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The electrophysiologic properties of normal neonatal and adult canine cardiac purkinje fibers
ABSTRACTS
CARDIAC RHYTHM IN SUDDEN INFANT DEATH SYNDROME Terrence j. Montague, MD; Philip C. Baqnell, MD; DOuglai L. Roy, MD; Eldon R. Smith, MD, Dalhousie University, Halifax, Nova Scotia, Canada.
TUESDAY, MARCH 11, 1980 AM CARDIAC FUNCTION 8:30- 12:OO
Although the etiology of sudden infant death syndrome (SIDS) remains uncertain, cardiac dysrhythm (particularly bradycardic arrest and dysrhythm associated with QT interval prolongation) continues to be proposed as a likely In an ongoing effort to assess this possibilmechanism. ity. we utilized continuous 24-48 hr electrocardiography (ECG) to monitor cardiac rate and rhythm in 9 patients There were 7 females and 2 (pts) with "near-miss" SIDS. males with an age range of 9 days to 20 weeks (wks). All were previously well although 2 had sibs die of SIDS. Each had normal physlcal and routine laboratory examinaand 12-lead ECG tions, including electroencephaloqraphy (lead II mean QTc = 0.407 2 0.029 [S.D.] set; lead Vl mean QTc = 0.393 t 0.013 SW). Sinus rhythm, ranging from 73 to 225 beats/min (mean Six pts 140 i 9) was the prevailing rhythm in all pts. had frequent episodes of mild sinus arrhythmia (SA); one Two pts also occasionally had wandering atria1 pacemaker. had infrequent moderate SA and another had one period of marked SA (adjacent cycle length variation > 100%). AtriQTc from monal ectopics occurred infrequently in 2 pts. itoring leads was normal in all (mean 0.393 ? 0.002) with the maximum variation during the monitoring period averaging 0.099 ? 0.025 sec. Because of marked SA, one pt reDespite documented apceived a pacemaker at age 4 wks. propriate function of the pacemaker the pt had another "near-miss" at 6 wks and died suddenly of indeterminable These observations suggest: (1) cardiac cause at 8 wks. dysrhythm (including QT prolongation) is not readily detected in a population at high risk of SIDS and (2) bradydysrhythm or bradycardic arrest is not the primary cause of death in all cases of SIDS.
LEFT VENTRICULAR FUNCTION AT REST AND DURING EXERCISE IN MARATHON RUNNERS Walter J. Paulsen MD, Derek R. Boughner MD., PhD., David A. Cunningham PM., University Hospital,London,Ontario.
TRE ELECTROPHYSIOLOGIC PROPERTIES OF NORMAL NEONATAL AND ADULT CANINE CARDIAC PURKINJE FIBERS. Robert Reder, MD, Dennis Miura, MD, Peter Danilo, Jr., PhD, Michael Rosen, MD, FACC, Columbia Univ., College of P&S, New York, NY To determine the basis for age-related changes in the transmembrane action potentials (AP) of canine cardiac Purkinje fibers (PF), we used standard microelectrode techniques to study PF from neonatal and adult beagles. Neonatal PF have a lower maximum diastolic potential (MDP) (-86.Z3.8 my -91.5t5.9 mV (M+SD)), AP amplitude (amp) (126.1k4.7 vs 1?0.8+-6.8 mV) and maximum upstroke velocity of phase 0 (V,,) (533+90 vs 634*103 V/set) than adults (Pc.05). AF duration measured at 50% (141.0'13.9 vs 185.4f19.9 msec) and 100% repolarization (245.4t22.7 vs 286.9+28.0 msec) was shorter and phases 1 (11.9+10.9 vs -1.927.2 mV) and 2 (11.9t10.9 vs 1.3f6.8 mV) occurred at higher levels of membrane potential in neonates (Pc.05). The lower MDP in neonates appears to result from a lower intracellular K activity (aft) (studied with a K+ sensitive microelectrode). Neonatal PF showed greater depression of AF amp and V,,, on superfusion with the rapid Na+ channel blocker, tetrodotoxin (TTX), than adults, attributable to an apparent age-related change in the fast Na+ channel. An outward K current blocker, 4-aminopyridine, altered phase 1 more in adults than neonates. Adult PF AP repolarization was more sensitive to ARR-2666, a putative inward Ca+2 blocker and less sensitive to TTX than neonates, suggesting that the contribution of Ca+2 to the AF plateau diminishes and that of Na+ increases with age. All drug-induced changes were significant (Pc.05). In summary, as age increases from the neonate to the adult there are significant changes in ak and MDP, in the East inward Na+ current, in an early repolarizing K+ current, and in the SlOW, inward Ca* and Na+ currents. These in part explain the age-related changes in Al' contour.
