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Differential responses to canine myosin atpase activity and ventricular tissue gases in the pressure overloaded ventricle dependent upon degree of obstruction: Mild versus severe pulmonic and aortic stenosis
ABSTRACTS
COMPARISON OF 2' INFRANODAL WITH 2' AV NODAL BLOCK. Michael B. Simson, M.D., Joseph F. Spear, Ph.D. and E. Neil Moore, D.V.M., Ph.D., F.A.C.C., Cardiovascular Section, Hospital of the University of Pennsylvania, Philadelphia, Pa. Experiments were performed to compare 2" infranodal block, produced by mechanical pressure on the bundle of His, with 2O AV nodal block, induced by rapid atria1 pacing, in 12 open chested anesthetized dogs. Conduction time through the damaged infranodal conduction system (proximal His bundle to left ventricular electrogram.H-V) and across the AV node (low atria1 to His bundle electrogram, A-H) were measured by an on-line computer. Similarities were noted in 2' block in both systems: 1) The first beat after a blocked beat was more rapidly conducted than any subsequent beat. 2)In 2:l block the second, normally blocked beat would conduct if the stimulus was delayed by less than 100 msec. 3) No reentry was observed when the stimulus for the normally blocked beat was interrupted. The observed differences between 2' infranodal and 2' AV nodal block were: 1) Refractory curves for the infranodal system were much flatter (maximal increase in H-V was 7-25 msec) than the AV node (maximal increase in A-H was 105-130 msec). 2) With rare exceptions 2" infranodal block occurred in even number ratios only (2:1, 4:3, 6:5) but the AV node produced stable odd number ratios (such as 3:2). 3) During 4:3 and 6:5 block the infranodal conduction time and effective refractory period oscillated and did not progressively increase, in contrast to the progressive increase in conduction time and effective refractory period observed during 2O AV nodal block.
DIFFERENTIAL RESPONSES TO CANINE MYOSlN ATPase ACTIVITY AND VENTRICULAR TISSUE GASES IN THE PRESSURE OVERLOADED VENTRICLE DEPENDENT UPON DEGREE OF OBSTRUCTION: MILD VERSUS SEVERE PULMONIC Af4D AORTIC STENOSIS Alan Smith, BS; Claudia Fenner, BS; Teiko Kamiyama, MD: Antone F. Salel, MD, FACC; Dean T. Mason, MD, FACC; Joan Wikman-Coffelt, PhD, University of California, Davis, CA Effects of mild compared to severe hemodynamic pressure overload of right (RV) and left (LV) ventricles on myosin enzymatic function and tissue gases of stressed myocardium were determined in intact canine preparations. Mild pulmonic stenosis (PS) performed by pulmonary artery banding elevated RV peak systolic pressure 60% and caused rise in RV myosin ATPase activity which peaked 35% above In contrast, normal in enzymatic Vmax value by 5 weeks. severe PS by Jacobson cuff inflation elevating RV peak systolic pressure 300% decreased RV myosin ATPase activity 12% (pc.01) by 6 weeks. CA?+ activated enzymatic V,, value of RV myosin was similarly depressed in severe BS. In additional dogs, mild aortic stenosis (AS) (peak gradient 30 mmHg) caused rise in LV myosin ATPase activity In contrast, severe AS (peak gradient 50 mm by 5 weeks. Hg) caused decline in LV myosin ATPase activity by 5 Thus a differential response of myosin ATPase acweeks. tivity occurs in the pressure overloaded ventricle dependent on degree of obstruction. Analyses of tissue gases (~0~ and pC02) by mass spectrometry showed that ventricles subjected to severe pressure overload were hypoxic by 5 In contrast, ventricular tissue subjected to mild weeks. pulmonic or aortic stenosis was not hypoxic. These observations demonstrate mild ventricular pressure overload enhances myosin enzymatic function with stressed myocardium remaining normoxic, whereas severe stenosis causes decline of myosin activity with overloaded ventricle becoming hypoxic.
EPICARDIAL ST-SEGMENT REDUCTION BY VERAPANIL lITHOUT CHANGE IN EXPERIMENTAL INFARCT SIZE Bramah N. Singh, M.D., Ming K. Heng, H.B., Thomas Peter, M.D., Robin M. Norris, M.D. Green Lane Hospital, Auckland New Zealand.
THE INCIDENCE OF MITRAL VALVE PROLAPSE IN 336 CONSECUTIVE LEFT-VENTRICULAR ANGICGRAMS WITH ECHOCARDIOGFAPHIC CORRELATION. Eldon R. Smith, MD; John W. Purdy, PhD; Robert N. Anderson, MD; David B. Fraser, MD, Dalhousie University, Halifax, Nova Scotia.
