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PubMed1996

Atherosclerotic disease of the aortic arch as a risk factor for recurrent ischemic stroke.

BACKGROUND: Atherosclerotic disease of the aortic arch is found in 60 percent of patients 60 years of age or older who have had brain infarction. The aim of this study was to determine whether atherosclerotic plaques in the aortic arch are a risk factor for recurrent brain infarction and for vascular events in general (i.e., brain infarction, myocardial infarction, peripheral embolism, and death from vascular causes). METHODS: For a period of two to four years, we followed a cohort of 331 patients 60 years of age or older who were consecutively admitted to the hospital with brain infarction (a total of 788 person-years of follow up). All patients underwent transesophageal echocardiography to determine whether atherosclerotic plaques were present in the aortic arch proximal to the ostium of the left subclavian artery. The patients were divided into three groups according to the thickness of the wall of the aortic arch ( < 1 mm, 1 to 3.9 mm, and > or = 4 mm). RESULTS: The incidence of recurrent brain infarction was 11.9 per 100 person-years in patients with an aortic-wall thickness of > or = 4 mm, as compared with 3.5 per 100 person-years in patients with a wall thickness of 1 to 3.9 mm and 2.8 per 100 person-years in patients with a wall thickness of < 1 mm (P < 0.001). The overall incidence of vascular events was 26.0, 9.1, and 5.9 per 100 person-years of follow-up in the respective groups (P < 0.001). After adjustment for the presence of carotid stenosis, atrial fibrillation, peripheral arterial disease, and other risk factors, aortic plaques > or = 4 mm thick (including the thickness of the aortic wall) were found to be independent predictors of recurrent brain infarction (relative risk, 3.8; 95 percent confidence interval, 1.8 to 7.8; P = 0.0012) and of all vascular events (relative risk, 3.5; 95 percent confidence interval, 2.1 to 5.9; P < 0.001). CONCLUSIONS: Atherosclerotic plaques > or = 4 mm thick in the aortic arch are significant predictors of recurrent brain infarction and other vascular events.

Aged↗
PubMed2002

Apoptotic activity is increased in brain cortex infarct after hypothermic circulatory arrest in a porcine model.

OBJECTIVE: It has been shown that apoptosis contributes to neuronal cell death after ischemia, and we evaluated the degree of apoptotic activity occurring in brain cortex of pigs after hypothermic circulatory arrest (HCA). DESIGN: Thirty-one pigs underwent 75 min of HCA at 20 degrees C. Histological examination of the brain was performed, and slides of brain cortex were evaluated for apoptotic activity by the TUNEL method. RESULTS: Ten animals died during the first postoperative day and 21 survived until the seventh postoperative day. Brain cortex infarcts were found in animals that survived 7 days and these were included in this study. The median histopathological score among animals that died on the first postoperative day was 3.0 (range, 2-4), whereas it was 4.0 (range, 2-4) among survivors (p = 0.019). The apoptotic index was particularly high in the area of the infarct, whereas only a few TUNEL-stained cells were observed in noninfarcted areas. The apoptotic index was nil in all pigs that died in the first postoperative period, whereas it was 2.0 (range, 0-6) among the animals that survived until the seventh postoperative day (p < 0.0001). CONCLUSION: The apoptotic index was significantly increased in brain cortex infarcts of animals that survived 7 days after HCA, whereas only a few apoptotic cells were observed in noninfarcted areas of these animals as well as in animals that died on the first postoperative day. Further studies are required to elucidate the timing of development of brain infarction after HCA and whether neuroprotective strategies targeting the apoptotic process may mitigate brain damage.

Animals↗
PubMed2004

[New aspects of Wallenberg syndrome and other brain stem infarctions].

Studies with MRI and non-invasive vascular imaging have modified previous conceptions on clinical spectrum and causes of different types of brain stem infarcts. Wallenberg's syndrome caused by lateral medullary infarction (LMI) often presents with patterns of sensory loss different from the "classical" crossed type. LMI carries a risk for respiratory and cardiovascular complications in the acute phase, warranting close patient monitoring. Medial medullary infarcts often present with a lacunar syndrome mimicking capsular or pontine small vessel disease. Cerebellar infarcts are most often caused by cardiac embolism. Isolated vertigo may be the only presenting symptom. Neurosurgical intervention of expansive cerebellar infarcts may be life-saving. Clinical features of progressive multifocal brain-stem symptoms are often suggestive of basilar artery occlusion. CT-angiography is a useful initial diagnostic tool. Based on observational studies, intraarterial thrombolysis is used in selected patients with basilar artery occlusion, but further studies are needed to define treatment criteria more precisely.

