Takao Mitsuoka

Asystole with syncope following strenuous exercise in a man without organic heart disease

A 29-year-old man without organic heart disease who had a history of six episodes of syncope following sudden cessation of strenuous exercise over the last 18 years was reported. Resting electrocardiogram and 24-hour electrocardiographic monitoring did not show any rhythm disturbance or ischemic changes. Sinus node recovery time, sinoatrial conduction time and A-V conduction were normal on electrophysiologic study. Asystole with syncope occurred immediately following sudden cessation of strenuous exercise and following release of intrathoracic pressure during Valsalvas maneuver performed after subcutaneous administration of 0.5 mg of epinephrine. However, Masters single two-step test and Valsalvas maneuver performed without epinephrine could not evoke asystole. It was assumed from these results that transient overactivity of the autonomic nervous system and sympathetic-parasympathetic interactions were the underlying factors responsible for the occurrence of asystole following sudden cessation of strenuous exercise in the present case.

Changes in T wave morphology during hypercalcemia and its relation to the severity of hypercalcemia

The effect of hypercalcemia on T wave morphology, polarity, and amplitude was studied in 14 patients with a primary diagnosis of malignant lymphoma (8 patients), adult T-cell leukemia (5 patients), and Hodgkins disease (1 patient). Hypercalcemia was severe to extreme in 11 (14.9-22.8 mg/dl), moderate in 1 (13.4 mg/dl), and mild in 2 (11.8 and 12.2 mg/dl) patients. Ten of the 11 patients (91%) with severe hypercalcemia showed inverted, biphasic, and notched T waves, mainly in the chest leads. Notched T waves were observed in all 10 of these patients in anterior to lateral, mid to lateral, or lateral chest leads. Biphasic and/or inverted T waves in anterior or anterior to midchest leads were present in 4 of these 10 patients who had extreme hypercalcemia (greater than 16 mg/dl). Changes in T wave morphology were not observed in moderate or mild hypercalcemia. T wave amplitude showed significant inverse correlation with serum calcium (T mV vs Ca, r = -0.60, p less than 0.001; T/R ratio vs Ca, r = -0.68, p less than 0.001; n = 35). Decrease in T wave amplitude was marked in severe hypercalcemia (p less than 0.0001) and moderate hypercalcemia, but there was no change in mild hypercalcemia. Changes in T wave morphology, polarity, and amplitude either appeared with development of hypercalcemia or disappeared with normalization of serum calcium level. It was concluded that in addition to shortening the QT interval, severe to extreme hypercalcemia can cause development of inverted, biphasic, or notched T wave with a marked decrease in amplitude of T waves.

Influence of sympathetic nerve activity on ventricular arrhythmogenicity in the dog with chronic hypokalemia

To examine the influence of sympathetic nerve activity on ventricular arrhyth mogenicity in the dog with chronic hypokalemia, an electrophysiologic study was performed before and after bilateral stellectomy (BS) in 10 dogs with chronic hypokalemia (2.8 ± 0.1 mEq/L), which was created by feeding a low-potassium diet and by administering furosemide over a four-week period, and the results were compared with those obtained from 10 dogs with normokalemia (4.7 ± 0.3 mEq/L) from being fed an ordinary diet over a four-week period. Before BS the incidence of electrically induced ventricular arrhythmias was higher in the hypokalemic than in the normokalemic dogs. After BS it was decreased considerably in the hypokalemic but not in the normokalemic dogs. Heterogeneity of effective refractory period (ΔERP), which was determined as the difference between the longest and shortest effective refractory periods in three sites of the right and left ventricles, was greater in the hypokalemic than in the normokalemic dogs before BS. The ΔERP decreased slightly in the two groups both before and after BS. There was, however, no significant difference in ΔERP in the two groups both before and after BS. Ventricular fibrillation threshold (VFT) was significantly lower in the hypokalemic dogs than in the nor mokalemic dogs before BS (p< 0.005). VFT was elevated in the two groups after BS. Percent increase in VFT after BS was significantly greater in the hypoka lemic than in the normokalemic dogs. In conclusion, sympathetic nerve activity may play an important role in the increase in ventricular arrhythmogenicity in the presence of chronic hypokalemia.

Twenty‐Seven‐Year Follow‐up of Arrhythmogenic Right Ventricular Dysplasia

OBATA, H., et al.: Twenty‐Seven‐Year Follow‐up of Arrhythmogenic Right Ventricular Dysplasia. This case report describes clinical features, especially of surface ECG changes, observed for 27 years in a patient with arrhythmogenic right ventricular dysplasia (ARVD). The course of this patient was characterized by progressive deterioration of right ventricular function and progression of delayed potentials (so‐called epsilon waves) following QRS complexes. However, the relation between ventricular arrhythmias and ECG changes or the degree of right ventricular abnormality was difficult to discern.

