Role of Nimodipine and Milrinone in Delayed Cerebral Ischemia

Kotwal, Abhishek; Ramalingaiah, Arvinda Hanumanthapura; Shukla, Dhaval; Radhakrishnan, Muthuchellappan; Konar, Subhas; Bharath, S; Chakrabarti, Dhritiman; Sundaram, Mouleeswaran

doi:10.1016/j.wneu.2022.06.150

Cited by 3 publications

(2 citation statements)

References 27 publications

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“…Another study, involving 13 patients, reported a decrease in V mean among those receiving IV milrinone. The effects of induced hypertension were not studied (11). As compared with these previous studies, the present one has strengths: 1) the delineation, in the same population, of the respective effects of induced hypertension and its combination with IV milrinone via an a priori defined stepwise implementation of these therapies, 2) the indexation of V mean to MBP or CO to assess V mean changes regardless of these parameters.…”

Section: Discussionmentioning

confidence: 99%

Cerebral Vasospasm After Subarachnoid Hemorrhage: Respective Short-Term Effects of Induced Arterial Hypertension and its Combination With IV Milrinone: A Proof-of-Concept Study Using Transcranial Doppler Ultrasound

Lakhal,

Fresco,

Hivert

et al. 2023

Critical Care Explorations

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OBJECTIVES: It is unclear whether IV milrinone relaxes spasmed cerebral arteries and therefore reduces cerebral blood mean velocity (Vmean). In patients treated for cerebral vasospasm, we aimed to assess and delineate the respective impacts of induced hypertension and its combination with IV milrinone on cerebral hemodynamics as assessed with transcranial Doppler. DESIGN: Observational proof-of-concept prospective study. SETTING: ICU in a French tertiary care center. PATIENTS: Patients with aneurysmal subarachnoid hemorrhage who received induced hypertension (mean arterial blood pressure [MBP] of 100–120 mm Hg) and IV milrinone (0.5 µg/kg/min) for moderate-to-severe cerebral vasospasm. We excluded patients who underwent invasive angioplasty or milrinone discontinuation within 12 hours after the diagnosis of vasospasm. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Vmean was measured at vasospasm diagnosis (TDIAGNOSIS), after the induction of hypertension (THTN), and 1 (THTN+MILRINONE_H1) and 12 hours after the adjunction of IV milrinone (THTN+MILRINONE_H12). Thirteen patients were included. Median Vmean was significantly lower (p < 0.01) at THTN+MILRINONE_H1 (99 [interquartile range (IQR) 89; 134] cm.s−1) and THTN+MILRINONE_H12 (85 [IQR 73–127] cm/s) than at TDIAGNOSIS (136 [IQR 115–164] cm/s) and THTN (148 [IQR 115–183] cm/s), whereas TDIAGNOSIS and THTN did not significantly differ. In all patients but one, Vmean at THTN+MILRINONE_H1 was lower than its value at TDIAGNOSIS (p = 0.0005). Vmean-to-MBP and Vmean-to-cardiac output (CO) ratios (an assessment of Vmean regardless of the level of MBP [n = 13] or CO [n = 7], respectively) were, respectively, similar at TDIAGNOSIS and THTN but were significantly lower after the adjunction of milrinone (p < 0.01). CONCLUSIONS: The induction of arterial hypertension was not associated with a significant decrease in Vmean, whereas the adjunction of IV milrinone was, regardless of the level of MBP or CO. This suggests that IV milrinone may succeed in relaxing spasmed arteries.

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Section: Discussionmentioning

confidence: 99%

Cerebral Vasospasm After Subarachnoid Hemorrhage: Respective Short-Term Effects of Induced Arterial Hypertension and its Combination With IV Milrinone: A Proof-of-Concept Study Using Transcranial Doppler Ultrasound

Lakhal,

Fresco,

Hivert

et al. 2023

Critical Care Explorations

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“…Nimodipine, the VGCC, was used to delay brain damage in early cerebral ischemia. It is found that nimodipine injection via intra-arterial administration protects the brain from cerebral ischemic injury after aneurysmal subarachnoid hemorrhage [ 90 ]. Treated with icaritin (ICT), the natural compound extracted from traditional Chinese herb ( Epimedium Genus ), can protect neuronal cell from glutamate-induced neuronal cell damage by inhibiting DAPK1 and GluN2B activation with promoting phosphorylation of ERK and GluN2A expression, which reduce neuronal cell death in ischemic rats [ 91 ].…”

