Suliman K, Flatau E, Shimoni Z, Garty I
Isr J Med Sci. 1985 May;21(5):445-50.
Two weeks following streptococcal tonsillitis two patients developed migratory arthralgia, fever and pericarditic chest pain, followed by an episode of severe coronary retrosternal pressure. The ECG during the latter episodes revealed ST elevation in the inferior wall leads, followed later by the appearance of pathological Q waves in the same leads which persisted for only a few days. Radionuclide scans and echocardiographic studies revealed localized involvement of the inferior left ventricle in both cases and, in addition, involvement of the right ventricle in have been suggested to explain the co-occurrence of viral myopericarditis and myocardial infarction (MI)-like picture during acute rheumatic fever can be explained either by coronary vasculitis resulting in myocardial ischemia, or by direct involvement of the myocardium because of an inflammatory process. Both mechanisms have been suggested to explain the co-occurrence of viral myopericarditis and myocardial necrosis. The transient Q waves were probably produced by stunning of the myocytes during the acute phase of the disease. Increased awareness will probably result in detection of similar cases and may contribute to understanding the pathogenesis of the MI-like picture of acute rheumatic fever.
链球菌性扁桃体炎发作两周后，两名患者出现游走性关节痛、发热和心包性胸痛，随后出现严重的冠状动脉胸骨后压榨感。在后一阶段发作期间，心电图显示下壁导联ST段抬高，随后同一导联出现病理性Q波，仅持续数天。放射性核素扫描和超声心动图研究显示，两例患者均为左心室下壁局部受累，此外，一例患者右心室也受累。有人提出，急性风湿热期间病毒感染性心肌心包炎与心肌梗死（MI）样表现同时出现，可通过导致心肌缺血的冠状动脉血管炎来解释，也可通过炎症过程直接累及心肌来解释。这两种机制都被认为可以解释病毒感染性心肌心包炎和心肌坏死的同时出现。短暂的Q波可能是在疾病急性期心肌细胞顿抑产生的。提高认识可能会发现类似病例，并有助于理解急性风湿热MI样表现的发病机制。
