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Biomedical subjects

M Kaste

Publications and source records attributed to M Kaste.

At least 91 records · Page 5Linked to original sources

Genetic risk factors and ischaemic cerebrovascular disease: role of common variation of the genes encoding apolipoproteins and angiotensin-converting enzyme.

DNA polymorphisms in genes encoding apolipoproteins (apo) A-I, C-III, B and E and angiotensin-converting enzyme (ACE) have been proposed to be associated with the risk of coronary artery disease (CAD). We studied whether the same genetic markers would also be associated with the occurrence and extent of atherosclerosis in cervical arteries. DNA samples from 234 survivors of stroke or a transient ischaemic attack aged 60 years or less were examined. The presence of atherosclerosis was assessed using aortic arch angiograms. The SstI polymorphism of apoA-I/C-III gene locus, the XbaI polymorphism of apoB gene, common apoE phenotypes and the insertion/deletion polymorphism of the ACE gene were analysed. The allele frequencies of the apoA-I/C-III, apoB, apoE or ACE gene did not differ between the groups with (n = 148) or without (n = 85) cervical atherosclerosis. However, when patients with at least one apoE4 allele and one X2 allele of apoB were combined and compared with those without either of them (E2E3 or E3E3 and X1X1), a significant association with the presence of cervical atherosclerosis was found (P = 0.03). The patients having the E2E3 phenotype had a significantly elevated serum triglyceride level compared with those with the E3E3 phenotype (P = 0.03). Serum high-density lipoprotein (HDL) cholesterol was lower in the patients with the E2E3 phenotype than in those with the E3E3 and E3E4 (P = 0.01 and P = 0.06, respectively). The apoB or ACE genotypes were not significantly associated with serum lipid or lipoprotein levels. There was no association between the ACE gene polymorphism and the occurrence of hypertension. In conclusion, the interaction of common apoB and apoE alleles may increase the risk of atherosclerosis in cervical arteries.

Alleles↗

Comparison of stroke features and disability in daily life in patients with ischemic stroke aged 55 to 70 and 71 to 85 years.

BACKGROUND AND PURPOSE: This study compared stroke features and poststroke disability in two age groups of patients with ischemic stroke: younger (55 to 70 years) and older (71 to 85 years). Stroke has an impact on daily living in many areas, but whether risk factors, stroke features, and poststroke disability differ between young and old patients with stroke is not so well established. METHODS: A cohort of 486 ischemic stroke patients aged 55 to 85 years admitted consecutively to the Helsinki University Central Hospital (Finland) between December 1, 1993, and March 31, 1995, were examined 3 months after the index stroke. Structured medical, neurological, and radiological (MRI or CT) examinations, mental status, and emotional examination and interview of a close informant were done. Prestroke and poststroke activities of daily living were assessed with five scales: the Index of ADL, Instrumental Activities of Daily Living Scale, Functional Activities Questionnaire, Blessed Functional Activities Scale, and Barthel Index. RESULTS: History of cardiac failure (P < .001), atrial fibrillation (P < .001), and cardioembolic stroke (P = .011) was more frequent in the older age group, whereas stroke due to large-artery atherosclerosis (P = .048) was more common in the younger age group. The older patients more often had major dominant stroke syndrome (P = .018). Comparison of activities of daily living before and after stroke showed that the older age group deteriorated significantly more than the younger age group after adjustment for sex, education, and living conditions (Barthel Index, P = .005; other scales, P < .0001). CONCLUSIONS: The stroke patients in young and old age groups had different risk profiles and stroke features. The older stroke patients were more dependent and disabled beforehand, and after stroke they were relatively even more dependent than the patients in the younger age group. Because older patients already constitute the majority of stroke victims, the importance of early active diagnosis, treatment, rehabilitation, and guidance is stressed.

Activities of Daily Living↗

Dementia three months after stroke. Baseline frequency and effect of different definitions of dementia in the Helsinki Stroke Aging Memory Study (SAM) cohort.

