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PubMed1991

Congestive heart failure, coronary events and atherothrombotic brain infarction in elderly blacks and whites with systemic hypertension and with and without echocardiographic and electrocardiographic evidence of left ventricular hypertrophy.

Hypertension was present in 50% of 196 blacks and in 36% of 382 whites (p less than 0.001). A prospective study of 84 elderly blacks (70% women) and 326 elderly whites (73% women) with hypertension correlated echocardiographic and electrocardiographic left ventricular (LV) hypertrophy with incidences of congestive heart failure (CHF), coronary events and atherothrombotic brain infarction (ABI). Echocardiographic LV hypertrophy (p less than 0.02) and concentric LV hypertrophy (p less than 0.001) were more prevalent in hypertensive blacks than in hypertensive whites. Hypertensive blacks were younger (78 +/- 9 years) than hypertensive whites (82 +/- 7 years) (p less than 0.001). Other coronary risk factors were similar, except for higher serum triglycerides in whites than in blacks (p less than 0.02). Follow-up was 37 +/- 18 months in blacks and 43 +/- 18 months in whites (p less than 0.01). Incidences of CHF and coronary events were not significantly different in blacks and whites. ABI incidence was 38% in blacks and 21% in whites (p less than 0.005). Multiple logistic regression analysis showed that prior CHF (p = 0.000), concentric LV hypertrophy (p = 0.018) and echocardiographic LV hypertrophy (p = 0.022) were independent risk factors for CHF. Echocardiographic LV hypertrophy (p = 0.001), serum total cholesterol (p = 0.002), concentric LV hypertrophy (p = 0.005) and prior coronary artery disease (p = 0.042) were independent risk factors for coronary events. Prior ABI (p = 0.001), echocardiographic LV hypertrophy (p = 0.001) and electrocardiographic LV hypertrophy (p = 0.034) were independent risk factors for ABI.

Aged↗
PubMed1994

Ancrod for the treatment of acute ischemic brain infarction. The Ancrod Stroke Study Investigators.

BACKGROUND AND PURPOSE: There is no acute therapy proven to be of benefit for ischemic stroke. Ancrod is a potentially effective therapy because of the advantageous consequences of fibrinogen lowering. METHODS: We studied the safety and efficacy of ancrod in patients with acute ischemic stroke administered within 6 hours of stroke onset. In a double-blind, randomized, placebo-controlled trial 64 patients received intravenous ancrod and 68 received placebo for 7 days. Neurological outcome, disability, and brain infarct volume were measured. RESULTS: There was no significant difference in overall mean scores on the Scandinavian Stroke Scale. No increase in bleeding occurred in the ancrod-treated patients. The target reduction of plasma fibrinogen levels of less than 100 mg/dL was achieved in only 15 (23%) of 64 ancrod-treated patients. Those patients with ancrod-induced 6-hour fibrinogen levels 130 mg/dL or less had a marginally significantly better neurological outcome on the Scandinavian Stroke Scale, mortality, and Barthel Index than ancrod-treated patients with higher fibrinogen levels. CONCLUSIONS: Ancrod appears safe and potentially effective when administered to patients within 6 hours of onset of ischemic stroke.

Acute Disease↗
PubMed1987

Risk factors for atherothrombotic brain infarction in persons over 62 years of age in a long-term health care facility.

A history of systolic (greater than or equal to 160 mm Hg) or diastolic (greater than or equal to 90 mm Hg) hypertension, diabetes mellitus (fasting venous plasma glucose greater than or equal to 140 mg/dl), a history of cigarette smoking, fasting serum total cholesterol greater than or equal to 200 mg/dl and greater than or equal to 250 mg/dl, and obesity (greater than or equal to 20% above ideal body weight) were examined as risk factors for atherothrombotic brain infarction (ABI) in 144 men, mean age 81 +/- 8 years, and 391 women, mean age 82 +/- 8 years, in a long-term health care facility. ABI occurred in 33 of 144 men (23%) and in 68 of 391 women (17%), P not significant. A history of systolic or diastolic hypertension correlated with ABI in both men and women (P less than 0.001). Diabetes mellitus correlated with ABI in both men and women (P less than 0.001). A history of cigarette smoking correlated with ABI in men (P less than 0.02) but not in women. Serum total cholesterol greater than or equal to 200 mg/dl and greater than or equal to 250 mg/dl did not significantly correlate with ABI in men or in women. Obesity did not significantly correlate with ABI in men or in women. Systolic or diastolic hypertension, diabetes mellitus, and cigarette smoking are risk factors for ABI in elderly men. Systolic or diastolic hypertension and diabetes mellitus are risk factors for ABI in elderly women.