Section: Reviewmentioning

confidence: 99%

The underlying mechanism of calcium toxicity-induced autophagic cell death and lysosomal degradation in early stage of cerebral ischemia

Sengking,

Mahakkanukrauh

2024

Anat Cell Biol

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Cerebral ischemia is the important cause of worldwide disability and mortality, that is one of the obstruction of blood vessels supplying to the brain. In early stage, glutamate excitotoxicity and high level of intracellular calcium (Ca 2+ ) are the major processes which can promote many downstream signaling involving in neuronal death and brain tissue damaging. Moreover, autophagy, the reusing of damaged cell organelles, is affected in early ischemia. Under ischemic conditions, autophagy plays an important role to maintain energy of the brain and its function. In the other hand, over intracellular Ca 2+ accumulation triggers excessive autophagic process and lysosomal degradation leading to autophagic process impairment which finally induce neuronal death. This article reviews the association between intracellular Ca 2+ and autophagic process in acute stage of ischemic stroke.

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Is Stent Retraction to ReLieve Arterial Cerebral VaSospasm Caused by SAH (Stent-ReLACSS) Using PRELAX the Long-awaited Solution for Treatment of Posthemorrhagic Cerebral Vasospasm?

Khanafer,

von Gottberg,

Albiña-Palmarola

et al. 2024

Clin Neuroradiol

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Purpose Recent observational studies have indicated the efficacy of stent retriever devices for the treatment of posthemorrhagic cerebral vasospasm (CVS), both by deployment and on-site withdrawal into the microcatheter (stent angioplasty, SA) and deployment followed by retraction through the target vessel similar to thrombectomy (StentRetraction to reLieve Arterial Cerebral vaSospasm caused by SAH, Stent-ReLACSS). This article reports the findings with each application of pRESET and pRELAX in the treatment of CVS. Methods We retrospectively enrolled 25 patients with severe CVS following aneurysmal subarachnoid hemorrhage. For the SA group, a stent retriever or a pRELAX was temporarily deployed into a narrow vessel segment and retrieved into the microcatheter after 3 min. For the Stent-ReLACSS group, a pRELAX was temporarily deployed into a narrow vessel and pulled back unfolded into the internal carotid artery. If intra-arterial vasodilators were administered, they were given exclusively after mechanical vasospasmolysis to maximize the effectiveness of the stent treatment. Results In this study fifteen patients and 49 vessels were treated with SA. All were technically successful without periprocedural complications; however, 8/15 patients (53.3%) required additional treatment of the CVS. A total of 10 patients and 23 vessel segments were treated with Stent-ReLACSS. All maneuvers were technically successful without periprocedural complications and all vessels showed significant angiographic improvement. No recurrent CVS requiring further endovascular treatment occurred in-hospital, and neither territorial ischemia in the treated vessels nor vascular injury were observed in follow-up angiography. Conclusion Based on the presented data it appears that Stent-ReLACSS with pRELAX does not pose any additional risks when used to treat CVS and might be superior to SA, especially concerning mid-term and long-term efficacy. The mechanism of action may be an effect on the endothelium rather than mechanical vasodilation. As many patients with CVS are diagnosed too late, prophylactic treatment of high-risk patients (e.g., poor grade, young, female) is potentially viable.

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Role of Nimodipine and Milrinone in Delayed Cerebral Ischemia

Cited by 3 publications

References 27 publications

Cerebral Vasospasm After Subarachnoid Hemorrhage: Respective Short-Term Effects of Induced Arterial Hypertension and its Combination With IV Milrinone: A Proof-of-Concept Study Using Transcranial Doppler Ultrasound

Cerebral Vasospasm After Subarachnoid Hemorrhage: Respective Short-Term Effects of Induced Arterial Hypertension and its Combination With IV Milrinone: A Proof-of-Concept Study Using Transcranial Doppler Ultrasound

The underlying mechanism of calcium toxicity-induced autophagic cell death and lysosomal degradation in early stage of cerebral ischemia

Is Stent Retraction to ReLieve Arterial Cerebral VaSospasm Caused by SAH (Stent-ReLACSS) Using PRELAX the Long-awaited Solution for Treatment of Posthemorrhagic Cerebral Vasospasm?

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