Carotid sinus baroreflex influence on electrophysiologic properties of the canine atrioventricular node and ventricle

This study examines the efferent mechanisms of carotid sinus baroreflex influence on ventricular repolarization and refractory period compared with effects on atrioventricular (AV) nodal conduction. Pressure was controlled in both carotid sinuses by the Moisejeff technique in 16 chloralose-anesthetized dogs. Increases in carotid sinus pressure during pacing produced graded prolongation of AV nodal conduction, ventricular repolarization and refractory period with a threshold at a carotid sinus pressure of 120 mm Hg and a peak response at 200 mm Hg. Atropine, 0.4 mg/kg, attenuated the peak percent change in ventricular repolarization interval by only 12 ± 14% (± standard error of the mean) despite a significantly greater attenuation (48 ± 11%, p <0.05) in peak percent change in AV nodal conduction. However, stellate ganglionectomy attenuated the peak percent change in ventricular repolarization (42 ± 19%), similar to effects on AV nodal conduction (59 ± 21%, p >0.25). Changes in mean arterial pressure, ventricular end-diastolic segment length or segment length shortening with systole (sonomicrometer technique) did not account for the electrophysiologic responses. Latency to peak effect on ventricular repolarization (43 ± 7 seconds) was slower than that on AV nodal conduction (23 ± 6 seconds, p <0.05). This difference in time course was not abolished by atropine. Thus, the carotid sinus baroreflex prolongs ventricular repolarization and refractoriness mainly by withdrawal of sympathetic influence; AV nodal conduction is prolonged by both vagal activation and sympathetic withdrawal. In addition, differences in time course between ventricular and AV nodal electrophysiologic responses are not explained by different efferent autonomic mechanisms.     

Paroxysmal tachycardia with atrioventricular dissociation in a patient with a variant of pre-excitation syndrome

We report a patient with a variant of the pre-excitation syndrome who has paroxysmal tachycardia with a pattern of left bundle branch block and ventriculo-atrial dissociation. The tachycardia is precipitated by exercise, reproduced by atrial pacing and terminated with lidocaine. Between attacks the electrocardiogram revealed prominent R waves in right precordial leads and the vectorcardiogram displayed anterior displacement of the mean QRS vector, but neither was diagnostic of pre-excitation. The resting P-R interval (140 msec) and A-H interval (60 msec) were within normal limits, but the H-V interval (30 msec) was at or slightly below normal limits. Increasing heart rate from 80 to 150/min with atrial pacing increased A-H from 70 to 160 msec, but did not change the H-V interval. With pacing at 160/min, A-H lengthened progressively from 160 to 190 msec, but A-V remained constant at the critical limit of 190 msec. Accordingly, the H-V interval decreased until the His spike disappeared into the QRS or did not occur because of A-V block. At this point, the QRS complex changed to that seen during spontaneous tachycardia. Pacing was stopped, but tachycardia continued at 160/min and ventriculoatrial dissociation appeared. Lidocaine promptly restored sinus rhythm. We speculate that the patient has anomalous conduction between the lower segment of the A-V node and the ventricular septum (Mahaim fibers) and a reciprocating tachycardia which results from antegrade conduction down the anomalous pathway and retrograde conduction up the His-Purkinje system and lower A-V node. Ventriculo-atrial Wenckebach during the tachycardia excludes participation of atria and upper part of the A-V node in the re-entrant tachycardia. This variant of pre-excitation syndrome could easily be mistaken for “true ventricular tachycardia” and serious heart disease.     

