Lesion patterns and etiology of ischemia in the anterior inferior cerebellar artery territory involvement: a clinical – diffusion weighted – MRI study

The topography and mechanism of stroke in the anterior inferior cerebellar artery (AICA) territory are delineated before, but the detailed clinical spectrum of lesions involving AICA territory was not studied by diffusion weighted imaging (DWI). We reviewed 1350 patients with posterior circulation ischemic stroke in our registry. We included patients if the diagnosis of AICA territory involvement was confirmed, and DWI, and magnetic resonance angiography were obtained in the 3 days of symptoms onset. The potential feeding arteries of the AICA territory were evaluated on magnetic resonance imaging (MRI) using a three-dimensional rotating cineoangiographic method. There were 23 consecutive patients with lesion involving AICA territory, six with isolated lesion in the AICA territory, six with posterior inferior cerebellar artery, 11 with multiple posterior circulation infarcts (MPCIs). The clinical feature of isolated AICA infarct was vertigo, tinnitus, dysmetria, ataxia, facial weakness, facial sensory deficits, lateral gaze palsy, and sensory-motor deficits in patients with pontine involvement. Patients with largest lesion extending to the anterior and inferolateral cerebellum showed mixed symptomatology of the lateral medullary (Wallenberg's syndrome) and AICA territory involvement. Patients with MPCIs presented various clinical pictures with consciousness disturbances and diverse clinical signs because of involvement of different anatomical structures. Large-artery atherosclerotic disease in the vertebrobasilar system was the main cause of stroke in 12 (52%) patients, cardioembolism (CE) in one (4%), and coexisting large-artery disease and a source of CE in four (17%). The main cause of stroke was atheromatous vertebrobasilar artery disease either in the distal vertebral or proximal basilar artery. The outcome was usually good except those with multiple lesions. The new MRI techniques and clinical correlations allow better definition of the diverse topographical and etiological spectrum of AICA territory involvement and associated infarcts which was previously based on pathological and conventional MRI studies.     

Spectrum of anterior cerebral artery territory infarction: clinical and MRI findings

To evaluate and review the clinical spectrum of anterior cerebral artery (ACA) territory infarction, we studied 48 consecutive patients who admitted to our stroke unit over a 6-year period. We performed magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA) in all patients, and diffusion magnetic resonance imaging (DWI) in 21. In our stroke registry, patients with ACA infarction represented 1.3% of 3705 patients with ischemic stroke. The main risk factors of ACA infarcts was hypertension in 58% of patients, diabetes mellitus in 29%, hypercholesterolemia in 25%, cigarette smoking in 19%, atrial fibrillation in 19%, and myocardial infarct in 6%. Presumed causes of ACA infarct were large-artery disease and cardioembolism in 13 patients each, small-artery disease (SAD) in the territory of Heubner's artery in two and atherosclerosis of large-arteries (<50% stenosis) in 16. On clinico-radiologic analysis there were three main clinical patterns depending on lesion side; left-side infarction (30 patients) consisting of mutism, transcortical motor aphasia, and hemiparesis with lower limb predominance; right side infarction (16 patients) accompanied by acute confusional state, motor hemineglect and hemiparesis; bilateral infarction (two patients) presented with akinetic mutism, severe sphincter dysfunction, and dependent functional outcome. Our findings suggest that clinical and etiologic spectrum of ACA infarction may present similar features as that of middle cerebral artery infarction, but frontal dysfunctions and callosal syndromes can help to make a clinical differential diagnosis. Moreover, at the early phase of stroke, DWI is useful imaging method to locate and delineate the boundary of lesion in the territory of ACA.     

Could a high resectability rate improve the long‐term survival of patients with proximal bile duct cancer?

BACKGROUND AND OBJECTIVES: This retrospective study was undertaken to evaluate if high resectability rate could improve the long-term outcome of patients with proximal bile duct cancer. METHODS: Between 1985 and 2001, 50 patients (34 male and 16 female) with proximal bile duct cancer were treated. Thirty-six patients (72%) were considered suitable for surgery, while 14 underwent nonsurgical palliative procedures. Twenty patients had bile duct resection only. Ten patients had Roux-en-Y cholangiojejunostomy with two or three divided segmental hepatic ducts; in 10 patients, the cholangiojejunostomy was performed with four or five divided segmental hepatic ducts. Three patients were treated by palliative transtumoral intubation with Kehr tube. Thirteen patients had bile duct resection plus hepatectomy. Despite the curative intention of the operation, only in 19 (52.7%) patients did the histopathological examination reveal tumor-free margins. RESULTS: There was no operative mortality. Postoperative morbidity was 25%. Overall 1-, 3-, and 5-year survival of the entire surgical group was 61%, 22.5%, and 9%, respectively. In the 19 patients treated with curative intent the survival at 1, 3, and 5 years was 63.1%, 31.5%, and 15.8%, respectively, while in the group that had palliative treatment it was 45%, 15%, and 0%, respectively. CONCLUSIONS: Only margins free from tumor can guarantee an improvement in long-term outcome. Increasing resectability improves survival and could offer a chance of better long-term survival.     

