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Biomedical subjects

M Yasaka

Publications and source records attributed to M Yasaka.

At least 19 recordsLinked to original sources
PubMed2003

Population-based distribution of plasminogen activity and estimated prevalence and relevance to thrombotic diseases of plasminogen deficiency in the Japanese: the Suita Study.

Reduced plasminogen activity with a normal level of antigen is commonly observed in Japanese individuals. The first reported patient with plasminogen deficiency was accompanied with deep vein thrombosis. The present study examines whether heterozygous or homozygous deficiency of plasminogen is a risk factor for thrombotic disease. This study measures the plasminogen activity of 4517 individuals in the general population, determines the cut-off to define plasminogen deficiency, and identifies plasminogen deficiencies in the control groups and thrombotic disease groups. In another study, we examined the phenotypes of consecutive patients with homozygous plasminogen deficiency detected in our hospital. We found 173 and two of 4517 individuals to have heterozygous and homozygous deficiency with normal plasminogen antigen level, respectively, and 19 to have heterozygous deficiency with reduced antigen levels. The incidence of plasminogen deficiency in an age- and sex-matched control group (13/324, 4.01% for deep vein thrombosis or 13/330, 3.94% for stroke) selected from the 4517 individuals was not significantly different from those in patients with deep vein thrombosis (3/108, 2.78%) or cardioembolic stroke (6/110, 5.55%). Among 19 patients with homozygous plasminogen deficiency showing about 10% plasminogen activity, none had deep vein thrombosis. These findings indicate that neither heterozygous nor homozygous plasminogen deficiency constitutes a significant risk factor for thrombotic disease.

Aged↗
PubMed2002

Effect of prothrombin complex concentrate on INR and blood coagulation system in emergency patients treated with warfarin overdose.

We investigated the effect of prothrombin complex concentrate (PCC) on the international normalized ratio (INR) and blood coagulation system in two emergent patients treated with warfarin for secondary prevention of cardioembolic stroke due to nonvalvular atrial fibrillation. An 80-year-old woman developed massive subcutaneous hemorrhage and swelling on her right upper extremity with weak pulsation of the right radial artery and had an INR above 10. An 83-year-old man had pleural effusion with an INR value of 6.69 and pleural puncture was immediately required. We administered 500 IU of PCC to the two patients (17.2 IU/kg and 12.5 IU/kg) with 10 mg of vitamin K. The INR decreased to 1.12 and 1.85, respectively, with an increase of plasma levels of protein C and coagulant factors IIa, VIIa, IXa, and Xa 10 min after administration. The plasma levels of the thrombin-antithrombin III complex increased (from 4.0 to 12.0 micro g/l and from 0.5 to 28.9 micro g/l, respectively, normal value <3.0), but prothrombin fragment 1+2 increased minimally 10 min after administration (from 0.4 to 1.1 nmol/ml and from 0.4 to 0.7 nmol/ml, respectively, normal value 0.4-1.4 nmol/ml). Plasma levels of D-dimer remained unchanged. The massive subcutaneous hemorrhage in the former patient improved in 14 days. Anticoagulation was restarted in the latter patient after 14 days of PCC administration. There were no embolic episodes during the month after PCC administration. In conclusion, a small amount of PCC may be effective in immediately correcting increased INR levels with increased plasma levels of protein C and coagulant factors IIa, VIIa, IXa, and Xa and may partially activate the coagulation system without any effects on plasma levels of D-dimer.

Aged↗
PubMed2001

Prediction of the final infarct volume within 6 h of stroke using single photon emission computed tomography with technetium-99m hexamethylpropylene amine oxime.

BACKGROUND: A simple method to predict the final infarct volume within 6 h of onset of hemispheric ischemic stroke based on the measurement of cerebral blood flow (CBF) using single photon emission computed tomography (SPECT) with techneticum-99m hexamethylpropylene amine oxime ((99m)Tc-HMPAO) was investigated in a clinical model involving patients without definite early reperfusion or clinical recovery. METHODS: A group of 16 patients (group 1) was used to establish the methodology, which was then validated in a second group of 14 patients (group 2). The final infarct volume was defined using computed tomography (CT) performed at least 7 days after stroke. The relative CBF threshold value, expressed as a percentage of the mean contralateral hemispheric value, which most closely estimated the final infarct size on coregistered CT was established for each patient. RESULTS: The mean threshold CBF value for group 1 was 63.7%. When this value was used to predict infarct size in group 2, a close correlation was observed between the actual and the estimated sizes (r = 0.973, p < 0.0001). This value was not time dependent. CONCLUSIONS: If no significant early reperfusion or clinical recovery occurs, a CBF threshold value of 63.7% on (99m)Tc-HMPAO SPECT performed within 6 h of stroke onset will reliably predict the final infarct size.

