Search

Electrophysiologic studies were conducted in 17 patients without apparent sinus node disease before and after intravenous administration of 1 to 2 mg of atropine. Mean values in milliseconds (+/- standard error of the mean) before and after administration of atropine were as follows: sinus cycle length 846 +/- 26.4 versus 647 +/- 20.0 (P less than 0.001); sinus nodal recovery time 1,029 +/- 37 versus 774 +/- 36 (P less than 0.001); mean calculated sinoatrial (S-A) conduction time 103 +/- 5.7 versus 58 +/- 3.9 (P less than 0.001); mean P-A interval 34 +/- 1.5 msec versus 31 +/- 1.5 (P less than 0.05); mean atrial effective and functional refractory periods during sinus rhythm 285 +/- 11.3 versus 238 +/- 7.9 and 331 +/0 11.6 versus 280 +/- 8.6, respectively (P less than 0.001 for both); mean atrial effective and functional refractory periods measured at equivalent driven cycle length 239 +/- 7.7 versus 213 +/- 7.4 and 277 +/- 11.4 versus 245 +/- 9.5, respectively (P less than 0.001 for both). In conclusion, atropine shortened sinus cycle length, sinus nodal recovery time and calculated S-A conduction time. The shortening of atrial refractory periods with atropine implies that vagotonia prolongs atrial refractoriness in man.

His bundle electrograms were recorded in a patient with pre-excitation and normal PR intervals to determine whether conduction was via anomalous A-V connection (Kent bundle) or infranodal bypass (Mahaim tract). During sinus rhythm (62/min) both P-delta and P-H measured 155 msec. With atrial pacing at 70 and 75/min, P-H prolonged while P-delta remained constant. At 80/min, the anomalous pathway failed and the QRS normalized. The effective refractory period (ERP) of the anomalous pathway was 700 msec. In summary, the normal PR interval represented slow Kent bundle conduction. Additional findings of depressed Kent bundle conduction included a prolonged ERP and block at a slow paced rate, implying that tachycardia would be unlikely. In WPW, the functional properties of both normal and anomalous pathways can be determined by His bundle recording and atrial pacing.

Thirty-three patients with severe hypertension were treated with rapidly injected intravenous diazoxide. Renal function was measured in nine patients and four underwent cardiac catheterization during renal function studies. Diazoxide had a rapid, profound hypotensive effect. Average decrease in mean arterial pressure was 26%, with an average duration of 16 hours. Drug resistance was not observed. Renal function was not impaired despite maintenance of arterial pressure at or near normal levels. Decreased mean arterial pressure was associated with a decrease in systemic vascular resistance and left ventricular end-diastolic pressure while an increase in cardiac index and heart rate occurred. Urine volume was unchanged, whereas the glomerular filtration rate and the effective renal plasma flow increased but urinary sodium excretion decreased markedly. Intravenous diazoxide is a practical effective agent for treatment of all forms of severe hypertension.

His bundle electrograms were obtained in 26 patients before and after intravenous administration of glucagon (50 μg/kg). The group consisted of 4 patients with normal conduction and 22 patients with conduction disease. The P-A interval, measured in all patients, was 35 ± 1.4 msec (mean ± standard error of the mean) before and 30 ± 1.5 msec after infusion of glucagon ( P P P In summary, glucagon increased sinus nodal automaticity, as manifested by an increase in sinus rate and decrease of sinus nodal recovery time, and improved intraatrial conduction as manifested by a reduction of the P-A interval and atrial functional and effective refractory periods. Glucagon had no effect on A-V nodal or intraventricular conduction.

A patient is reported who had left bundle branch block at age 21 and complete heart block at age 31. Electrophysiological studies revealed complete block distal to the His bundle with normal A-H interval, suggesting bilateral bundle branch disease. Hemodynamic studies revealed elevated left ventricular (LV) end-diastolic pressures which normalized with ventricular pacing, and slight increase of LV volumes. Coronary arteriography was normal. These findings suggest a diagnosis of Lenegre's disease. We believe this to be the youngest reported patient with this diagnosis. This case suggests that “benign” left bundle branch block in young adults may be a forerunner of progressive conduction disease. Electrophysiological studies in the catheterization laboratory may allow correct diagnosis prior to the development of heart block.

We have previously reported that 25 micrograms/kg of intravenous (i.v.) delta-9-tetrahydrocannabinol (delta-9-THC) produces marked increases in heart rate, prolongation of left ventricular ejection time corrected for heart rate (LVETc), and a shortening of the pre-ejection period in normal volunteers. Beta-adrenergic blockade partially attenuates these responses. To elucidate further the mechanism of action of delta-9-THC, we gave 10 normal volunteers 0.1 mg/kg of i.v. propranolol and 2 mg of i.v. atropine before they received 25 micrograms/kg of i.v. delta-9-THC. Systolic time intervals were compared in the denervated subjects before and after delta-9-THC. Post delta-9-THC responses were measured at a time approximating peak psychologic high. Mean +/- SEM heart rate before and after delta-9-THC was 89 +/- 4 and 87 +/- 3 beats/min (NS); mean +/- SEM pre-ejection period before and after delta-9-TCH was 107 +/- 5 and 109 +/- 4 ms (NS); and mean +/- SEM LVETc before and after delta-9-THC was 433 +/- 6 and 429 +/- 6 ms (NS). Since previous denervation of our subjects with atropine and propranolol totally abolished changes in heart rate and systolic time intervals, the cardiac effects of delta-9-THC appear to be mediated totally via the autonomic nervous system, probably reflecting direct central nervous system stimulation.

His bundle electrograms were obtained in 42 patients with heart disease before, during and after intravenous isoproterenol infusion. The group consisted of 5 patients with normal conduction and 37 patients with atrioventricular or intraventricular conduction disease. The A-H interval could be measured in 38 patients. In 30 patients with a normal A-H interval ( The following improvements in conduction were noted in the patients with second and third degree atrioventricular (A-V) block during isoproterenol infusion: (1) total reversal of second degree block proximal to the His bundle in two patients; (2) development of 2:1 conduction in one of three patients with third degree A-V block and “split” H potentials; and (3) development of 3:1 conduction in one of three patients with third degree A-V block distal to the His bundle. We conclude that administration of isoproterenol may facilitate both normal and depressed conduction in the A-V node and His-Purkinje system. This effect may lead to partial or total reversal of second or third degree A-V block proximal to, in and distal to the His bundle.

A patient undergoing double aortocoronary bypass grafting had Wolf-Parkinson-White syndrome without troublesome arrythmia preoperatively. Electrocardiographic, vectorcardiographic, and electrophysiological studies defined the functional properties of the anomalous bypass tract and suggested a posterior left ventricular insertion. Epicardial mapping identified early activation of the posterobasal portion of the left ventricle just to the left of the interventricular sulcus, beginning simultaneously with the onset of the delta wave.