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首页> 外文期刊>Peptides: An International Journal >Plasma brain natriuretic peptide at rest and after adenosine-induced myocardial ischemia in normotensive and essential hypertensive patients with suspected coronary artery disease.
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Plasma brain natriuretic peptide at rest and after adenosine-induced myocardial ischemia in normotensive and essential hypertensive patients with suspected coronary artery disease.

机译：血压正常和原发性高血压可疑冠心病患者的血浆脑钠肽在静息状态和腺苷诱发的心肌缺血后的状态。

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This study investigated plasma brain natriuretic peptide (BNP) levels in normotensive and hypertensive patients with suspected coronary artery disease during radionuclide pharmacological stress testing. Twenty-seven normotensive patients (15 males, aged 63.0+/-4.5 years and 12 females, aged 63.0+/-4.1 years) and 38 essential hypertensive patients (25 males, aged 63.3+/-3.3 years and 13 females, aged 64.6+/-2.6 years) with chest pain and exercise stress testing inconclusive for coronary artery disease underwent myocardial perfusion single-photon emission computed tomography (SPECT) using adenosine infusion. SPECT identified patients without (16 normotensive and 22 hypertensive) and patients with (11 normotensive and 16 hypertensive) transient perfusion defects. Basal BNP levels in normotensive patients without transient myocardial ischemia (3.1+/-1.2fmol/ml) were significantly (P<0.01) lower than those observed in normotensive patients with transient ischemia (8.2+/-1.2fmol/ml), whereas BNP levels in hypertensive patients without transient ischemia (8.2+/-1.0fmol/ml) did not significantly differ from those in hypertensive patients with transient ischemia (8.1+/-2.0fmol/ml). No significant difference was found in BNP levels between males or females either in normotensive or hypertensive patients without or with ischemia. Adenosine infusion did not significantly change BNP levels in any subject group without or with myocardial perfusion defects. Our findings show that increases in BNP allow early detection of myocardial ischemia in normotensive patients, but not in hypertensive patients with suspected coronary artery disease. Adenosine-induced myocardial ischemia does not affect BNP production already activated by coronary artery disease in normotensive patients and by hemodynamic changes in hypertensive patients.
机译：这项研究调查了在放射性核素药理学压力测试期间可疑冠状动脉疾病的血压正常和高血压患者的血浆脑利钠肽（BNP）水平。二十七例血压正常的患者（男15例，年龄63.0 +/- 4.5岁，女性12例，年龄63.0 +/- 4.1岁）和38例原发性高血压患者（男25例，年龄63.3 +/- 3.3岁，女性13例，年龄64.6岁） +/- 2.6岁），对于胸痛和运动压力测试尚无定论，对冠心病进行了心肌灌注，使用腺苷灌注进行了单光子发射计算机断层扫描（SPECT）。 SPECT识别出无（16例正常血压和22例高血压）患者和（11例正常血压和16例高血压）短暂性灌注缺陷的患者。没有短暂性心肌缺血的血压正常患者的基础BNP水平（3.1 +/- 1.2fmol / ml）显着（P <0.01）低于短暂性心肌缺血的血压正常患者（8.2 +/- 1.2fmol / ml），而BNP没有短暂性缺血的高血压患者（8.2 +/- 1.0fmol / ml）的水平与短暂性缺血的高血压患者（8.1 +/- 2.0fmol / ml）的水平没有显着差异。在没有缺血或有缺血的血压正常或高血压患者中，男性或女性的BNP水平无显着差异。在没有或有心肌灌注缺陷的任何受试者组中，腺苷灌注均不会显着改变BNP水平。我们的研究结果表明，BNP的增加可在血压正常的患者中早期检测出心肌缺血，但在怀疑患有冠状动脉疾病的高血压患者中则无法检测出心肌缺血。腺苷诱导的心肌缺血不会影响正常血压患者的冠状动脉疾病和高血压患者的血流动力学变化已经激活的BNP产生。

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