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Ventricular tachycardia and atrioventricular reciprocation produced by, and myopotential inhibition of, normally-functioning DVI (AV sequential) pacemakers
ABSTRACTS
MODIFIED RADIOFFEOUENCY SYSTEM FOR ELECTROPHYSIOLOGICAL STUDIES Boris Strasberg, MD; Joseph Fetter, HFEE; Edwin PalileO, MD, FACC; Steven Hess, MD; Sidney Levitsky, MD, FACC; Kenneth Rosen, MD, FACC, university of Illinois, Chicago. A modified radiofrequency (RF) pacemaker system that allows performance of complete electrophysiologic stimulation protocols (EsP) including ventricular extrastimulation (Vl-V2: Vl-V3) is described. An RF transmitter (Medtronic 5998T/2324) was modified by adding an input jack providing connection to the output of a programmable stimulator (Medtronic 5325) resulting in a programmed pulse output from the transmitter. Two patients who underwent ventricular aneurysmectomy and endocardial resection for treatment of ventricular tachycardia had a RF pacemaker (Medtronic 5998) and epicardial lead implanted. In both patients, ESP were done before discharge using the modified RF system without recourse to catheterization. In one patient, sustained VT was inducible (Vl-V3 stimulation) while in the second, only nonsustained VT (maximum 5 beats) was induced (Vl-V3). In the former patient, additional ESP with serial drug testing were repeated postoperatively without the need of recatheterization. In patients receiving modified RF system, ESP can be performed to determine the success of therapy. The system seems especially applicable for testing new drugs as they become available (in drug resistant patients), and for serial testing of long half-life drugs such as amiodarone.
VENTRICULAR TACHYCARDIA AND ATRIOVENTRICULAR RECIPROCATION PRODUCED BY, AND MYOPOTENTIAL INHIBITION OF, NORMALLY-FUNCTIONING DVI (AV SEQUENTIAL) PACEMAKERS Richard M. Luceri, MD; Antonio V. Ramirez, MD; Victor Medina-Ravell. MD: Richard J. Tburer. MD. FACC:Aaustin Castellanos, i&l, FACC; Robert J. Myerburg, MD,'FjiCC, Division of Cardiology, University of Miami School of Medicine, Miami, Florida. Meticulous attention to details of operation showed how some problems,that in initial generations of DVI(AV sequential) pacemakers (Pace)were attributed to complications, really constituted "eccentricities" (unexpected variations of normal function). In 3 patients with the antitachycardia DVI,MN Pace, magnet application produced the expected reversion to DO0 pacing.During this modality of stimulation, paced atria1 impulses occurring early in the sinus cycle initiated runs of tachycardia when the corresponding ventricular impulses fell while the ventricles were "effectively" refractory. All episodes of tachycardia, thus induced, were subsequently terminated by AV pacing itself, Two patients with unipolar DVI,M Pace, with "committed" ventricular stimuli had induced (and spontaneous) myopotential inhibition which was corrected noninvasively(using an external programmer) by decreasing the sensitivity. One patient with this same type of Pace had left ventricular extrasystoles that were non-sensed (as expected) due to their occurrence late in diastole. Delivery of the ineffective atria1 stimuli at the end of the QRS complexes allowed the "committed" stimuli to fall on the T wave so as to trigger runs of ventricular tachycardia. In conclusion, ventricular, as well as supraventricular, tachycardias may be induced by (and myopotential inhibition occurs in patients with) normally-functioning DVI pacemakers.
