Background and Purpose-The importance of cancer-associated hypercoagulability as a possible stroke etiology in patients with cancer has received relatively little attention to date. A recent study has suggested that cancer-associated hypercoagulation may be of special importance in the absence of conventional stroke mechanisms. Methods-We identified patients with ischemic stroke sequentially admitted to our stroke center with the additional diagnosis of active and malignant cancer from 2002 to 2011. By using our prospectively collected stroke, MRI, and laboratory data banks, the etiology and risk factors of stroke, types of cancer, deep vein thrombosis/pulmonary embolism, d-dimer levels, and diffusion-weighted imaging lesion patterns were compared to an age-and sex-matched control group. Patients with cancer with a conventional stroke etiology and patients with an unidentified and/or cancer-associated stroke etiology were analyzed separately. Results-One hundred forty patients with cancer and 140 control subjects were included. Unidentified stroke (P<0.001) and infarction in multiple vascular territories (P<0.001) were significantly more frequent and d-dimer levels significantly higher (P<0.05) in patients with cancer. Vice versa, risk factors such as hypertension (P<0.05) and hyperlipidemia (P<0.01) were more prevalent in control subjects. Deep vein thrombosis and pulmonary embolism were more frequent (P<0.01) and d-dimer levels higher (P<0.01) in the patients with unidentified and/or cancerassociated stroke etiology compared to the patients with cancer with a conventional stroke etiology. Lung and pancreatic cancer were significantly overrepresented and d-dimer levels higher in these patients compared with other patients with cancer (P<0.01). Conclusions-Our data confirm the concept of cancer-associated hypercoagulation as a widely underestimated important stroke risk factor in patients with cancer, especially in those with severely elevated

Background: Hemorrhagic transformation (HT) after acute ischemic stroke is frequently detected using magnetic resonance imaging (MRI), in particular in patients treated with tissue plasminogen activator (tPA). Knowledge about causes and early clinical consequences of HT mostly arises from computed tomography-based studies. We analyzed potential predictors and early outcome of HT after stroke detected by MRI with T₂*-weighted gradient echo sequences (T₂*-MRI). Methods: 122 consecutive stroke patients (mean age 65.5 years, 41% women) who underwent T₂*-MRI within 6–60 h after stroke onset were included. 25.4% of patients were treated with tPA; the overall detection rate of HT on T₂*-MRI was 20.5%. Potential predictors of HT, such as age, sex, blood pressure, stroke etiology, prior antithrombotic medication, neurological deficit on admission, tPA treatment, and specific MRI findings, were analyzed. In addition, we evaluated the effect of HT on early outcome: a decrease of >4 points on the National Institute of Health Stroke Scale (NIHSS) on day 5 was considered early improvement, and an increase of >4 points was considered early deterioration. Results: The main predictor for occurrence of HT was tPA treatment (48.4 vs. 11.1%; odds ratio 7.50; 95% confidence interval 2.9–19.7; p < 0.001). Furthermore, the development of HT was associated with a severer neurological deficit on admission (mean NIHSS score 9.9 vs. 5.9; p = 0.003), and territorial infarction (88 vs. 58.8%; p = 0.007). 19 patients (15.6%) showed early improvement which was associated with the occurrence of HT (p = 0.011) and tPA treatment (p < 0.001). Conclusions: HT is a frequent finding on T₂*-MRI in patients with acute ischemic stroke associated with tPA treatment, territorial infarction and severer neurological deficits on admission. However, HT does not cause clinical deterioration; it is rather related to a favorable early outcome likely reflecting early recanalization and better reperfusion in these patients.

Background: Acute ischemic stroke patients may occasionally suffer from concomitant acute coronary syndrome (ACS). Troponin I and T are established biomarkers to detect ACS. Recently introduced high-sensitive cardiac troponin (hs-TNI and hs-TNT) assays are increasingly used to identify ACS in stroke patients even without signs or symptoms of ACS. These new test systems very often detect elevated values of hs-troponin, although clinical relevance and consequences of elevated hs-TNI values in these patients are unclear so far. Patients and Methods: We examined hs-TNI values in 834 consecutive ischemic stroke patients admitted to our Comprehensive Stroke Center during a 1-year period. hs-TNI was measured immediately after admission and after 3 h if initial hs-TNI was elevated above the 99th percentile of normal values (>0.045 ng/ml). Patients with elevated values were divided into two groups: (1) constant and (2) dynamic hs-TNI values. The dynamic approach was defined as a 30% rise or fall of the hs-TNI value above the critical value within 3 h. All patients received stroke diagnostic and continuous monitoring according to international stroke unit standards, including a 12-lead ECG, blood pressure, body temperature and continuous ECG monitoring, as well as regular 6-hourly neurological and general physical examination (including NIHSS scores). The cardiologists - as members of the Stroke Unit team - evaluated clinical symptoms/examination, as well as laboratory, echocardiographic and ECG findings for the diagnosis of ACS. Results: 172/834 (20.6%) patients showed elevated hs-TNI levels on admission. Patients with elevated hs-TNI values exhibited a significantly (p < 0.001) increased rate of hypertension (89 vs. 77.2%), history of stroke (24.4 vs. 14.8%), history of coronary artery disease (65.7 vs. 34.1%), history of myocardial infarction (22.1 vs. 7.6%), heart failure (12.8 vs. 5.7%) and atrial fibrillation (44.2 vs. 23.6%). 82/136 patients showed constant and 54/136 patients dynamic hs-TNI values: among the latter, 5 patients were diagnosed with ST segment elevation myocardial infarction (STEMI) and 24 with non-STEMI (NSTEMI). Conclusion: Our data demonstrate that hs-TNI was elevated in about 20.6% of acute ischemic stroke patients but therapeutically relevant ACS was diagnosed only in the dynamic group. hs-TNI elevations without dynamic changes may occur in stroke patients without ACS due to different reasons that stress the heart. Therefore, we suppose that hs-TNI is a sensitive marker to detect high-risk patients but serial measurements are mandatory and expert cardiological workup is essential for best medical treatment and to accurately diagnose ACS in acute ischemic stroke patients.

Real-time ultrasound perfusion imaging (rt-UPI) allows visualization of microbubbles flowing through the cerebral microvasculature. We hypothesized that analysis of microbubble tissue replenishment would enable for characterization of perfusion deficits in acute middle cerebral artery (MCA) territory stroke. Twenty-three patients (mean age 70.2±13.2 years, 9 weeks) were included. Sequential images of bubble replenishment were acquired by transcranial rt-UPI at low mechanical index immediately after microbubble destruction. Different parameters were calculated from regions of interest (ROIs): real-time time to peak (rt-TTP), rise rate (b), and plateau (A) of acoustic intensity, and A¾b was used as an index of blood flow. Results were compared with diffusion-weighted and perfusion magnetic resonance imaging. Parameters of rt-UPI had lower values in ROIs of ischemic as compared with normal tissue (b = 0.58 ± 0.40 versus 1.25 ± 0.83; P = 0.001; A = 1.44 ± 1.75 versus 2.63 ± 2.31; P = 0.05; A¾b = 1.14 ± 2.25 versus 2.98 ± 2.70; P = 0.01). Real-time time to peak was delayed in ischemic tissue (11.43 ± 2.67 versus 8.88 ± 1.66 seconds; P < 0.001). From the analysis of receiver operating characteristic curves, b and A¾b had the largest areas under the curve with optimal cutoff values of b < 0.76 and A¾b < 1.91. We conclude that rt-UPI with analysis of microbubble replenishment correctly identifies ischemic brain tissue in acute MCA stroke.