1.
Use of levosimendan in the treatment of cerebral vascular vasospasm: a case study.
Onichimowski, D, Nosek, K, Goraj, R, Jalali, R, WiĆska, A, Pawlos, A, Tuyakov, B
Drug design, development and therapy. 2018;:1777-1783
Abstract
Despite the progress in the management of cerebral arterial aneurysms, subarachnoid hemorrhage (SAH) remains the major cause of neurological disability. While SAH-related deaths usually occur as a result of brain impairment due to hemorrhage, permanent neurological deficits are caused by cerebral ischemia due to edema and spasm of cerebral arteries. Additionally, ~20%-30% of patients with SAH develop secondary cardiomyopathy; this phenomenon is known as neurogenic stress cardiomyopathy (NSC), which is associated with increased mortality and poor long-term prognosis. Levosimendan is a new inotropic drug that causes calcium sensitization of troponin C, thus increasing contraction force of myofilaments. The drug also causes opening of ATP-dependent potassium channels in vascular smooth muscles, which results in dilatation of veins and arteries, including cerebral arteries. To date, there have been several reports of levosimendan application in patients with SAH and neurogenic stress cardiomyopathy, and the effect of the drug on vasospasm has been previously advocated. This paper presents a case report of a 57-year-old patient with massive SAH, where levosimendan was used for reducing vasospasm.
2.
Reversible cerebral vasoconstriction syndrome.
Yancy, H, Lee-Iannotti, JK, Schwedt, TJ, Dodick, DW
Headache. 2013;(3):570-6
Abstract
Reversible cerebral vasoconstriction syndrome (RCVS) is a cerebrovascular disorder with a clinical picture that continues to be refined. It has presented to multiple subspecialties over the past several decades, bringing with it many questions regarding risk factors, diagnosis, and management. Answers have been forthcoming but many questions remain. RCVS presents with recurrent, secondary thunderclap headaches and predominantly affects young women. The mechanism of vasoconstriction is unclear, but there has been speculation regarding a hyperadrenergic state. Diagnosis requires physician awareness, vascular imaging, and knowledge of the differential. The hallmark of its diagnosis is reversibility. Management is empiric, usually with calcium-channel blockers, as there are no controlled treatment trials for RCVS. Randomized controlled trials are needed.