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SUMMARY Analysis of early deaths after stroke is important, since some deaths may be preventable. Previous studies have relied on retrospective and often incomplete clinical data, for comparison with pathological findings.The present study is based on 1073 consecutive stroke patients admitted to an intensive care stroke unit from a well-defined population. There were 212 deaths within the first 30 days, yielding a mortality rate of 20%. Clinical, radiological, and laboratory data were collected prospectively according to a standardized protocol. Autopsies were performed on 90 of the 212 patients, and CT scanning on a further 27.Early mortality after stroke exhibits a bimodal distribution. One peak occurs during the first week, and a second during the second and third weeks. The majority of deaths in the first week are due to transtentorial herniation. Of these, deaths due to hemorrhage usually occur within the first three days, whilst deaths due to infarction peak between the third and sixth day post ictus. After the first week, deaths due to relative immobility (pneumonia, pulmonary embolism and sepsis) predominate, peaking towards the end of the second week. Cardiac deaths occur throughout the first month, and unfortunately account for many deaths in patients with small functional deficits.Stroke VOL 15, No 3, 1984

Our objectives were to investigate the utility of the Hachinski Ischemic Score (HIS) in differentiating patients with pathologically verified Alzheimer's disease (AD), multi-infarct dementia (MID), and "mixed" (AD plus cerebrovascular disease) dementia, and to identify the specific items of the HIS that best discriminate those dementia subtypes. Investigators from six sites participated in a meta-analysis by contributing original clinical data, HIS, and pathologic diagnoses on 312 patients with dementia (AD, 191; MID, 80; and mixed, 41). Sensitivity and specificity of the HIS were calculated based on varied cutoffs using receiver-operator characteristic curves. Logistic regression analyses were performed to compare each pair of diagnostic groups to obtain the odds ratio (OR) for each HIS item. The mean HIS (+/- SD) was 5.4 +/- 4.5 and differed significantly among the groups (AD, 3.1 +/- 2.5; MID, 10.5 +/- 4.1; mixed, 7.7 +/- 4.3). Receiver-operator characteristic curves showed that the best cutoff was < or = 4 for AD and > or = 7 for MID, as originally proposed, with a sensitivity of 89.0% and a specificity of 89.3%. For the comparison of MID versus mixed the sensitivity was 93.1% and the specificity was 17.2%, whereas for AD versus mixed the sensitivity was 83.8% and the specificity was 29.4%. HIS items distinguishing MID from AD were stepwise deterioration (OR, 6.06), fluctuating course (OR, 7.60), hypertension (OR, 4.30), history of stroke (OR, 4.30), and focal neurologic symptoms (OR, 4.40). Only stepwise deterioration (OR, 3.97) and emotional incontinence (OR, 3.39) distinguished MID from mixed, and only fluctuating course (OR, 0.20) and history of stroke (OR, 0.08) distinguished AD from mixed. Our findings suggest that the HIS performed well in the differentiation between AD and MID, the purpose for which it was originally designed, but that the clinical diagnosis of mixed dementia remains difficult. Further prospective studies of the HIS should include additional clinical and neuroimaging variables to permit objective refinement of the scale and improve its ability to identify patients with mixed dementia.

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SUMMARY The possibility that acute stroke produces an increase in sympathetic tone with resultant cardiac abnormalities was examined in 100 stroke patients admitted to a stroke ICU and in 50 controls found to have diagnoses other than stroke or TIA after admission to the Unit. Continuous 24 hour Holter ECG tapings were performed and serum cardiac enzymes and plasma norepinephrine concentrations were measured within 48 hours after admission. Significantly, (p < .001) more serious arrhythmias were observed during 24 hour Holter ECG monitoring in stroke patients compared with controls and the difference remained (p < .01) after matching for age and co-existing heart disease. Arrhythmias were more common in older stroke (p < .001) and older control (p = .05) patients and with infarction of the cerebral hemispheres (p < .05) as compared to brainstem lesions. Arrhythmia occurrence was independent of the presence of co-existing heart disease and the level of sympathetic activity. However, the 15 stroke patients with abnormally high CK values (mean 34.3 units) had a higher (p < .02) mean plasma norepinephrine concentration (650.4 pg/ml) than stroke patients with normal CK (427.7 pg/ml). Acute stroke may cause cardiac arrhythmias and myocardial cell damage, the latter through stroke induced increases in sympathetic tone.

SUMMARY Serum cardiac enzyme levels (CK, LDH, SCOT) were estimated and the ECG recorded for 4 days following admission of 288 patients (Group I) to a stroke intensive care unit. Sixty-four of these patients, subsequently found not to have strokes, served as controls. Mean serum levels of all 3 cardiac enzymes were elevated in 8% of the 224 patients with stroke. The mean serum enzyme levels in patients with transient ischemic attacks (TIA) did not differ from controls.In a second group of 230 patients with stroke (Group II) serum CK levels were measured and the isoenzymes were fractionated to determine the tissue source of the enzymes. One hundred and one patients had raised total CK values and 25 of these (11%) had raised CK-MB (heart) iso-enzyme, the remainder having CK-MM (skeletal muscle) fraction. No serum CK-BB (brain) iso-enzyme was detected in any patient. Patients with positive serum levels of CK-MB had more evidence of acute myocardial ischemia on ECG (p < 0.05), and more cardiac arrhythmias (p < 0.001) than those with normal CK levels. Scattered areas of myocytolysis were found in the myocardium at autopsy in one patient.The acute rise in serum cardiac enzymes which we have recorded in the initial stages of stroke suggest that acute myocardial involvement is a commoner complication than is generally recognized. Also, since the CK-MB rises were modest and progressive, it is more likely that this acute myocardial dysfunction is a consequence, rather than a cause, of the acute cerebrovascular lesion.

SUMMARY One hundred and eighty-four consecutive patients admitted to an Investigative Stroke Unit with transient ischemic attacks (TIA) and cerebral infarction (stroke) had 48-hour automated arrhythmia monitoring, 55 patients had additional Holter monitoring and 127 patients had 2-D echocardiography. One hundred and sixteen presented with stroke (63%) and 68 patients with TIA (37%). One hundred and twenty-two were men (66.3%) and 62 were women (33.7%), mean age 63.5 years, range 25-86.The monitoring identified twelve (6.5%) patients with significant arrhythmias undetected by history, examination and admission electrocardiogram: six with atrial fibrillation (AF), four with 2° heart block type Mobitz II and one each with 3° heart block and sick sinus syndrome. Two-D echocardiography showed a previously unknown potential source for cardiac emboli in 22 patients (17.3%): segmental ventricular disease in eleven, mitral valve prolapse in seven, left ventricular thrombus in six, left ventricular aneurysm in three and one each with mitral valve endocarditis and global myocardial dysfunction. Only the mitral valve findings were expected on the basis of a previous M-mode echocardiographic study carried out in our city on healthy elderly volunteers.From the clinical history and all cardiac investigations, we found 59 patients (32%) with a possible cardiac source for cerebral emboli. After cerebral angiography, 29 of these 59 patients also showed a vascular lesion in the appropriate carotid artery and we could not decide definitely which lesion was responsible for the cerebral embolus. In the remaining 30 patients (16.4%), the evidence implicated the heart as the most likely source. These findings illustrate the common coincidence of cardiac and arterial lesions and the difficulties of diagnosing cardiac embolism confidently.Arrhythmia monitoring and 2-D echocardiography detected a previously unrecognized possible cardiac source for emboli in 28 patients (15.2%). The specific identification of potentially treatable conditions by these investigations suggests that they are valuable in arriving at therapeutic decisions for TIA and stroke patients.