TUESDAY, APRIL 27, 7982 PM CORONARY ARTERY SPASM 2:00-3:30 CORONARY SPASM IN THE CAT PRODUCED BY INCREASING CENTRAL SYMPATHETIC OUTFLOW TO THE HEART Sharon A. Segal, BA; David L. Pearle, MD, FACC; Richard . . 1 lS, Ph.D, Georgetown University, Washington, D.C. Clinical data suggest that an increase in sympathetic nervous system activity can precede the occurrence of coronary spasm in some patients with variant angina pectoris, and may be one pathophysiologic mechanism responsible for the increase in coronary vascular resistance (CVR). Hence, it should be possible to experimentally produce coronary spasm by increasing cardiac sympathetic nerve activity. To test this we administered picrotoxin, a drug known to act in the brain to increase sympathetic outflow, to chloralose-anesthetized cats. Picrotoxin, 600 ug, was injected into the lateral cerebral ventricle of 7 vagotcmized animals while monitoring arterial pressure (BP), coronary blood flow measured directly (electromagnetic flow probe on the LAD coronary artery), and ST segment changes on a 6 lead ECG. Coronary constriction occurred in each animal as measured by an increase in CVR (I= 30 + 8.6X, p
PLATELET INHIBITION REDUCES LIPID ACCUMULATION IN VEIN GRAFTS OF HYPERLIPEMIC PRIMATES Lawrence E. Boer-boom, PhD; Gordon N. Olinger, MD, FACC; Lawrence I. Bonchek, MD, FACC; James Munns, MD: Lawrence Hutchinson, MD; Ahmed H. Kissebah, MD, PhD; Medical College of Wisconsin, Milwaukee, Wisconsin We recently showed that the increased uptake of cholesterol (C) and B-apoprotein (B) caused by controlled barotrauma to autologous veins grafted into arteries of normolipemic macaques could be dramatically ameliorated by antiplatelet therapy. This study tests whether platelet inhibition can also be effective in this model when animals are mlipemic. Cephalic veins were interposed in femoral arteries of 11 macaques previously rendered and maintained uniformly hyperlipemic by diet (serum C 463 _t.60 mg/dl). Before grafting, one-half of each vein was distended at high pressure (700 torr-HP) and the other at low pressure (350 torr-LP). Seven animals were treated (Rx) with aspirin (80 mg/day) and dipyridamole (50 mg/day); 4 were controls. Graft tissue C and B were measured at 12 weeks. Rx markedly reduced C and 8 in both LP and HP veins as well as C in ungrafted veins (UV) (all p< 0.005). This reduction of graft lipid accumulation even in the adverse presence of severe hyperlipidemia further supports our assertion that platelet inhibition can be a potent attenuator of vein graft atherogenesis and reaffirms our current routine practice of prescribing these drugs clinically. Cholesterol (mg/lOUmK) B-apoprotein (uE/lUOmE) uv LP HP UV LP HP Control 0.13 0.56 1.05 7.5 261 449 (S.D.) 2.03 5.07 2.05 +l.O +41 -+54 Rx
March 1982
0.08 +.Ol -
0.24 2.05
0.69 2.08
7.1 23.9
The American Journal of CARDIOLOGY
161 240
Volume 49
308 -+51
953
MODIFIED RADIOFFEOUENCY SYSTEM FOR ELECTROPHYSIOLOGICAL STUDIES Boris Strasberg, MD; Joseph Fetter, HFEE; Edwin PalileO, MD, FACC; Steven Hess, MD; Sidney Levitsky, MD, FACC; Kenneth Rosen, MD, FACC, university of Illinois, Chicago. A modified radiofrequency (RF) pacemaker system that allows performance of complete electrophysiologic stimulation protocols (EsP) including ventricular extrastimulation (Vl-V2: Vl-V3) is described. An RF transmitter (Medtronic 5998T/2324) was modified by adding an input jack providing connection to the output of a programmable stimulator (Medtronic 5325) resulting in a programmed pulse output from the transmitter. Two patients who underwent ventricular aneurysmectomy and endocardial resection for treatment of ventricular tachycardia had a RF pacemaker (Medtronic 5998) and epicardial lead implanted. In both patients, ESP were done before discharge using the modified RF system without recourse to catheterization. In one patient, sustained VT was inducible (Vl-V3 stimulation) while in the second, only nonsustained VT (maximum 5 beats) was induced (Vl-V3). In the former patient, additional ESP with serial drug testing were repeated postoperatively without the need of recatheterization. In patients receiving modified RF system, ESP can be performed to determine the success of therapy. The system seems especially applicable for testing new drugs as they become available (in drug resistant patients), and for serial testing of long half-life drugs such as amiodarone.
