Malignant cerebral infarction after ChAdOx1 nCov-19 vaccination: a catastrophic variant of vaccine-induced immune thrombotic thrombocytopenia.

Vaccine-induced thrombotic thrombocytopenia with cerebral venous thrombosis is a syndrome recently described in young adults within two weeks from the first dose of the ChAdOx1 nCoV-19 vaccine. Here we report two cases of malignant middle cerebral artery (MCA) infarct and thrombocytopenia 9-10 days following ChAdOx1 nCoV-19 vaccination. The two cases arrived in our facility around the same time but from different geographical areas, potentially excluding epidemiological links; meanwhile, no abnormality was found in the respective vaccine batches. Patient 1 was a 57-year-old woman who underwent decompressive craniectomy despite two prior, successful mechanical thrombectomies. Patient 2 was a 55-year-old woman who developed a fatal bilateral malignant MCA infarct. Both patients manifested pulmonary and portal vein thrombosis and high level of antibodies to platelet factor 4-polyanion complexes. None of the patients had ever received heparin in the past before stroke onset. Our observations of rare arterial thrombosis may contribute to assessment of possible adverse effects associated with COVID-19 vaccination.

Plasma creatinine levels, estimated glomerular filtration rate and carotid intima media thickness in middle-aged women: a population based cohort study.

BACKGROUND AND AIM: The relationships between high Creatinine (Cr) levels or low estimated Glomerular Filtration Rate (eGFR) and common carotid Intima Media thickness (IMT) have been evaluated in a population-based cohort study in women, aged 30-69 (Progetto ATENA). METHODS AND RESULTS: Serum Cr and eGFR were measured in 310 women, as a part of 5.062. In this group carotid ultrasound examination (B-Mode imaging) was performed and mean max IMT was calculated. Women were classified by Cr levels >1 mg/dL or eGFR < 56 ml/min. Women with Cr > 1 mg/dL (90th percentile of creatinine distribution) or eGFR less than 56 ml/min (5th percentile of eGFR distribution) had relatively more carotid plaques as compared to the rest of the cohort. Multivariate logistic analysis, after adjustment for age, demonstrated a significant association between Cr (>1 mg/dL) and IMT (≥1.2 mm): OR 4.12 (C.I 1.22-13.86), p = 0.022; or eGFR (<56 ml/min) and IMT (≥1.2 mm): OR 4.31 (C.I 1.27-14.66), p = 0.019. CONCLUSIONS: These findings on an independent relationship between Cr and common carotid plaques in this population of middle aged women, independently of age, suggest the value of screening for early carotid disease in asymptomatic middle aged-women with mild renal insufficiency, in order to predict those at relatively higher risk for future cardiovascular events.

Carotid artery wall hypertrophy in children with metabolic syndrome.

Preclinical vascular changes (increased stiffness and/or wall thickness) have been observed in children with known metabolic risk factors. Aim of the present study was to evaluate different carotid parameters, representative of vascular health, in children with and without metabolic syndrome (MS). We studied 38 children with MS (mean age 9.6+/-2.6 years; range 6-14 years) and 45 healthy age-matched subjects. Children who met three or more of the following criteria qualified as having the MS: fasting glucose >110 mg dl(-1), fasting triglyceride concentration >100 mg dl(-1), fasting high-density lipoprotein cholesterol concentration <50 mg dl(-1) for females or <45 mg dl(-1) for the males, waist circumference >75th percentile for age and gender and systolic or diastolic blood pressure >90th percentile for age, gender and height. Carotid B-mode ultrasound examinations were performed and intima-media thickness and diameters were measured in all subjects. Arterial geometry was further characterized by calculation of carotid cross-sectional area. Carotid intima-media thickness and lumen diameters were increased in children with MS as compared to children without MS. Moreover, carotid cross-sectional area was significantly higher in the group of children with MS 9.83+/-1.86 mm(2) [mean+/-s.d.] compared with the control group: 7.77+/-1.72 mm(2), P<0.001, even after adjustment for age, gender and height. Carotid hypertrophy is already detectable in children with MS. High-resolution B-mode ultrasound could provide a valuable tool for the cardiovascular risk stratification of children.

