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Left ventricular ejection rate during the first third of systole in patients with aortic insufficiency
ABSTRACTS
LEFT VENTRICULAR DYSFUNCTION IN PATIENTS WITH MITRAL REGURGITATION Lewis C. Lipson, MD, Kenneth M. Kent, XD, FACC, Robert 0. Bonow, MD, Douglas R.Rosing. MD, Charles L.McIntosh, MD, Michael Jones, MD, Andrew G.Morrow, IfD, Stephen E. Epstein, MD, FACC, NHLBI, NIH, Bethesda, TId.
MONDAY, MARCH 16, 1961 PM DIASTOLIC MECHANICS OF THE HEART AND PERICARDIUM 4:00-5:30
To determine optimum time for valve replacement in pta c with mitral regurgitation (MR), we prospectively studied echo, radionuclide (RN) angiography, and hemodynamics in 21 pts with MR and severe symptoms who subsequently underwent operation (op). These studies were compared to those obtained in 17 mildly symptomatic pts who were followed (nonop). Pre-op. there were no significant differences between op and nonop pts in echo LV diastolic dimension (64~11 vs. 6e_ll), RN ejection fraction at rest (EFrest) (53+9 vs.51+8) or during exercise (EFex)(57+11 vs.56+12). At rest op pts had higher RA pressure (1124 ~6.523, pc.001) and PAW pressures (26+8 vs. 1455, p<.OOl), but similar CI (2.3+.7 vs 2.5+.7, MS) compared to nonop pts. During supine exercise, d:spite similar elevations of PAW pressure (38+9 op vs. 31214 nonop, NS) np pts had a lower CI (3.4+1.2 vs. 5.5+1.8, pc.005) than nonop pts. Postoa, despite-improvement-in RA (11+4 to 854, n=13, pc.05) and PAW pressures (24+8 to 1826, n=13, p<.OS), CI was unchanged (2.2k.6 preop vs. 2.65.8 postop, n=13. pc.05). Postop there was a marked reduction in EFrest (38+10 vs. 51+10 preop, n=13, pc.05) and EFex (41+12 vs.56~12 preop, n=12, pc.01); lo/l3 pts had subnormal (<45%).EFrest and 11/12 pts had subnormal (~54%) EFex. Postop EFex was inversely related to preop LVDD and PAW at rest. We conclude that in pts with MR (1) LV dilatation occurs before severe symptoms develop and (2) by the time pts become severely symptomatic, irreversible LV dysfunction has occurred despite normal preop RN EF, a result of LV decompression into a low pressure LA.
SYSTOLIC IOAIItEPENDExY OF LQT =m REw[ATIoNIS INE'LmBYBEI1\ ~ICxxiEAIuD~~~ Alvin S. Blaustein IQ, William H. Gaasch MD E'ACC,John D. CaXYOll~,DanAdamPhDandHe?ZbertJ. L.evineIQ FACC. Tufts-NewhglandMedical Center Hospital and Harvsxd-Beth IsraelHospital, Fzoat.cm,m. The relation between LV relaxation velocity and systolic load (pressure) was examined in18 open &e&anesthetized (ohloral-w) dogs (constant heart rate,2 Hz). LV pressure (P) wasmasuredwithamiorananamz tarand the time anstant (T,ms) of LVisovolumic P declinewas taken as an index of LV relaxaticm velocity. A progressive increase inLVsystolicPwaapraluo=dby abrupt diastolic cross cl-of the descending thoracic aorta; the clamp wasmaintained for 3beats andthenreleased,thus generating 4 end systolic (Es) P-Tcoorclinates. Over awide range of ESP (95-200 tig.) the ESP-T relation was linear (least squares best fit, *0.98).By definition,the slope (k) of this relation reflects the load dew of T. Values of T and k were debefore (ccntrol, C) and after each of three interventions: isoproterenol (Isob propr~lol (Pro), and LV asynchrony (Aayn). A.syruW~~~y was prc&zed by RV free wall pacing; all other stties wereperfox.n&withRApacing. DatabelowaremeanfSE; *=p
LEFT VE~RICULAR EJECTION RATE DURING THE FIRST THIRD OF SYSTOLE IN PATIENTS WITH AORTIC INSUFFICIENCY Lyme L. Johnson, MD, Mitchell Marshall, BS, Yvonne E. Johnson, MD, Paul J. Cannon, MD, FACC, Columbia UNew York
MECHANISMS OF LOAD INDEPENDENCE OF RELAXATION DURING HYPOXIA IN MAMMALIAN CARDIAC MUSCLE Stanislas U S I; Philippe R. Hourmans, M.D.; Eric R. Van &Dirk L. Brutsaert, M.D., Ph.D. Dept .of Physiology, University of Antwerp, Antwerp, Belgium.