To determine the cardiac adaptations to prolonged endurance training left ventricular echocardiograms were performed in 8 active marathon runners, mean age 27 yrs. These recordings were made at rest and during 12 mins of supine bicycle ergometer exercise with workloads increasing by 25 watts every 3 mins to a maximum of 125 watts. When compared to 10 sedentary controls the significant differences (p< 0.01) for runners versus controls were as folincreased maximum oxygen consumption, 72.8+5 vs 41k lows: 56 ml/kg/min; left ventricular end diastolic diameter 56+_2 vs 52+5 nun; left ventricular posterior wall thickness,l0.3 5.7 vs 8.5+1.0 mm; left ventricular mass 316+28 vs 187544 gm. There were decreases in resting heart rate 54+4 vs 73-&9 beats/ruin; resting pressure-rate product, 6248+888 vs 8430+_1370; and resting peak velocity of circumferential fiber shortening (peak Vcf), 1.420.1 vs 1.7+0.2 circumfsec During exercise at a workload of 125 watts there were decreases in heart rate 11257 vs 144215 beats/min; pressure-rate product 20684+2260 vs 28430+_1247; and peak Vcf, 2.5IlIO.lvs 3.eO.3 circ/sec. However, peak Vcf has been shown to vary directly with pressure-rate product. When peak Vcf was corrected for changes in pressure-rate product, there was no significant difference between the runners and controls either at rest or during exercise. These data indicate that prolonged endurance training results in an increased left ventricular chamber size and wall thickness but echocardiographic estimates of myocardial contractility remain unchanged.
CORONARY ARTERY CONSTRICTION AND HEMODYNA!4IC RESPONSES DURING ISOMETRIC HANDGRIP IN PATIENTS (pts) WITH CORONARY ARTERY DISEASE (CAD) B Greg Brown MD PhD Robert B Petersen, PhD, Cynthia D A-. Pierce, BS, Maylene Wang, MD, Wadsworth VA Hosp., L.A., CA; Edward Bolson, MS, Harold T Dodge, MD FACC, Universiv of Washington, Seattle, WA. The effect of handgrip (HGP) on arterial caliber and on resistance to flow in large and in small coronary vessels (CVR) is unknown. Twelve pts with CAD underwent catheterization and coronary arteriography. Coronary sinus flow (CSF) was measured by thermodilution. All hemodynamic measurements and selected coronary arteriograms were made just before (CON), and at 4-S minutes during sustained HGP at 11 kgt2-SD (25% of max.) A computer-based angiographic analysis estimated dimensional changes during HGP in 30 diseased coronary artery segments in these pts. Lumen cross-sectional area in the "normal" part of the segment (An), minimum stenosis area (Amin), and stenosis flow resistance (R,) were estimated. Results: (increase 4; decrease 4) CVR MEAN An CSF SYST. HEART Amin Rs PERCENT CHANGE FROM ml A PR WEDGE CONTROL VALUE (G) (b::::") (m$) (m?) 69 CON 101 2S* ll%r-' 9%+' 29%fX 27%+' 170X HGP 184* 84x NS = not significant; *=pc.OS; x=p<.Ol. CON "s HGP: -All pts had forearm pain and fatigue; two had chest pain and one, PVC's. Pressure-rate product rose 58%'. Small vessels dilated with increased metabolic demand, but diseased arteries constricted in spite of increased systemic pressure. HGP thus can impair the distribution of coronary flow in CAD, and should enhance ischemic abnormalities detected by non-invasive techniques.
