Connelly C M, McLaughlin R J, Vogel W M, Apstein C S
Whitaker Cardiovascular Institute, Boston University School of Medicine, MA 02118.
Circulation. 1991 Jul;84(1):387-99. doi: 10.1161/01.cir.84.1.387.
Left ventricular aneurysm formation after myocardial infarction (MI) has been associated with elongation of infarcted tissue in response to wall stress. Such elongation most commonly occurs in acutely infarcted or partially healed regions during the early post-MI period; however, recent reports have indicated that mature (15-week-old) healed infarct regions also undergo elongation after stress.
To assess factors contributing to post-MI left ventricular aneurysm formation, we subjected isolated strips (n = 50) of rabbit myocardial tissue from acutely ischemic (noninfarcted left ventricular), acutely infarcted (24 hours after MI), and healed infarct (3 and 15 weeks after MI) regions to a range of loading conditions and measured the reversible and irreversible length changes that occurred. The isolated strips were repetitively stretched for 1 hour at 4 Hz to impose cyclical physiological peak and resting stresses of 2.0 and 0.2 g/mm2. During a second hour, either peak stress ("afterload") or resting stress ("preload") was tripled, and the increase in strip length (strain) was measured. During a third hour, peak and resting stresses were returned to the initial values to assess the reversibility of length changes occurring during increased load. Elongation was expressed as the increase in natural strain from the first hour. Increasing afterload caused similar irreversible length increases of 4-5%/hr in acutely infarcted and 3- and 15-week-old healed infarct strips; acutely ischemic tissue length increased by 7.4%/hr (p less than 0.05 versus acutely infarcted tissue and scars). Increasing preload in acutely ischemic and acutely infarcted tissue caused a reversible length increase of less than 1%/hr. (Scar strips were not tested for the effect of preload.)
Since an irreversible length increase may represent an early event in aneurysm formation, our results suggest that 1) afterload increases are more likely to lead to aneurysm development than preload increases, 2) acutely ischemic tissue is the most vulnerable to increased afterload, and 3) for a given wall stress level, healing scar tissue is as susceptible to irreversible length changes as is acutely infarcted tissue. The observation that even mature post-MI scar elongated in response to increases in afterload implies that long-term pharmacological management of afterload in post-MI patients may be beneficial in preventing tissue elongation and aneurysm formation and that factors that increase wall stress (e.g., hypertension and exercise stress) have the potential to promote aneurysm formation in healed infarct scars.
心肌梗死（MI）后左心室动脉瘤的形成与梗死组织因壁应力而伸长有关。这种伸长最常发生在心肌梗死后早期急性梗死或部分愈合的区域；然而，最近的报告表明，成熟的（15周龄）愈合梗死区域在应激后也会发生伸长。
为了评估促成心肌梗死后左心室动脉瘤形成的因素，我们对来自急性缺血（非梗死左心室）、急性梗死（心肌梗死后24小时）和愈合梗死（心肌梗死后3周和15周）区域的兔心肌组织分离条带（n = 50）施加一系列加载条件，并测量发生的可逆和不可逆长度变化。将分离条带以4 Hz重复拉伸1小时，以施加2.0和0.2 g/mm2的周期性生理峰值和静息应力。在第二个小时内，要么将峰值应力（“后负荷”）要么将静息应力（“前负荷”）增加两倍，并测量条带长度（应变）的增加。在第三个小时内，将峰值和静息应力恢复到初始值，以评估在负荷增加期间发生的长度变化的可逆性。伸长表示为第一个小时后自然应变的增加。增加后负荷在急性梗死以及3周和15周龄愈合梗死条带中引起类似的不可逆长度增加，为4 - 5%/小时；急性缺血组织长度增加7.4%/小时（与急性梗死组织和瘢痕相比，p < 0.05）。在急性缺血和急性梗死组织中增加前负荷引起的可逆长度增加小于1%/小时。（未测试瘢痕条带的前负荷效应。）
由于不可逆长度增加可能代表动脉瘤形成的早期事件，我们的结果表明：1）后负荷增加比前负荷增加更可能导致动脉瘤发展；2）急性缺血组织对后负荷增加最敏感；3）对于给定的壁应力水平，愈合瘢痕组织与急性梗死组织一样容易发生不可逆长度变化。即使成熟的心肌梗死后瘢痕在增加后负荷时也会伸长这一观察结果意味着，对心肌梗死后患者的后负荷进行长期药物管理可能有助于预防组织伸长和动脉瘤形成，并且增加壁应力的因素（如高血压和运动应激）有可能促进愈合梗死瘢痕中的动脉瘤形成。