Basilar Artery↗
PubMed2001

[Myocardial injury in acute stroke assessed by troponin I].

BACKGROUND: Acute ischaemic or haemorrhagic cerebrovascular events may produce myocardial damage. Cardiac troponin I is an indicator of cardiac cell injury with very high sensitivity and specificity. MATERIAL AND METHODS: We measured troponin I in 149 acute stroke patients admitted to the stroke unit of Trondheim University Hospital, Norway, in January to June 1999. RESULTS: 40 patients (27%) had troponin I values at 0.4 microgram/l or higher, indicating myocardial injury. 10 patients (6.7%) had troponin I values above 2.0 micrograms/l. Similarly, the mean value of CK-MB vas higher in the patients with myocardial injury, and these patients had more often ECG findings suggesting myocardial ischaemia. Patients with myocardial injury had a higher rate of previous TIA and heart failure. ECG showed atrial fibrillation in 13 of 39 patients with myocardial damage. Patients with detectable levels of troponin I had more embolic brain infarctions than thrombotic brain infarctions. Patients with myocardial injury did more often have abnormal values of CRP. 9 of 10 patients with troponin I-values above 2.0 micrograms/l had abnormal CRP values. No differences in glycosylated haemoglobin, cholesterol, heart rate, blood pressure or body temperature were found. Patients with the highest troponin I values had lower systolic blood pressure, and a higher heart rate, but these differences were not statistically significant. Patients with troponin I values above 2.0 micrograms/l had lower functional and neurological scores at admittance. Patients with myocardial injury were more often discharged to nursing homes. INTERPRETATION: Many patients with an acute stroke have at the same time a myocardial injury, determined by elevated troponin I values.

Activities of Daily Living↗
PubMed2004

[Cytokines in clinical and experimental ischemic stroke].

Inflammatory reaction following acute cerebral ischaemia exacerbates infarct size and neurological deficit. Brain resident cells localised within ischaemic region rapidly synthesise cytokines, proteins involved in cellular communication. The cytokines become important mediators of endothelial-leukocyte interactions leading to the influx of haematogenous inflammatory cells into the brain ischaemic region. Proinflammatory cytokines: tumour necrosis factor-alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta) initiate inflammatory reaction and induce expression of other cytokines and inflammatory mediators. The presence of cytokines in brain infarct region has been shown in human and animal autopsy studies. Suppression of proinflammatory cytokines expression reduces brain infarct size in animal models of stroke. Increased levels of proinflammatory cytokines in cerebrospinal fluid and/or in serum of acute ischaemic stroke patients correlate with brain infarct volume and stroke severity and may have a predictive value for stroke outcome. This review presents cytokines studied in clinical and experimental strokes documenting that the molecules may exert not only detrimental but also neuroprotective effect on ischaemic brain.

Acute Disease↗
PubMed1997

Mitral valve strands and the risk of ischemic stroke in elderly patients. The French Study of Aortic Plaques in Stroke (FAPS) Investigators.

BACKGROUND AND PURPOSE: Strands are thin and filamentous attachments on the cardiac valves shown by transesophageal echocardiography. Their nature and their potential for embolization are largely unknown. The objective was to estimate the risk of brain infarction in patients with mitral valve strands. METHODS: Using transesophageal echocardiography, we compared the frequency of strands on native mitral valves in 284 consecutive patients admitted with brain infarction and 276 control patients, all older than 60 years. In a second part, case subjects were followed up over a 2- to 4-year period, and the risk of recurrence of brain infarction was estimated in patients with and without strands. RESULTS: In the case-control study, mitral valve strands were found in 22.5% of the case patients and in 12.1% of the control subjects. In case subjects, mitral valve strands were more frequent in those with mitral valve dystrophy (52.4% versus 37.4%; P = .03). Strands were not associated with mitral valve prolapse, annular calcifications, or left atrial spontaneous echocardiographic contrast. After adjustment for age, sex, and mitral valve dystrophy, the odds ratio for ischemic stroke among patients with mitral strands was 2.2 (95% confidence interval, 1.4 to 3.6; P = .005). The frequency of strands was not different in patients with a known cause of brain infarction (24.4%) from that in patients with no other apparent cause (20.9%). During 646 per 100 person-years of follow-up, the incidence of recurrent brain infarction was 6.0 person-years in patients with strands and 4.2 in those without. In the Cox analysis, including potential confounders and poststroke treatment, mitral valve strands did not appear as independent predictors of recurrent brain infarction (relative risk, 1.3; 95% confidence interval, 0.5 to 3.0; P = .54). CONCLUSIONS: The present study shows an independent association between mitral valve strands and the risk of brain infarction. However, the lack of an increased relative risk of recurrence raises doubts about the potential causal relation with brain infarction in patients aged 60 years or older.