February 1990
The American Journal of CARDIOLOGY
Volume 45
431
CARDIAC RHYTHM IN SUDDEN INFANT DEATH SYNDROME Terrence j. Montague, MD; Philip C. Baqnell, MD; DOuglai L. Roy, MD; Eldon R. Smith, MD, Dalhousie University, Halifax, Nova Scotia, Canada.
TUESDAY, MARCH 11, 1980 AM CARDIAC FUNCTION 8:30- 12:OO
Although the etiology of sudden infant death syndrome (SIDS) remains uncertain, cardiac dysrhythm (particularly bradycardic arrest and dysrhythm associated with QT interval prolongation) continues to be proposed as a likely In an ongoing effort to assess this possibilmechanism. ity. we utilized continuous 24-48 hr electrocardiography (ECG) to monitor cardiac rate and rhythm in 9 patients There were 7 females and 2 (pts) with "near-miss" SIDS. males with an age range of 9 days to 20 weeks (wks). All were previously well although 2 had sibs die of SIDS. Each had normal physlcal and routine laboratory examinaand 12-lead ECG tions, including electroencephaloqraphy (lead II mean QTc = 0.407 2 0.029 [S.D.] set; lead Vl mean QTc = 0.393 t 0.013 SW). Sinus rhythm, ranging from 73 to 225 beats/min (mean Six pts 140 i 9) was the prevailing rhythm in all pts. had frequent episodes of mild sinus arrhythmia (SA); one Two pts also occasionally had wandering atria1 pacemaker. had infrequent moderate SA and another had one period of marked SA (adjacent cycle length variation > 100%). AtriQTc from monal ectopics occurred infrequently in 2 pts. itoring leads was normal in all (mean 0.393 ? 0.002) with the maximum variation during the monitoring period averaging 0.099 ? 0.025 sec. Because of marked SA, one pt reDespite documented apceived a pacemaker at age 4 wks. propriate function of the pacemaker the pt had another "near-miss" at 6 wks and died suddenly of indeterminable These observations suggest: (1) cardiac cause at 8 wks. dysrhythm (including QT prolongation) is not readily detected in a population at high risk of SIDS and (2) bradydysrhythm or bradycardic arrest is not the primary cause of death in all cases of SIDS.
LEFT VENTRICULAR FUNCTION AT REST AND DURING EXERCISE IN MARATHON RUNNERS Walter J. Paulsen MD, Derek R. Boughner MD., PhD., David A. Cunningham PM., University Hospital,London,Ontario.
TRE ELECTROPHYSIOLOGIC PROPERTIES OF NORMAL NEONATAL AND ADULT CANINE CARDIAC PURKINJE FIBERS. Robert Reder, MD, Dennis Miura, MD, Peter Danilo, Jr., PhD, Michael Rosen, MD, FACC, Columbia Univ., College of P&S, New York, NY To determine the basis for age-related changes in the transmembrane action potentials (AP) of canine cardiac Purkinje fibers (PF), we used standard microelectrode techniques to study PF from neonatal and adult beagles. Neonatal PF have a lower maximum diastolic potential (MDP) (-86.Z3.8 my -91.5t5.9 mV (M+SD)), AP amplitude (amp) (126.1k4.7 vs 1?0.8+-6.8 mV) and maximum upstroke velocity of phase 0 (V,,) (533+90 vs 634*103 V/set) than adults (Pc.05). AF duration measured at 50% (141.0'13.9 vs 185.4f19.9 msec) and 100% repolarization (245.4t22.7 vs 286.9+28.0 msec) was shorter and phases 1 (11.9+10.9 vs -1.927.2 mV) and 2 (11.9t10.9 vs 1.3f6.8 mV) occurred at higher levels of membrane potential in neonates (Pc.05). The lower MDP in neonates appears to result from a lower intracellular K activity (aft) (studied with a K+ sensitive microelectrode). Neonatal PF showed greater depression of AF amp and V,,, on superfusion with the rapid Na+ channel blocker, tetrodotoxin (TTX), than adults, attributable to an apparent age-related change in the fast Na+ channel. An outward K current blocker, 4-aminopyridine, altered phase 1 more in adults than neonates. Adult PF AP repolarization was more sensitive to ARR-2666, a putative inward Ca+2 blocker and less sensitive to TTX than neonates, suggesting that the contribution of Ca+2 to the AF plateau diminishes and that of Na+ increases with age. All drug-induced changes were significant (Pc.05). In summary, as age increases from the neonate to the adult there are significant changes in ak and MDP, in the East inward Na+ current, in an early repolarizing K+ current, and in the SlOW, inward Ca* and Na+ currents. These in part explain the age-related changes in Al' contour.