Aged↗
PubMed1978

[Survived brain infarction in old age - clinical and morphological findings. II. Risk factors (author's transl)].

208 hospitalized patients, nearly 80 years old, were investigated because of risk factors and complicating diseases. Hypertension (58.2%), typical myocardial infarctions (37.2%) and diabetes (45.2%) were twice often as in our comparable cases without stroke. Corresponding we found signs of left ventricular hypertrophy in more than 50% post mortem. The dimensions of heart failure by hypertension are visible in ECG indicating LVH with many dysrhythmias. Early mortality (40%) as survival time are dependent on the size of the stroke. Cardiovascular causes of death were found mainly. The differences to younger patients with brain infarction seem to be only of gradually nature and especially to refer to the more intensive damaged heart.

Age Factors↗
PubMed1993

Accelerated brain infarction in hypertension complicated by hereditary heterozygous protein C deficiency.

BACKGROUND: Protein C deficiency leads to reduced inhibition of coagulation and an increased likelihood of thrombosis. It is widely accepted that the most common syndromes associated with protein C deficiency are venous thrombosis and pulmonary thromboembolism, whereas arterial thrombosis is rare. Here we describe two patients with hypertension and hereditary heterozygous protein C deficiency who developed multiple lacunar infarcts. CASE DESCRIPTIONS: Patient 1 was a 46-year-old man with a history of hypertension who developed a right upper quadrantanopia and gradually progressive intellectual and behavioral deterioration. Patient 2 was a 61-year-old man with history of hypertension and two episodes of right-sided motor weakness who developed left sixth and seventh cranial-nerve palsies and reduced pinprick sensation in the right extremities. In both patients, magnetic resonance imaging revealed multiple small lesions in the pons as well as the bilateral basal ganglia, thalamus, corona radiata, and other subcortical structures, which are consistent with lacunar infarcts. Protein C activity and antigen levels were reduced to approximately one half of normal in these two patients, as well as in some of their family members who had no other serological or coagulation abnormalities. A diagnosis of heterozygous protein C deficiency type 1 was thus established. CONCLUSIONS: Although it remains uncertain whether protein C deficiency itself increases the risk of cerebral artery thrombosis, it may predispose a patient to develop multiple brain infarctions in association with hypertension.

Blood Coagulation Disorders↗
PubMed2003

[Ischemia brain infarct and rupture of an infrarenal anortic aneurysm].

An 86-year old lady with aphasia, left sided hemiparesis, a heart rate of 110 bpm and a blood pressure of 110/60 mmHg was intubated by the emergency physician. She was given 1000 ml crystalloid fluid IV and brought to our department with suspected stroke. Clinical examination revealed a pulsatile abdominal mass, while immediate CT-scan excluded an intracranial hemorrhage. The patient developed shock and lactic acidosis, and ultrasound examination confirmed the diagnosis of a ruptured abdominal aortic aneurysm. The patient underwent emergency laparotomy, and after cross clamping of the aorta a tube prosthesis was inserted. The following day a CT-scan revealed an ischemic brain infarction in the territory of the right middle cerebral artery. On duplex examination, no relevant stenoses of the extracranial arteries could be found. Postoperatively, the patient suffered from bilateral pleural effusions and pneumonia. Finally, she was weaned successfully from the respirator and transferred to a neurologic rehabilitation clinic on day 52 after admission. Even focal neurological deficits, especially when combined with hypotension, may have systemic causes such as anemia and volume depletion, as in this patient with at first hand unnoticed bleeding.

