Marin-Neto J A, Marzullo P, Marcassa C, Gallo Júnior L, Maciel B C, Bellina C R, L'Abbate A
Medical School of Ribeirão Preto, University of São Paulo, Brazil.
Am J Cardiol. 1992 Mar 15;69(8):780-4. doi: 10.1016/0002-9149(92)90505-s.
Most patients with chronic Chagas' heart disease complain of chest pain. The pathophysiology of this symptom is unknown, although myocardial necrosis and fibrosis are frequent necropsy findings and cardiac autonomic impairment is a prominent feature of the disease. To evaluate the possibility of an ischemic cause for these abnormalities in 23 patients (18 men, aged 32 to 60 years, mean 42) with chronic Chagas' disease complaining of chest pain, thallium-201 myocardial scintigraphy was performed after maximal effort and 4-hour redistribution. Regional wall motion was assessed by radionuclide and contrast angiography. Heart rate responses to sinus respiratory arrhythmia, atropine, phenylephrine and Valsalva maneuver were evaluated in all patients and in 22 normal control subjects. Coronary angiography was performed in 16 patients. Only 1 patient had chest pain and no ischemic electrocardiographic changes occurred in any case during the effort test. Scintigraphic analysis of 7 segments per patient showed perfusion defects in at least 1 segment in all patients. Of 161 myocardial segments 16 showed fixed, 10 reversible, and 22 paradox defects (reverse redistribution). The majority (75%) of the fixed perfusion defects occurred in dyssynergic regions, whereas reverse redistribution predominated in regions with normal wall motion (82%). The reversible defects were present in normal or mildly hypokinetic regions. Markedly impaired parasympathetic cardiac control was present but no significant coronary abnormalities were seen in any of the 16 patients undergoing angiography. It is concluded that whereas fixed defects are likely to correspond to fibrotic or necrotic lesions, reversible and paradox perfusion defects may be caused by regional flow or metabolism derangements, possibly related to abnormal parasympathetic control of the coronary microcirculation.
大多数慢性恰加斯心脏病患者主诉胸痛。尽管心肌坏死和纤维化是尸检常见发现，且心脏自主神经功能障碍是该病的一个突出特征，但这种症状的病理生理学尚不清楚。为评估23例（18例男性，年龄32至60岁，平均42岁）主诉胸痛的慢性恰加斯病患者出现这些异常的缺血性病因的可能性，在最大运动负荷后及4小时再分布后进行了铊-201心肌闪烁扫描。通过放射性核素和对比血管造影评估局部室壁运动。在所有患者及22名正常对照者中评估了对窦性呼吸性心律失常、阿托品、去氧肾上腺素和瓦尔萨尔瓦动作的心率反应。16例患者进行了冠状动脉造影。仅1例患者有胸痛，运动试验期间在任何情况下均未出现缺血性心电图改变。每位患者7个节段的闪烁扫描分析显示所有患者至少1个节段存在灌注缺损。在161个心肌节段中，16个显示为固定缺损，10个为可逆缺损，22个为矛盾缺损（反向再分布）。大多数（75%）固定灌注缺损出现在运动失调区域，而反向再分布在室壁运动正常区域占主导（82%）。可逆缺损出现在正常或轻度运动减弱区域。存在明显受损的副交感神经心脏控制，但在接受造影的16例患者中均未发现明显的冠状动脉异常。结论是，固定缺损可能对应于纤维化或坏死性病变；而可逆和矛盾灌注缺损可能由局部血流或代谢紊乱引起，可能与冠状动脉微循环的异常副交感神经控制有关。
