Significantly higher values of cardiac biomarkers were observed in SAH patients complicated with NPE. Elevated values of cardiac biomarkers appear to play an active role in prediction of NPE, although white blood cell count may be involved in the prediction of NPE. There is an influence of SAH therapy on predictors of NPE.
Background. Mortality rates following aneurysmal subarachnoid haemorrhage (aSAH) have decreased due to improvements in diagnoses and the management of complications, as well as early obliteration of the aneurysms. Neurogenic pulmonary oedema (NPO) is a clinical syndrome associated with an acute increase in intracranial pressure and a release of catecholamines into the circulation. This study investigated independent predictors of unfavourable outcomes (Glasgow Outcome Scores 1, 2 or 3) in patients with aSAH.
Materials and methods.A total of 262 patients with aSAH (162 females) were included in this prospective study. Clinical characteristics were assessed, and electrocardiographic, serum cardiac and inflammatory biomarker measurements were recorded on admission. Outcomes were assessed three months after admission. Univariate and multivariate analyses of these data were used to predict unfavourable outcomes.
Results.A total of 156 patients (59.54%) had unfavourable outcomes. Compared to those who had favourable outcomes, patients with unfavourable outcomes were significantly older (54.37 ± 10.56 vs. 49.13 ± 10.77 years; p < 0.001) and had more severe aSAHs (Hunt and Hess grades ≥ 3: 82.7% vs. 39.6%; p < 0.001). Patients with unfavourable outcomes were more likely to have NPO (10.3% vs. 2.8%; p = 0.023), hydrocephalus (34.0% vs. 20.8%; p = 0.02), and aneurysm reruptures (28.2% vs. 3.8%; p < 0.001). Independent predictors of an unfavourable outcome included Hunt and Hess grades ≥ 3 (odds ratio [OR], 4.291; 95% confidence interval [CI], 2.168-8.491; p < 0.001), increased systolic blood pressure on admission (OR, 1.020; 95% CI, 1.002-1.038; p = 0.03), increased heart rate (HR) on admission (OR, 1.024; 95% CI, 1.001-1.048; p = 0.04), and aneurysm rerupture (OR, 4.961; 95% CI,; p = 0.01).Conclusions. These findings suggest that aneurysm reruptures, as well as increased blood pressure and HR, are associated with unfavourable outcomes in patients with aSAH.
Introduction. Subarachnoid haemorrhage (SAH) can be followed by cardiac abnormalities. We describe a patient with Takotsubo cardiomyopathy and neurogenic pulmonary edema (NPE) after aneurysmal SAH. Case report. A previously healthy, postmenopausal woman, suffered from aneurysmal SAH with consequent hydrocephalus. After external ventricular drainage, craniotomy and clipping of the posterior inferior cerebellar artery aneurysm, the patient developed acute heart failure and NPE. Transthoracic echocardiogram showed the left ventricular apical ballooning and hypercontractile basal segments. On chest radiography, bilateral pulmonary infiltrates were seen. Seventeen days after the SAH attack, the patient was discharged from hospital. Postponed coronary angiography revealed no signs of coronary artery disease. Conclusion. This case and review of the relevant literature suggest that Takotsubo cardiomyopathy and neurogenic pulmonary edema are not uncommon after aneurysmal SAH.
SumarryIntroduction: Neurogenic pulmonary edema (NPE) is a clinical syndrome characterized by the acute onset of pulmonary edema after sudden raise of intracranial pressure. NPE is the result of release of catecholamines into the circulation immediately after intracranial hemorrhage. The aim of this study is to investigate a possible correlation between the values of cardiac biomarkers on admission and incidence of NPE in patients with aneurysmal subarachnoid hemorrhage (SAH). Methods: Prospective study includes 262 patients with SAH (162 females). Clinical characteristics, serum cardiac and inflammatory biomarkers were measured on admission and on the day of development of NPE. These data were analysed by tests of statistical significance and binary logistic regression analysis in order to predict the development of NPE. Results: 19 patients (7.25%) developed NPE. Statistical analysis revealed that patients who subsequently developed NPE experienced more severe SAH. Cardiac damage was more severe in these patients, as represented by significantly higher number of patients with elevated values of all examined cardiac biomarkers (P from < 0.001 to 0.004). Multivariate regression analysis revealed that elevated troponin I (OR 4.980; P = 0.021) and white blood cells count (OR 22.195; P < 0.001) were predictors of NPE. Conclusion: Significantly higher number of patients with elevated values of cardiac biomarkers had SAH complicated with NPE. Elevated values of cardiac biomarkers might play an active role in prediction of NPE, although white blood cells count may be involved in the prediction of NPE.
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