Aged↗
PubMed2001

Hypertension and neurovascular compression of the left lateral medulla oblongata in ischemic stroke.

Hypertension is a major risk factor for stroke. Neurovascular compression (NC) of the left ventrolateral medulla oblongata may cause arterial hypertension. We evaluated the relationship between the two ischemic stroke patients. We classified 69 patients under 50 years old (49 men and 20 women, aged 43.6 +/- 7.3 years) based on magnetic resonance imaging findings as follows: NC patients (n = 38; 10 with NC on the right side, 18 with NC on the left side, and 10 with NC on both sides) and non-NC patients (n = 31). We compared the following clinical characteristics between the two groups: (1) risk factors for stroke, including hypertension, diabetes mellitus, hypercholesterolemia, and smoking and (2) stroke subtype. Hypertension was more frequent in the NC group than in the non-NC group (58 vs. 19%, p = 0.001). Hypertension was more frequent in patients with left-side NC than in those with right-side NC (78 vs. 20%, p = 0.005). No other differences were observed between the two groups. Twelve patients presented with atherothrombotic stroke, 16 with cardioembolic stroke, 24 with lacunar stroke and 17 with stroke of miscellaneous etiology. NC was significantly more common in patients with lacunar stroke as compared with those affected by other stroke subtypes (p = 0.015). We found a significant relationship between hypertension and NC of the ventrolateral medulla oblongata on the left side in ischemic stroke patients younger than 50 years of age. Some patients with lacunar stroke may have hyptertension related to NC.

Adolescent↗
PubMed2001

Blood flow in the left atrial appendage and embolic stroke in nonvalvular atrial fibrillation.

It is unclear if low flow velocity in the left atrial appendage (LAA) is a predisposing factor to stroke in patients with nonvalvular atrial fibrillation (NVAF). We investigated flow velocity in the LAA in NVAF patients in relation to a past history of stroke and other potential embolic sources. We measured and analyzed peak flow velocities into (FV-in) and out of (FV-out) the LAA in a middle portion of the LAA in 35 NVAF patients by transesophageal echocardiography (TEE). We divided the NVAF patients into 3 groups: the Eaf group had a history of embolic stroke without any other potential embolic sources; the Emulti group had other potential embolic sources, and the control group had no embolic history. FV-in and FV-out in the Eaf group (12.3 +/- 6.7 and 10.2 +/- 7.3 cm/s) were significantly lower than those in the control group (24.3 +/- 11.3 and 19.9 +/- 8.8 cm/s; multicomparison Scheffé's test, p = 0.0123 and 0.0395, respectively). The Emulti group varied in those values from less than 5 to above 35. Low flow velocity in the LAA seems to be a predisposing factor for stroke in NVAF patients without any other sources of emboli.

Aged↗
PubMed2001

Secondary prevention of stroke in patients with nonvalvular atrial fibrillation: optimal intensity of anticoagulation.

