Polski merkuriusz lekarski : organ Polskiego Towarzystwa Lekarskiego · 2020
Takotsubo syndrome after nimodipine-induced hypotension treated with norepinephrine in a female with subarachnoid hemorrhage.
Клинический случайСтатьяНазвание и аннотация: Перевод в очереди
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Elikowski Waldemar, Małek-Elikowska MaŁgorzata, Piestrzeniewicz Rafał, Fertała Natalia, Zawodna Magdalena, Ganowicz-Kaatz Teresa, Baszko Alina, Smól Sławomir
Аннотация
UNLABELLED: The prevalence of takotsubo syndrome (TTS) in patients with subarachnoid hemorrhage (SAH) is much higher than in the general population. Clinical and experimental observations confirm secondary to brain damage catecholamine-mediated cardiac injury resulting in reversible left ventricular (LV) dysfunction. However, other triggers can also be involved in TTS development e.g. manipulations during surgical or endovascular treatment of a bleeding intracranial aneurysm, concomitant hyponatremia or infection, intubation, blood transfusion and pharmacologic treatment. Nimodipine is recommended in SAH to prevent cerebral arteries vasospasm but can cause hypotension, so vasopressors, e.g. norepinephrine (NE) are commonly used to reach target blood pressure.
A CASE REPORT: The authors present a case of a 72-year-old woman with SAH in whom the disease began with a headache, syncope, decreased level of consciousness and vomiting; there were no cardiac symptoms at admission. Endovascular coiling of internal carotid artery aneurysm was performed. On day 2, she developed TTS presenting in echocardiography as apical ballooning; immediately before TTS onset, NE was started to treat nimodipine-induced hypotension. Despite severe heart failure (HF), the patient's neurological status did not deteriorate. HF symptoms remitted after a few days and LV function returned to normal after a week. Negative T waves in ECG which appeared at TTS onset disappeared after 50 days. At that moment no neurological deficits were observed.
CONCLUSIONS: The authors underline that in SAH patients nimodipine administration should be cautious to avoid an excessive blood pressure decrease especially in view of further catecholamines use.
A CASE REPORT: The authors present a case of a 72-year-old woman with SAH in whom the disease began with a headache, syncope, decreased level of consciousness and vomiting; there were no cardiac symptoms at admission. Endovascular coiling of internal carotid artery aneurysm was performed. On day 2, she developed TTS presenting in echocardiography as apical ballooning; immediately before TTS onset, NE was started to treat nimodipine-induced hypotension. Despite severe heart failure (HF), the patient's neurological status did not deteriorate. HF symptoms remitted after a few days and LV function returned to normal after a week. Negative T waves in ECG which appeared at TTS onset disappeared after 50 days. At that moment no neurological deficits were observed.
CONCLUSIONS: The authors underline that in SAH patients nimodipine administration should be cautious to avoid an excessive blood pressure decrease especially in view of further catecholamines use.