BACKGROUND AND PURPOSE: Vascular dementia is a common cause of dementia, and cerebrovascular disease is related to a higher risk of dementia. The frequency of dementia associated with ischemic stroke and the effects of different definitions of dementia in the diagnosis are still incompletely known. We evaluated the frequency of cognitive decline and dementia 3 months after ischemic stroke in a large stroke cohort. METHODS: Our cohort consisted of consecutively admitted ischemic stroke patients (n = 486) aged 55 to 85 years in the Helsinki (Finland) Stroke Aging Memory Study (SAM). Subjects were assessed by structured medical, neurological, and radiological examinations and interview with a close informant, as well as by the Mini-Mental State Examination and detailed clinical mental status examination of defined cognitive domains. The criteria for dementia were those of the Diagnostic and Statistical Manual of Mental Disorders (DSM) (DSM-III, DSM-III-R, and DSM-IV), the National Institute of Neurological Disorders and Stroke-Association Internationale pour la Recherche et l'Enseignement en Neurosciences (NINDS-AIREN), and the International Classification of Diseases, 10th Revision (ICD-10). RESULTS: We found that 451 (92.8%) of the patients were testable, 239 (49.2%) of the patients were women, and the mean age was 71.2 years. Any cognitive decline was present in 61.7%. In the groups aged 55 to 64, 65 to 74, and 75 to 85 years, the frequency of any cognitive decline was 45.7%, 53.8%, and 74.1% (P = .0008), respectively. The frequency of dementia was 25.5% by DSM-III, 20.0% by DSM-III-R, 18.4% by DSM-IV, 21.1% by NINDS-AIREN, and 6.0% by ICD-10 criteria. The frequency increased with increasing age: by the DSM-III definition, frequency in the aforementioned age groups was 19.3%, 23.7%, and 25.5%, respectively (P = .014). There was an overlap in the cases diagnosed as demented according to the different guidelines. Compared with standard diagnosis, the DSM-III was the most sensitive and ICD-10 the most specific. Concordance was moderate between the DSM criteria and NINDS-AIREN criteria but was poor between ICD-10 and the other criteria. CONCLUSIONS: Cognitive decline and dementia were frequent in the cohort of ischemic stroke patients, and the frequency increased with increasing age. Different definitions gave different frequency estimates, and overlap in the cases was observed. Our findings question the validity of current criteria for dementia in the setting of cerebrovascular disease and emphasize the need for further debate and studies to refine the categories of cognitive impairment related to cerebrovascular disease.

Aged↗

Hemostasis and fibrinolysis activation after subarachnoid hemorrhage.

The authors assessed hemostasis and fibrinolysis serially: on admission and on the 1st and 7th days after surgery for subarachnoid hemorrhage (SAH), examining the complications of aneurysm rupture and its surgical repair. Of 32 patients, 25 with SAH were compared with seven control patients who underwent surgery for an unruptured intracranial aneurysm. On admission, patients with SAH had higher thrombin-antithrombin III complex (TAT) levels (13.3 +/- 3.8 vs. 3.8 +/- 0.6 ng/ml, p = 0.01), fibrin degradation product, D-dimer levels (1310 +/- 220 vs. 556 +/- 89 ng/ml, p = 0.0001), and leukocyte counts (14.6 +/- 0.7 vs. 10.6 +/- 1.8 x 10(9) cells/L, p < 0.05) than did control patients. Postoperative D-dimer values (p = 0.007) remained higher in the SAH group. Furthermore, admission D-dimer levels were higher in the patients in poor clinical condition than in those in good condition (2017 +/- 377 vs. 934 +/- 208 ng/ml, p = 0.007), and D-dimer levels were associated with the outcome at 3 months after admission. Additionally, thrombin generation and fibrinolytic markers measured on admission were related to clinical grade, amount of subarachnoid blood seen on computerized tomography (CT) scanning, and patient fatality. Patients with hypodense lesions verified on follow-up CT scanning or with persistent neurological deficits at 3 months had higher prothrombin fragments 1 and 2, TAT, D-dimer, and plasminogen activator inhibitor-1 values on the 1st day postoperatively than did patients without such lesions. In short, in patients with SAH, activation of coagulation and fibrinolysis was strongly associated with clinical state, patient fatality, and outcome at 3 months, and postoperatively this activation correlated with the development of brain infarction.

Adult↗

[Thrombolytic therapy in stroke. What do clinical tests prove?].

Despite the increased risk of intracranial haemorrhage associated with the use of thrombolytic treatment of stroke. American studies have shown patients treated with rt-PA (recombinant plasminogen activator) within three hours of the onset of symptoms to manifest 30 per cent less disability at three-month follow-up than those placebo. However, until satisfactory criteria for the use of rt-PA are available, caution is essential, and thrombolytic therapy should be restricted to specialised centres. It is also important to promote public awareness of the stroke patient's need of immediate treatment at a specialised stroke unit.

Acute Disease↗

Endothelial ICAM-1 expression associated with inflammatory cell response in human ischemic stroke.

BACKGROUND: After focal brain ischemia, leukocytes adhere to the perturbed endothelium and are believed to aggravate reperfusion injury. Although ischemia-induced upregulation of endothelial adhesion molecules, intercellular adhesion molecule-1 (ICAM-1) and P-selectin, has been observed in experimental animals, the mechanism of cerebral leukocyte infiltration and thus therapeutic possibilities to reduce it in humans are uncertain. METHODS AND RESULTS: We counted the granulocytes, mononuclear phagocytes, and the percentages of cerebral microvessels expressing ICAM-1 by applying immunohistochemistry on brain sections showing a variable degree of neuronal damage from 11 human subjects who died 15 hours to 18 days after ischemic stroke and from normal control brains. In infarcted regions, granulocytes were detected as early as at 15 hours after injury (11.3 versus 0.5 cells/mm2 in noninfarcted hemisphere); their amount exceeded 200 cells/mm2 by 2.2 days but was back to normal level at 6.3 and 8.5 days. Acute infarctions (0.6 to 8.5 days) harbored significantly more ICAM-1-stained microvessels (up to 97% of microvessels at 1.8 days) than the noninfarcted hemisphere (P < .001), although the noninfarcted hemisphere (1.8 to 6.3 days) also showed higher ICAM-1 expression than controls. In the absence of ICAM-1 upregulation, macrophages (> 200/mm2) were abundant in the core of neuronal damage at 17 and 18 days. CONCLUSIONS: The striking upregulation of endothelial ICAM-1 expression, functioning in concert with chemotactic factors, may cause granulocyte infiltration during the first 3 days after stroke. This study may support the usage and timing of antibody infusions to block endothelial adhesion molecules in an attempt to reduce leukocyte-induced damage in stroke.

