Brown E J, Swinford R D, Gadde P, Lillis O
Department of Medicine, State University of New York, Health Sciences Center, Stony Brook 1794-8171.
J Am Coll Cardiol. 1991 Jun;17(7):1641-50. doi: 10.1016/0735-1097(91)90660-2.
The purpose of this study was to characterize the effects of late reperfusion on myocardial infarct shape and to quantitate associated changes in left ventricular volume. Reperfusion was delayed until there was no salvage of ischemic myocardium. Dogs underwent 6.5 h of left anterior descending coronary artery occlusion (n = 5) or 5.5 h of occlusion and 1 h of reperfusion (n = 5). Infarct shape was measured with pairs of ultrasonic crystals implanted circumferentially in the mid myocardium. Infarct stiffness was determined from end-diastolic pressure-segment length curves produced by aortic clamping. Left ventricular volume was measured with three pairs of endocardial ultrasonic crystals and the effect of infarct shape change on left ventricular volume was determined. Infarct size, expressed as a percent of the area at risk, was similar in reperfused (97 +/- 1%) and nonreperfused (98 +/- 1%) hearts. After coronary artery occlusion, infarct segments became akinetic and functional dilation, measured as end-diastolic ultrasonic crystal separation, increased to a similar extent in reperfused (24 +/- 7%) and nonreperfused (19 +/- 3%) hearts. In 13 additional dogs that underwent reperfusion and instrumentation with endocardial ultrasonic crystals for volume measurement, left ventricular volume increased 42 +/- 6% over the preocclusion level (p less than 0.001). Within minutes of reperfusion, the infarct stiffened, infarct dilation decreased to 1 +/- 4% over the baseline preocclusion level (p less than 0.05 vs. prereperfusion) and left ventricular volume decreased to 16 +/- 11% over the baseline level (p less than 0.01 vs. postocclusion). Thus, coronary artery reperfusion reverses initial infarct dilation. Changes in infarct dilation occur immediately after reperfusion and are accompanied by infarct stiffening and a decrease in left ventricular volume. Reperfusion can affect infarct shape and stiffness at a point in time when myocardial salvage is no longer possible.
本研究的目的是描述晚期再灌注对心肌梗死形状的影响,并对左心室容积的相关变化进行定量分析。再灌注延迟至无存活的缺血心肌。犬接受6.5小时左前降支冠状动脉闭塞(n = 5)或5.5小时闭塞及1小时再灌注(n = 5)。用环形植入心肌中层的成对超声晶体测量梗死形状。梗死硬度由主动脉夹闭产生的舒张末期压力-节段长度曲线确定。用三对心内膜超声晶体测量左心室容积,并确定梗死形状改变对左心室容积的影响。梗死面积以危险区面积的百分比表示,在再灌注心脏(97±1%)和未再灌注心脏(98±1%)中相似。冠状动脉闭塞后,梗死节段变为运动不能,以舒张末期超声晶体间距测量的功能性扩张在再灌注心脏(24±7%)和未再灌注心脏(19±3%)中增加程度相似。在另外13只接受再灌注并植入心内膜超声晶体以测量容积的犬中,左心室容积比闭塞前水平增加了42±6%(p<0.001)。再灌注后数分钟内,梗死变硬,梗死扩张降至比闭塞前基线水平高1±4%(与再灌注前相比,p<0.05),左心室容积降至比基线水平高16±11%(与闭塞后相比,p<0.01)。因此,冠状动脉再灌注可逆转最初的梗死扩张。梗死扩张的变化在再灌注后立即发生,并伴有梗死变硬和左心室容积减小。在心肌挽救不再可能的时间点,再灌注可影响梗死形状和硬度。