Focal cerebral ischaemia induces corticotropin releasing factor (CRF) vascular immunoreactivity in rat occluded hemisphere.

Corticotropin-releasing factor (CRF) induces the dilatation of cerebral blood vessels and increases cerebral blood flow (CBF). CRF receptor antagonists reduce ischaemic damage in the rat. In the present study, the expression of CRF around cerebral vessels has been investigated in the rat. No CRF immunoreactivity was identified around pial or intracerebral vessels in the absence of cerebral ischaemia. Four hours after middle cerebral artery occlusion (MCAo), intensely CRF-positive blood vessels were evident on the ischaemic cortical surface and in the peri-infarct and infarct zone. Increased CRF immunoreactivity was also detected in swollen axons in subcortical white matter, caudate nucleus and lateral olfactory tract of the ipsilateral hemisphere, consistent with the failure of axonal transport. These data provide morphologic support for a role of CRF in the pathophysiology of cerebral ischaemia.

Impaired endothelium-dependent vascular reactivity in patients with familial combined hyperlipidaemia.

BACKGROUND: Familial combined hyperlipidaemia (FCHL) is associated with a markedly increased risk of premature coronary artery disease. This study was designed to evaluate whether preclinical atherosclerotic functional abnormalities are detectable in the arteries of patients with FCHL. METHODS: 60 subjects were recruited for the study: 30 probands of families with FCHL (mean (standard deviation (SD)) age 48 (10) years, 77% men), defined by fasting total plasma cholesterol or triglyceride concentration >250 mg/dl (>6.5 mmol/l cholesterol, >2.8 mmol/l triglyceride) and by the occurrence of multiple lipoprotein phenotypes within a family, and 30 age-matched and sex-matched healthy controls. All subjects underwent high-resolution B-mode ultrasound examination and the brachial arterial reactivity, a marker of endothelial function, was measured by a semiautomated computerised program. Lipid profile, resting blood pressure, body mass index (BMI), smoking status, insulin and homocysteine levels were also determined. RESULTS: Compared with controls, patients with FCHL had significantly higher BMI, diastolic blood pressure and insulin levels. No difference was observed in baseline brachial diameter between the two groups (mean (SD) 3.45 (0.51) mm for FCHL v 3.60 (0.63) mm for controls; p = 0.17). In response to flow increase, the arteries of the controls dilated (mean (SD) 8.9% (4.9%), range 2.3-20.8%), whereas in the patients with FCHL, brachial arterial reactivity was significantly impaired (5.5% (2.5%), range 0-10.1%; p = 0.002). In multivariate linear regression analysis, apolipoprotein B and BMI were independent determinants of brachial artery response to reactive hyperaemia. CONCLUSIONS: The findings of our study suggest that vascular reactivity is impaired in the arteries of patients with FCHL.

Specific therapies for ischaemic stroke: rTPA and others.

In the last few years there have been several important advances in the understanding of cerebrovascular disorder pathophysiology that have impacted on stroke management. The development of timely and effective treatment strategies was and is still considered a high priority issue. Therapeutic options dramatically increased both in the prevention and overall in the treatment of acute ischaemic stroke (AIS). At present, whereas neuroprotection remains experimental, intravenous (i.v.) thrombolysis is the only specific therapy effective in reducing mortality and disability associated with stroke. The efficacy and safety of the antithrombotic therapy in AIS treatment are not well established, and few issues in clinical stroke management are more controversial. However, some studies have brought new light and new doubts on the roles of these traditional therapies.

An intelligent controller for automated operation of sequencing batch reactors.

In this paper the results are presented of original research into the automatic and "intelligent" detection of breakpoints in Dissolved Oxygen (DO) profiles. The research has been based on a large body of data collected from laboratory SBRs operating on synthetic wastewater. Two different approaches were followed to identify the endpoints. The paper analyses and evaluates the results of automatic detection on the basis of geometric features in the DO profiles. This was followed by classification of the detected breakpoints using different soft computing techniques based on Neural Network (NN), Fuzzy Neural Network (FuNN) and Evolving Fuzzy Neural Network (EfuNN) software systems for breakpoint classification. A high rate of successful detection and classification was obtained with up to 96% of the decisions made correctly. In order to overcome the limitations of this system to adapt to dynamically changing process conditions, an intelligent control model was developed by a combination between an Evolving Fuzzy Neural Net (EfuNN) combined with a logic decision unit. This system has the ability to "learn on-the-fly" and adjust its response pattern in order to maintain a high rate of successful breakpoint detection under varying changing process conditions. This software system has been sucessfully embedded on a small programmable controller for integration into larger process control systems for the operation of SBR plants.

