Kramer, Christopher L.

Background: Given the uncertainty regarding clinical applicability of early treatment trials and lack of data on long-term disease progression, we evaluated the progression of stenosis and development of symptoms on patients with asymptomatic carotid artery stenosis (ACAS) treated with contemporary medical therapy over a prolonged follow up. Methods: Retrospective review of bilateral carotid arteries from consecutive patients diagnosed with moderate or severe ACAS, at our institution between 2000 and 2001. Patient vascular risk factors and treatments, cerebrovascular imaging, ipsilateral symptoms, and revascularization were recorded. Progression of stenosis was defined by change category of stenosis. Factors associated with symptomatic carotid disease were sought using univariate and multivariate logistic regression analysis. Results: We identified 214 patients (58.8% men; median age 70 years) and collected data on 349 vessels. Severe stenosis (>70%) upon diagnosis was present in 92(26.4%) vessels. All patients were on antithrombotics, 97% on antihypertensives, and 95% on statins. Median length of follow up was 13 years (range 5-14) and the mean number of time points with follow-up imaging was 8.1±3.9. Progression of stenosis was observed in 237(67.9%) vessels. 72(20.6%) patients developed symptomatic carotid stenosis (TIA in 14.4%, non-disabling stroke in 4%, and disabling stroke in 2.2%). Median time to appearance of first symptom was 6 years (range 1-13). Revascularization procedures were performed in 118(33.8%) vessels, including 73(61.9%) vessels which had become symptomatic. On multivariate analysis, baseline stenosis (OR 1.65, 95%CI 1.12-2.44), intracranial stenosis > 50% (OR 2.87, 95%CI 1.46-5.62), plaque ulceration (OR 3.41, 95%CI 1.34-8.69), silent infarction (OR 4.25, 95%CI 2.30-7.83), and previous history of TIA/stroke (OR 2.73, 95%CI 1.14-6.54) were associated with development of TIA/stroke ipsilateral to the carotid stenosis. Conclusions: There is a substantial rate of progression of stenosis in patients with asymptomatic carotid atherosclerosis over time despite adequate medical therapy. Over long-term follow up, one in five patients with ACAS developed ipsilateral TIA/stroke.

Background: Fever has been associated with worse clinical outcomes in aneurysmal subarachnoid hemorrhage (aSAH). However, the impact of the cause, severity, and duration of fever is not clear. We conducted this study to evaluate the impact of fever and subfebrile load and fever characteristics on functional outcome. Methods: We collected detailed information on fever onset, cause, severity, and duration during the ICU stay in a cohort of 586 consecutive patients with aSAH. Fever was defined as core body temperature ≥ 38.3°C. Subfebrile measurements were those between 37 and 38.2°C. Febrile and subfrebile loads were defined as number of hours with fever or subfebrile measurements. Poor outcome was defined as modified Rankin score (mRS) > 2. Univariate and multivariate logistic regression models were developed to define predictors of outcome using various categorizations of fever cause, severity, and duration. Results: 532/586 patients (90.9%) had fever for a mean of 2.1±3.0 days. Fever started within 24 hours in 69 (11.8%) and within 72 hours in 110 (18.8%). Poor outcome occurred in 175 patients (29.9%). On univariate analysis, days of fever, febrile load, fever onset within 24 hours, and fever onset within 72 hours were associated with poor outcome (all p<0.001), but subfebrile load was not (p=0.58). On multivariate model constructed with all variables associated with outcome on univariate analyses (including age, WFNS grade, modified Fisher grade) days of fever remained independently associated with poor outcome (OR 1.14 of poor outcome per day of fever, 95% CI 1.06-1.22; p=0.0006) displacing all other fever measures from the final model. Conclusions: The great majority of patients with aSAH are febrile during their ICU stay. Early onset of fever, number of hours with fever, and especially days of fever are associated with poor functional outcome. Conversely, the number of hours with elevated but subfebrile temperature does not influence clinical outcome. These data suggest that prolonged fever should be avoided, but subfebrile temperatures do not justify intervention.

ABSTRACTIntroductionWe sought to determine the specificity of compound muscle action potential (CMAP) durations and amplitudes in a large critical illness neuromyopathy (CINM) cohort relative to controls with other neuromuscular conditions.MethodsFifty‐eight patients with CINM who had been seen over a 17‐year period were retrospectively studied. Electrodiagnostic findings of the CINM cohort were compared with patients with axonal peripheral neuropathy and myopathy due to other causes.ResultsMean CMAP durations were prolonged, and mean CMAP amplitudes were severely reduced both proximally and distally in all nerves studied in the CINM cohort relative to the control groups. The specificity of prolonged CMAP durations for CINM approached 100% if they were encountered in more than 1 nerve.DiscussionProlonged, low‐amplitude CMAPs occur more frequently and with greater severity in CINM patients than in neuromuscular controls with myopathy and axonal neuropathy and are highly specific for the diagnosis of CINM. Muscle Nerve 57: 395–400, 2018