ST elevation identifies a group with reduced vulnerability to the initiation of ventricular tachycardia during programmed stimulation because in 8 of 13 such individuals that arrhythmia was induced by means of the protocol used. Had all patients undergone testing free of antiarrhythmic drug treatment, some of the 8 who were not inducible while receiving drugs would have been vulnerable to programmed stimulation. Because such patients were equally represented at all levels of ST elevation, it is unlikely that the conclusions of this study would have been altered. Of 6 patients with right bundle branch block, only 1 had ST elevation >l mm. Repolarization abnormalities secondary to the bundle branch block offset what might have been persistent ST elevation. Exclusion of these patients does not, however, unmask a difference. Ventricular tachycardia was induced in 4 of the 6. Thus, clinical electrophysiologic testing does not identify a basis for persistence of ST elevation after healing of a myocardial infarction. Additional hypotheses must be proposed and tested.

Differentiation between late potentials of right ventricular and of left ventricular origin

The aim of this study was to determine whether late potentials of right and left ventricular origin could be differentiated with the use of a signal-averaging technique. Nineteen patients with both late potentials and recurrent sustained ventricular tachycardia were divided into 2 groups according to the origin of their late potentials. Group I consisted of 10 patients with late potentials that originated from the right ventricle. Group II consisted of 9 patients with late potentials originating from the left ventricle. Signal-averaged electrocardiograms (Marquette Electronics MAC I unit) were recorded using 3 bipolar and 3 augmented unipolar leads (the electrode positions were V1, V5 and V6R) with a band-pass filter of 100 to 300 Hz. The augmented unipolar V5 lead (aV5) was used for left-side recording and the augmented unipolar V1 lead (aV1) was used for right-side recording. In group I, the mean maximal late potential amplitude was larger in lead aV1 than in lead aV5 (5.1 +/- 2.5 vs 3.7 +/- 1.8 microV, p less than 0.005) and the maximal late potential amplitude was larger in lead aV1 in all except 1 patient. In group II, however, the mean maximal late potential amplitude was smaller in lead aV1 than in lead aV5 (4.0 +/- 3.0 vs 5.7 +/- 3.2 microV, p less than 0.005) and the maximal late potential amplitude was smaller in lead aV1 in all patients. Thus, the origin of late potentials (right ventricular vs left ventricular origin) can be determined by comparing the maximal amplitudes of late potentials in the right- and left-sided leads. This method might be useful in determining ventricular tachycardia origins.

Narrow QRS Complex Tachycardia with Atrioventricular Dissociation

We describe the case of a 22‐year‐old man who had frequent episodes of narrow QRS complex tachycardia with atrioventricular dissociation. The ECG during sinus rhythm showed normal PR and QRS intervals, hut it showed a left bundle branch block configuration during atrial pacing or after injection of verapamil. An electrophysiological study demonstrated that the patient had nodoventricular Mahaim fibers. The narrow QRS complex tachycardia was explained by a circuit involving antegrade conduction via the atrioventricular nodo‐His axis and retrograde conduction via the nodoventricular bypass tract.

The effects of lying position on ventricular volume in congenital absence of the pericardium

In patients with congenital absence of the left pericardium, the heart is supported by the existing right pericardium in the right lateral position, while it is not in the left lateral position. To investigate the change in ventricular size resulting from postural change, seven patients with this malformation were examined. Ventricular volumes were calculated by computed tomography, integrating areas of computed tomographic cross sections measured at 1 cm intervals from the cardiac apex to the aortic arch. In the right lateral position, right ventricular (RV) and left ventricular (LV) volumes were no different from those of five control subjects. With a change in the lying position to the left, the increase in the ventricular volume was significantly greater than that in the control subjects (35 +/- 11 versus 3 +/- 3 ml in the right ventricle and 15 +/- 13 versus 3 +/- 8 ml in the left ventricle). The increases in RV and LV end-diastolic pressure, however, were almost the same as those in the 11 control subjects. It is concluded that the cardiac ventricle, especially the right ventricle, dilates significantly with a small increase in preload in patients with congenital absence of the pericardium. It may be a clue for clarifying the ventricular distensibility being freed from physiologic restraint of the pericardium for a long period.