C
February
1991
The American
Journal
of CARDIOLOGY
C
PrO
27+4* 2023 .ll+.Ol .2%.04*
C
Asyn
2422 30_13* .09+.02 .25f.04*
Thus, the tikamstantof LVprfGsure deciineisioad dewti thisloaddependencyisdecreasedbyisopro~ enoland hxeasedbypmpanololand asyntiony. Changes in synpathetictom presumbly influencerelaxation throughsubcellularorbiochemicalprocesses,~leasynchronylikely influencestheloaddependencyof Tby changing the distributionofla3dover fmctioningrtyofibrils and/orby causingtenporaldispersionof relaxation
In previous studies the rate of LV volume change during the first l/3 of systole was shown to be a more sensitive index of cardiac performance than ejection fraction (EF) in coronary disease. To test the hypothesis that a noninvasive index of the ejection rate in early systole can also identify subtle abnormalities of LV performance in aortic insufficiency (AI) the rate of change of LV counts during the first l/3 of systole was measured by firstpass radionuclide angiography in 26 patients. By weighted least squares a monoexponential equation was fit to the LV counts obtained at 0.025 second intervals during the first l/3 of systole; the slope was divided by theaverage counts in the first l/3 to give a rate constant (RC) proportional to LV volume change during early systole. The patients were divided into two groups based uponthe response of EF to exercise 6.EF). In group I restingEF was .59+.08and increased .10+_.04during exercise; in group II resting EF was not different (.5e.O8) but fell during exercise (-.08+.06) (p<.OOl). The RC obtained at rest wss 15.73.0 in group I and was significantly lower in group II, 9.523.0 (p<.OOl). Using an RC of 12.0 as a cut-off and applying the Fisher exact test, separation of the groups was excellent (p<.OOl) with only one group I patient with RCc12.0 and 2 in group II with RC) 12.0. When RC ias plotted vs EF for the 26 patients, there was a significant direct relationship, r * 0.76 (d.01) but with wide confidence limits. The data indicate that a non-invasive index of the rate of LV volume change during the first l/3 of systole can identify abnormal LV reserve in patients with AI and normal EF at rest.
410
IS0
22f3* T120 2622 k .16_L.O1 .09+.01*
In mammalian cardiac muscle relaxation, which is very sensitive to the prevailing load, was recently shown to become largely load-independent during hypoxia. This effect was ascribed to a delayed removal of the actiwting myoplasmic calcium. To further elucidate the underlying mechanisms of this effect of ow studied in 20 cat pa&lary muscles hypoxia, relaxation “of (29’ C; 12/min; (6 $. 2.5 mM) at low (6 ), (1.0, 0.5, 0.375mM)oraftervempamil (10m6 M). Load dependence of relaxation was quantified by comparing force and time coordinates at the onset of the isometric relaxation phase in seveml afterlooded isotonic twitch contractions with the.y&xation of the isometric control contraction. Low wmpamil and hypoxia reversed relaxation from2+ (G ),, load-dependent into load-independent. Although low (Ca ). and vempamil had a more marked negative inotropic effect on the contmction ph.se than hypoxia, the reversal of relaxation from load-dependent into Id-independent was significantly more pronounced wihhypoxia . Even when hypoxia was superimposed on low (6 ), or vempamil, the same marked degree of load dependence was attai@ as during hypoxia alone. The mechanisms by which low (Ca ). and vempamil result in load-independence of relaxation, probably by slowing down the removal of activating myoplasmic calcium, are still not fully understood. However, hypoxia exerts an additional disturbing effect on relaxation through other, probably energetically linked aspects, e g. the ATP-dependent detachment of the actinomyosin intemctions.
