12. Angiotensin-II type-1 receptor blockade decreased T2 signal intensity in spinal cord compression in symptomatic cervical spondylotic myelopathy.

Cervical spondylosis may lead to spinal cord compression, poor vascular perfusion, and ultimately cervical myelopathy. The process whereby chronic compression may cause spinal cord damage has not been fully understood. However, multiple mechanisms such as inflammation, apoptosis, and vascular variations, are thought to be responsible for the neuronal loss, axonal degeneration, and myelin impairment seen in cervical spondylotic myelopathy (CSM). Studies reported a beneficial effect of renin-angiotensin system (RAS) blockers in the central nervous system, particularly in brain inflammation and stroke, but data on their influence on the spinal cord are limited. We aimed to determine if RAS blockers are correlated with preoperative functional status and radiological markers of spinal cord damage secondary to compression in patients with CSM. Retrospective cohort study. Symptomatic cervical spondylosis patients. Functional status (including modified Japanese Orthopedic Association [mJOA] and Nurick grading scales) and imaging characteristics (including % maximum canal compromise [MCC], % maximum spinal cord compromise [MSCC], increased signal intensity [ISI], signal intensity ration [SIR] and ISI surface area), all of which were evaluated on midsagittal T2-weighted MRIs. Adults with symptomatic degenerative cervical stenosis patients were included. Demographic data, comorbidities, antihypertensive medications (particularly RAS blockers), and functional status were collected. We assessed % canal compromise, % cord compromise, surface area of T2 signal cord change, and pixel intensity of signal cord change compared to normal cord on T2-weighted MRI sequences. Of the 267 patients, 41.6% were female and 58.1% male; median age of 57.2 years; 20.6% smokers; 24.7% diabetics. One hundred forty-nine patients (55.8%) had hypertension, of which 142 (95.3%) were taking antihypertensive medications: 37 angiotensin-II receptor blockers [ARBs], 44 angiotensin-converting enzyme inhibitors [ACEIs], and 61 other medications). Patients treated with ARBs displayed a higher signal intensity ratio (lower signal intensity change in the compressed cord area) compared to those untreated non-hypertensive patients (p=.004). Hypertensive patients had worse preoperative mJOA and Nurick scores compared to non-hypertensive patients (p<.001). In the multivariate analysis, ARBs remained an independent beneficial factor for lower signal intensity change (p=.04), while hypertension remained a risk factor for worse preoperative neurological status (p<.01), after adjusting for covariables that were significant in the univariate analyses or were considered relevant. In cervical spinal cord compression patients, hypertensive subjects treated with RAS inhibitors were associated with less signal intensity change (higher SIR) than untreated non-hypertensive patients. Also, hypertensive subjects under any antihypertensive medication displayed worse mJOA and Nurick scores compared to untreated non-hypertensive individuals. Further studies are warranted to verify the effect of RAS inhibitors in spinal cord damage. This abstract does not discuss or include any applicable devices or drugs. [ABSTRACT FROM AUTHOR]