Effects of the volume conductor on the apparent orientation of a known cardiac dipole

The surface electrocardiogram (EKG) is dependent on two major factors: the cardiac generator and the volume conductor. This investigation assessed the effects of the volume conductor in man on the apparent orientation of a simulated cardiac dipole. The apparent orientation of the dipole was calculated from measured surface potentials from about 60 locations on the body of five patients with implanted cardiac pacemakers. The real orientation of the dipole (an implanted pacemaker) was determined radiographically. The effects of both inhomogeneity and boundary characteristics of the volume conductor on the apparent orientation of the dipole were assessed using a new inverse algorithm. The difference between the orientation of the real and the calculated dipoles averaged 30 degrees (range 15 degrees--40 degrees) when the torso was assumed to be an infinite-homogeneous volume conductor. When the configuration of the torso was accounted for, however, the difference between the orientation of the real and calculated dipoles was reduced to 9 degrees (range 5 degrees--13 degrees). Thus, by taking into account the geometry of the torso and neglecting the inhomogeneities in the volume conductor, it is possible to calculate the orientation of a dipole in the cardiac region with an accuracy of about 9 degrees. It is reasonable to assume that the orientation of real activation wave fronts from localized areas of the heart could be calculated with a similar degree of accuracy.     

Spontaneous return of sinus rhythm in older patients with chronic atrial fibrillation and rheumatic mitral valve disease. Description of three patients

Three patients with rheumatic mitral stenosis had had atrial fibrillation for over ten years before spontaneously restoring normal sinus rhythm. Each had undergone a closed mitral commissurotomy ten to twelve years before the conversion. Their ages at the time of resuming normal rhythm were 47, 59, and 71 years. This unusual phenomenon has no satisfactory explanation by our present knowledge of the natural history of mitral valve disease and the pathogenesis of atrial fibrillation.     

Distribution of local repolarization changes produced by efferent vagal stimulation in the canine ventricles

The purpose of this study was to compare the distribution of effects of right and left efferent vagal stimulation on ventricular recovery properties in the in situ heart. To measure these effects in many areas simultaneously, local repolarization changes (local QT intervals) were recorded with bipolar electrodes in nine ventricular sites from 38 anesthetized dogs. In initial experiments, this method was shown to correlate with effective refractory period changes measured in the same test site after QT recording; vagal nerve stimulation prolonged the local QT interval by 1 ms for each 0.82 ms prolongation in effective refractory period (r = 0.87). Simultaneous local QT recordings during vagal nerve stimulation demonstrated uniform prolongation with two exceptions. First, left vagal efferent stimulation prolonged local QT interval in the posterior left ventricular base more than did right vagal stimulation (5.9 +/- 1.0 mean +/- standard error of the mean versus 3.7 +/- 0.9%, p less than 0.05). This probably resulted from an interaction with the left sympathetic nerves because left stellate ganglionectomy or norepinephrine infusion eliminated differences between effects of right and left vagal stimulation. Second, it was also found that vagal stimulation from either side did not prolong local QT interval time in the anterior right ventricle despite attempts to augment vagal effects with bilateral vagal stimulation alone or during isoproterenol or physostigmine administration. These regional differences in ventricular repolarization exhibited in response to efferent vagal nerve stimulation in the dog may provide a basis for understanding how autonomic influences could contribute to the genesis of ventricular arrhythmias.     

Anomalous origin of the left anterior descending coronary artery from the pulmonary artery

Three children were identified as having anomalous origin of the left anterior descending coronary artery (LAD) from the pulmonary artery (PA). Two had had congestive heart failure in infancy with clinical diagnosis of endocardial fibroelastosis and all had abnormal ECGs. The correct diagnosis was delayed in each case, and two patients required selective coronary angiography. Surgery was accomplished in the three children although ECG abnormalities have persisted and one child has dyskinesis of the left ventricular apex. Because this diagnosis may be difficult to make when intercoronary anastomoses are inadequate to outline the left anterior descending coronary flow into the PA, patients with clinical findings suggestive of anomalous coronary artery may require selective coronary studies to exclude this anomaly.     

Evaluation of regional myocardial function in ischemic heart disease by echocardiography

Echocardiography can display motion abnormalities of acutely or chronically ischemic myocardium. In experimental studies, this permits the evaluation of the effect on regional dyskinesis of potentially therapeutic interventions. In clinical studies, the demonstration of segmental dyskinesis has been primarily useful for diagnostic purposes. As more experience is gained with the newer two-dimensional cross-sectional ultrasound techniques, it appears likely that these will afford a major advance in the diagnosis of ischemic heart disease by permitting the routine noninvasive demonstration of segmental ventricular dyskinesis and assessment of regional myocardial function.     

