Myocardial Injury and Left Ventricular Performance After Subarachnoid Hemorrhage

Abstract

Background and Purpose-Electrocardiographic abnormalities and elevations of the creatine kinase myocardial isoenzyme (CK-MB) occur frequently after subarachnoid hemorrhage. In some patients, a reversible and presumably neurogenic form of left ventricular dysfunction is demonstrated by echocardiography. It is not known whether cardiac injury of this type adversely affects cardiovascular hemodynamic performance. Methods-We retrospectively studied 72 patients admitted to our neuro-ICU for aneurysmal subarachnoid hemorrhage over a 2.5-year period. We selected patients who met the following criteria: (1) CK-MB levels measured within 3 days of onset, (2) pulmonary artery catheter placed, (3) echocardiogram performed, and (4) no history of preexisting cardiac disease. Hemodynamic profiles were recorded on the day after surgery (nϭ67) or on the day of echocardiography (nϭ5) if surgery was not performed (mean, 3.3Ϯ1.7 days after onset). The severity of cardiac injury was classified as none (peak CK-MB Ͻ1%, nϭ36), mild (peak CK-MB 1% to 2%, nϭ21), moderate (peak CK-MB Ͼ2%, nϭ6), or severe (abnormal left ventricular wall motion, nϭ9). Results-Abnormal left ventricular wall motion occurred exclusively in patients with peak CK-MB levels Ͼ2% (PϽ0.0001), poor neurological grade (Pϭ0.002), and female sex (Pϭ0.02). Left ventricular stroke volume index and stroke work index were elevated above the normal range in patients with peak CK-MB levels Ͻ1% and fell progressively as the severity of cardiac injury increased, with mean values for patients with abnormal wall motion below normal (both PϽ0.0001 by ANOVA). Cardiac index followed a similar trend, but the effect was less pronounced (PϽ0.0001). Using forward stepwise multiple logistic regression, we found that thick subarachnoid clot on the admission CT scan (odds ratio, 1.9; 95% confidence interval [95% CI], 1.0 to 3.4; Pϭ0.04) and depressed cardiac index (odds ratio, 2.1; 95% CI, 1.0 to 4.1; Pϭ0.04) were independent predictors of symptomatic vasospasm. Conclusions-Myocardial enzyme release and echocardiographic wall motion abnormalities are associated with impaired left ventricular performance after subarachnoid hemorrhage. In severely affected patients, reduction of cardiac output from normally elevated levels may increase the risk of cerebral ischemia related to vasospasm. (Stroke. 1999;30:780-786.)

Randomized, Double-Blind Trial of the Effect of Fluid Composition on Electrolyte, Acid–Base, and Fluid Homeostasis in Patients Early After Subarachnoid Hemorrhage

“…Myocardial dysfunction is related to the severity of subarachnoidal hemorrhage [31]. Myocardial dysfunction may have influenced renal function and water clearance in our study as well.…”

Myocardial Stunning Following Combined Modality Combretastatin‐Based Chemotherapy: Two Case Reports and Review of the Literature

“…2 Myocardial stunning is reported following subarachnoid hemorrhage. 3 A total of 95% of cases in 1 series occurred in women. 2 Another series following subarachnoid hemorrhage found that all women were postmenopausal.…”

“…2 Another series following subarachnoid hemorrhage found that all women were postmenopausal. 3 Patients present within 1 to 5 hours with chest pain or dyspnea. 2,4 Some develop pulmonary edema and cardiogenic shock.…”

Clinical Significance of Elevated Natriuretic Peptide Levels and Cardiopulmonary Parameters After Subarachnoid Hemorrhage

“…10) Various electrocardiography studies on rhythm disturbances have detected both minor abnormalities such as bradycardia, ST-T changes, and QTc prolongation, as well as less common but life-threatening arrhythmias such as ventricular tachycardia and ventricular fibrillation. 9,11) Cardiac muscle injury associated with SAH has been confirmed by histological findings of myofibrillar degeneration, myocytolysis, and inflammatory cell infiltration, 2,5) in addition to increased serum levels of myocardium-specific markers such as plasma phosphokinase myocardial fraction (CK-MB) 12) and troponin I. 26) Most patients also develop neurogenic pulmonary edema.…”