Concealed conduction in the reentrant pathway as a mechanism of stable ventricular quadrigeminy

This is the first report on the stable occurrence of ventricular quadrigeminy as a manifestation of concealed bigeminy in a case of fixed and late coupled ventricular extrasystoles. A 46-year-old man is reported in whom the period of ventricular bigeminy alternated with the period of ventricular quadrigeminy. Coupling intervals of the extrasystoles were fixed and much longer than sinus QT intervals. When the heart rate is decreased, the period of bigeminy changed to the period of quadrigeminy without gradual decrease in coupling of the preceding extrasystoles. Once such a change occurred, stable quadrigeminy is maintained for a period. These findings suggest the possibility that concealed electrotonic conduction of blocked impulses and interference of conducted impulses may occur in the reentrant extrasystolic pathway as a mechanism of stable ventricular quadrigeminy.

Effect of Bilateral Stellectomy on Electrical Instability of the Atrium in the Dog with Hypokalemia

To investigate the effect of sympathetic nerve activity on electrical instability of the atrium in the presence of hypokalemia, open chest elecfrophysiological study was performed before and after bilateral stellectomy (BS) in 15 dogs with hypokalemia (hypokalemia group) and in 15 dogs with normo‐kalemia (control group). Hypokalemia was created by infusion of 5.0 g/kg of polystyrene sulfonic acid calcium into the colon. Serum level of potassium was significantly lower in the hypokalemia group (2.94 ± 0.52 mEq/L) than in the control group (4.86 ± 0.51 mEq/L, P < 0.01) before BS. There was no significant change in serum level of potassium in the two groups after BS. Incidence of electrically induced atrial fibrillation (AF) was significantly higher in the hypokalemia group (80%) than in the control group (13%, P < 0.001) before BS. It was significantly reduced in (he hypokalemia group (40%, P < 0,05), but not in the control group (6%) after BS. Dispersion of effective refractory period of the atrium (AEHP) was significantly greater in the hypokalemia group (26.1 ± 2.8 msec) than in the control group (22.0 ± 3.3 msec, P < 0.005) before BS. ft was significantly decreased to 23.1 ± 3.2 msec in the hypokalemia group (P < 0.001) and to 20.6 ± 2.5 msec in the control group (P < 0.01) after BS. Maximum conduction delay in the atrium (MaxCD) was 36.1 ± 3.5 msec before and 36.2 ± 4.1 msec after BS in the hypokalemia group and 31.1 ± 4.2 msec before and 32.3 ± 4.9 msec after BS in the control group. There was a significant difference in MaxCD betiveen the two groups before BS. Atrial fibrillation threshold (AFT) was significantly lower in the hypokalemia group (3.9 ± 0.7 mA) than in the control group (33.8 ± 3.1 mA, P < 0.001) before BS. It was significantly increased both in the hypokalemia group (6.5 ± 1.3 mA, P < 0.001) and in the control group (15.0 ± 2.7 mA, P < 0.005) after BS. It is concluded that sympathetic nerve activity may play some role in the increase in electrical instability of the atrium in the presence of hypokalemia.

Effect of verapamil directly administered into A-V node artery on A-V junctional automaticity and A-V conduction in dogs.

Summary: We investigated the direct effects of verapamil, which was infused into the A-V node artery at two doses of 0.01 and 0.1 μg/kg/min on the A-V conduction and the A-V junctional automaticity in the dog with experimentally induced A-V junctional rhythm. Verapamil significantly prolonged the A-H interval, but not the H-V interval, in the His bundle electrogram during atrial pacing at a rate of 100 beats/min. Effective and functional refractory periods of the A-V node also were prolonged significantly by verapamil. On the other hand, verapamil showed less propensity to decrease the spontaneous A-V junctional rate and to prolong the A-V junctional recovery time after atrial overdrive at a rate of 100 beats/min for 60 s. These results indicate that suppressive effects of verapamil on the A-V junctional automaticity are much weaker when compared with that on the A-V conduction.

Suppression of Exercise-Induced Ventricular Arrhythmias by Propranolol and Diltiazem in a Woman Without Organic Heart Disease—A Case Report

A thirty-five-year-old woman without organic heart disease who has exercise-induced ventricular arrhythmias suppressed by propranolol and diltiazem is reported. Treadmill exercise provoked reproducibly nonsustained ventricular tachycardia (NSVT) and salvos of ventricular premature contraction (VPC). QRS morphology of these ventricular arrhythmias showed left bundle branch block pattern and right axis deviation. Oral propranolol (20 mg) and diltiazem (90 mg) prevented exercise provocation of NSVT and VPC. However, oral mexiletine (200 mg) and procainamide (500 mg) could not prevent exercise provocation of these ventricular arrhythmias. No ventricular arrhythmias could be induced by any form of ventricular extrastimulations. Right ventricular pacing at a rate of 210 beats/minute provoked NSVT of which the QRS morphology was similar to that of exercise-induced NSVT. Triggered activity may be a possible electrophysiologic mechanism for exercise-induced ventricular arrhythmias in this patient, although other mechanisms such as reentry and enhanced automaticity could not be completely excluded.