Bodí V, Sanchis J, Llàcer A, Insa L, Chorro F J, López-Merino V
Cardiology Department, University Clinic Hospital, Cardiology Unit, Marina Baixa Hospital, Avda Partida Galandú 5, 03570 La Vila-Joiosa, Spain.
Am Heart J. 1999 Jun;137(6):1107-15. doi: 10.1016/s0002-8703(99)70370-4.
Resting ST-segment elevation on Q leads after an acute myocardial infarction has been related to a greater infarct size. Otherwise, the relation between exercise-induced ST-segment elevation and myocardial viability is controversial. We investigated the relation between ST-segment elevation on Q leads at rest and during exercise and regional dysfunction and its evolution, contractile reserve, left ventricular dilation, and coronary patency.
Exercise testing and cardiac catheterization were performed at the first week after infarction in 51 patients. The study group was divided according to the existence (in 2 or more Q leads; n = 36) or not (n = 15) of resting ST-segment elevation and according to the existence (n = 28) or not (n = 23) of exercise-induced ST-segment elevation. Left ventricular end-diastolic and end-systolic volumes (mL/m2), regional wall motion (SD/chord), contractile reserve (wall motion percentage improvement with low-dose dobutamine), and coronary patency in the culprit artery were analyzed. Cardiac catheterization was repeated at the sixth month in 35 patients; systolic recovery (wall motion percentage improvement), left ventricular volumes, and coronary patency were again evaluated. Patients with resting ST-segment elevation showed poorer wall motion (2.1 +/- 0.8 SD/chord vs 1.2 +/- 1 SD/chord, P =.002), lesser contractile reserve (17% [0% to 39%] vs 41% [4% to 92%], P =.04), greater end-systolic volume (32 +/- 15 mL/m2 vs 23 +/- 11 mL/m2, P =.04), and higher percentage of occlusion (36% vs 7%, P =.04) than did patients without ST-segment elevation. Likewise, patients with exercise-induced ST-segment elevation showed lesser contractile reserve (8% [0% to 40%] vs 35% [12% to 86%], P =.03) than did patients without exercise-induced ST-segment elevation. The only independent predictors of contractile reserve were wall motion <2 SD/chord (odds ratio [OR] 7.1, confidence interval [CI] 6.3 to 7.9, P =.01) and the absence of exercise-induced ST-segment elevation (OR 5.7, CI 4.9 to 6.5, P =. 02). There were no significant differences between patients with and those without ST-segment elevation (at rest or during exercise) in systolic recovery or left ventricular volumes at the sixth month.
ST-segment elevation on Q leads at rest is related to a poorer systolic function (more severe regional dysfunction, greater end-systolic volume, and less response to dobutamine). ST-segment elevation during exercise is independently related to a lesser contractile reserve. ST-segment elevation (at rest or during exercise) is not related to the evolution of volumes or regional dysfunction during the first 6 months after infarction.
急性心肌梗死后Q导联静息ST段抬高与更大的梗死面积相关。否则,运动诱发的ST段抬高与心肌存活能力之间的关系存在争议。我们研究了静息和运动时Q导联ST段抬高与局部功能障碍及其演变、收缩储备、左心室扩张和冠状动脉通畅情况之间的关系。
对51例患者在心肌梗死后第一周进行运动试验和心脏导管检查。根据静息ST段抬高的有无(2个或更多Q导联;n = 36)或无(n = 15)以及运动诱发的ST段抬高的有无(n = 28)或无(n = 23)将研究组进行分组。分析左心室舒张末期和收缩末期容积(mL/m²)、局部室壁运动(SD/弦)、收缩储备(低剂量多巴酚丁胺时室壁运动改善百分比)以及罪犯血管的冠状动脉通畅情况。35例患者在第六个月重复进行心脏导管检查;再次评估收缩恢复情况(室壁运动改善百分比)、左心室容积和冠状动脉通畅情况。静息ST段抬高的患者显示出较差的室壁运动(2.1±0.8 SD/弦对1.2±1 SD/弦,P = 0.002)、较小的收缩储备(17%[0%至39%]对41%[4%至92%],P = 0.04)、更大的收缩末期容积(32±15 mL/m²对23±11 mL/m²,P = 0.04)以及更高的闭塞百分比(36%对7%,P = 0.04),与无ST段抬高的患者相比。同样,运动诱发ST段抬高的患者显示出比无运动诱发ST段抬高的患者更小的收缩储备(8%[0%至40%]对35%[12%至86%],P = 0.03)。收缩储备的唯一独立预测因素是室壁运动<2 SD/弦(比值比[OR]7.1,置信区间[CI]6.3至7.9,P = 0.01)和无运动诱发的ST段抬高(OR 5.7,CI 4.9至6.5,P = 0.02)。在第六个月时,有或无ST段抬高(静息或运动时)的患者在收缩恢复或左心室容积方面没有显著差异。
静息时Q导联ST段抬高与较差的收缩功能相关(更严重的局部功能障碍、更大的收缩末期容积以及对多巴酚丁胺反应较小)。运动时ST段抬高独立地与较小的收缩储备相关。ST段抬高(静息或运动时)与梗死后前6个月容积或局部功能障碍的演变无关。