Aged↗
PubMed2005

Ten year recurrence after first ever stroke in a Japanese community: the Hisayama study.

BACKGROUND: Very few population based cohort studies have focused on the long term recurrence of stroke. OBJECTIVE: To examine 10 year cumulative recurrence rates for stroke in a Japanese cohort according to pathological type and clinical subtype of brain infarction. METHODS: During a 32 year follow up of 1621 subjects >/=40 years of age, 410 developed first ever stroke. These were followed up prospectively for 10 years after stroke onset. RESULTS: During follow up, 108 (26%) experienced recurrent stroke. The cumulative recurrence rates were 35.3% at five years and 51.3% at 10 years. The 10 year recurrence rates of subarachnoid haemorrhage (SAH), brain haemorrhage, and brain infarction were 70.0%, 55.6%, and 49.7%, respectively; the difference between SAH and brain infarction was significant (p = 0.004). Most recurrent episodes after SAH or brain haemorrhage happened within a year after the index stroke, whereas recurrence of brain infarction increased consistently throughout the observation period. Cardioembolic stroke had a higher recurrence rate (75.2%) than lacunar infarction (46.8%) (p = 0.049). The 10 year risk of stroke recurrence increased with age after lacunar or atherothrombotic brain infarction, but not after the other types or subtypes. After atherothrombotic brain infarction, cardioembolic stroke, or SAH, the type and subtype of most recurrent strokes were the same as for the index stroke, but recurrence after lacunar infarction or brain haemorrhage showed divergent patterns. CONCLUSIONS: Japanese people have higher recurrence rates of stroke than other populations. Recurrence rate after a first brain infarct increases consistently through the next 10 years.

Adult↗
PubMed2003

Diagnosis of acute brain-stem infarcts using diffusion-weighed MRI.

There are many reports on acute cerebral infarcts diagnosed by diffusion-weighted MRI (DWI), but few describe brain-stem infarcts diagnosed by this method. Using the apparent diffusion coefficient (ADC), we studied 18 consecutive patients with brain-stem infarcts who underwent DWI during the acute phase. We calculated and compared the ADC ratio (lesion ADC/contralateral ADC) in 10 patients with brain-stem and 23 with supratentorial cortical infarcts examined within 24 h of the onset of stroke. Ischaemic brain-stem lesions were detected in all 15 patients who underwent DWI more than 3 h after the onset, but not in two who had DWI within 3 h of the onset; their ADC ratio was more than 0.95. ADC ratios in patients with brain-stem infarcts decreased as the interval between onset and DWI increased; the decrease was slower than in patients with supratentorial cortical infarcts.

Acute Disease↗
PubMed2005

Continuous EEG monitoring for the detection of seizures in traumatic brain injury, infarction, and intracerebral hemorrhage: "to detect and protect".

Brain injury results in a primary pathophysiologic response that enables the brain to have seizures. Seizures occur frequently after traumatic and nontraumatic intracerebral bleeding. These seizures can be nonconvulsive, and if one does not monitor for seizures, one will not know they are occurring. The use of continuous EEG monitoring (cEEG) to detect brain arrhythmias after a primary insult, much in way that cardiac arrhythmias are detected after myocardial infarction, can influence treatment decisions and mitigate some of the pathophysiologic natural history of brain injuries. Seizures after brain injury worsen clinical outcome and need to be treated. In summary, cEEG is a valuable clinical instrument "to detect and protect," i.e., to detect seizures and protect the brain from seizure-related injury in critically ill patients, whose brains are often in a particularly vulnerable state.

