Tung Poyee, Kopelnik Alexander, Banki Nader, Ong Ken, Ko Nerissa, Lawton Michael T, Gress Daryl, Drew Barbara, Foster Elyse, Parmley William, Zaroff Jonathan
Division of Cardiology, UCSF Medical Center, USA.
Stroke. 2004 Feb;35(2):548-51. doi: 10.1161/01.STR.0000114874.96688.54. Epub 2004 Jan 22.
Subarachnoid hemorrhage (SAH) frequently results in myocardial necrosis with release of cardiac enzymes. Historically, this necrosis has been attributed to coronary artery disease, coronary vasospasm, or oxygen supply-demand mismatch. Experimental evidence, however, indicates that excessive release of norepinephrine from the myocardial sympathetic nerves is the most likely cause. We hypothesized that myocardial necrosis after SAH is a neurally mediated process that is dependent on the severity of neurological injury.
Consecutive patients admitted with SAH were enrolled prospectively. Predictor variables reflecting demographic (age, sex, body surface area), hemodynamic (heart rate, systolic blood pressure), treatment (phenylephrine dose), and neurological (Hunt-Hess score) factors were recorded. Serial cardiac troponin I measurements and echocardiography were performed on days 1, 3, and 6 after enrollment. Troponin level was treated as a dichotomous outcome variable. We performed univariate and multivariate analyses on the relationships between the predictor variables and troponin level.
The study included 223 patients with an average age of 54 years. Twenty percent of the subjects had troponin I levels >1.0 microg/L (range, 0.3 to 50 microg/L). By multivariate logistic regression, a Hunt-Hess score >2, female sex, larger body surface area and left ventricular mass, lower systolic blood pressure, and higher heart rate and phenylephrine dose were independent predictors of troponin elevation.
The degree of neurological injury as measured by the Hunt-Hess grade is a strong, independent predictor of myocardial necrosis after SAH. This finding supports the hypothesis that cardiac injury after SAH is a neurally mediated process.
蛛网膜下腔出血（SAH）常导致心肌坏死并伴有心肌酶释放。过去，这种坏死被归因于冠状动脉疾病、冠状动脉痉挛或氧供需不匹配。然而，实验证据表明，心肌交感神经去甲肾上腺素的过度释放是最可能的原因。我们推测SAH后的心肌坏死是一个神经介导的过程，取决于神经损伤的严重程度。
前瞻性纳入连续收治的SAH患者。记录反映人口统计学（年龄、性别、体表面积）、血流动力学（心率、收缩压）、治疗（去氧肾上腺素剂量）和神经学（Hunt-Hess评分）因素的预测变量。在入组后的第1、3和6天进行连续心肌肌钙蛋白I测量和超声心动图检查。肌钙蛋白水平被视为二分结局变量。我们对预测变量与肌钙蛋白水平之间的关系进行了单变量和多变量分析。
该研究纳入了223例平均年龄为54岁的患者。20%的受试者肌钙蛋白I水平>1.0μg/L（范围为0.3至50μg/L）。通过多变量逻辑回归分析，Hunt-Hess评分>2、女性、较大的体表面积和左心室质量、较低的收缩压以及较高的心率和去氧肾上腺素剂量是肌钙蛋白升高的独立预测因素。
以Hunt-Hess分级衡量的神经损伤程度是SAH后心肌坏死的一个强有力的独立预测因素。这一发现支持了SAH后心脏损伤是一个神经介导过程的假说。