Nonvalvular atrial fibrillation (NVAF) is frequently seen in elderly people and has become a main cause of cardioembolic stroke. The efficacy of anticoagulation for primary prevention of stroke or transient ischaemic attacks (TIAs) in patients with NVAF has been established by prospective, randomised and controlled trials. Warfarin decreased the frequency of all strokes by 68% and the rate of the combined outcome of stroke, systemic embolism or death by 48%. Anticoagulation with warfarin using international normalised ratios (INRs) ranging from 2.0 to 3.0 is recommended for patients with NVAF, who have any of the risk factors identified by the Atrial Fibrillation Investigators (AFI) [previous stroke or TIA, history of hypertension, diabetes mellitus, advanced age (> or = 65 years old), congestive heart failure and coronary artery disease], the American College of Chest Physicians (ACCP) [increased age (> 75 years old), prior stroke, hypertension and heart failure], or the Stroke Prevention in Atrial Fibrillation (SPAF) investigators [women > 75 years old, prior stroke, systolic blood pressure > 160mm Hg, recent heart failure, and fractional shortening < 25% on echocardiography]. For the secondary prevention of stroke, the efficacy of adjusted-dose warfarin therapy has been demonstrated by 2 major randomised trials. SPAF III (INR 2.0 to 3.0) demonstrated a lower incidence of ischaemic stroke or systemic embolism (3.4 %/year) compared with low fixed-dose warfarin plus aspirin (acetylsalicylic acid) [11.9%]. The European Atrial Fibrillation Trial [EAFT] (INR 2.5 to 4.0) showed a lower incidence of all stroke (4.0 %/year) with adjusted-dose warfarin compared with placebo (12.0 %/year). The incidence of major bleeding in the adjusted-dose warfarin group in SPAF III and EAFT was 2.4 and 2.8 %/year, respectively. EAFT incidence rates for the occurrence of a first ischaemic or haemorrhagic complication analysed by INR range indicated that the rate was lowest at INRs of 2.0 to 2.9, and higher with INRs of 3.0 to 3.9. Therefore, the optimal intensity of anticoagulation for prevention of recurrent stroke seems to be an INR of between 2.0 and 3.0, as for primary prevention. Retrospective and prospective studies from Japan reported that in the elderly, haemorrhagic complications occur frequently with INRs above 2.6 and major ischaemic events cannot be prevented at INRs below 1.6. Therefore, an INR target between 1.6 and 2.6 may be an alternative for secondary prevention of stroke in elderly patients with NVAF who have a potential risk of bleeding, to avoid both major ischaemic and haemorrhagic events. Antiplatelets may be administered in patients who are unable to manage taking warfarin properly or who have a high risk of falling and subsequently sustaining a head injury, although the efficacy of antiplatelets for secondary prevention of stroke in NVAF has not yet been established.

Anticoagulants↗
PubMed2001

Optimal intensity of international normalized ratio in warfarin therapy for secondary prevention of stroke in patients with non-valvular atrial fibrillation.

OBJECTIVE: To determine optimal intensity of international normalized ratio (INR) of warfarin therapy for the prevention of ischemic events in patients with non-valvular atrial fibrillation (NVAF), we evaluated the risk of severe recurrent stroke, systemic embolism and major hemorrhagic complications according to INR and age. METHODS: We carried out the National Cardiovascular Center (NCVC) NVAF Secondary Prevention Study and analyzed data with those of Japanese Nonvaluvular Atrial Fibrillation-embolism Secondary Prevention Cooperative Study to elucidate relationships of major stroke and hemorrhage with INR and age. In both studies, all patients with cardioembolic stroke were given warfarin, monitored with INR every month, and followed up for primary endpoints of stroke and embolism to other parts of the body, and for secondary endpoints of major hemorrhagic complications requiring blood transfusion or hospitalization. We regarded ischemic stroke with NIH stroke scale (NIHSS) score > or = 10 or systemic embolism as a major ischemic event and ischemic stroke with NIHSS score <10 as a minor ischemic event. There were 203 patients enrolled in total (152 men and 51 women). We investigated the relationship of occurrence of the events with INR and age, and calculated the incidence rates of major and minor ischemic events and major hemorrhagic events. RESULTS: During the mean follow-up of 653 days, major ischemic stroke and systemic embolism occurred in only 4 patients with INR <1.6, minor ischemic stroke in 10 patients with INR 1.50-2.66, and major hemorrhage in 9 patients with INR 2.30-3.56. Patients with major ischemic or hemorrhagic events were significantly older than those without any events (75+/-4 years vs. 67+/-7 years, p<0.001 unpaired t test). Incidence rates of any events at INR < or = 1.59, 1.60-1.99, 2.00-2.59 and > or = 2.60 were 8.6%, 3.8%, 4.9%, and 25.7%/year, respectively. CONCLUSIONS: Major ischemic or hemorrhagic events occur often in the elderly NVAF patients, in whom an INR value of between 1.6 and 2.6 seems optimal to prevent such events.

Aged↗
PubMed2001

Massive pontine hemorrhagic infarction associated with embolic basilar artery occlusion.

We report here an autopsy case of massive pontine hemorrhagic infarction secondary to embolic basilar artery occlusion. A large embolus appeared to have traversed the vertebral artery into the basilar artery as a result of basilarization of the vertebral artery due to severe stenosis of the contralateral vertebral artery. Extensive ischemia due to embolic occlusion of the entire length of the basilar artery, and migration of the embolus are assumed to have resulted in a massive pontine hemorrhagic infarction.

Aged↗
PubMed2000

Lesions visualized by contrast-enhanced magnetic resonance imaging in transient ischemic attacks.