Volume
47
LEFT VENTRICULAR DYSFUNCTION IN PATIENTS WITH MITRAL REGURGITATION Lewis C. Lipson, MD, Kenneth M. Kent, XD, FACC, Robert 0. Bonow, MD, Douglas R.Rosing. MD, Charles L.McIntosh, MD, Michael Jones, MD, Andrew G.Morrow, IfD, Stephen E. Epstein, MD, FACC, NHLBI, NIH, Bethesda, TId.
MONDAY, MARCH 16, 1961 PM DIASTOLIC MECHANICS OF THE HEART AND PERICARDIUM 4:00-5:30
To determine optimum time for valve replacement in pta c with mitral regurgitation (MR), we prospectively studied echo, radionuclide (RN) angiography, and hemodynamics in 21 pts with MR and severe symptoms who subsequently underwent operation (op). These studies were compared to those obtained in 17 mildly symptomatic pts who were followed (nonop). Pre-op. there were no significant differences between op and nonop pts in echo LV diastolic dimension (64~11 vs. 6e_ll), RN ejection fraction at rest (EFrest) (53+9 vs.51+8) or during exercise (EFex)(57+11 vs.56+12). At rest op pts had higher RA pressure (1124 ~6.523, pc.001) and PAW pressures (26+8 vs. 1455, p<.OOl), but similar CI (2.3+.7 vs 2.5+.7, MS) compared to nonop pts. During supine exercise, d:spite similar elevations of PAW pressure (38+9 op vs. 31214 nonop, NS) np pts had a lower CI (3.4+1.2 vs. 5.5+1.8, pc.005) than nonop pts. Postoa, despite-improvement-in RA (11+4 to 854, n=13, pc.05) and PAW pressures (24+8 to 1826, n=13, p<.OS), CI was unchanged (2.2k.6 preop vs. 2.65.8 postop, n=13. pc.05). Postop there was a marked reduction in EFrest (38+10 vs. 51+10 preop, n=13, pc.05) and EFex (41+12 vs.56~12 preop, n=12, pc.01); lo/l3 pts had subnormal (<45%).EFrest and 11/12 pts had subnormal (~54%) EFex. Postop EFex was inversely related to preop LVDD and PAW at rest. We conclude that in pts with MR (1) LV dilatation occurs before severe symptoms develop and (2) by the time pts become severely symptomatic, irreversible LV dysfunction has occurred despite normal preop RN EF, a result of LV decompression into a low pressure LA.
SYSTOLIC IOAIItEPENDExY OF LQT =m REw[ATIoNIS INE'LmBYBEI1\ ~ICxxiEAIuD~~~ Alvin S. Blaustein IQ, William H. Gaasch MD E'ACC,John D. CaXYOll~,DanAdamPhDandHe?ZbertJ. L.evineIQ FACC. Tufts-NewhglandMedical Center Hospital and Harvsxd-Beth IsraelHospital, Fzoat.cm,m. The relation between LV relaxation velocity and systolic load (pressure) was examined in18 open &e&anesthetized (ohloral-w) dogs (constant heart rate,2 Hz). LV pressure (P) wasmasuredwithamiorananamz tarand the time anstant (T,ms) of LVisovolumic P declinewas taken as an index of LV relaxaticm velocity. A progressive increase inLVsystolicPwaapraluo=dby abrupt diastolic cross cl-of the descending thoracic aorta; the clamp wasmaintained for 3beats andthenreleased,thus generating 4 end systolic (Es) P-Tcoorclinates. Over awide range of ESP (95-200 tig.) the ESP-T relation was linear (least squares best fit, *0.98).By definition,the slope (k) of this relation reflects the load dew of T. Values of T and k were debefore (ccntrol, C) and after each of three interventions: isoproterenol (Isob propr~lol (Pro), and LV asynchrony (Aayn). A.syruW~~~y was prc&zed by RV free wall pacing; all other stties wereperfox.n&withRApacing. DatabelowaremeanfSE; *=p
LEFT VE~RICULAR EJECTION RATE DURING THE FIRST THIRD OF SYSTOLE IN PATIENTS WITH AORTIC INSUFFICIENCY Lyme L. Johnson, MD, Mitchell Marshall, BS, Yvonne E. Johnson, MD, Paul J. Cannon, MD, FACC, Columbia UNew York
MECHANISMS OF LOAD INDEPENDENCE OF RELAXATION DURING HYPOXIA IN MAMMALIAN CARDIAC MUSCLE Stanislas U S I; Philippe R. Hourmans, M.D.; Eric R. Van &Dirk L. Brutsaert, M.D., Ph.D. Dept .of Physiology, University of Antwerp, Antwerp, Belgium.