Brain Infarction↗
PubMed2004

Usefulness of brain natriuretic peptide levels to discriminate patients with stable angina pectoris without and with electrocardiographic myocardial ischemia and patients with healed myocardial infarction.

Brain natriuretic peptide (BNP) levels were measured in 100 patients with coronary heart disease (CHD) who underwent myocardial stress thallium-201 single-photon emission computed tomography (30 with stable angina without basal electrocardiographic ischemia and no perfusion defects, 31 with angina with electrocardiographic ischemia and reversible perfusion defects, and 39 with myocardial infarction and irreversible defects) and in 42 controls. BNP levels progressively increased in patients with CHD and were significantly greater in patients with ischemia (p <0.01) and infarction (p <0.001) compared with controls and subjects with angina. BNP concentration was correlated positively (r = 0.923, p <0.001) with perfusion defect extent and inversely (r = -0.690, p <0.001) with the left ventricle ejection fraction (not different in the subjects examined).

Analysis of Variance↗
PubMed1996

Weekend and holiday increase in the onset of ischemic stroke in young women.

BACKGROUND AND PURPOSE: Chronobiological analyses of stroke onset may throw some light on the mechanisms that trigger stroke. Observations may generate new hypotheses for identifying significant causal relationships. METHODS: In the present study, both the circadian and the weekend and holiday versus workday times of the onset of ischemic cerebral infarction were determined for 723 consecutive subjects, aged 16 to 60 years, who were admitted for hospital treatment in the acute phase without any selection. RESULTS: Among young adults (16 to 40 years) and women, more infarctions occurred during weekends and holidays than were expected. Young women in particular had an increased risk for brain infarction during weekends and holidays (odds ratio [OR], 2.14; 95% confidence interval [CI], 1.26 to 3.63). In a multivariate analysis, age of 16 to 30 years (OR, 3.13; 95% CI, 1.57 to 6.50), female sex (OR 1.71; 95% CI, 1.12 to 2.63), and recent drinking of alcohol (P < .01) were associated with the onset of brain infarction during weekends and holidays, whereas current cigarette smoking was associated with the onset of brain infarction during workdays (P < .001). A morning increase in the onset of brain infarction was observed among middle-aged people during both weekends/holidays and workdays. Among young adults, however, an evening increase was also seen during weekends/holidays and workdays. CONCLUSIONS: We found that young adults and women are frequently stricken by brain infarction during weekends and holidays and that the circadian distribution of the onset of brain infarction among young adults is different from that of middle-aged people. These observations suggest that there may be stroke-triggering activities that are associated with lifestyle.

Adolescent↗
PubMedDate not supplied

Outcome of 314 patients with transient ischemic attacks.

Between 1967 and 1976, 314 patients with transient ischemic attack (TIA) were evaluated and treated. Follow-up has been from 2.8 to 13.2 years (mean 7.8). As of 1979, 55 of the patients had succumbed to cardiovascular disease (28), cerebrovascular disease (9), malignancy (10), and other causes (8). During the follow-up period, 15 patients suffered brain infarction (4.8% under the risk) while 40 had myocardial infarction (12.7%) under the risk). Brain infarction occurred as often in patients with carotid TIA as in those with vertebral-basilar TIA, and was more common in patients under anticoagulation therapy than in those without it (p less than 0.05). Arterial hypertension, heart disease, peripheral arterial disease and diabetes did not increase the risk of brain infarction, but all (except diabetes) increased the risk of myocardial infarction. Combination of TIA with arterial hypertension, heat disease, or peripheral arterial disease increased the mortality (p less than 0.001). A life table analysis of surviving 1, 5, and 10 years gave probabilities of 99 and 100%, 89 and 91%, and 60 and 75% for males and females respectively. In the case of normotensive and hypertensive patients, a life table analysis of chances of surviving 1, 5, and 10 years gave probabilities of 100 and 95%. 94 and 80%, and 76 and 49% in both groups respectively. The result clearly emphasize treating of arterial hypertension, and demonstrate that TIA is not only a warning sign of impending stroke but also that of myocardial infarction.