Increased carotid intima-media thickness in children-adolescents, and young adults with a parental history of premature myocardial infarction.

AIMS: The present study was designed to test whether early carotid structural changes are demonstrable (by high resolution B-mode ultrasound) in children, adolescents and young adults with a history of premature parental myocardial infarction. METHODS AND RESULTS: One hundred and fourteen healthy young (5 to 30 years) subjects with a parental history of premature myocardial infarction and 114 age- and sex-matched control subjects were enrolled in the study. They were divided into two age groups: children and adolescents (age 5 to 18 years) (54 individuals with a parental history of premature myocardial infarction and their control subjects; mean age 12.8+/-3.8 years) and young adults (age 19 to 30 years) (60 individuals with a parental history and their controls; mean age 23.8+/-3.3 years). All subjects underwent high resolution B-mode ultrasonographic evaluation of common carotid artery intima-media thickness. Lipid profile, resting blood pressure, body mass index and smoking status were also evaluated. In both age groups, compared to controls, subjects with a parental history of premature myocardial infarction had increased intima-media thickness of common carotid arteries (mean of combined sites: age 5-18 years: 0.45+/-0.076 mm vs 0.40+/-0.066 mm in controls, P=0.008; age 19-30 years: 0.48+/-0.077 mm vs 0.45+/-0.078 mm in controls,P =0.007) Offspring of coronary patients showed an unfavourable lipid profile, however, the association between a parental history of premature myocardial infarction and carotid intima-media thickness was independent of lipids, apolipoproteins and other traditional risk factors. CONCLUSIONS: Vascular structural changes associated with a parental history of premature myocardial infarction are already detectable in childhood and adolescence and occur independently of several traditional cardiovascular risk factors.

Aortic atheroma. An unknown source of ischemic stroke.

Cerebrovascular mortality represents 25% of all cardiovascular mortality. Defining the pathological mechanism of an episode of ischemic stroke is important for epidemiological, prognostic and overall therapeutic purposes. About 1/4 of ischemic strokes are defined as being of unknown cause. The use of transesophageal echocardiography for studying the aortic arch and thoracic aorta, revealed that aortic atheroma can be considered as an embolic source. Retrospective studies documented a significant prevalence of atheroma >4 mm in the aortic arch in patients with previous stroke (15%); while prospective studies documented an increased risk for cardiovascular events in patients with plaque of =/> 4 mm in thickness at the level of the thoracic aorta compared with controls without these lesions: in particular, the incidence of recurrent stroke is 12%/year, while the incidence of cardiovascular events is 26%. Plaques defined unstable and at risk of embolic event are protrudent, >4 mm in thickness, without calcification and have on their surface mobile thrombus. Embolization from a protrudent atheroma can have a iatrogenic cause, that is cardiac catheterization or placement of an intra-aortic balloon- pump or during cardiopulmonary bypass. The management of the subject with aortic atheroma is not well defined. Encouraging dates with the use of statins are from a recent meta-analysis also anticoagulant treatment versus antiplatelet treatment, reduced incidence of stroke in a significant manner. The surgical therapy of aortic endoarterectomy, has, at this moment, a limited indication, because is not without risk. Transesophageal ecocardiography is a method of choice for the study of the aortic atheroma and it should be done in every patient with stroke by unknown cause.

[Media-intima thickness: what is it? how is it measured? what is its clinical significance? what are the pending problems?]. / Lo spessore medio-intimale: che cosa è? Come si misura? Qual è il suo significato clinico? Quali sono i problemi da risolvere?