Comparative effects of catecholamines in cardiac tamponade: Experimental and clinical studies

In experimental cardiac tamponade, catecholamines improve hemodynamic variables. To determine whether hemodynamic changes result in increased blood flow to critical organs, tamponade was produced in nine spontaneously breathing, anesthetized dogs. Infusion of dopamine, isoproterenol or norepinephrine doubled cardiac output, but only norepinephrine increased mean arterial pressure. All catecholamines increased blood flow to the myocardium, but not to the brain or kidney. Isoproterenol caused a significant decrease in the endocardial/epicardial blood flow ratio, which was shown to be due to tachycardia.To determine whether catecholamines increase cardiac output and mean arterial pressure in patients with tamponade, eight patients with tamponade due to neoplasms were studied before therapeutic pericardiocentesis. Cardiac output increased only 50 percent with dopamine and isoproterenol and not at all with norepinephrine. Cardiac filling pressure did not decrease with isoproterenol or dopamine, as in experimental tamponade. Only norepinephrine increased mean arterial pressure.Thus, although catecholamines improve hemodynamics in experimental tamponade, the heart is the only critical organ to which blood flow is improved. The hemodynamic benefits of catecholamine administration to patients may be more limited than previous experimental studies have suggested.     

Termination of recurrent supraventricular tachycardia by right ventricular endocardial pacing but not by left ventricular epicardial pacing

Externally controlled ventricular pacing was employed in a patient with recurrent disabling supraventricular tachycardia and frequent sinus pauses between attacks of tachyarrhythmia. A permanent transthoracic demand pacemaker was inserted after electrophysiologic study demonstrated the effectiveness of ventricular stimulation in terminating induced supraventricular tachycardia. Subsequently, spontaneous recurrences of tachyarrhythmia failed to respond to fixed rate left ventricular stimulation accomplished by placing a magnet externally over the pacemaker pack. During an induced supraventricular tachycardia, repeat electrophysiologic study demonstrated that paced left ventricular beats failed to invade the A-V junctional area before it was depolarized previously by the corresponding tachycardia beat. Right ventricular stimulation from a transvenous pacemaker could depolarize the site of the reentrant circuit and terminate an induced supraventricular tachycardia. The addition of propranolol increased the ease by which spontaneous attacks of tachyarrhythmia could be terminated by right ventricular endocardial pacing.     

Sudden unexpected death as a result of anomalous origin of the right coronary artery from the left sinus of Valsalva

The association of sudden unexpected death with coronary artery anomalies has been limited to cases of anomalous origin of the left main coronary artery, either from the right sinus of Valsalva or from the main pulmonary artery. In contrast, anomalies involving the origin of the right coronary artery have been considered to be benign. Postmortem examination in a patient who died suddenly at 23 years of age disclosed that the right coronary artery originated anomalously from the left sinus of Valsalva. The findings in this patient: (1) constitute the first necropsy documentation of premature sudden unexpected death in a patient whose sole pathologic abnormality was anomalous origin of the right coronary artery; (2) have important implications regarding previously proposed mechanisms of sudden death due to anomalous origin of the left main coronary artery; and (3) support recent suggestions that markedly acute angulation of either coronary artery, even when located in the appropriate sinus of Valsalva, may predispose to sudden unexpected death.     

Congenital complete heart block and long Q-T syndrome requiring ventricular pacing for control of refractory ventricular tachycardia and fibrillation.

A three-year-old girl with congenital complete heart block presented with repeated bouts of ventricular tachycardia and ventricular fibrillation. The ECG was remarkable for both complete heart block and a long Q-T interval, when corrected for rate. The Q-T interval was longer than the Q-T interval of children with congenital complete heart block and of children without heart disease. Overdrive ventricular pacing was necessary to control the arrhythmias. A prolonged Q-T interval in patients with complete heart block, even in the presence of a normal QRS duration, may predispose the patient to sudden death. Permanent pacing can suppress these arrhythmias by overdriving.     

