Jaffe A S, Biello D R, Sobel B E, Geltman E M
Int J Cardiol. 1987 Apr;15(1):77-89. doi: 10.1016/0167-5273(87)90294-4.
To define effects of nifedipine on regional metabolism in jeopardized myocardium we quantified accumulation of carbon-11 labeled palmitate ([11C]palmitate) in patients with acute myocardial infarction by positron emission tomography in a randomized, double-blind, placebo controlled study. Tomographic studies were performed prior to treatment as soon as possible after hospital admission. Subsequent studies were performed seven days later. Twenty-two patients with acute myocardial infarction were randomized to treatment with nifedipine (n = 13) or placebo (n = 9). The dosage of active medication was guided by a "third party observer" to avoid iatrogenic hypotension. Treatment was initiated within 9.6 +/- 1 hours after the onset of symptoms of infarction. The extent of the zone of abnormal accumulation of [11C]palmitate was similar in pre-treatment positron emission tomograms from patients subsequently given nifedipine compared with those given placebo. In subsequent positron emission tomography studies, patients treated with nifedipine exhibited improved metabolism of [11C]palmitate (by 16 +/- 10%, SE, P less than 0.05) compared with no change in patients given placebo. Neither enzymatic estimates of infarct size nor scintigraphic estimates of left ventricular ejection fraction differed in the two groups. Patients given nifedipine and manifesting substantial improvement in accumulation of [11C]palmitate had a high incidence of chest pain and recurrent infarction compared with those given placebo in whom no improvement was evident. These observations suggest that some regions of myocardium were benefited transiently by nifedipine but that they remained at high risk for recurrent injury. Thus, patients benefited transiently by drugs early after the onset of infarction may require aggressive intervention such as angioplasty or early coronary bypass surgery. Accordingly, they should be evaluated angiographically early for identification of lesions with unusually high risk.
为了确定硝苯地平对濒危心肌区域代谢的影响，我们在一项随机、双盲、安慰剂对照研究中，通过正电子发射断层扫描对急性心肌梗死患者中碳-11标记的棕榈酸酯（[11C]棕榈酸酯）的蓄积进行了定量分析。断层扫描研究在入院后尽快于治疗前进行。随后的研究在七天后进行。22例急性心肌梗死患者被随机分为硝苯地平治疗组（n = 13）或安慰剂组（n = 9）。活性药物的剂量由“第三方观察者”指导，以避免医源性低血压。治疗在梗死症状出现后9.6±1小时内开始。与给予安慰剂的患者相比，随后给予硝苯地平的患者治疗前正电子发射断层扫描图中[11C]棕榈酸酯异常蓄积区域的范围相似。在随后的正电子发射断层扫描研究中，与给予安慰剂的患者无变化相比，接受硝苯地平治疗的患者[11C]棕榈酸酯代谢有所改善（提高16±10%，标准误，P<0.05）。两组间梗死面积的酶学估计值和左心室射血分数的闪烁显像估计值均无差异。与[11C]棕榈酸酯蓄积无明显改善的安慰剂组患者相比，给予硝苯地平且[11C]棕榈酸酯蓄积有显著改善的患者胸痛和再发梗死的发生率较高。这些观察结果表明，心肌的某些区域短暂受益于硝苯地平，但它们仍处于再发损伤的高风险中。因此，梗死发作后早期短暂受益于药物的患者可能需要积极干预，如血管成形术或早期冠状动脉搭桥手术。相应地，应尽早对他们进行血管造影评估，以识别具有异常高风险的病变。