Adolescent↗
PubMedDate not supplied

Xenon contrast-enhanced CT imaging of supratentorial hypoperfusion in patients with brain stem infarction.

BACKGROUND AND PURPOSE: The characteristics of hypoperfusion in the supratentorial region of patients with brain stem infarction are unclear. We investigated the relationships between the presence of hypoperfusion and the location, number, and size of the infarcts with xenon contrast-enhanced CT. METHODS: One hundred five patients with brain stem infarction detected by MR imaging underwent xenon contrast-enhanced CT to measure the regional CBF (rCBF) in the frontal, temporal, parietal, and occipital regions and in the putamen and thalamus. A decrease of more than 10% from the mean rCBF value for normal individuals was considered to indicate hypoperfusion. RESULTS: Thirty-six patients had supratentorial hypoperfusion. The mean rCBF values (measured in mL/100 g/minute) were as follows: frontal region, 36.2 +/- 5.1 (-14.8%, n = 28); parietal region, 42.3 +/- 4.7 (-19.1%, n = 29); temporal region, 41.5 +/- 2.8 (-12.6%, n = 12); and thalamus, 50.1 +/- 3.2 (-19.6%, n = 7). Supratentorial hypoperfusion was associated with pontine infarction in 33 patients (upper pons in 15, middle pons in 18, and lower pons in seven), midbrain infarction in two, and medulla infarction in one. Twenty-three patients had infarcts that were larger than 5 mm, and 11 had infarcts that were 2 to 5 mm. Only two had infarcts that were smaller than 2 mm. Seven patients each had one infarct, 13 each had two, and 16 each had three. CONCLUSION: Supratentorial hypoperfusion was associated with larger infarcts, with more infarcts, and with pontine infarction.

Aged↗
PubMed1998

Impaired clearance of emboli (washout) is an important link between hypoperfusion, embolism, and ischemic stroke.

OBJECTIVE: To explore the relationship between hypoperfusion, embolism, and brain infarction. DESIGN: We studied 4 situations in which brain infarction is related to hypoperfusion: extracranial and intracranial occlusive vascular disease, reduced functional vascular reserve in patients with carotid artery occlusive disease, reduced collateral blood flow in patients given thrombolytic treatment, and cardiac surgery. We reviewed results of emboli monitoring using transcranial Doppler ultrasonography. RESULTS: Hypoperfusion is strongly linked to brain ischemia and infarction. The evidence includes close correlation of (1) the severity of arterial stenosis with brain infarction; (2) impaired functional blood flow reserve in patients with carotid artery disease and subsequent brain infarction; (3) reduced collateral blood flow with poor prognosis after thrombolysis; and (4) stroke-related neurologic deficits after cardiac surgery to hypoperfusion during surgery. Microembolization is common in patients with severe symptomatic carotid artery stenosis and during and after cardiac surgery. CONCLUSIONS: Hypoperfusion and embolism often coexist and their pathophysiological features are interactive. Arterial lumenal narrowing and endothelial abnormalities stimulate clot formation and subsequent embolization. Reduced perfusion limits the ability of the bloodstream to clear or wash out emboli and microemboli and reduces available blood flow to regions rendered ischemic by emboli that block supply arteries. The brain border zones are a favored destination for microemboli that are not cleared. We posit that impaired washout is an important but neglected concept that intertwines hypoperfusion, embolization, and brain infarction.

Arterial Occlusive Diseases↗
PubMed1998

Cyclooxygenase-2 is induced globally in infarcted human brain.

Cyclooxygenase (COX) catalyzes synthesis of prostanoids after liberation of arachidonic acid, an important biochemical sequela of cerebral ischemia that aggravates brain injury. We investigated expression of inducible COX-2 in infarcted human brains (symptom duration, 15 hours to 18 days) and found that COX-2 protein was present in both neuronal and glial cells throughout the brain in accord with infarct topography and duration. These results emphasize the global yet temporally regulated nature of COX-2 induction during focal ischemia in humans, clearly different from the circumscribed acute expression reported in experimental animal models. We speculate that early induction of COX-2 may fuel tissue damage through prostanoids and free radicals, and delayed induction in remote brain areas may promote reconstitutive processes in the face of tissue scarring and remodeling of the surviving neural networks.

Adult↗