C
February
1991
The American
Journal
of CARDIOLOGY
C
PrO
27+4* 2023 .ll+.Ol .2%.04*
C
Asyn
2422 30_13* .09+.02 .25f.04*
Thus, the tikamstantof LVprfGsure deciineisioad dewti thisloaddependencyisdecreasedbyisopro~ enoland hxeasedbypmpanololand asyntiony. Changes in synpathetictom presumbly influencerelaxation throughsubcellularorbiochemicalprocesses,~leasynchronylikely influencestheloaddependencyof Tby changing the distributionofla3dover fmctioningrtyofibrils and/orby causingtenporaldispersionof relaxation
In previous studies the rate of LV volume change during the first l/3 of systole was shown to be a more sensitive index of cardiac performance than ejection fraction (EF) in coronary disease. To test the hypothesis that a noninvasive index of the ejection rate in early systole can also identify subtle abnormalities of LV performance in aortic insufficiency (AI) the rate of change of LV counts during the first l/3 of systole was measured by firstpass radionuclide angiography in 26 patients. By weighted least squares a monoexponential equation was fit to the LV counts obtained at 0.025 second intervals during the first l/3 of systole; the slope was divided by theaverage counts in the first l/3 to give a rate constant (RC) proportional to LV volume change during early systole. The patients were divided into two groups based uponthe response of EF to exercise 6.EF). In group I restingEF was .59+.08and increased .10+_.04during exercise; in group II resting EF was not different (.5e.O8) but fell during exercise (-.08+.06) (p<.OOl). The RC obtained at rest wss 15.73.0 in group I and was significantly lower in group II, 9.523.0 (p<.OOl). Using an RC of 12.0 as a cut-off and applying the Fisher exact test, separation of the groups was excellent (p<.OOl) with only one group I patient with RCc12.0 and 2 in group II with RC) 12.0. When RC ias plotted vs EF for the 26 patients, there was a significant direct relationship, r * 0.76 (d.01) but with wide confidence limits. The data indicate that a non-invasive index of the rate of LV volume change during the first l/3 of systole can identify abnormal LV reserve in patients with AI and normal EF at rest.
410
IS0
22f3* T120 2622 k .16_L.O1 .09+.01*
In mammalian cardiac muscle relaxation, which is very sensitive to the prevailing load, was recently shown to become largely load-independent during hypoxia. This effect was ascribed to a delayed removal of the actiwting myoplasmic calcium. To further elucidate the underlying mechanisms of this effect of ow studied in 20 cat pa&lary muscles hypoxia, relaxation “of (29’ C; 12/min; (6 $. 2.5 mM) at low (6 ), (1.0, 0.5, 0.375mM)oraftervempamil (10m6 M). Load dependence of relaxation was quantified by comparing force and time coordinates at the onset of the isometric relaxation phase in seveml afterlooded isotonic twitch contractions with the.y&xation of the isometric control contraction. Low wmpamil and hypoxia reversed relaxation from2+ (G ),, load-dependent into load-independent. Although low (Ca ). and vempamil had a more marked negative inotropic effect on the contmction ph.se than hypoxia, the reversal of relaxation from load-dependent into Id-independent was significantly more pronounced wihhypoxia . Even when hypoxia was superimposed on low (6 ), or vempamil, the same marked degree of load dependence was attai@ as during hypoxia alone. The mechanisms by which low (Ca ). and vempamil result in load-independence of relaxation, probably by slowing down the removal of activating myoplasmic calcium, are still not fully understood. However, hypoxia exerts an additional disturbing effect on relaxation through other, probably energetically linked aspects, e g. the ATP-dependent detachment of the actinomyosin intemctions.
Volume
47