Predictors of left ventricular regional wall motion abnormalities after subarachnoid hemorrhage

Introduction: Cardiac abnormalities that have been reported after subarachnoid hemorrhage (SAH) include the release of cardiac biomarkers, electrocardiographic changes, and left ventricular (LV) systolic dysfunction. The mechanisms of cardiac dysfunction after SAH remain controversial. The aim of this study was to determine the prevalence of LV regional wall motion abnormalities (RWMA) after SAH and to quantify the independent effects of specific demographic and clinical variables in predicting the development of RWMA. Methods: Three hundred patients hospitalized with SAH were prospectively studied with serial echocardiography. The primary outcome measure was the presence of RWMA. The predictor variables included the admission Hunt & Hess grade, age, gender, cardiac risk factors, aneurysm location, plasma catecholamine levels, cardiac troponin I (cTi) level, heart rate (HR), blood pressure, and phenylephrine dose. Univariate and multivariate logistic regression was performed with adjustment for serial measurements, reporting odds ratios (OR) and 95% confidence intervals (CI). Results: In this study, 817 echocardiograms were analysed. RWMA were detected in 18% of those studied. The prevalence of RWMA in patients with Hunt & Hess grades 3 - 5 was 35%. Among patients with a peak cTi level greater than 1.0 m g/L, 65% had RWMA. Multivariate analysis demonstrated that high Hunt & Hess grade (OR 4.22 for grade 3 - 5 versus grade 1 - 2, p = 0.046), a cTi level greater than 1.0 μg/L (OR 10.47, p = 0.001), a history of prior cocaine or amphetamine use (OR 5.50, p = 0.037), and higher HR (OR 1.34 per 10 bpm increase, p = 0.024) were predictive of RWMA. Conclusions: RWMA were frequent after SAH. High-grade SAH, an elevation in cTi levels, a history of prior stimulant drug use, and tachycardia are independent predictors of RWMA. Copyright © 2006 Humana Press Inc. All rights of any nature whatsoever are reserved

Hypernatremia predicts adverse cardiovascular and neurological outcomes after SAH

Introduction: Abnormalities of serum sodium are common after subarachnoid hemorrhage (SAH) and have been linked to poor outcome. This study analyzed whether abnormal serum sodium levels are associated with cardiac outcomes and mortality after subarachnoid hemorrhage (SAH). Methods: In a prospective cohort study of SAH patients, the primary predictor variable was subjects\u27 sodium level. Hypernatremia was defined as sodium \u3e143 mmol/L and hyponatremia was \u3c133 mmol/L. Cardiac troponin I (cTi) was measured and echocardiography was performed on three study days. Dichotomous outcome variables were cTi \u3e 1.0 μg/L, left-ventricular ejection fraction (LVEF) \u3c50%, presence (vs absence) of regional wall motion abnormalities (RWMA) of the LV, pulmonary edema, and death. Additional analyses studied the degree of hypernatremia and sodium supplementation, and the temporal relationship between hypernatremia and cardiac outcomes. Results: The study included 214 subjects. Forty-eight subjects (22%) were hypernatremic on at least one study day, and 45 (21%) were hyponatremic. After multivariate adjustment, hypernatremia was an independent predictor of LVEF \u3c50% (OR 4.7, CI 1.3-16.2, p = 0.015), elevated cTi (OR 3.7, CI 1.2-11.9, p = 0.028), and pulmonary edema (OR 4.1 CI 1.4-1.5, p = 0.008). It was not, however a statistically significant predictor of mortality (p = 0.075). Conclusion: In the acute period after SAH, hypernatremia is associated with adverse cardiac outcomes and death. SAH patients with hypernatremia should be monitored for evidence of cardiac dysfunction. Copyright © 2006 Humana Press Inc. All rights of any nature whatsoever are reserved

Cardiac injury after subarachnoid hemorrhage is independent of the type of aneurysm therapy

