High-Dose Adenosine Overcomes the Attenuation of Myocardial Perfusion Reserve Caused by Caffeine
High-Dose Adenosine Overcomes the Attenuation of Myocardial Perfusion Reserve Caused by Caffeine
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DOI：
10.1016/j.jacc.2008.08.052
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发表时间：
2008-12-09
影响因子：
24
通讯作者：
Underwood, S. Richard
中科院分区：
文献类型：
--
作者：
Reyes, Eliana;Loong, Chee Y.;Underwood, S. Richard
目的我们研究腺苷剂量的增加是否能克服咖啡因对腺苷介导的冠状动脉血管舒张的拮抗作用。背景咖啡因是腺苷受体的竞争性拮抗剂，但咖啡中的咖啡因是否改变外源性腺苷的作用尚不清楚，方法采用心肌灌注显像（MPS）技术，观察腺苷对心肌缺血再灌注损伤的影响。在30名患者中，在摄入咖啡（咖啡因）之前（基线）和之后（基线）诱导充血。在基线时，患者接受140 μ g/kg/min的腺苷联合低水平运动。对于咖啡因研究，12名患者在摄入咖啡因（200 mg）后接受140 μ g/kg/min腺苷（标准），18名患者接受210 μ g/kg/min（高剂量）。结果咖啡因可降低腺苷诱发的心肌灌注异常的程度（以SDS评分为标准），咖啡因可降低腺苷诱发的心肌灌注异常的程度（以SDS评分为标准）（基线时12.0 +/- 4.4 vs.咖啡因后4.1 +/- 2.1，p < 0.001）以及缺损大小（18% [ 3%至38%] vs. 8% [ 0%至22%]，p < 0.01），而它对高剂量腺苷引起的异常没有影响（SDS，基线时7.7 +/- 4.0 vs.咖啡因后7.8 +/- 4.2，p = 0.7）。在高剂量组中，基线和咖啡因研究的节段性缺损类别（kappa = 0.72，95%置信区间：0.65至0.79）之间具有良好的一致性。咖啡因摄入后腺苷的增加是很好的tolerable.Conclusions咖啡中的咖啡因衰减腺苷诱导的冠状动脉充血，因此，检测灌注异常腺苷MPS。这可以通过增加腺苷剂量来克服，而不影响试验耐受性。（J Am科尔心脏病学杂志2008;52：2008-16）（C）美国心脏病学会基金会2008年
Objectives We studied whether an increase in adenosine dose overcomes caffeine antagonism on adenosine-mediated coronary vasodilation.Background Caffeine is a competitive antagonist at the adenosine receptors, but it is unclear whether caffeine in coffee alters the actions of exogenous adenosine, and whether the antagonism can be surmounted by increasing the adenosine dose.Methods Myocardial perfusion scintigraphy (MPS) was used to assess adenosine-induced hyperemia in 30 patients before (baseline) and after coffee ingestion (caffeine). At baseline, patients received 140 mu g/kg/min of adenosine combined with low-level exercise. For the caffeine study, 12 patients received 140 mu g/kg/min of adenosine (standard) and 18 patients received 210 mu g/kg/min (high dose) after caffeine intake (200 mg). Myocardial perfusion was assessed semiquantitatively and quantitatively, and perfusion defect was characterized according to the presence of reversibility.Results Caffeine reduced the magnitude of perfusion abnormality induced by standard adenosine as measured by the summed difference score (SDS) (12.0 +/- 4.4 at baseline vs. 4.1 +/- 2.1 after caffeine, p < 0.001) as well as defect size (18% [ 3% to 38%] vs. 8% [ 0% to 22%], p < 0.01), whereas it had no effect on the abnormalities caused by high-dose adenosine (SDS, 7.7 +/- 4.0 at baseline vs. 7.8 +/- 4.2 after caffeine, p = 0.7). There was good agreement between baseline and caffeine studies for segmental defect category (kappa = 0.72, 95% confidence interval: 0.65 to 0.79) in the high-dose group. An increase in adenosine after caffeine intake was well tolerated.Conclusions Caffeine in coffee attenuates adenosine-induced coronary hyperemia and, consequently, the detection of perfusion abnormality by adenosine MPS. This can be overcome by increasing the adenosine dose without compromising test tolerability. (J Am Coll Cardiol 2008;52:2008-16) (C) 2008 by the American College of Cardiology Foundation