Sympathetic denervation limited to a region of acutely ischemic canine myocardium increases excitability threshold and duration of bipolar electrograms

This study determines the direct effects of sympathetic denervation on excitability threshold and bipolar electrograms in acutely ischemic myocardium. Regional denervation was performed by application of phenol to the epicardium surrounding the ischemic zone in order to eliminate the possible hemodynamic effects that global cardiac denervation may exert on the ischemic zone. Data were obtained during serial occlusions (≤6 minutes in duration) of left anterior coronary artery in open-chest dogs with sympathetic denervation performed before the last occlusion. Late diastolic threshold was measured every 5 seconds by a constant voltage pacemaker which automatically registered threshold in stimulus duration. During ischemia, regional denervation (n = 9) increased peak excitability threshold from 240 ± 51 (standard error of the mean) to 552 ± 182 μs (p < 0.05) and prolonged electrographic duration in epicardium from 19 ± 3 to 25 ± 4 ms (p < 0.025) and in endocardium from 20 ± 3 to 25 ± 4 ms (p < 0.01). Phenol application did not alter aortic pressure, ischemic wall motion (sonomicrometer technique), or ischemic zone blood flow (microsphere technique). Thus, acute sympathetic denervation when limited to ischemic myocardium increases the peak excitability threshold and concomitantly prolongs duration of bipolar electrograms.     

Mitral valve prolapse in anxiety neurosis (panic disorder)

Our purpose was to determine the incidence of mitral valve prolapse in patients with anxiety neurosis or panic disorder, with symptoms including recurrent anxiety attacks, dyspnea, palpitations, chest pain, dizziness, and paresthesias. Twenty-one patients and 20 age- and sexmatched normal controls were studied. Objective cardiac abnormalities were significantly (p < 0.05) more frequent in the patient group as compared to the control group; these comprised echocardiographic prolapse, ST-T abnormalities on resting ECG, premature ventricular contractions on exercise ECG, and the combination of echo prolapse with clicks/murmurs or exercise-induced PVC. We conclude that patients with anxiety neurosis or panic disorder may also have evidence of an organic abnormality-the mitral prolapse syndrome.     

Total, phasic, and regional myocardial blood flow in aortic stenosis.

The effect of aortic stenosis on total, phasic, and regional myocardial flow was studied in 16 anesthetized, open-chested dogs. An adjustable catheter device was used to produce increasing aortic obstruction, the severity of which was judged from the left ventricular aortic peak systolic gradient as mild (< 25 mm. Hg), moderate (26 to 50 mm. Hg) and severe (> 50 mm. Hg). The supply/demand index was estimated from the ratio of diastolic pressure time index to systolic pressure time index ($\text{DPTI}\text{SPTI}$). The ratio of diastolic to systolic coronary blood flow ($\text{DIAS}\text{SYS}$) was determined from the flow tracings. Total myocardial flow and endocardial/epicardial flow ratios ($\text{ENDO}\text{EPI}$) were determined by injecting four differently-labeled 7 to 9 micron microspheres in the left atrium during control, mild, moderate, and severe aortic stenosis.The supply/demand ($\text{DPTI}\text{SPTI}$) index decreased significantly at all levels of aortic stenosis because of a decrease in DPTI and an increase in SPTI. The $\text{DIAS}\text{SYS}$ coronary flow ratio and the $\text{ENDO}\text{EPI}$ myocardial flow ratio were not significantly changed during aortic stenosis. The total myocardial flow was significantly higher than control only during severe aortic stenosis.The results indicate that, for all degrees of experimental aortic stenosis, there were significant decreases in $\text{DPTI}\text{SPTI}$ but no significant changes in $\text{DIAS}\text{SYS}$ coronary flow ratio or the distribution of myocardial perfusion. Thus, in acute, experimental aortic stenosis, there is evidence of increased myocardial oxygen demand, but endocardial perfusion is not changed significantly.