Acidosis, Lactic↗
PubMed1995

Silent brain infarcts and transient ischemic attacks. A three-year study of first-ever ischemic stroke patients: the Klosterneuburg Stroke Data Bank.

BACKGROUND AND PURPOSE: We undertook to study the clinical relevance of silent strokes and history of transient ischemic attacks (TIAs) and their individual and combined effects on outcome variables of neurological and epidemiological interest in first-ever stroke patients. METHODS: We performed univariate and multivariate analyses of data prospectively collected in the Klosterneuburg Stroke Data Bank, a hospital-based registry in Austria that includes a 3-year follow-up program. RESULTS: Of 728 patients (mean age, 68 +/- 10 years) with a first-ever ischemic stroke, 110 (15%) had had a previous TIA, and 66/618 (11%) patients did not have a history of TIA but showed evidence of silent brain infarct on CT. Outcome variables of neurological interest were not significantly different between groups, including time between stroke and study entry, activities of daily living status at first presentation, median time of hospitalization, 30-day mortality, or 3-year mortality. Univariate analyses of epidemiologically important risk factors showed either history of TIA or evidence of silent infarct to be more frequently associated with hypertension (P = .007). Cox models of survival showed that neither history of TIA nor evidence of silent infarct were significantly associated with an increase in 3-year mortality. CONCLUSIONS: Over a period of 3 years, neither history of TIA nor evidence of silent infarct diagnosed at the time of the presenting major stroke in first-ever ischemic stroke patients exert an important influence on neurological or epidemiological outcome variables.

Adult↗
PubMed1996

Enzyme-histochemical and morphological characteristics of fast- and slow-twitch skeletal muscle after brain infarction in the rat.

The right middle cerebral artery was permanently occluded in 12-week-old male spontaneously hypertensive rats. After the surgery the rats were subjected to repeated behavioural tests during the observation period. Fourteen weeks after surgery the fast-twitch extensor digitorum longus (EDL) and the slow-twitch soleus muscle of both sides were removed and examined with regard to muscle fibre characteristics obtained by histochemical and morphometrical methods. Comparisons were made with age-matched controls. Limb placement and the ability to traverse a beam or a rotating pole were repeatedly tested 2-13 weeks after the operation. In spite of permanent sensorimotor deficits in limb placement and when traversing a rotating pole or beam, no increase in pathological changes was noted in either EDL or soleus. The number and proportion of fibre types remained unchanged in both muscles. There was no difference in muscle fibre size in either EDL or soleus. It is concluded that brain infarction in the rat, although causing marked impairment of contralateral motor function, does not have a major influence on the muscle-fibre morphology or fibre-type composition, irrespective of muscle type.

Animals↗
PubMed1991

[A case of brain infarction associated with viral encephalitis: MRI and pathological findings].

A 10-year-old girl had an infarction in the left brain during an acute viral meningoencephalitis. She initially showed seizure, unconsciousness and fever, and right hemiplegia gradually developed. She died at the 48th day of disease from respiratory disturbance and renal failure. Cranial MRI during the acute phase of the disease, when there was no clinical sign of right hemiplegia, showed a high intensity lesion in the left parietal and occipital areas on T-2 weight image. Autopsy disclosed the findings suggesting viral encephalitis, including multiple focal necrosis, perivascular round cell infiltration, proliferation of glial cells and spongy degeneration with some intranuclear inclusion bodies, and infarction in the left hemisphere. These findings suggest that T-2 high intensity lesion on MRI reflected infarction.

Cerebral Infarction↗
PubMed2004

Fas and activated caspase 8 in normal, Alzheimer and multiple infarct brains.

Using immunohistochemistry, Fas and caspase 8 positive sites were localized in the brains of Alzheimer patients and those with multiple infarcts as well as age-matched normal. The frontal, occipital and hippocampal regions were dissected out from these patients and normal individuals shortly after death. Positive Fas neurons were found in all these regions of normal individuals and Alzheimer patients, but not in the brains of patients with multiple infarct. Activated caspase 8 protein was found only in the brains of Alzheimer patients and not in the other groups. Plaques in the Alzheimer patients were positive for Fas and activated caspase 8. The former was localized in the membrane and the inside of the plaque whereas activated caspase 8 was only present in the interior of the plaque, as revealed by confocal microscopy. Our study shows that caspase 8 was activated in the Alzheimer brain and the presence of Fas and activated caspase 8 points to a possibility that at least some plaques were of intracellular origin as Fas was a cell membrane receptor and caspase 8 was a intracellular enzyme downstream to Fas. Furthermore, we had confirmed that in most neurons Fas and caspase 8 did not exist concomitantly and that the glial cells (astrocytes) did not express caspase 8 in Alzheimer patients.