In vivo effects of caffeic acid phenethyl ester on myocardial ischemia-reperfusion injury and apoptotic changes in rats

Ischemia/reperfusion (I/R) has been reported to induce apoptotic cellular death in myocardium. This study tested the hypothesis that caffeic acid phenethyl ester (CAPE), one of the active components of propolis, may ameliorate myocardial apoptosis and oxidative myocardial injury. Wistar rats were divided into 4 groups: (i) sham operated, (ii) I/R, (iii) I/R+CAPE, and (iv) I/R+glutathione (GSH). CAPE (10 micromol/kg) was infused iv 10 min before occlusion of the left anterior descending coronary artery (30 min) followed by reperfusion (120 min). GSH (5 mg/kg) was infused iv after the occlusion and immediately before reperfusion. The TdT-mediated in situ nick end-labeling (TUNEL) method was used to evaluate apoptotic activity. I/R resulted in myocardial apoptosis, alterations of antioxidant status, elevation of serum creatine kinase (CK) and aspartate aminotransferase (AST) activities, evidence of lipid peroxidation, and elevated nitric oxide levels, compared to the sham-operation group. No apoptotic cells were found in the myocardial tissue of sham-operated rats. The TUNEL-positive myocardial cells averaged 60%, 30%, and 40% in the I/R, I/R+CAPE, and I/R+GSH groups, respectively. This study demonstrates that pretreatment with CAPE provides cardio-protection from I/R injury. The I/R+CAPE group showed reduced apoptosis, attenuated NO production, elevated myocardial superoxide dismutase (SOD) activity, and diminished serum CK and AST activities, compared to the I/R group.     

Genetic basis of apnoea of prematurity and caffeine treatment response: role of adenosine receptor polymorphisms: genetic basis of apnoea of prematurity

Aim: Caffeine treatment reduces the frequency of apnoea of prematurity (AOP) and eliminates the need for mechanical ventilation by acting as a nonspecific inhibitor of adenosine A1 and adenosine 2A receptors. Patients with AOP have demonstrated variant responses to caffeine therapy. We proposed to investigate the role of A1 and 2A polymorphisms in the development of AOP and individual differences in caffeine response. Secondly, we aimed to determine whether these polymorphisms have any effect on bronchopulmonary dysplasia (BPD) development. Methods: Cord blood samples were collected from infants born with gestational ages between 24 and 34 weeks. Two groups were defined: patients without apnoea (n = 60) and patients with apnoea (n = 55). Patients with apnoea were divided into two subgroups: a caffeine‐responsive group (n = 30) and an unresponsive group (n = 25). Six single‐nucleotide polymorphisms were chosen for genotyping. Results: Patients with apnoea over 28 weeks of gestational age who responded to the caffeine treatment were found to carry the rs16851030 C/C genotype rather than the C/T or T/T genotype. Logistic regression analysis showed a significant correlation between rs35320474‐C/T and T/T genotypes and apnoea and BPD development. Conclusion: Our results indicate a role for adenosine receptor gene polymorphisms in susceptibility to AOP and BPD and in interindividual variability to caffeine response.     

Serum level of lipoprotein (a) is inversely associated with the development of coronary collateral circulation

BACKGROUND: This study sought to determine the relationship between serum lipoprotein (a) levels and angiographically visible coronary collateral circulation and to evaluate whether lipoprotein (a) exerts any effect on vascular endothelial cell growth factor. METHODS: The study population included 60 patients (39 men, mean age 59+/-13 years) with angiographically documented total occlusion in one of the major coronary arteries. Development of collaterals was classified by Rentrop's method. Patients were defined as having poorly developed collaterals for grades 0 and 1 (group 1), or well-developed collaterals for grades 2 and 3 (group 2). Serum lipoprotein (a) and vascular endothelial cell growth factor levels were determined by enzyme-linked immunosorbent assay. RESULTS: In group 1, lipoprotein (a) levels were significantly higher and vascular endothelial cell growth factor levels were significantly lower than in group 2 (34+/-19 vs. 20+/-12 mg/dl, P<0.001, and 2.5+/-0.7 vs. 3.4+/-0.8 ng/dl, P<0.001, respectively). Poorly developed collaterals were significantly more frequent in patients with lipoprotein (a) levels >or=30 mg/dl than in patients with levels <30 mg/dl (72 vs. 37%, P=0.008). A strong negative correlation was observed between lipoprotein (a) and vascular endothelial cell growth, factor (r=-0.708, P<0.0001). Multivariate analysis revealed that a high level of lipoprotein (a) negatively affected the development of collaterals, whereas the duration of angina had a positive effect. CONCLUSION: This study demonstrated for the first time that the high level of lipoprotein (a) negatively affects the formation of coronary collateral vessels in human beings. Reduced production or bioactivity of vascular endothelial cell growth factor caused by high levels of lipoprotein (a) may be the possible responsible mechanisms of hyperlipoprotein (a)-related poor collateral formation.     

Electrocardiographic changes after coronary artery surgery

The electrocardiographic changes early after uncomplicated coronary artery bypass with complete revascularization were examined preoperatively and on the 1st and 3rd postoperative days in 53 patients. Heart rate, PR index, corrected PR interval, corrected P dispersion, corrected duration of QRS complex, corrected QT dispersion, corrected QT interval, rhythm, QRS axis, ST-segment changes, and blocks were determined. Changes in new parameters obtained by different combinations of R, S, and T waves were also studied. On the 1st postoperative day, atrial fibrillation was significantly less prevalent, right bundle branch block increased significantly, and QRS axis was significantly more positive but returned to baseline on the 3rd postoperative day. Postoperative heart rate and PR index were significantly higher than preoperative values. In the postoperative period, corrected PR interval was significantly lower, corrected QRS complex duration was significantly shorter, corrected QT interval was significantly longer, and corrected QT dispersion showed a significant increase on the 1st postoperative day. This study defines electrocardiographic changes in uncomplicated patients with complete revascularization. Any deviations from these findings may alert us to the need for further evaluation of an undesired event.