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Electrophysiological effects of nitroglycerin during experimental coronary occlusion
ABSTRACTS
MAHAIM FIBERS AS A BASIS FOR A UNIQUE VARIETY OF PREEXCITATION Maurice Lev, MD, FACC; Samuel M. Fox, III, MD, FACC; Saroja Bharati, MD; Kenneth M. Rosen, MD, FACC; Richard Isngendorf, MB, FACC; Alfred Pick, MD, FACC, Hektoen Institute for Medical Research, Chicago, Ill. This report concerns pathological findings in a 54 year old female wi,th intermittent preexcitation, who died of breast carcinoma. Electrocardiograms (ECG) revealed predominantly normal sinus rhythm with normal PR and narrow QHS. Episodes of sinus rhythm, short PH, and QRS widening (with delta wave) were also recorded. During preexcitation; QS complexes were noted in leads II, III, AVR, AVF, Vl, and V4_6; R waves were noted in leads I and AVL; and rS complexes in V2 and V3. ECG during paroxysmal atria1 fibrillation revealed groups of narrow complexes alternating with groups of wide complexes identitle to the anomalous &RS described above. QRS morphology defies classification of this case into any known variety of preexcitation. Complete serial sections were cut through the entire condsystem and both AV rims totaling 18,600 sections. These revealed no bundle of Instead Mahaim fibers histologicalFidentified as Kent. His bundle tissue were given off from the AV bundle both to the right and left sides of the septum associated with the normal fibers of James. The short PR interval is thus explained as produced by James fibers bypassing most of the AV node. Preexcitation appeared to start at the summit of the ventricular septum on both sides and spread anteriorly on both free walls from epicardium to endocardium producing the bizarre lX!G. This case revealed that fibers of Mahaim must have the property of conduction; and atria1 arrhythmias in WPW are not of necessity caused by reentry but produced by concomitant disease, in this instance carcinwatons atria1 involvement.
ELECTROPHYSIOLOGICAL EFFECTS OF NITROGLYCERIN DURING EWERIMENTAL CORONARY OCCLUSION Rafael Levites, MD; Monty Rodenheimer, MD; Richard H. Helfant, MD, FACC, Presbyterian-University of Pennsylvania Medical Center, Philadelphia, Pennsylvania Previous studies have shown that nitroglycerin (NTG) decreases ventricular premature complexes and increases the ventricular fibrillation threshold after acute coronary occlusion. In order to determine the electrophysiological effects of NTG after occlusion, experiments were performed in 13 mongrel dogs, with heart rate controlled by atria1 pacing. Conduction time from the onset of the QRS to local electrogram onset and refractory periods obtained by the extrastimulus method, were determined in normal and ischemic areas of left ventricular myocardium prior to and after variable periods of occlusion, as well as following the IV administration of NTG (300ug bolus followed by an infusion titrated to reduce arterial pressure POmmHg). Following 15 min of occlusion, refractory periods in the normal area remained unchanged while it shortened in the ischemic area to 82% of control (p<.OOl), creating an 18% mean dispersion of refractory periods. After NTG, refractory periods in the normal area were unaffected while prolongation in the ischemic area to 90% of control occurred thus decreasing the dispersion of refractory periods to 10% (pc.001). However, following periods of occlusion %O min, NTG had inconsistent effects on ischemic refractory periods, and did not significantly affect refractory period dispersion. NTG had no effects on conduction times of normal or ischemic areas. These observations suggest that 1) NTG enhances the electrical stability of the acutely ischemic ventricle by decreasing the dispersion of refractoriness between normal and ischemic areas in the immediate period following occlusion and 2) NTG has inconsistent effects after more prolonged periods of occlusion.
152
January 1975
The American Journal of CARDlOLOGY
CONDUCTION SYSTEM IN SUDDEN CARDIAC DEATH J.T. Lie, M.D., Departments of Pathology, Royal Melbourne Hospital, Melbourne, Australia, and Baylor College of Medicine Houston, Texas 77025 Sudden cardiac death (SCD) has been attributed to the development of lethal dysrhythmias in coronary heart disease victims, and several recent autopsy surveys showed that 10 to 47% of SCD patients had unsuspected acute myocardial infarction (AMI). The present study concerned histopathologic findings of the conduction system in 49 SCD (within 6 hours of the onset of acute symptoms) patients; 39 with established AMI (Group A) and 10 without (Group B). Both groups showed high incidence of cardiome&y, significant coronary artery disease affecting two or more vessels, and acute myocardial ischemia undetectable by Stenosis of nutrient conventional histological techniques. vessels of the conduction system was present in about SO% of the atrioventricular (AV) node arteries and about 25% of the sinoatrial (SA) node arteries in both groups of SCD patients. Nonspecific “degenerative” changes (fibrosis, fatty infiltration or both) of the conduction tissue, which might or might not represent results of old ischemic injury, also occurred with similar frequencies. Acute changes (infarction, hemorrhage) of the AV node and bundle branches were found only in two Thus, Group A patients, both had massive septal infarction. the conduction tissue appeared more resistant to ischemlc injury and was overtly damaged only on rare occasions in fatal AMI. ‘Ihe scarcity of acute lesions in the conduction system itself suggested that lethal dysrhythmia in SCD was probably due to electrical instability of the acutely ischemic myocardium rather than a direct injury to the specialized tissue of the heart.
