Lanza G A
Istituto di Cardiologia, Università Cattolica del Sacro Cuore, Roma, Italy.
Herz. 1999 Apr;24(2):97-106. doi: 10.1007/BF03043848.
Syndrome X is likely to be caused by a dysfunction of small coronary arteries. Several authors suggested that an increased adrenergic activity could be involved in the pathogenesis of syndrome X, but studies investigating this topic by indirect methods led to conflicting results. We directly investigated cardiac sympathetic nerve function in syndrome X by myocardial radionuclide studies with 123I-metaiodobenzylguanidine (MIBG). Twelve syndrome X patients and 10 healthy controls were enrolled in the study. Cardiac MIBG uptake was assessed calculating the heart/mediastinum (H/M) ratio and a semiquantitative MIBG uptake score. Cardiac MIBG images were normal in all but 1 of controls (10%). Conversely, abnormalities in cardiac MIBG uptake were found in 9 syndrome X patients (75%, p < 0.01). In 5 patients the heart was totally or almost totally invisible on radionuclide MIBG images, while regional defects were found in other 4 patients. The H/M ratio was lower and cardiac MIBG uptake score strikingly higher in syndrome X patients. At 3 hours the H/M ratio was 1.70 +/- 0.6 in patients and 2.19 +/- 0.3 in controls (p = 0.03), while MIBG uptake score was 36.7 +/- 31 and 4.0 +/- 2.5 (p = 0.003) in the 4 groups, respectively. There were no differences between patients and controls in lung and salivary MIBG uptake. Reversible perfusion defects on stress thallium scintigraphy were found in 5 syndrome X patients (45%), all of whom also had abnormal MIBG scintigrams, while all 3 patients with normal MIBG scintigraphy also had normal thallium images. Thus, the function of efferent cardiac adrenergic nerve fibers is strongly impaired in the majority (i.e., 75%) of syndrome X patients. This abnormal function likely contributes significantly to the pathophysiologic and clinical features of syndrome X. We speculate that also the increased perception of cardiac pain reported in these patients could be an expression of the abnormal function of cardiac nerves, reflecting alterations of afferent nociceptive cardiac nerve fibers, as the abnormalities in MIBG uptake reflect alterations of efferent cardiac adrenergic nerve fibers.
X综合征可能由小冠状动脉功能障碍引起。几位作者认为，肾上腺素能活性增加可能参与X综合征的发病机制，但通过间接方法对此主题进行研究的结果相互矛盾。我们通过使用123I-间碘苄胍（MIBG）的心肌放射性核素研究直接调查了X综合征患者的心脏交感神经功能。12例X综合征患者和10名健康对照者纳入本研究。通过计算心脏/纵隔（H/M）比值和半定量MIBG摄取评分来评估心脏MIBG摄取情况。除1名对照者（10%）外，所有对照者的心脏MIBG图像均正常。相反，9例X综合征患者发现心脏MIBG摄取异常（75%，p<0.01）。5例患者在放射性核素MIBG图像上心脏完全或几乎完全不可见，而其他4例患者发现有局部缺损。X综合征患者的H/M比值较低，心脏MIBG摄取评分显著较高。3小时时，患者的H/M比值为1.70±0.6，对照者为2.19±0.3（p=0.03），而4组的MIBG摄取评分分别为36.7±31和4.0±2.5（p=0.003）。患者和对照者在肺部和唾液MIBG摄取方面无差异。5例X综合征患者（45%）在运动铊闪烁显像中发现可逆性灌注缺损，所有这些患者的MIBG闪烁显像也异常，而所有3例MIBG闪烁显像正常的患者铊图像也正常。因此，大多数（即75%）X综合征患者的传出心脏肾上腺素能神经纤维功能严重受损。这种异常功能可能对X综合征的病理生理和临床特征有显著影响。我们推测，这些患者中报告的心脏疼痛感知增加也可能是心脏神经功能异常的一种表现，反映了传入伤害性心脏神经纤维的改变，就像MIBG摄取异常反映传出心脏肾上腺素能神经纤维的改变一样。
