THE CARDIAC CONSEQUENCES OF HEMISPHERIC STROKE

自1995年11月17日以来，我们已经招募了70名患者参加正在进行的 学习。这个特定的项目涉及识别 卒中对心脏结局的影响。患者已在 术后1个月、3个月、9个月和12个月 中风，这使得他们有必要在Osler 5号进入GCRC。 入院后，他们将接受全面的临床心脏病学和神经病学检查。 再加上神经学评分，胸部X光，心电图， 较晚的潜在评估，以及带有特殊 构建了为评估收集一小时数据的平台 心率、血压和呼吸变异性。此外，a 一些生化和血液流变学的评估是在这些 病人。到目前为止，我们的流失率约为16%，这意味着 所有登记的患者中有16%已经从研究中失去了。它 是这项研究的统计设计的一个基本特征，我们 不要询问我们的终点，因为它与心脏病的结果相关 中风的位置，直到研究结束，这将是在四个 好几年了。然而，我们正在查询数据库中的其他中风 相关数据。例如，我们已经确定大约15%-20% 我们那些被认为患有腔隙性脑梗塞的患者 高血压，有显著的潜在结构性心脏病 这表明这就是他们缺憾的原因。原则： 图示左心房内有新鲜的、可移动的血栓。 附属物。这些数据目前正在进行评估，以便在 随后的临床会议。此外，我们还发现了一种新的 这种现象我们称之为“神经源性顿抑心肌”。 这些患者也没有冠状动脉疾病的证据。 根据临床检查或病史或腺苷铊扫描； 然而，他们有局灶性或全局性运动障碍的证据 不能简单地根据潜在的冠状动脉来解释 疾病或糖尿病。这些数据将在即将到来的 美国心脏协会关于卒中和中风的国际联合会议 1997年2月的《脑循环》。这一现象很重要 因为这表明大脑和心脏之间可能存在某种联系 而不是通过影响冠状动脉循环。因此，它同意 与我们之前的动物实验工作表明，损伤在 大脑的某些部分可能会改变心脏自主神经平衡， 将其转向更具同情心的驱动力。这增加了 交感神经输出会直接导致心肌损伤， 结构受损，伸缩性降低。我们也在监视CPK- 这些患者体内的MB水平，看看是否有具体的证据表明 对心脏肌肉系统的损伤。

Since November 17, 1995, we have recruited 70 patients into our ongoing study. This particular project is concerned with identifying the influence of stroke on cardiac outcome. Patients have been assessed at one month, three months, nine months and twelve months following their stroke and this has necessitated their admission to the GCRC on Osler 5. When admitted, they receive a full clinical cardiological and neurological assessment together with a neurological score, a chest x-ray, an ECG, late potential evaluations, as well as assessment with a specially constructed platform which accrues one hour of data for assessment of heart rate, blood pressure and respiratory variability. In addition, a number of biochemical and hemorheological assessments are made in these patients. To date, we have an approximately 16% attrition rate, meaning that 16% of all the enrolled patients have been lost from the study. It is a fundamental feature of the statistical design of this study that we do not interrogate our endpoints which correlate cardiological outcomes with stroke location until the end of the study, which will be in four years time. However, we are interrogating the database for other stroke related data. For example, we have identified that approximately 15-20% of our patients who were thought to have lacunar infarctions on the basis of hypertension, have significant underlying structural cardiac disease suggesting that this is the etiology of their lacune. Principle amongst these is the presence of a fresh, mobile clot in the left atrial appendage. These data are being evaluated currently for communication at a subsequent clinical meeting. In addition, we have identified a new phenomenon which we have termed "the neurogenic stunned myocardium". These are patients who have no evidence of coronary artery disease, either from clinical examination or on history or on adenosine thallium scanning; however, they have evidence of either focal or global dyskinesias which cannot be explained easily on the basis of underlying coronary artery disease or diabetes. These data will be communicated at the forthcoming American Heart Association International Joint Conference on Stroke and Cerebral Circulation in February 1997. This phenomenon is important because it indicates a possible connection between the brain and the heart other than by influencing the coronary circulation. As such, it agrees with our previous animal experimental work which suggests that lesions in certain parts of the brain may alter cardiac autonomic balance, shifting it towards increased sympathetic drive. This increased sympathetic output can directly result in damage to the myocardium, structural damage, and reduced contractility. We are also monitoring CPK- MB levels in these patients to see whether there is specific evidence for damage to the cardiac musculature.