OBJECTIVE: Subarachnoid hemorrhage (SAH) is associated with cardiac injury and dysfunction. Whether aneurysm clipping versus coiling has a differential effect on the risk of troponin release and left ventricular (LV) dysfunction after SAH is unknown. It is hypothesized that aneurysm treatment does not affect the risk of developing cardiac injury and dysfunction. METHODS: The study included 172 consecutive SAH patients who underwent clipping (n = 109) or coiling (n = 63) aneurysm therapy. Hemodynamic data were collected, cardiac troponin I was measured, and echocardiography was performed on the 1st, 3rd, and 6th days after enrollment. A cardiac troponin I measurement of more than 1.0 microg/L was considered abnormal. For each echocardiographic examination, a blinded observer measured LV ejection fraction (abnormal if \u3c50%) and quantified LV regional wall motion abnormalities. The incidence of cardiac outcomes in the treatment groups was compared using odds ratios (ORs). RESULTS: The coiled patients were older than the clipped patients (mean age, 59 +/- 13 yr versus 53 +/- 12 yr; t test, P \u3c 0.001) and were more likely to have posterior aneurysms (33% versus 18%; chi(2) test, P = 0.019). There were no significant between-group differences in the risk of cardiac troponin I release (coil 21% versus clip 19%; OR = 0.89, P = 0.789), regional wall motion abnormalities (33% versus 28%; OR = 0.76, P = 0.422), or LV ejection fraction lower than 50% (16% versus 17%; OR = 1.06, P = 0.892). No patient died of cardiac causes (heart failure, myocardial infarction, or arrhythmia). CONCLUSION: Surgical and endovascular aneurysm therapies were associated with similar risks of cardiac injury and dysfunction after SAH. The presence of neurocardiogenic injury should not affect aneurysm treatment decisions

Acute neurocardiogenic injury after subarachnoid hemorrhage

BACKGROUND: Left ventricular (LV) systolic dysfunction has been reported in humans with subarachnoid hemorrhage (SAH), and its underlying pathophysiology remains controversial. Possible mechanisms include myocardial ischemia versus excessive catecholamine release from sympathetic nerve terminals. METHODS AND RESULTS: For 38 months, echocardiography and myocardial scintigraphy with technetium sestamibi (MIBI) and meta-[(123)I]iodobenzylguanidine (MIBG) were performed on 42 patients admitted with SAH to assess myocardial perfusion and sympathetic innervation, respectively. A blinded observer interpreted the scintigraphic images. Cardiac troponin I (cTI) was measured to quantify the degree of myocyte necrosis. Blinded observers calculated the LV ejection fraction and graded each LV segment as normal (score=1), hypokinetic (score=2), or akinetic (score=3). A wall-motion score was calculated by averaging the sum of the 16 segments. All subjects with interpretable scans (N=41) had normal MIBI uptake. Twelve subjects had either global (n=9) or regional (n=3) absence of MIBG uptake. In comparison with patients with normal MIBG uptake, those with evidence of functional denervation were more likely to have LV regional wall-motion abnormalities (92% versus 52%, P=0.030) and cTI levels \u3e1 microg/L (58% versus 21%, P=0.029). CONCLUSIONS: LV systolic dysfunction in humans with SAH is associated with normal myocardial perfusion and abnormal sympathetic innervation. These findings may be explained by excessive release of norepinephrine from myocardial sympathetic nerves, which could damage both myocytes and nerve terminals

Plasma B-type natriuretic peptide levels are associated with early cardiac dysfunction after subarachnoid hemorrhage

Background and Purpose - Serum B-type natriuretic peptide (BNP) is elevated after subarachnoid hemorrhage (SAH), as well as in the setting of congestive heart failure and myocardial infarction. The aim of this study was to prospectively quantify the relationship between BNP levels and cardiac outcomes after SAH. Methods - Plasma was collected for BNP measurements as soon as possible after enrollment; a mean of 5±4 days after SAH symptom onset. On days 1, 3, and 6 after enrollment, troponin I (cTi) was measured and 2-dimensional echocardiography was performed. The following cardiac variables were collected and treated dichotomously: left ventricular ejection fraction (LVEF), regional wall motion abnormalities (RWMA), diastolic dysfunction, pulmonary edema, and cTi. Results - There were 57 subjects. The median BNP level was 141 pg/mL (range, 0.8 to 3330 pg/mL). Higher mean BNP levels were present in those with RWMA (550 versus 261 pg/mL; P=0.012), diastolic dysfunction (360 versus 44; P=0.011), pulmonary edema (719 versus 204; P=0.016), elevated cTi (662 versus 240; P=0.004), and LVEF \u3c50% (644 versus 281; P=0.015). Conclusion - Early after SAH, elevated BNP levels are associated with myocardial necrosis, pulmonary edema, and both systolic and diastolic dysfunction of the left ventricle. These findings support the hypothesis that the heart releases BNP into the systemic circulation early after SAH. © 2005 American Heart Association, Inc