During the past 20 years, several hundred peer-reviewed publications have documented the critical scientific steps in the determination of the usefulness of B-mode ultrasound measurements of the carotid artery intima-media thickness (IMT) for the detection and monitoring of artery wall atherosclerotic disease. Since the initial validation study of the IMT, carotid ultrasound IMT measurements have been performed in a large number of individuals with "traditional" and "non traditional" cardiovascular risk factors, have been shown to correlate with the severity of atherosclerotic lesions in other vascular territories, and have been used as outcome measures in clinical trials evaluating the various effects of treatment on the progression/regression of atherosclerosis. Furthermore, in longitudinal studies, carotid IMT has been shown to be an independent predictor of stroke and coronary events. However, before this powerful indicator of arterial wall atherosclerotic disease can be used in clinical settings as a routine test for the prediction of an individual's cardiovascular risk, some unresolved issues need to be addressed.

[Instability determinants of the carotid plaque: from histology to ultrasound]. / Determinanti dell'instabilità della placca carotidea: dall'istologia agli ultrasuoni.

Over the last decade, it has become progressively clear that the most important mechanism responsible for acute coronary and cerebrovascular events is atherosclerotic plaque rupture with superimposed thrombus formation. Anatomo-pathological studies have shown that the risk of rupture depends on plaque type rather than plaque size. The determinants of carotid plaque vulnerability to rupture are similar to those responsible for coronary instability: 1) size and consistency of the lipid-rich atheromatous core, 2) ongoing inflammation and repair processes within the fibrous cap, and 3) the thickness of the fibrous cap covering the core. Unstable plaques contain a soft, lipid-rich core that is covered by a thin and inflamed cap of fibrous tissue. External factors such as mechanical and hemodynamic stresses may be important not only in precipitating disruption of vulnerable plaques, but also in their cellular differentiation. Several imaging techniques have been used to identify plaques at high risk of events. High-resolution B-mode ultrasound is a noninvasive, inexpensive technique which allows a characterization of carotid plaque dimension, internal structure and surface. Nevertheless, such a method is not perfect. The subjective evaluation of plaque morphology on B-mode ultrasound, the need of improving reproducibility and the lack of a uniform terminology are critical issues, which need to be addressed.

[Non-invasive evaluation of the endothelial function using high-resolution B-mode ultrasonography]. / Valutazione non invasiva della funzione endoteliale mediante ultrasonografia B-mode ad alta risoluzione.

The vascular endothelium has a central role in regulating vasomotor tone, smooth muscle cell proliferation, platelet and leukocyte adhesion to the arterial wall, thrombosis and fibrinolysis. Disturbances of these endothelial functions have been suggested to be important in the early and advanced phases of atherosclerosis. The development of a simple, valid ultrasound-based method allowed to non-invasively evaluate endothelial function in a large number of individuals with traditional and non-traditional cardiovascular risk factors. The ultrasound technique measures changes in brachial artery diameter in response to an increase in blood flow (reactive hyperemia) and thus in shear stress, which causes endothelium-dependent dilation. This methodology is not yet perfect. The critical issues today involve the definition of "normal values", and standardized scanning and reading protocols to reduce variability.

Arterial abnormalities in the offspring of patients with premature myocardial infarction.

BACKGROUND: Findings from epidemiologic and autopsy studies suggest that the offspring of patients with premature coronary disease may be at increased risk for atherosclerosis. We undertook a study to determine whether changes in brachial-artery reactivity and thickness of the carotid intima and media, two markers of early atherosclerosis, are present in adolescents and young adults with a parental history of premature myocardial infarction. METHODS: We enrolled 40 healthy young people whose parents had had premature myocardial infarction (48 percent male; mean [+/-SD] age, 19.0+/-5.2 years) and 40 control subjects who were matched with the first group according to age and sex. All the subjects underwent high-resolution B-mode ultrasound examinations for the measurement of the brachial-artery vasodilatory response after arterial occlusion (i.e., reactive hyperemia) and the intima-media thickness of the distal common carotid arteries. Lipid profiles, blood pressure while at rest, body-mass index, and smoking status were also determined. RESULTS: As compared with the control subjects, the offspring of patients with premature myocardial infarction had lower flow-mediated reactivity of the brachial arteries (5.7+/-5.0 percent, vs. 10.2+/-6.6 percent in the control subjects; P=0.001) and greater mean intima-media thickness of the common carotid artery (0.49+/-0.08 mm, vs. 0.44+/-0.07 mm in the control subjects, P=0.004). In the subjects with a parental history of premature myocardial infarction, an inverse association was found between brachial-artery reactivity and carotid intima-media thickness (r=-0.46, P=0.003). In a conditional logistic-regression analysis, both brachial-artery reactivity and carotid intima-media thickness were significantly and independently correlated with a parental history of premature myocardial infarction. CONCLUSIONS: Structural and functional changes are present at an early age in the arteries of persons with a parental history of premature myocardial infarction.