THE EFFECTS OF GLUCOSE-INSULIN-POTASSIUM THERAPY IN GLOBAL MYOCARDIAL ISCHEMIA A. James Liedtke, M.D., Howard C. Hughes, V.M.D., and James R. Neely, Ph.D., Penna. State Univ., Hershey, Pa. The metabolic benefits of glucose-insulin-potassium(GIK) administration during myocardial ischemia have recently been questioned as has the proposed clinical efficacy of its use in the management of patients with ischemic heart disease. To test this intervention experimentally in an intact, working swine heart preparation, GIK enriched medium(32.4 mM glucose, .025 units/ml insulin, and 5.9mM potassium)was provided during coronary perfusion in nine control hearts and nine hearts rendered ischemic by reducing total coronary blood flow from 157 to 82 ml/rain. In another group of 14 hearts(six control and eight ischemic)coronary perfusate contained 11.8 mH glucose, 5.9 mM potassium, and no insulin. In hearts without GIK, ischemia increased left ventricular end-diastolic pressure ((LVEDP)from 8 to 15 mmllg, p<.05)and resulted in declines of myocardial oxygen consumption((MV02)from .80 to .68 rmnol/hr/g, p<.O5), free fatty acid(FFA)oxidation(from 31 to 21 pmol/hr/g, pc.O25), and tissue creatine phosphate ((CP)from 47 to 21 umol/g). Data for control hearts with GIK were similar to controls without GIK except that glucose uptake was increased to 430 ?.mol/hr/g. Ischemia had similar effects in GIK-treated hearts(LVEDP:22 mmHg;MVO2: .51 mmol/hr/g; FFA oxidation: 25 pmol/hr/g;CP;24 umol/g). Glucose uptake was reduced to 240 pmol/hr/g and average survival time during ischemia was 10 minutes less than in hearts receiving no GIK. These data indicate that in global ischemia GIK provides essentially no metabolic advantages to jeopardized myocardium and suggest any therapeutic benefit derived from such treatment in regional ischemia probably occurs in the uninvolved myocatdium.
Volume 35
MAHAIM FIBERS AS A BASIS FOR A UNIQUE VARIETY OF PREEXCITATION Maurice Lev, MD, FACC; Samuel M. Fox, III, MD, FACC; Saroja Bharati, MD; Kenneth M. Rosen, MD, FACC; Richard Isngendorf, MB, FACC; Alfred Pick, MD, FACC, Hektoen Institute for Medical Research, Chicago, Ill. This report concerns pathological findings in a 54 year old female wi,th intermittent preexcitation, who died of breast carcinoma. Electrocardiograms (ECG) revealed predominantly normal sinus rhythm with normal PR and narrow QHS. Episodes of sinus rhythm, short PH, and QRS widening (with delta wave) were also recorded. During preexcitation; QS complexes were noted in leads II, III, AVR, AVF, Vl, and V4_6; R waves were noted in leads I and AVL; and rS complexes in V2 and V3. ECG during paroxysmal atria1 fibrillation revealed groups of narrow complexes alternating with groups of wide complexes identitle to the anomalous &RS described above. QRS morphology defies classification of this case into any known variety of preexcitation. Complete serial sections were cut through the entire condsystem and both AV rims totaling 18,600 sections. These revealed no bundle of Instead Mahaim fibers histologicalFidentified as Kent. His bundle tissue were given off from the AV bundle both to the right and left sides of the septum associated with the normal fibers of James. The short PR interval is thus explained as produced by James fibers bypassing most of the AV node. Preexcitation appeared to start at the summit of the ventricular septum on both sides and spread anteriorly on both free walls from epicardium to endocardium producing the bizarre lX!G. This case revealed that fibers of Mahaim must have the property of conduction; and atria1 arrhythmias in WPW are not of necessity caused by reentry but produced by concomitant disease, in this instance carcinwatons atria1 involvement.
