Prevalence of Positive Troponin and Echocardiogram Findings and Association With Mortality in Acute Ischemic Stroke.

BACKGROUND AND PURPOSE: Acute ischemic stroke (AIS) patients may have raised serum cardiac troponin levels on admission, although it is unclear what prognostic implications this has, and whether elevated levels are associated with cardiac causes of stroke or structural cardiac disease as seen on echocardiogram. We investigated the positivity of cardiac troponin and echocardiogram testing within a large biracial AIS population and any association with poststroke mortality. METHODS: Within a catchment area of 1.3 million, we screened emergency department admissions from 2010 using International Classification of Diseases, Ninth Edition, discharge codes 430 to 436 and ascertained all physician-confirmed AIS cases by retrospective chart review. Hypertroponinemia was defined as elevation in cardiac troponin above the standard 99th percentile. Multiple logistic regression was performed, controlling for stroke severity, history of cardiac disease, and all other stroke risk factors. RESULTS: Of 1999 AIS cases, 1706 (85.3%) had a cardiac troponin drawn and 1590 (79.5%) had echocardiograms. Hypertroponinemia occurred in 353 of 1706 (20.7%) and 160 of 1590 (10.1%) had echocardiogram findings of interest. Among 1377 who had both tests performed, hypertroponinemia was independently associated with echocardiogram findings (odds ratio, 2.9; 95% confidence interval, 2-4.2). When concurrent myocardial infarctions (3.5%) were excluded, hypertroponinemia was also associated with increased mortality at 1 year (35%; odds ratio, 3.45; 95% confidence interval, 2.1-5.6) and 3 years (60%; odds ratio, 2.91; 95% confidence interval, 2.06-4.11). CONCLUSIONS: Hypertroponinemia in the context of AIS without concurrent myocardial infarction was associated with structural cardiac disease and long-term mortality. Prospective studies are needed to determine whether further cardiac evaluation might improve the long-term mortality rates seen in this group.

The location of origin of spontaneous extracranial internal carotid artery dissection is adjacent to the skull base.

INTRODUCTION: The traditional view is that spontaneous extracranial internal carotid artery (ICA) dissection (CAD) extends cranially from an intimal tear located just beyond the carotid bulb. This paper demonstrates that CAD originates in and primarily involves a more distal segment of the artery. METHODS: A retrospective study of 54 dissected ICAs in 50 consecutive patients with spontaneous or traumatic CAD was undertaken. The site of the dissection, presence of ICA redundancy, rate of acute or delayed ischaemic stroke and vessel remodelling were determined. RESULTS: Of the 51 dissections that occurred spontaneously or after indirect trauma, 25/51 (49.0%) were solely in the distal third of the artery, and 49/51 (96.1%) involved the distal two-thirds. Only 2/51 (3.9%) originated in the proximal third. ICA redundancy was seen in 27/36 (75%) of patients with spontaneous CAD, compared with only 1/11 (9.1%) of those with CAD due to indirect trauma (P = 0.0002). Acute stroke occurred in 10/12 (83.3%) of patients with ICA occlusion secondary to CAD and in 14/38 (36.8%) with non-occlusive CAD (P = 0.0074). Where follow-up was available, only 2/32 (6.3%) patients had a stroke after diagnosis, and 19/33 (57.6%) ICAs recanalised or remodelled. CONCLUSION: CAD occurring spontaneously or due to indirect trauma most frequently involves the distal extracranial ICA. Spontaneous CAD is associated with vessel redundancy, and the risk of acute stroke is greatest with occlusive CAD. The prognosis is good with treatment, with a low rate of recurrent stroke and a high rate of vessel remodelling.