The effect of intravenous verapamil on infarct size in dogs with left anterior descending coronary artery (LAD) ligation was studied. Myocardial blood flow (MBF, ml/min /lOOg) was measured by radioactive microsphere6 and infarct size quantitated by myocardial creatine phosphokIn inase (CPK) depletion 24 hr after LAD ligation. untreated animals (n=8) summated ST-segment elevation (&ST:,;t+l5 min after LAD ligation, was 4.9 + 0.9 mV , - 14) in the border zone and 11.2 - 1.6 mV (MBF. 30 + 6) in the center zones; normal areas had zero Changes in MBF at 24 hr were &-ST (MBF, 169 + 11). In animals (n=8) pretreated similar to those at 15 min. ST in the border zone was with+verapamil (0.79 mg&) 5.1 - 1.6 mV (MBF, 129 - 10) and 3.6 f 1.2 mV (P40.025; Verapamil MBF 39 + 6) in the center zones of infarct+. increased MBF in the normal areas to 216 - 14 (p
The systolic click - late systolic murmur syndrome (CMS) is a poorly understood clinical entity characterized angiographically by late systolic bulging of one or more scallops of the posterior mitral leaflet (PML). Recently, angiographic mitral valve prolapse (AMVP), often without a click or murmur, has been reported as common in patients (pts) with ASD, severe coronary artery disease (CAD) and in those with angina-like chest pain without CAD. To determine the overall incidence of AMVP, bi-plane left-ventricular angiograms from 336 consecutively studied pts were analysed. There were 223 males and 113 females with a mean age of 47 years (range 13-71). The clinical diagnosis was CMS in 6 pts and all had AMVP. AMVF' was also present in 62/131 pts with CAD (40%), 3/19 with cardiomyopathy (16%), 27/84 with valvular disease (32%), 5/12 with congenital disease (42%) and in 50/84 (59%) of normals (no CAD). Of these, the AMVF' was uni-scalloped in 94, bi-scalloped in 43 and tri-scalloped in 6. Technically satisfactory echocardiograms were available on 140 pts from this group. Analysis revealed evidence of PML prolapse (mid or pan-systolic) in only 9 pts, 6 of whom had CMS clinically. Thus, in this series, AMVE was present in 43% of cases, without predilection in any diagnostic subgroup. Conversely, echographic mitral prolapse was uncommon but correlated well with the presence of a click and/or murmur. We conclude that end-systolic bulging of one or more scallops of the PML is a common angiographic pattern and, at least in the absence of other features of CMS, probably should not be considered a pathologic finding.
January 1976
The American Journal of CARDIOLOGY
Volume 37
173
COMPARISON OF 2' INFRANODAL WITH 2' AV NODAL BLOCK. Michael B. Simson, M.D., Joseph F. Spear, Ph.D. and E. Neil Moore, D.V.M., Ph.D., F.A.C.C., Cardiovascular Section, Hospital of the University of Pennsylvania, Philadelphia, Pa. Experiments were performed to compare 2" infranodal block, produced by mechanical pressure on the bundle of His, with 2O AV nodal block, induced by rapid atria1 pacing, in 12 open chested anesthetized dogs. Conduction time through the damaged infranodal conduction system (proximal His bundle to left ventricular electrogram.H-V) and across the AV node (low atria1 to His bundle electrogram, A-H) were measured by an on-line computer. Similarities were noted in 2' block in both systems: 1) The first beat after a blocked beat was more rapidly conducted than any subsequent beat. 2)In 2:l block the second, normally blocked beat would conduct if the stimulus was delayed by less than 100 msec. 3) No reentry was observed when the stimulus for the normally blocked beat was interrupted. The observed differences between 2' infranodal and 2' AV nodal block were: 1) Refractory curves for the infranodal system were much flatter (maximal increase in H-V was 7-25 msec) than the AV node (maximal increase in A-H was 105-130 msec). 2) With rare exceptions 2" infranodal block occurred in even number ratios only (2:1, 4:3, 6:5) but the AV node produced stable odd number ratios (such as 3:2). 3) During 4:3 and 6:5 block the infranodal conduction time and effective refractory period oscillated and did not progressively increase, in contrast to the progressive increase in conduction time and effective refractory period observed during 2O AV nodal block.
