Robert Boxer

Method for recording electrical activity of the sinoatrial node and automatic atrial foci during cardiac catheterization in human subjects

A method for recording electrical activity of the sinoatrial (S-A) node and automatic atrial foci in human subjects is described. To record S-A nodal electrograms, an electrode catheter was inserted percutaneously into the femoral vein and advanced under fluoroscopic control to the superior vena caval-right atrial junction. The distal terminal of the catheter was placed in the area of the S-A node and the proximal terminal on the free right atrial wall or in the right atrial lumen. Polarity was reversed from the conventional electrocardiographic recording; high amplification (about 100 microV/cm) and selective filters (0.1 to 20 hertz) were used. S-A nodal electrograms recorded with this method in human subjects were similar to electrograms obtained previously from the dog and rabbit and revealed negatively directed diastolic and upstroke slopes preceding the P wave of the electrocardiogram. Sinoatrial conduction time measured from the S-A nodal electrograms in 15 cases was 34.9 +/- 2.1 ms(mean +/- standard error of the mean) for a sinus cycle length of 736.4 +/- 38.6 ms. The coronary sinus electrograms in a patient with coronary sinus rhythm were recorded by the same technique except that the distal terminal of the catheter was placed at the coronary sinus ostium. A negatively directed diastolic slope preceding the P wave was consistently recorded. This method for recording electrograms of the S-A node and ectopic automatic atrial foci should prove useful in (1) assessment of both normal and abnormal S-A nodal function, (2) direct determination of conduction time from the S-A nodal pacemaker to the atrium, and (3) localization of automatic atrial foci.

Electrograms From the Canine Sinoatrial Pacemaker Recorded in Vitro and in Situ

We have identified extracell potential changes associated with the electrical activity of the canine sinoatrial pacemaker. Small nonpolarizable electrodes and low frequency high gain amplification were used to record unipolar electrograms from both the epicardial and the endocardial surfaces of the canine sinus node. Initially in vitro studies were performed so that transmembrane action potential changes could be recorded simultaneously with the extracell potentials. The sinus nodal electrogram showed two characteristic potentials when the electrode was in immediate proximity to pacemaking cells: (1) During phase 4 there was a steady slope of about -30 to -100 muv/sec, and (2) during the transition from phase 4 to phase 0 of the transmembrane action potential the slope of the electrogram increased smoothly to approximately -400 to -1,000 muv/sec. These potentials were followed by high frequency deflections as cells in the surrounding atrium depolarized. Tetrodotoxin (5 mg/liter) rendered the atrial muscle inexcitable and delayed and then abolished the high frequency activity in the sinus electrogram, which then appeared as a continuous smooth tracing similar to the sinus pacemaker action potential but reversed in polarity. We then recorded these small localized potentials from the in situ canine heart. Sinus nodal electrograms could be obtained from beating hearts with hand held probes on the epicardial surface and with conventional recording catheters on the endocardial surface. The results demonstrate that the canine sinus node gives rise to detectable and characteristic changes in extracell potential and suggest that similar potentials can be recorded from man to evaluate sinus nodal function.

CONDUCTION DEFECTS FOLLOWING VENTRICULAR SEPTAL DEFECT CLOSURE WITH AND WITHOUT A RIGHT VENTRICULOTOMY

It has been reported from our institution that almost all patients (pts) with tetralogy of Fallot develop a right bundle branch block pattern (RBBBP) postop and in addition 8.7% develop a left anterior hemiblock pattern (LAHP). To evaluate the occurrence of postop ventricular conduction defects the surgical procedures and pre and postop electrocardiograms of 70 pts with isolated ventricular septal defect (VSD) in whom the repair was carried out via a right ventriculotomy and 52 pts with VSD repaired via the atrium were reviewed. Of the 70 pts who had a right ventriculotomy 57 (81%) developed an RBBBP and 13 (19%) had no conduction abnormalities. No pt developed LAHP. Among the 52 pts repaired without a right ventriculotomy 13 (25%) developed an RBBBP and in addition 3 of the 13 had LAHP. The other 39 (75%) pts had no conduction defects after surgery. VSD size, location and use of suture vs. patch closure for VSD repair were similar for both groups. Our results indicate that 1) the incidence of RBBBP following VSD closure via the atrium is less frequent than previously reported; 2) RBBBP is more frequent when VSD is repaired via a right ventriculotomy suggesting that most lesions following ventriculotomy are due to peripheral injury of the right bundle branch; 3) when RBBBP and LAHP develop following VSD repair via the atrium, the lesion must be considered central in origin.

Echocardiography in infants with anomalous origin of the left coronary artery

SummaryEchocardiograms were performed on four infants with anomalous origin of the left coronary artery from the pulmonary artery. Common features included (1) a large, dilated, poorly contractile left ventricle, (2) posterior position of the mitral valve, (3) an abnormal pattern of septal motion with exaggerated septal excursion, (4) decreased excursion and delayed onset of posterior left ventricular wall contraction, and (5) an enlarged left atrium. These findings in infants are similar to those seen in adult patients with coronary artery disease. Septal motion was similar to the pattern described in adults with left bundle branch block. The characteristic echocardiographic features described are useful in both the diagnosis and the follow-up of left ventricular function of patients with anomalous origin of the left coronary artery from the pulmonary artery.