[Presence and severity of carotid atherosclerosis in asymptomatic hypertension patients with left ventricular hypertrophy]. / Presenza e severità dell'aterosclerosi carotidea in soggetti ipertesi asintomatici con ipertrofia ventricolare sinistra.

BACKGROUND AND PURPOSE: Arterial hypertension is associated with structural changes in the cardiovascular system. In hypertensives, a relationship has been found between left ventricular hypertrophy and carotid wall thickness, whereas the association with atherosclerotic plaque is less defined. The aim of this study was to evaluate the occurrence and severity of carotid atherosclerosis in hypertensive patients with or without left ventricular hypertrophy (LVH). MATERIALS AND METHODS: We studied 122 hypertensive subjects (62 men and 60 women), aged 60.1 +/- 12.1. Subjects were considered to have left ventricular hypertrophy if their left ventricular mass index (LVMI) at echocardiography exceeded 110 g/m2 in women and 135 g/m2 in men. Carotid intima-media thickness (IMT), external diameter and atherosclerotic plaques were evaluated by high resolution echo-color Doppler. RESULTS: IMT in both common carotid and bifurcation was significantly greater in hypertensives with LVH (p < 0.01), whereas external diameter did not differ significantly in the two groups. Increased presence (73.4 vs 32.8%) and severity (18.7 vs 5.2% for stenosis > 40%) of atherosclerotic plaque were found in the hypertrophic group. A weak but significant association was present among left ventricular mass index, ventricular wall thicknesses and carotid intima-media thickness, and plaque. CONCLUSIONS: In asymptomatic hypertensive subjects, LVH is associated with an increased risk of plaque formation and progression. Vascular hypertrophy may represent a distinct prognostic factor in hypertension and the association of cardiac and vascular hypertrophy may identify a group at high risk of future cardiovascular events.

Motor fluctuations in Parkinson's disease: pathophysiology and treatment.

At the initial stages of Parkinson's disease (PD), levodopa (LD) is able to reduce most motor symptoms and to significantly improve the patient's quality of life. However, in the vast majority of patients with prolonged LD usage, some decline in efficacy occurs and motor complications eventually begin to appear. These complications consist not only of daily fluctuations in the voluntary motor performance often accompanied by involuntary movements, but also of fluctuations in cognitive, autonomic, and sensory functions. Several recent studies on LD complications in PD have led to a better understanding of their pathophysiology and of the possible therapeutic interventions, and a summary of these findings is presented in this review. Different observations now suggest that postsynaptic pharmacodynamic factors play a major role in determining fluctuations in PD. Two explanations are given: chronic intermittent dopaminergic therapy may lead to postsynaptic receptor downregulation in PD; or, receptor changes in the striatum may occur independently of treatment as a result of structural adaptation of the postsynaptic dopaminergic system to the progressive decline of the nigrostriatal pathway. The hypothesis of reversible postsynaptic changes as the main mechanism underlying a fluctuating response to LD lends itself to a possible pharmacological manipulation of the dopaminergic response to reverse, or even avoid, motor fluctuations (initial monotherapy with dopamine agonists and early combination LD/dopamine agonists). The role of peripheral pharmacokinetics factors is also critical and the use of controlled release LD formulations, of monoamine oxidase (MAO)-B and of catechol-O-methyltransferase (COMT) inhibitors may all, to a different degree, improve such phenomena. In the last decade, there has been a resurgence in surgical therapies in advanced PD, due to higher levels of accuracy and safety provided by the new surgical devices, and to a more precise localization of the target areas allowed by the neurophysiological mapping techniques. The surgical procedures currently used in advanced PD are stereotactic brain lesions (internal globus pallidus and subthalamic nucleus), chronic brain stimulation (of the same nuclei) and striatal grafting of dopamine-producing cells. All these procedures have already shown their efficacy in the management of severe fluctuations in PD, but their indications, and relative advantages and disadvantages, are still the subject of considerable debate and controversy.