DIFFERENTIAL RESPONSES TO CANINE MYOSlN ATPase ACTIVITY AND VENTRICULAR TISSUE GASES IN THE PRESSURE OVERLOADED VENTRICLE DEPENDENT UPON DEGREE OF OBSTRUCTION: MILD VERSUS SEVERE PULMONIC Af4D AORTIC STENOSIS Alan Smith, BS; Claudia Fenner, BS; Teiko Kamiyama, MD: Antone F. Salel, MD, FACC; Dean T. Mason, MD, FACC; Joan Wikman-Coffelt, PhD, University of California, Davis, CA Effects of mild compared to severe hemodynamic pressure overload of right (RV) and left (LV) ventricles on myosin enzymatic function and tissue gases of stressed myocardium were determined in intact canine preparations. Mild pulmonic stenosis (PS) performed by pulmonary artery banding elevated RV peak systolic pressure 60% and caused rise in RV myosin ATPase activity which peaked 35% above In contrast, normal in enzymatic Vmax value by 5 weeks. severe PS by Jacobson cuff inflation elevating RV peak systolic pressure 300% decreased RV myosin ATPase activity 12% (pc.01) by 6 weeks. CA?+ activated enzymatic V,, value of RV myosin was similarly depressed in severe BS. In additional dogs, mild aortic stenosis (AS) (peak gradient 30 mmHg) caused rise in LV myosin ATPase activity In contrast, severe AS (peak gradient 50 mm by 5 weeks. Hg) caused decline in LV myosin ATPase activity by 5 Thus a differential response of myosin ATPase acweeks. tivity occurs in the pressure overloaded ventricle dependent on degree of obstruction. Analyses of tissue gases (~0~ and pC02) by mass spectrometry showed that ventricles subjected to severe pressure overload were hypoxic by 5 In contrast, ventricular tissue subjected to mild weeks. pulmonic or aortic stenosis was not hypoxic. These observations demonstrate mild ventricular pressure overload enhances myosin enzymatic function with stressed myocardium remaining normoxic, whereas severe stenosis causes decline of myosin activity with overloaded ventricle becoming hypoxic.
EPICARDIAL ST-SEGMENT REDUCTION BY VERAPANIL lITHOUT CHANGE IN EXPERIMENTAL INFARCT SIZE Bramah N. Singh, M.D., Ming K. Heng, H.B., Thomas Peter, M.D., Robin M. Norris, M.D. Green Lane Hospital, Auckland New Zealand.
THE INCIDENCE OF MITRAL VALVE PROLAPSE IN 336 CONSECUTIVE LEFT-VENTRICULAR ANGICGRAMS WITH ECHOCARDIOGFAPHIC CORRELATION. Eldon R. Smith, MD; John W. Purdy, PhD; Robert N. Anderson, MD; David B. Fraser, MD, Dalhousie University, Halifax, Nova Scotia.
The effect of intravenous verapamil on infarct size in dogs with left anterior descending coronary artery (LAD) ligation was studied. Myocardial blood flow (MBF, ml/min /lOOg) was measured by radioactive microsphere6 and infarct size quantitated by myocardial creatine phosphokIn inase (CPK) depletion 24 hr after LAD ligation. untreated animals (n=8) summated ST-segment elevation (&ST:,;t+l5 min after LAD ligation, was 4.9 + 0.9 mV , - 14) in the border zone and 11.2 - 1.6 mV (MBF. 30 + 6) in the center zones; normal areas had zero Changes in MBF at 24 hr were &-ST (MBF, 169 + 11). In animals (n=8) pretreated similar to those at 15 min. ST in the border zone was with+verapamil (0.79 mg&) 5.1 - 1.6 mV (MBF, 129 - 10) and 3.6 f 1.2 mV (P40.025; Verapamil MBF 39 + 6) in the center zones of infarct+. increased MBF in the normal areas to 216 - 14 (p
The systolic click - late systolic murmur syndrome (CMS) is a poorly understood clinical entity characterized angiographically by late systolic bulging of one or more scallops of the posterior mitral leaflet (PML). Recently, angiographic mitral valve prolapse (AMVP), often without a click or murmur, has been reported as common in patients (pts) with ASD, severe coronary artery disease (CAD) and in those with angina-like chest pain without CAD. To determine the overall incidence of AMVP, bi-plane left-ventricular angiograms from 336 consecutively studied pts were analysed. There were 223 males and 113 females with a mean age of 47 years (range 13-71). The clinical diagnosis was CMS in 6 pts and all had AMVP. AMVF' was also present in 62/131 pts with CAD (40%), 3/19 with cardiomyopathy (16%), 27/84 with valvular disease (32%), 5/12 with congenital disease (42%) and in 50/84 (59%) of normals (no CAD). Of these, the AMVF' was uni-scalloped in 94, bi-scalloped in 43 and tri-scalloped in 6. Technically satisfactory echocardiograms were available on 140 pts from this group. Analysis revealed evidence of PML prolapse (mid or pan-systolic) in only 9 pts, 6 of whom had CMS clinically. Thus, in this series, AMVE was present in 43% of cases, without predilection in any diagnostic subgroup. Conversely, echographic mitral prolapse was uncommon but correlated well with the presence of a click and/or murmur. We conclude that end-systolic bulging of one or more scallops of the PML is a common angiographic pattern and, at least in the absence of other features of CMS, probably should not be considered a pathologic finding.
January 1976
The American Journal of CARDIOLOGY
Volume 37
173