TY - JOUR
T1 - Acute effects of parenteral beta-blockade on regional ventricular function of infarct and noninfarct zones after reperfusion therapy in humans
AU - Grines, Cindy L.
AU - Booth, David C.
AU - Nissen, Steven E.
AU - Gurley, John C.
AU - Bennett, Kim A.
AU - DeMaria, Anthony N.
PY - 1991
Y1 - 1991
N2 - Although the mechanism is unknown, clinical trials have suggested that intravenous beta-adrenergic blockade may prevent early cardiac rupture after myocardial infarction. Previous studies have examined effects of beta-blockers on global left ventricular function after myocardial infarction; however, few data exist regarding their immediate effects on regional function or in patients after successful reperfusion. Therefore, 65 patients in whom thrombolysis with or without coronary angioplasty achieved reperfusion at 4.6 ± 1.7 h from symptom onset were studied. Low osmolarity contrast ventriculograms were obtained immediately before and after administration of 15 mg of intravenous metoprolol (n = 54) or placebo (n = 11). Intravenous metoprolol immediately decreased heart rate (from 92 to 76 beats/min, p < 0.0001), increased left ventricular diastolic volume (from 150 to 163 ml, p < 0.0001) and systolic volume (from 72 to 77 ml, p < 0.0005) but did not change systolic and diastolic pressures. Although there was no difference in ejection fraction after metoprolol, centerline chord analysis revealed reduced noninfarct zone motion (from 0.41 to 0.12 SD/ chord, p < 0.05), improved infarct zone motion (from −3.1 to −2.9 SD/chord, p < 0.01) and smaller circumferential extent of hypokinesia (from 30 to 27 chords, p < 0.05). Patients with dyskinesia of the infarct zone had the most striking improvement in infarct zone wall motion. Because these changes occurred immediately after beta-blockade, they could not be attributed to myocardial salvage. No significant changes in heart rate, left ventricular volumes or regional wall motion were apparent in the control group. Thus, intravenous beta-blockade reduced wall motion of the noninfarct zone and enhanced infarct zone wall motion after reperfusion in humans, independent of myocardial salvage. Whether these changes are due to alteration in heart rate, reduction in ischemia or reduction in forces from the opposing hypercontractile wall will require further investigation.
AB - Although the mechanism is unknown, clinical trials have suggested that intravenous beta-adrenergic blockade may prevent early cardiac rupture after myocardial infarction. Previous studies have examined effects of beta-blockers on global left ventricular function after myocardial infarction; however, few data exist regarding their immediate effects on regional function or in patients after successful reperfusion. Therefore, 65 patients in whom thrombolysis with or without coronary angioplasty achieved reperfusion at 4.6 ± 1.7 h from symptom onset were studied. Low osmolarity contrast ventriculograms were obtained immediately before and after administration of 15 mg of intravenous metoprolol (n = 54) or placebo (n = 11). Intravenous metoprolol immediately decreased heart rate (from 92 to 76 beats/min, p < 0.0001), increased left ventricular diastolic volume (from 150 to 163 ml, p < 0.0001) and systolic volume (from 72 to 77 ml, p < 0.0005) but did not change systolic and diastolic pressures. Although there was no difference in ejection fraction after metoprolol, centerline chord analysis revealed reduced noninfarct zone motion (from 0.41 to 0.12 SD/ chord, p < 0.05), improved infarct zone motion (from −3.1 to −2.9 SD/chord, p < 0.01) and smaller circumferential extent of hypokinesia (from 30 to 27 chords, p < 0.05). Patients with dyskinesia of the infarct zone had the most striking improvement in infarct zone wall motion. Because these changes occurred immediately after beta-blockade, they could not be attributed to myocardial salvage. No significant changes in heart rate, left ventricular volumes or regional wall motion were apparent in the control group. Thus, intravenous beta-blockade reduced wall motion of the noninfarct zone and enhanced infarct zone wall motion after reperfusion in humans, independent of myocardial salvage. Whether these changes are due to alteration in heart rate, reduction in ischemia or reduction in forces from the opposing hypercontractile wall will require further investigation.
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U2 - 10.1016/S0735-1097(10)80151-2
DO - 10.1016/S0735-1097(10)80151-2
M3 - Article
C2 - 1673133
AN - SCOPUS:0025878731
SN - 0735-1097
VL - 17
SP - 1382
EP - 1387
JO - Journal of the American College of Cardiology
JF - Journal of the American College of Cardiology
IS - 6
ER -