Posterior circulation infarcts simulating anterior circulation stroke. Perspective of the acute phase.

BACKGROUND AND PURPOSE: Ischemic stroke patients whose initial clinical presentation suggests an involvement of the anterior circulation (AC) are sometimes found to have a posterior circulation (PC) infarct, a fact that may generate erroneous decisions in clinical management. We investigated the prevalence of this misdiagnosis in the first few hours after stroke onset. METHODS: We performed a cohort study of 158 patients hospitalized within 5 hours of onset of a presumed AC ischemic stroke, as diagnosed on clinical grounds. RESULTS: Final CT or pathology diagnosis was AC infarct in 128 patients (81%), a repeatedly negative CT in 14 (9%), PC infarct (5 pons, 1 midbrain and cerebellum, 6 supratentorial territory of the posterior cerebral artery) in 12 (8%), and other or undiagnosed lesions in 4 (3%). AC and PC stroke patients did not differ in terms of age, vascular risk factors, and initial severity, but the latter were more frequently men (83% versus 53%; P = .04), were hospitalized later (mean +/- SD, 168 +/- 86 versus 109 +/- 55 minutes; P = .001), and presented a pure motor hemiparesis or a sensorimotor stroke (50% versus 33%) more often than their counterparts. At baseline CT, PC stroke patients never exhibited an early parenchymal hypodensity in the carotid territory or a hyperdense middle cerebral artery, which were instead found in 59% (P = .0003) and 31% (P = .02) of AC stroke patients, respectively. Early neurological deterioration, 1 month case-fatality rate, and disablement in survivors were comparable in the two groups. CONCLUSIONS: Shortly after onset the clinical discrimination between AC and nontypical PC infarcts is not reliable, which explains the frequent occurrence of this misdiagnosis. Emergency CT scan helps in the differential diagnosis only when it demonstrates an early focal hypodensity within the carotid territory.

Thrombolysis acute ischemic stroke.

Thrombolysis is an attractive but potentially dangerous they for cerebral ischemia: it is capable of dissolving an arterial thrombus, but can also transform a pale infarct into a hematoma and/or may cause severe oedema and herniation. The safety and efficacy of the treatment critically depend on the timing of intervention ad on patient selection. In recent studies on ischemic stroke, spontaneous hemorrhagic transformation of an infarct seems to be related to the size of the lesion, and can be reliably predicted as early as five hours from stroke onset by the presence of focal hypodensity in the CT scan. That is why in the European Co-operative Acute Stroke (ECASS), a randomised, double blind trial on intravenous rt-PA in hemispheric stroke, patients showing, on the admission CT scan, extended early hypodensity, involving more than one third of the territory of the middle cerebral artery, were excluded from the day. Other ongoing trials on thrombolytic agents are expected to provide further indications on how to identify those patients most likely to benefit and least likely to experience adverse effects from this treatment.

Clinical and prognostic correlates of stroke subtype misdiagnosis within 12 hours from onset.

