THE CARDIAC CONSEQUENCES OF HEMISPHERIC STROKE

自1995年11月17日以来，我们招募了70名患者参加我们正在进行的 study. 这个特别的项目涉及到识别 卒中对心脏预后影响。 患者已在 一个月，三个月，九个月和十二个月后，他们的 中风，这使他们有必要在奥斯勒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， 评估连同神经学评分、胸部X光、ECG， 延迟的潜在评价，以及具有特别 构建的平台，积累一个小时的数据，用于评估 心率血压和呼吸变异性。 另外还有按 许多生化和血液流变学评估是在这些 患者 到目前为止，我们有大约16%的流失率，这意味着 16%的入选患者已经从研究中消失。 它 是本研究统计设计的一个基本特征， 不询问与心脏结局相关的终点 中风的位置，直到研究结束，这将是在四个 年的时间。 但是，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% 我们的患者被认为有腔隙性脑梗死， 高血压，有明显的潜在结构性心脏病 提示这是其腔隙的病因。 原则中 左心房内存在新鲜的移动的凝块 附属物 目前正在评估这些数据，以便在 随后的临床会议。 此外，我们还发现了一种新的 我们称之为“神经源性顿抑心肌”。 这些患者也没有冠心病的证据 临床检查或病史或腺苷铊扫描; 然而，他们有证据表明局部或整体运动障碍， 不能根据潜在冠状动脉轻易解释 疾病或糖尿病。 这些数据将在即将举行的 美国心脏协会国际中风联合会议， 1997年2月，脑循环。 这个现象很重要 因为这表明大脑和心脏之间可能存在联系 而不是通过影响冠状动脉循环。 因此，它同意 我们之前的动物实验工作表明， 大脑的某些部分可以改变心脏自主平衡， 将其转向增强的交感冲动 这种增加的 交感神经输出可直接导致心肌损伤， 结构性损伤和收缩性降低。 我们也在监视CPK- 这些患者的MB水平，看看是否有具体的证据， 心脏肌肉组织受损

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.