Adult↗

Complement activation in the central nervous system following blood-brain barrier damage in man.

The central nervous system (CNS) is virtually isolated from circulating immunological factors such as complement (C), an important mediator of humoral immunity and inflammation. In circulation, C is constantly inhibited to prevent attack on host cells. Since a host of diseases produce an abnormal blood-brain/cerebrospinal fluid (blood-brain/CSF) permeability allowing C protein extravasation, we investigated if C activation occurs in CSF in vitro and in CNS in vivo during subarachnoid hemorrhage (SAH) or brain infarction. After SAH (n = 15), the terminal complement complex (TCC) concentration on days 0 to 2 was higher in the CSF, 210 +/- 61 ng/ml, than in the plasma, 63 +/- 17 ng/ml, but null in the CSF of controls (n = 8) or patients with an ischemic stroke (n = 7). TCC was eliminated from the CSF after SAH (24 +/- 10 ng/ml on days 7 to 10). Incubation of normal human CSF with serum in vitro also activated the terminal C pathway. In 10 fatal ischemic brain infarctions, immunohistochemical techniques demonstrated neuronal fragment-associated deposition of C9 accompanied by neutrophil infiltration. We conclude that the C system becomes activated intrathecally in SAH and focally in the brain parenchyma in ischemic stroke. By promoting chemotaxis and vascular perturbation, C activation may instigate nonimmune inflammation and aggravate CNS damage in diseases associated with plasma extravasation.

Adult↗

Patients with traumatic brain injury referred to a rehabilitation and re-employment programme: social and professional outcome for 508 Finnish patients 5 or more years after injury.

We studied influence of age and educational level before injury on the social and vocational outcome among a group of traumatic brain injury (TBI) patients with post-injury problems in their education and employment. Patients with TBI, followed up for at least 5 years, and who were admitted to a rehabilitation and re-employment programme, were selected for evaluation of long-term outcome. We used the Glasgow Coma Scale (GCS) scores at the time of emergency admission to the hospital to measure brain injury severity. Age at the time of TBI and educational status before TBI were correlated with the outcome measures at the end of follow-up separately in each category of brain injury severity. The study was carried out at the Kauniala outpatient neurological clinic, which specializes in brain injuries in Finland; it works closely with the Departments of Neurology and Neurosurgery at the Helsinki University Central Hospital. Main outcome measures were functional outcome measured by the Glasgow Outcome Scale (GOS), the educational level reached, and post-injury occupation, as well as the incapacity for work at the end of follow-up. In the severe category of brain injuries, children 7 years or younger at the time of injury suffered severe disability as measured by the GOS scores more often than did the older age groups (p = 0.010, chi 2). They were less often capable of independent employment (p = 0.011, chi 2) than the children injured at the age of 8-16. Patients with a higher education usually had a better outcome. In the category of mild brain injuries the majority of the patients, regardless of age, recovered well according to the GOS, and were capable of independent employment at the end of follow-up. Our patients were selected from the TBI population as survivors with problems in education and re-employment. Those with severe injury sustained early in life (childhood and early teens) coupled with poor educational attainment had relatively worse social and vocational outcome; better outcomes were enjoyed by those severely injured individuals whose injuries were sustained later (late teens or early adulthood). In the groups of patients with moderate and mild brain injuries such a relationship was not found between age or pre-injury education and outcome.

Adolescent↗

Declining incidence and mortality rates of stroke in Finland from 1972 to 1991. Results of three population-based stroke registers.

BACKGROUND AND PURPOSE: We aimed to determine trends in stroke incidence, mortality rates, case-fatality rates, and their relation in Finland. METHODS: We compared the results of three population-based stroke registers that included first-ever strokes in people aged > or = 15 years. Two registers were kept in Espoo-Kauniainen, the first in 1972 to 1973 (EK 72-73) and the second in 1978 to 1980 (EK 78-80). The present register of the Finnish Heart Association (FHA 89-91) was kept in four districts in Finland in 1989 to 1991. RESULTS: The age-adjusted incidence rates were 240.9, 174.4, and 191.6, and the 1-year mortality rates were 121.9, 77.0, and 65.3 in the EK 72-73, EK 78-80, and FHA 89-91 registers, respectively. The overall decline from 1972 to 1991 was 20% in the stroke incidence rate and 46% in the stroke mortality rate. One-month case-fatality rates decreased from 34.8% to 29.4% in the EK 72-73 and EK 78-80 registers and to 23.3% in the present register. CONCLUSIONS: The decline in the stroke incidence rate during the 1970s stabilized during the late 1980s and early 1990s; however, the case-fatality rate is still decreasing. Their combined effects may explain the continuing decline in stroke mortality.

Adolescent↗