BACKGROUND AND PURPOSE: Pure motor hemiparesis and sensorimotor stroke syndromes are not accurate predictors of lacunar infarct when described in the first 12 hours of stroke onset. We evaluate here whether this inaccuracy of clinical diagnosis might have influenced the planning of patient management either in routine practice or in therapeutic trials. METHODS: A consecutive hospital series of 517 first-ever ischemic hemispheric stroke patients presented lacunar or nonlacunar syndromes at the first examination within 12 hours of the event. A distinction was subsequently made, by means of a CT scan or autopsy performed within 15 +/- 2 days of stroke, between patients affected by lacunar or nonlacunar infarcts. We compared stroke risk factors, considered to be indicative of potential pathogenetic mechanisms, and the clinical outcome of lacunar infarct versus nonlacunar infarct patients and those of lacunar syndrome versus nonlacunar syndrome patients. RESULTS: Two hundred nineteen patients (42%) presented a lacunar syndrome and 298 (58%) a nonlacunar syndrome, while 170 (33%) had lacunar infarcts and 347 (67%) nonlacunar infarcts. Lacunar infarct patients were more frequently associated with hypertension and a previous transient ischemic attack and less frequently with atrial fibrillation when compared with their nonlacunar infarct counterparts, whereas no differences were apparent between lacunar syndrome and nonlacunar syndrome patients. Logistic regression analysis showed that hypertension and a previous transient ischemic attack on the one hand and atrial fibrillation on the other were strongly correlated with the diagnosis of lacunar infarct and nonlacunar infarct, respectively, while no risk factor was correlated with the diagnosis of lacunar syndrome. Twenty-two percent of lacunar infarct patients and 68% of nonlacunar infarct subjects had a poor outcome (death plus disability of survivors) as opposed to 40% of lacunar syndrome and 63% of nonlacunar syndrome patients. Logistic regression selected age, severity of neurological deficit at entry, cardiopathies, diabetes, and lacunar infarct, but not lacunar syndrome, as predictors of outcome. CONCLUSIONS: The inaccurate clinical diagnosis of lacunar infarct made in the first 12 hours of stroke might lead to no distinction being made between stroke subgroups with potentially different pathogenetic mechanisms and prognostic estimates, thus negatively influencing the planning of patient management.

Influence of hyperglycaemia on infarct size and clinical outcome of acute ischemic stroke patients with intracranial arterial occlusion.

We investigated the effects of hyperglycaemia on infarct size of 82 acute ischaemic stroke patients with angiographically diagnosed intracranial occlusion in middle cerebral artery territory. There were 9 diabetics, 40 non-diabetic hyperglycaemics and 33 non-diabetic normoglycaemics (mean age 67 +/- 8 SD years, male/female ratio 1:1). For each patient the infarct at CT was compared to that predicted from the location of the arterial occlusion. The extent of the infarct was then classified as equal to, smaller than and larger than estimated, taking a standard anatomical template of arterial territories as reference. The results were analysed separately according to the presence or absence of a collateral blood supply (CBS) at angiography. The clinical outcome at 30 days was also evaluated. The 35 patients lacking CBS had a high frequency of equal to estimated lesions (75%), without substantial differences among the three subgroups (72% of hyperglycaemics, 82% of normoglycaemics and 67% of diabetics; Fisher's exact test not significant for any of the pairwise comparisons). On the contrary, the 47 patients with CBS exhibited an overall predominance of smaller than estimated lesions (66%) but with a very uneven distribution among hyperglycaemics, normoglycaemics and diabetics (82%, 64% and 0%, respectively; p < 0.05 at Fisher's exact test for diabetics vs hyperglycaemics). Finally, the clinical outcome was bad (death and neurological impairment) in 89% of diabetics, 72% of hyperglycaemics and 54% of normoglycaemics (p < 0.05). These results suggest that in patients with intracranial arterial occlusion associated with CBS the effects of hyperglycaemia might be beneficial in non-diabetics and harmful in diabetics.(ABSTRACT TRUNCATED AT 250 WORDS)

Muscarinic cholinergic receptors in the human right coronary artery: a receptor binding and autoradiographic study.

We used a combination of radioreceptor binding and autoradiographic techniques to study the pharmacological characteristics and anatomical localization of [3H]-quinuclidinyl benzilate (QNB) binding sites in the human right coronary artery. The ligand was bound to sections of the human right coronary artery in a manner consistent with the labelling of muscarinic receptors. The addition of pirenzepine or of carbachol to the incubation medium to generate displacement curves was indicative of the presence of M1 and M2 receptors in the right coronary artery. Autoradiography showed the localization of M1 sites primarily in the medial layer of the right coronary artery. M2 sites were located primarily in the adventitia. No [3H]-QNB binding sites were observed in the endothelium. A possible role of muscarinic receptors in the pathogenesis of coronary vasospasm is discussed.