VENTRICULAR TACHYCARDIA AND ATRIOVENTRICULAR RECIPROCATION PRODUCED BY, AND MYOPOTENTIAL INHIBITION OF, NORMALLY-FUNCTIONING DVI (AV SEQUENTIAL) PACEMAKERS Richard M. Luceri, MD; Antonio V. Ramirez, MD; Victor Medina-Ravell. MD: Richard J. Tburer. MD. FACC:Aaustin Castellanos, i&l, FACC; Robert J. Myerburg, MD,'FjiCC, Division of Cardiology, University of Miami School of Medicine, Miami, Florida. Meticulous attention to details of operation showed how some problems,that in initial generations of DVI(AV sequential) pacemakers (Pace)were attributed to complications, really constituted "eccentricities" (unexpected variations of normal function). In 3 patients with the antitachycardia DVI,MN Pace, magnet application produced the expected reversion to DO0 pacing.During this modality of stimulation, paced atria1 impulses occurring early in the sinus cycle initiated runs of tachycardia when the corresponding ventricular impulses fell while the ventricles were "effectively" refractory. All episodes of tachycardia, thus induced, were subsequently terminated by AV pacing itself, Two patients with unipolar DVI,M Pace, with "committed" ventricular stimuli had induced (and spontaneous) myopotential inhibition which was corrected noninvasively(using an external programmer) by decreasing the sensitivity. One patient with this same type of Pace had left ventricular extrasystoles that were non-sensed (as expected) due to their occurrence late in diastole. Delivery of the ineffective atria1 stimuli at the end of the QRS complexes allowed the "committed" stimuli to fall on the T wave so as to trigger runs of ventricular tachycardia. In conclusion, ventricular, as well as supraventricular, tachycardias may be induced by (and myopotential inhibition occurs in patients with) normally-functioning DVI pacemakers.
TUESDAY, APRIL 27, 7982 PM CORONARY ARTERY SPASM 2:00-3:30 CORONARY SPASM IN THE CAT PRODUCED BY INCREASING CENTRAL SYMPATHETIC OUTFLOW TO THE HEART Sharon A. Segal, BA; David L. Pearle, MD, FACC; Richard . . 1 lS, Ph.D, Georgetown University, Washington, D.C. Clinical data suggest that an increase in sympathetic nervous system activity can precede the occurrence of coronary spasm in some patients with variant angina pectoris, and may be one pathophysiologic mechanism responsible for the increase in coronary vascular resistance (CVR). Hence, it should be possible to experimentally produce coronary spasm by increasing cardiac sympathetic nerve activity. To test this we administered picrotoxin, a drug known to act in the brain to increase sympathetic outflow, to chloralose-anesthetized cats. Picrotoxin, 600 ug, was injected into the lateral cerebral ventricle of 7 vagotcmized animals while monitoring arterial pressure (BP), coronary blood flow measured directly (electromagnetic flow probe on the LAD coronary artery), and ST segment changes on a 6 lead ECG. Coronary constriction occurred in each animal as measured by an increase in CVR (I= 30 + 8.6X, p
PLATELET INHIBITION REDUCES LIPID ACCUMULATION IN VEIN GRAFTS OF HYPERLIPEMIC PRIMATES Lawrence E. Boer-boom, PhD; Gordon N. Olinger, MD, FACC; Lawrence I. Bonchek, MD, FACC; James Munns, MD: Lawrence Hutchinson, MD; Ahmed H. Kissebah, MD, PhD; Medical College of Wisconsin, Milwaukee, Wisconsin We recently showed that the increased uptake of cholesterol (C) and B-apoprotein (B) caused by controlled barotrauma to autologous veins grafted into arteries of normolipemic macaques could be dramatically ameliorated by antiplatelet therapy. This study tests whether platelet inhibition can also be effective in this model when animals are mlipemic. Cephalic veins were interposed in femoral arteries of 11 macaques previously rendered and maintained uniformly hyperlipemic by diet (serum C 463 _t.60 mg/dl). Before grafting, one-half of each vein was distended at high pressure (700 torr-HP) and the other at low pressure (350 torr-LP). Seven animals were treated (Rx) with aspirin (80 mg/day) and dipyridamole (50 mg/day); 4 were controls. Graft tissue C and B were measured at 12 weeks. Rx markedly reduced C and 8 in both LP and HP veins as well as C in ungrafted veins (UV) (all p< 0.005). This reduction of graft lipid accumulation even in the adverse presence of severe hyperlipidemia further supports our assertion that platelet inhibition can be a potent attenuator of vein graft atherogenesis and reaffirms our current routine practice of prescribing these drugs clinically. Cholesterol (mg/lOUmK) B-apoprotein (uE/lUOmE) uv LP HP UV LP HP Control 0.13 0.56 1.05 7.5 261 449 (S.D.) 2.03 5.07 2.05 +l.O +41 -+54 Rx
March 1982
0.08 +.Ol -
0.24 2.05
0.69 2.08
7.1 23.9
The American Journal of CARDIOLOGY
161 240
Volume 49
308 -+51
953