In patients with transient ischemic attacks (TIAs), contrast-enhanced magnetic resonance imaging (MRI) is more sensitive to visualize the recent ischemic lesions than conventional MRI. We examined the clinical characteristics of TIA patients presenting with enhanced lesions visualized by contrast-enhanced MRI. We retrospectively evaluated 64 patients with carotid TIAs. We evaluated the frequency and topography of TIA associated infarcts on contrast-enhanced MRI and compared the clinical background of patients with and without such lesions. Twenty-three patients underwent plain MRI only, while the remaining 41 patients underwent contrast-enhanced MRI. Of the latter 41 patients, 16 had abnormal enhanced lesions (39%: group L), while 25 had no lesions (61%: group NL). In group L, all lesions were spotty, and they were located in the cerebral cortex in 13 patients (81%), the subcortex in two (12%), and the perforator territory in one (6%). Aphasia or confusional state, hypertension, and emboligenic cardiac or arterial disease (stenosis > or =50%) were more frequently observed in group L than in group NL (38 vs. 8%, 81 vs. 48%, and 93 vs. 60%, respectively, P<0. 05). The TIA patients with enhanced lesions on MRI may be associated with an emboligenic cardiac or arterial disease, severe neurologic symptom compared to those without them.

Aged↗
PubMed2000

Evaluation of posterior cerebral artery flow velocity by transcranial color-coded real-time sonography.

Using transcranial color-coded real-time sonography (TCCS), we measured peak-systolic flow velocities (PSVs) in segment P2 of 102 posterior cerebral arteries (PCAs) in 61 patients, with angiography. We divided 102 PCAs into four groups: control group (n = 70) with no significant stenotic lesions; PCS group (n = 7) with stenosis >/= 50% of P2 segment; Col (+) group (n = 13) and Col (-) group (n = 12) had occlusive lesions in the carotid system with or without collateral flow from PCA to the middle cerebral artery through the leptomeningeal anastomosis. In the PCS group, PSV (255.7 +/- 67.2 cm/s) was higher than in the other three groups (p < 0.0001). PSV was higher in the Col (+) group (127.6 +/- 31.2) than in the Col (-) (86.6 +/- 20.1) and control (83.8 +/- 24.8) groups (p < 0.001). The measurement of PSV in the P2 segment of PCA using TCCS may help to identify a significant stenosis in PCA.

Blood Flow Velocity↗
PubMed1999

The duration of symptoms in transient ischemic attack.

BACKGROUND: The majority of TIAs last from 2 to 15 minutes, although some may be of long duration. OBJECTIVE: We examined factors related to the duration of TIAs to identify the relationship to clinical characteristics. METHODS: We performed brain imaging studies as well as angiographic and cardiac examinations in 81 consecutive patients (64 men and 17 women, age 65.8+/-9.9 years) with carotid TIAs. We evaluated risk factors (hypertension, diabetes mellitus, hyperlipidemia, alcohol consumption, and smoking), potential cardiac sources of emboli, and arterial stenosis > or =50% in diameter in the carotid or middle cerebral arteries. Recent infarcts were assessed with CT or MRI. We correlated duration of symptoms with clinical data. RESULTS: The presence of emboligenic cardiac or arterial diseases was significantly related to the duration of symptoms. With sensitivity-specificity curve analysis for detecting such diseases, the duration of symptoms could be divided into short-duration TIAs (<60 minutes, n = 41) or long-duration TIAs (> or =60 minutes, n = 40). Patients with long-duration TIAs had emboligenic cardiac or arterial diseases more frequently than those with short-duration TIAs (86% versus 46%, p < 0.001). Recent infarcts were also more frequent in patients with long-duration TIAs than they were in patients with short-duration TIAs (45% versus 21%, p < 0.05). CONCLUSIONS: Short-duration and long-duration TIAs can be separated based on symptom duration of < 1 hour or > or = 1 hour. Patients with long-duration TIAs should be examined more closely for the presence of cardiac and arterial diseases than those with short-duration TIAs.

Aged↗
PubMed1999

Nimodipine and perfusion changes after stroke.