Abnormal septal motion in patients with postoperative right bundle branch block pattern

Echocardiograms were performed on 25 patients with postoperative right bundle branch block pattern 3 to 93 months after surgery to assess the possible effects of abnormal cardiac excitation on septal motion. Each of the 25 patients demonstrated a unique pattern of septal motion characterized by the presence of an early systolic anterior septal notch, brief in duration and unrelated to subsequent systolic septal motion, right ventricular size, or surgical procedure. Beginning approximately 70 to 80 msec. after the initial QRS deflection, the septum abruptly moved anteriorly 2 to 7 mm. and then returned to a baseline position. The total duration of this abnormal septal motion lasted 78 to 155 msec. This echocardiographic pattern was not seen in any of 30 patients in two control groups. Twenty had a normal QRS pattern and ten demonstrated right ventricular hypertrophy. In addition, patients who underwent open heart surgery and had normal right ventricular conduction postoperatively did not show this echocardiographic pattern with either normal or paradoxical septal motion. This previously undescribed echocardiographic pattern demonstrates that septal motion is uniquely affected in patients with postoperative right bundle branch block pattern.

ECHOCARDIOGRAPHIC OBSERVATIONS IN PATIENTS WITH RIGHT VENTRICULAR CONDUCTION DELAY

The echocardiographic (E) pattern of an early systolic anterior septal notch (ESASN) in post-op patients (pts) with complete right bundle branch block has been recently reported. This study evaluates the E findings in 35 pts with a right ventricular (RV) conduction delay (CD) on ECG (rsR^ pattern in VI with QRS duration ≤.08secs). 24 pre-op pts with catheterization diagnoses of secundum atrial septal defect (2°ASD) (17), normal heart (2), mild pulmonic stenosis (2), obstructed pulmonary veins (1), ventricular septal defect (1) and IHSS (1) were evaluated. In each pt, ESASN was recorded, regardless of RV dimensions or type of septal motion. The onset of ESASN after the QRS, its amplitude and duration were 84±9msec, 2.3±55mm and 114±11msec (mean±S.D.) respectively. Time intervals were corrected for heart rate using the square root of the RR interval. 11 pts were evaluated 2-7(M=3.S) years after surgical closure of a 2°ASD. In 8 of 11 pts with, and 2 of 3 pts without a residual RVCD, an identical ESASN was noted. In 20 normal pts without an RVCD, no ESASN was observed. Our observations indicate: 1) an ESASN is a characteristic pattern of septal motion associated with RVCD on ECG; 2) the occurrence of ESASN in pts with normal hearts and both systolic and diastolic overload, regardless of RV size or type of septal motion suggests a direct relationship to the ECG pattern of RVCD; 3) the presence of ESASN in pts with normal ECG after 2°ASD repair suggests that the echocardiogram may be a more sensitive indicator than the ECG for detection of residual RVCD.

88 EFFECT OF OXYGEN ON THE SYSTEMIC VASCULAR BED IN PATIENTS WITH TETRALOGY OF FALLOT

The mechanism by which oxygen (O2) administration improves systemic arterial saturation (SA sat) in patients (pts) with Tetralogy of Fallot (ToF) has not been previously elucidated. In order to explain this phenomenon, hemodynamic measurements were made before and after 90-100% 02 administration to 16 pts, age 4 mos. - 8 yrs. (M= 3.4 yrs.).During O2 administration, mean SA sat increased from 76.5±1.7%(M±SEM) to 90.9±1.9%(p<.001), mean SA pressure increased from 68.3±3.1 mmHg to 76.5±4. lmmHg(p<.02), mean systemic flow index decreased from 4.6±0.4L/min/m2 to 3.3±0.2L/min/m2 (p <.01), and mean systemic vascular resistance (SVR) increased from 15.6±1.2 Units/m2 to 24.4±1.3 Units/m2 (p <.001). Mean pulmonary flow index increased from 2.4±0.4L/min/m2 to 2.7±0.6L/min/m2 (p>.05). The mean % right to left (R→L)shunt decreased from 51.4±3.6% in room air to 35.5±4.6% in O2(p<.001). In room air, 4 pts had bidirectional shunts. However, with O2, an additional 7 pts developed bidirectional shunts. In all pts, the increment in oxygen saturation was significantly greater than could be due to dissolved O2 alone.It is concluded that O2 administration in pts with ToF increases SA sat by inducing systemic vasoconstriction. The resultant increased SVR causes a decrease in the R→L shunt and improved oxygenation. Thus, in ToF, the beneficial effect of O2 results primarily from its effect on the systemic vascular bed.