Aged↗
PubMed2001

Metabolism of 99mTc-ethylcysteinate dimer in infarcted brain tissue of rats.

UNLABELLED: Brain SPECT with 99mTc-ethylcysteinate dimer (99mTc-ECD) reveals a subacute cerebral infarct as a hypoactive area, even in the presence of postischemic hyperperfusion. The brain retention of 99mTc-ECD depends on hydrophilic conversion mediated by enzymes, and impaired enzymatic trapping is hypothesized to depress the retention efficiency in the infarcted region. The aim of this study was to determine whether the metabolic rate of 99mTc-ECD is actually reduced in infarcted brain tissue. METHODS: In 50 mmol/L phosphate buffer (pH 7.4), 99mTc-ECD was incubated for 30 min with homogenates of rat brain tissue with and without triphenyltetrazolium chloride (TTC) staining. The ratio of polar products was determined by thin-layer chromatography as a function of incubation time, and metabolic rates were obtained. Permanent focal ischemia was induced by occlusion of the right middle cerebral artery (MCA) in rats. The brain was removed 24 h after MCA occlusion, and the infarcted area was defined by TTC staining. The metabolic rate of 99mTc-ECD was determined in homogenates of infarcted tissue, contralateral noninfarcted tissue, and tissue sampled from sham-operated rats. The infarct volume was measured by direct and indirect methods to assess volume expansion caused by edema, and the metabolic rate in infarcted tissue was corrected for the effect of edema. RESULTS: TTC staining had no effect on the metabolic rate of 99mTc-ECD. The metabolic rates in the infarcted tissue were 0.222%/min +/- 0.054%/min and 0.285%/min +/- 0.064%/min before and after correction for edema, respectively. These rates were significantly lower than those in the contralateral noninfarcted tissue (0.426%/min +/- 0.028%/min) and the tissue sampled from the sham-operated rats (0.439%/min +/- 0.031%/min). No substantial difference in rates was observed between the contralateral tissue and the tissue from the sham-operated rats. CONCLUSION: The results of this study showed that infarction decreases the activity of enzymes that mediate the hydrophilic conversion of 99mTc-ECD in the brain and suggest that reduced metabolic activity is related to decreased accumulation of 99mTc-ECD in hyperperfused infarcts.

Animals↗
PubMed2002

Silent brain infarcts are rare in Kuwaiti children with sickle cell disease and high Hb F.

Overt stroke is rare among sickle cell disease (SCD) patients in Kuwait. However, there are no previous studies of silent cerebral infarcts, which have been described in up to 20% of American children with Hb SS. We have carried out a prospective brain MRI study among otherwise normal SCD patients, who were consecutive patients seen in a 1-year period to document the prevalence of silent cerebral infarcts in children with sickle cell disease in Kuwait. Any patient with a previous seizure or other neurological abnormality was excluded. MRI was done with a 1.5 Tesla unit with super-conducting magnet. T1- and T2-weighted sagittal and axial sections and proton density axial images were obtained in 5-mm thick sections. The study group consisted of 30 (23 SS and 7 Sbeta(0)Thal) patients-19 males and 11 females-whose ages ranged from 6 to 17 (mean of 9.8 +/- 3.5) years. Hb F ranged from 11% to 35% with a mean of 22.8% +/- 5.7%. Only one patient, a 10-and-a-half-year-old boy with Hb SS, showed hyperintense signals in the parietal white matter, consistent with small infarcts, thus giving a prevalence of 3.3%. Silent brain infarcts are uncommon in our patients, and the protective factors remain to be fully elucidated.

Adolescent↗