BACKGROUND AND PURPOSE: Meta-analysis of previous trials of oral nimodipine in acute stroke has suggested a benefit when commenced within 12 hours of onset. We sought to study the effect of oral nimodipine on reperfusion after acute stroke and the relation between reperfusion and outcome. METHODS: Fifty patients with acute middle cerebral artery territory cortical infarction were blindly randomized within 12 hours of onset to either oral nimodipine (30 mg every 6 hours) or placebo. Treatment was continued for 2 weeks. Cerebral blood flow was assessed with the use of 99mTc-hexamethylpropyleneamine oxime single-photon emission CT before therapy, 24 hours later, and at 3 months. Hypoperfusion was measured by a validated volumetric technique. Neurological impairment and functional outcome were assessed with the Canadian Neurological Scale and Barthel Index, respectively. Tissue loss was measured with CT at 3 months. Four patients were excluded from analysis for technical reasons. RESULTS: Twenty-three patients received nimodipine, and 23 received placebo. In the nimodipine group, there was early reperfusion that was not maintained at outcome (P=0.01). In the placebo group, mean infarct hypoperfusion volumes showed no overall change. Nonnutritional reperfusion in nimodipine-treated patients was associated with adverse neurological (P=0.05) and functional outcome (P=0.06). There was, however, no difference in clinical outcome between the 2 groups. CONCLUSIONS: Oral nimodipine administered within 12 hours enhanced acute reperfusion, but this was largely nonnutritional. Larger studies using a shorter treatment delay are required to evaluate the clinical efficacy of nimodipine in acute ischemic stroke.

Acute Disease↗
PubMed1999

[A case with frequent episodes of transient ischemic attack presenting the Wallenberg syndrome before and after the onset of brain infarction].

A 52-year-old man with diabetes mellitus, hyperlipidemia and smoking habit, experienced transient ischemic attacks (TIAs) with symptoms of left orbital pain, left blepharoptosis and hoarseness lasting for five minutes on March 10, 1997. Subsequently, the same symptoms repeated once or twice daily. On March 28, he had dysphagia, numbness and disturbance of pain and temperature sensation (segmental dissociated sensory disturbance) on the right side of the body above the level of the Th10, the right upper limb and face. The deficits persisted for more than 24 hours. Angiographic studies revealed an occlusion of the left vertebral artery immediately after branching of the posterior inferior cerebellar artery. MRI demonstrated a hyperintense lesion on MRI T2 weighted image in the left lateral medulla. About three months after the completed stroke, he had six episodes of TIAs of left Horner's sign and hoarseness. To our knowledge, this is the rare case that had frequent TIAs presenting the Wallenberg syndrome before and after the onset of lateral medullary infarction. We speculate that the TIAs resulted from microembolism from the proximal end of occluted left vertebral artery and failure of the microcirculation in and around the lateral portion of the medulla oblongata.

Cerebral Infarction↗
PubMed1999

[Homolateral ataxia and crural paresis following anterior cerebral artery territory infarction].

Homolateral ataxia and crural paresis (HACP) is defined as predominantly crural paresis with ipsilateral ataxia, a variant of ataxic hemiparesis (AH), by Fisher and his colleagues. HACP usually resulted from lacunar infarction in the basis pontis at the junction of the upper one-third and inferior two-third of the pons, or in the posterior limb of the internal capsule. We reported a patient with HACP which was caused by an infarct in the paracentral gyrus irrigated by the anterior cerebral artery (ACA). He had had no cerebellar signs before the onset of HACP, although he had old small infarcts in the right pons, right thalamus and left cerebellar hemisphere. Neuroimaging and other clinical studies suggested that the mechanism of the present infarction was the most-likely embolic, but not lacunar. As far as we know, there has been only one abstract presentation of a patient with HACP due to ACA territory infarction in Japan, although five such cases were recently reported by Bogousslavsky and others.

Aged↗
PubMed1998

Oscillating thromboemboli within the extracranial internal carotid artery demonstrated by ultrasonography in patients with acute cardioembolic stroke.

We detected oscillating thromboemboli at the extracranial internal carotid artery (ICA) by duplex carotid ultrasonography in patients with acute cardioembolic stroke. Using B-mode ultrasonography, we evaluated the extracranial ICA in 11 patients with acute cardioembolic ICA occlusion. A homogeneous, elastic, oscillating intraluminal mass echo originating in the extracranial ICA extended distally in 5 (46%) of these patients. The echoes moved quickly and distally during the systolic phase of the cardiac cycle and returned slowly to the original position during the diastolic phase. We performed a postmortem study 24 days after stroke onset in 1 patient with an oscillating intraluminal mass echo that had been demonstrated by duplex ultrasonography. The ICA lumen was obstructed with a fresh string-like thrombus. The findings of oscillating intraluminal mass echo may help establish a diagnosis of acute embolic ICA occlusion.

Acute Disease↗