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      Left Ventricular Outflow Tract Obstruction in Patients Treated With Milrinone for Cerebral Vasospasm: Case Report and Literature Review

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          Abstract

          Subarachnoid hemorrhage is associated with high morbidity and mortality, and cerebral arterial vasospasm is one of its main complications that determines neurological prognosis. The use of intravenous milrinone is becoming more common in the treatment of vasospasm. This molecule has positive inotropic and vasodilating properties by inhibiting phosphodiesterase-3. Its most described side effects are cardiac arrhythmias and arterial hypotension. In this paper, we raise a new issue concerning milrinone and discuss an undescribed side effect of this treatment, left ventricular outflow tract obstruction (LVOTO). Dynamic LVOTO is a clinical situation favored by hypovolemia, decreased left ventricular afterload, and excessive inotropism that can lead to severe hemodynamic failure and pulmonary edema. To our knowledge, this is the first study describing milrinone-induced LVOTO. This could compromise cerebral perfusion and therefore the neurological prognosis of patients. While it is known that catecholamines may induce LVOTO, milrinone-induced LVOTO appears to be a new pathophysiological entity of which neurosurgical intensivists should be aware.

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          Most cited references30

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          Stroke epidemiology: a review of population-based studies of incidence, prevalence, and case-fatality in the late 20th century

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            Hypertrophic cardiomyopathy phenotype revisited after 50 years with cardiovascular magnetic resonance.

            Our purpose was to characterize the pattern and distribution of left ventricular (LV) hypertrophy by cardiovascular magnetic resonance (CMR) to more precisely define phenotypic expression and its clinical implications in hypertrophic cardiomyopathy (HCM). Based on prior pathologic and 2-dimensional echocardiographic studies, HCM has been regarded as a disease characterized by substantial LV wall thickening. Cine and late gadolinium enhancement CMR were performed in 333 consecutive HCM patients (age 43 +/- 17 years). Basal anterior LV free wall and the contiguous anterior ventricular septum were the most commonly hypertrophied segments (n = 256; 77%). LV hypertrophy was focal (involving or = 8 segments [> or = 50% of LV]) in 180 patients (54%); 42 patients (13%) showed hypertrophied segments separated by regions of normal thickness. The number of hypertrophied segments was greater in patients with LV outflow tract obstruction (> or = 30 mm Hg) than without (10 +/- 4 vs. 8 +/- 4 per patient; p = 0.0001) and was associated with an advanced New York Heart Association functional class (p = 0.007). LV wall thickness was greater in segments with late gadolinium enhancement than without (20 +/- 6 mm vs. 16 +/- 6 mm; p < 0.001). We also identified 40 (12%) of HCM patients with segmental LV hypertrophy largely confined to the anterolateral free wall, posterior septum, or apex, which was underestimated or undetected by echocardiography. Although diverse, patterns of LV hypertrophy are usually not extensive in HCM, involving < or = 50% of the chamber in about one-half the patients, and are particularly limited in extent in an important minority. Contiguous portions of anterior free wall and septum constituted the predominant region of wall thickening, with implications for clinical diagnosis. These observations support an emerging role for CMR in the contemporary evaluation of patients with HCM.
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              Clinical review: Prevention and therapy of vasospasm in subarachnoid hemorrhage

              Vasospasm is one of the leading causes of morbidity and mortality following aneurysmal subarachnoid hemorrhage (SAH). Radiographic vasospasm usually develops between 5 and 15 days after the initial hemorrhage, and is associated with clinically apparent delayed ischemic neurological deficits (DID) in one-third of patients. The pathophysiology of this reversible vasculopathy is not fully understood but appears to involve structural changes and biochemical alterations at the levels of the vascular endothelium and smooth muscle cells. Blood in the subarachnoid space is believed to trigger these changes. In addition, cerebral perfusion may be concurrently impaired by hypovolemia and impaired cerebral autoregulatory function. The combined effects of these processes can lead to reduction in cerebral blood flow so severe as to cause ischemia leading to infarction. Diagnosis is made by some combination of clinical, cerebral angiographic, and transcranial doppler ultrasonographic factors. Nimodipine, a calcium channel antagonist, is so far the only available therapy with proven benefit for reducing the impact of DID. Aggressive therapy combining hemodynamic augmentation, transluminal balloon angioplasty, and intra-arterial infusion of vasodilator drugs is, to varying degrees, usually implemented. A panoply of drugs, with different mechanisms of action, has been studied in SAH related vasospasm. Currently, the most promising are magnesium sulfate, 3-hydroxy-3-methylglutaryl-CoA reductase inhibitors, nitric oxide donors and endothelin-1 antagonists. This paper reviews established and emerging therapies for vasospasm.

                Author and article information

                Contributors
                Journal
                JMIRx Med
                JMIRx Med
                JMIRxMed
                Jmirx Med
                JMIR Publications (Toronto, Canada )
                2563-6316
                Apr-Jun 2022
                11 April 2022
                : 3
                : 2
                : e31019
                Affiliations
                [1 ] Anesthesia and Intensive Care Department Rouen University Hospital Rouen France
                [2 ] Intensive Care Unit Elbeuf General Hospital Elbeuf France
                [3 ] Cardiology Department Rouen University Hospital Rouen France
                Author notes
                Corresponding Author: Charles Baulier charles.baulier@ 123456gmail.com
                Author information
                https://orcid.org/0000-0003-1817-5055
                https://orcid.org/0000-0002-4384-7522
                https://orcid.org/0000-0003-0029-9586
                https://orcid.org/0000-0001-8407-8793
                https://orcid.org/0000-0002-0014-7518
                https://orcid.org/0000-0002-4990-1438
                https://orcid.org/0000-0001-8630-7537
                Article
                v3i2e31019
                10.2196/31019
                10337478
                28da8335-f855-496f-abd3-f08a6435be19
                ©Charles Baulier, Marc Lessert, Jean-Louis Chauvet, Pauline Garel, Alexandre Bergis, Julie Burdeau, Thomas Clavier. Originally published in JMIRx Med (https://med.jmirx.org), 11.04.2022.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License ( https://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work, first published in JMIRx Med, is properly cited. The complete bibliographic information, a link to the original publication on https://med.jmirx.org/, as well as this copyright and license information must be included.

                History
                : 7 June 2021
                : 29 August 2021
                : 5 September 2021
                : 27 January 2022
                Categories
                Case Report
                Case Report

                ventricular outflow obstruction,subarachnoid hemorrhage,vasospasm,intracranial,milrinone,hemorrhage,neurosurgery,neurology,surgery,pharmaceutical

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