To determine the cardiac adaptations to prolonged endurance training left ventricular echocardiograms were performed in 8 active marathon runners, mean age 27 yrs. These recordings were made at rest and during 12 mins of supine bicycle ergometer exercise with workloads increasing by 25 watts every 3 mins to a maximum of 125 watts. When compared to 10 sedentary controls the significant differences (p< 0.01) for runners versus controls were as folincreased maximum oxygen consumption, 72.8+5 vs 41k lows: 56 ml/kg/min; left ventricular end diastolic diameter 56+_2 vs 52+5 nun; left ventricular posterior wall thickness,l0.3 5.7 vs 8.5+1.0 mm; left ventricular mass 316+28 vs 187544 gm. There were decreases in resting heart rate 54+4 vs 73-&9 beats/ruin; resting pressure-rate product, 6248+888 vs 8430+_1370; and resting peak velocity of circumferential fiber shortening (peak Vcf), 1.420.1 vs 1.7+0.2 circumfsec During exercise at a workload of 125 watts there were decreases in heart rate 11257 vs 144215 beats/min; pressure-rate product 20684+2260 vs 28430+_1247; and peak Vcf, 2.5IlIO.lvs 3.eO.3 circ/sec. However, peak Vcf has been shown to vary directly with pressure-rate product. When peak Vcf was corrected for changes in pressure-rate product, there was no significant difference between the runners and controls either at rest or during exercise. These data indicate that prolonged endurance training results in an increased left ventricular chamber size and wall thickness but echocardiographic estimates of myocardial contractility remain unchanged.
CORONARY ARTERY CONSTRICTION AND HEMODYNA!4IC RESPONSES DURING ISOMETRIC HANDGRIP IN PATIENTS (pts) WITH CORONARY ARTERY DISEASE (CAD) B Greg Brown MD PhD Robert B Petersen, PhD, Cynthia D A-. Pierce, BS, Maylene Wang, MD, Wadsworth VA Hosp., L.A., CA; Edward Bolson, MS, Harold T Dodge, MD FACC, Universiv of Washington, Seattle, WA. The effect of handgrip (HGP) on arterial caliber and on resistance to flow in large and in small coronary vessels (CVR) is unknown. Twelve pts with CAD underwent catheterization and coronary arteriography. Coronary sinus flow (CSF) was measured by thermodilution. All hemodynamic measurements and selected coronary arteriograms were made just before (CON), and at 4-S minutes during sustained HGP at 11 kgt2-SD (25% of max.) A computer-based angiographic analysis estimated dimensional changes during HGP in 30 diseased coronary artery segments in these pts. Lumen cross-sectional area in the "normal" part of the segment (An), minimum stenosis area (Amin), and stenosis flow resistance (R,) were estimated. Results: (increase 4; decrease 4) CVR MEAN An CSF SYST. HEART Amin Rs PERCENT CHANGE FROM ml A PR WEDGE CONTROL VALUE (G) (b::::") (m$) (m?) 69 CON 101 2S* ll%r-' 9%+' 29%fX 27%+' 170X HGP 184* 84x NS = not significant; *=pc.OS; x=p<.Ol. CON "s HGP: -All pts had forearm pain and fatigue; two had chest pain and one, PVC's. Pressure-rate product rose 58%'. Small vessels dilated with increased metabolic demand, but diseased arteries constricted in spite of increased systemic pressure. HGP thus can impair the distribution of coronary flow in CAD, and should enhance ischemic abnormalities detected by non-invasive techniques.
February 1990
The American Journal of CARDIOLOGY
Volume 45
431