Takotsubo cardiomyopathy in aneurysmal subarachnoid hemorrhage: A case report

Milakovic, Branko; Nastasovic, Tijana; Lepić, Milan; Novaković, Nenad; Matić, Siniša; Savić, Andrija; Rasulic, Lukas

doi:10.2298/vsp170705179m

Cited by 3 publications

(3 citation statements)

References 43 publications

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“…Previous studies have also described electrocardiographic abnormalities and myocardial enzyme release in patients with aSAH [3,29,39], but the effect of cardiac dysfunction on aSAH outcome remains unclear. Serum cardiac biomarkers have been used to predict negative outcomes [21,22,25,43,44,46]. In our study, only mean CPK-MB levels were significantly increased in patients with unfavourable outcomes.…”

Section: Discussionmentioning

confidence: 60%

Predictors of unfavourable outcome in aneurysmal subarachnoid haemorrhage

Nastasovic

Milakovic

Stosic

et al. 2019

Neurol Neurochir Pol.

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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.

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Section: Discussionmentioning

confidence: 60%

Predictors of unfavourable outcome in aneurysmal subarachnoid haemorrhage

Nastasovic

Milakovic

Stosic

et al. 2019

Neurol Neurochir Pol.

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“…Nonetheless, the most frequent triggers are brain- In large series of TTS due to SAB, however, NPE has not been described [93,94]. NOP, number of patients; ns, not specified; NPE, neurogenic pulmonary edema; AVM, arterio-venous malformation; SAB, subarachnoid bleeding; TTS, Takotsubo syndrome.…”

Section: Discussionmentioning

confidence: 99%

Neurological Perspectives of Neurogenic Pulmonary Edema

Finsterer¹

2019

Eur Neurol

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Background: Neurogenic pulmonary edema (NPE) is characterized by acute respiratory distress triggered by acute, severe compromise of the central nervous system (CNS). This review aims at summarizing and discussing recent and previous findings about the type and frequency of CNS triggers of NPE, pathogenesis, diagnosis, treatment, and outcome of patients experiencing NPE. Key Messages: NPE is diagnosed in the presence of pink, frothy sputum, pulmonary edema, bilateral opacities on X-ray, PaO2:PiO2 <200 mm Hg, acute CNS compromise with increased intra-cranial pressure, rapid resolution within 48–72 h, and the absence of alternative causes of respiratory distress. The most common cerebral triggers of NPE include enterovirus-71-associated brainstem encephalitis, subarachnoid bleeding, intracerebral bleeding, traumatic brain injury, epilepsy, ischemic stroke, intracranial/spinal surgery, multiple sclerosis, electroconvulsive therapy, subdural/epidural hematoma, intoxication, hypoxia, and hydrocephalus. Simultaneous treatment of CNS and pulmonary compromise is required. Cerebral treatment involves infectiologists, neurologists, and neurosurgeons. Pulmonary treatment is mainly supportive, but if ineffective, extracorporeal membrane oxygenation or thermodilution are alternative options. Applying intensive care measures, the outcome of NPE has improved. Summary: CNS-disease triggering NPE is more variegated than anticipated. Delineation of NPE from other pulmonary or cardiac conditions mimicking NPE is crucial to take appropriate measures and improve the outcome of these patients.

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“…First, we had no possibility to use transthoracic echocardiography (TTE) examination of the heart structure and function. This could enable to assess role of the heart dysfunction in pathophysiology of NPE 23 . Zaroff et al 10 found that the great majority of patients with NPE were complicated by concomitant wall motion abnormality.…”

Section: Discussionmentioning

confidence: 99%

How to predict neurogenic pulmonary edema in aneurysmal subarachnoid hemorrhage?: Neurogenic pulmonary edema in aneurysmal SAH

Nastasovic¹,

Milakovic²,

Stosic³

et al. 2019

Serb J Anest Inten Therapy

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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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Takotsubo cardiomyopathy in aneurysmal subarachnoid hemorrhage: A case report

Cited by 3 publications

References 43 publications

Predictors of unfavourable outcome in aneurysmal subarachnoid haemorrhage

Predictors of unfavourable outcome in aneurysmal subarachnoid haemorrhage

Neurological Perspectives of Neurogenic Pulmonary Edema

How to predict neurogenic pulmonary edema in aneurysmal subarachnoid hemorrhage?: Neurogenic pulmonary edema in aneurysmal SAH

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