ELECTROPHYSIOLOGICAL EFFECTS OF NITROGLYCERIN DURING EWERIMENTAL CORONARY OCCLUSION Rafael Levites, MD; Monty Rodenheimer, MD; Richard H. Helfant, MD, FACC, Presbyterian-University of Pennsylvania Medical Center, Philadelphia, Pennsylvania Previous studies have shown that nitroglycerin (NTG) decreases ventricular premature complexes and increases the ventricular fibrillation threshold after acute coronary occlusion. In order to determine the electrophysiological effects of NTG after occlusion, experiments were performed in 13 mongrel dogs, with heart rate controlled by atria1 pacing. Conduction time from the onset of the QRS to local electrogram onset and refractory periods obtained by the extrastimulus method, were determined in normal and ischemic areas of left ventricular myocardium prior to and after variable periods of occlusion, as well as following the IV administration of NTG (300ug bolus followed by an infusion titrated to reduce arterial pressure POmmHg). Following 15 min of occlusion, refractory periods in the normal area remained unchanged while it shortened in the ischemic area to 82% of control (p<.OOl), creating an 18% mean dispersion of refractory periods. After NTG, refractory periods in the normal area were unaffected while prolongation in the ischemic area to 90% of control occurred thus decreasing the dispersion of refractory periods to 10% (pc.001). However, following periods of occlusion %O min, NTG had inconsistent effects on ischemic refractory periods, and did not significantly affect refractory period dispersion. NTG had no effects on conduction times of normal or ischemic areas. These observations suggest that 1) NTG enhances the electrical stability of the acutely ischemic ventricle by decreasing the dispersion of refractoriness between normal and ischemic areas in the immediate period following occlusion and 2) NTG has inconsistent effects after more prolonged periods of occlusion.
152
January 1975
The American Journal of CARDlOLOGY
CONDUCTION SYSTEM IN SUDDEN CARDIAC DEATH J.T. Lie, M.D., Departments of Pathology, Royal Melbourne Hospital, Melbourne, Australia, and Baylor College of Medicine Houston, Texas 77025 Sudden cardiac death (SCD) has been attributed to the development of lethal dysrhythmias in coronary heart disease victims, and several recent autopsy surveys showed that 10 to 47% of SCD patients had unsuspected acute myocardial infarction (AMI). The present study concerned histopathologic findings of the conduction system in 49 SCD (within 6 hours of the onset of acute symptoms) patients; 39 with established AMI (Group A) and 10 without (Group B). Both groups showed high incidence of cardiome&y, significant coronary artery disease affecting two or more vessels, and acute myocardial ischemia undetectable by Stenosis of nutrient conventional histological techniques. vessels of the conduction system was present in about SO% of the atrioventricular (AV) node arteries and about 25% of the sinoatrial (SA) node arteries in both groups of SCD patients. Nonspecific “degenerative” changes (fibrosis, fatty infiltration or both) of the conduction tissue, which might or might not represent results of old ischemic injury, also occurred with similar frequencies. Acute changes (infarction, hemorrhage) of the AV node and bundle branches were found only in two Thus, Group A patients, both had massive septal infarction. the conduction tissue appeared more resistant to ischemlc injury and was overtly damaged only on rare occasions in fatal AMI. ‘Ihe scarcity of acute lesions in the conduction system itself suggested that lethal dysrhythmia in SCD was probably due to electrical instability of the acutely ischemic myocardium rather than a direct injury to the specialized tissue of the heart.
THE EFFECTS OF GLUCOSE-INSULIN-POTASSIUM THERAPY IN GLOBAL MYOCARDIAL ISCHEMIA A. James Liedtke, M.D., Howard C. Hughes, V.M.D., and James R. Neely, Ph.D., Penna. State Univ., Hershey, Pa. The metabolic benefits of glucose-insulin-potassium(GIK) administration during myocardial ischemia have recently been questioned as has the proposed clinical efficacy of its use in the management of patients with ischemic heart disease. To test this intervention experimentally in an intact, working swine heart preparation, GIK enriched medium(32.4 mM glucose, .025 units/ml insulin, and 5.9mM potassium)was provided during coronary perfusion in nine control hearts and nine hearts rendered ischemic by reducing total coronary blood flow from 157 to 82 ml/rain. In another group of 14 hearts(six control and eight ischemic)coronary perfusate contained 11.8 mH glucose, 5.9 mM potassium, and no insulin. In hearts without GIK, ischemia increased left ventricular end-diastolic pressure ((LVEDP)from 8 to 15 mmllg, p<.05)and resulted in declines of myocardial oxygen consumption((MV02)from .80 to .68 rmnol/hr/g, p<.O5), free fatty acid(FFA)oxidation(from 31 to 21 pmol/hr/g, pc.O25), and tissue creatine phosphate ((CP)from 47 to 21 umol/g). Data for control hearts with GIK were similar to controls without GIK except that glucose uptake was increased to 430 ?.mol/hr/g. Ischemia had similar effects in GIK-treated hearts(LVEDP:22 mmHg;MVO2: .51 mmol/hr/g; FFA oxidation: 25 pmol/hr/g;CP;24 umol/g). Glucose uptake was reduced to 240 pmol/hr/g and average survival time during ischemia was 10 minutes less than in hearts receiving no GIK. These data indicate that in global ischemia GIK provides essentially no metabolic advantages to jeopardized myocardium and suggest any therapeutic benefit derived from such treatment in regional ischemia probably occurs in the uninvolved myocatdium.
Volume 35