Massive infarcts involving the territory of the anterior choroidal artery and cardioembolism

BACKGROUND AND PURPOSE: At neuropathological examination, the territory of the anterior choroidal artery is frequently found to be involved in massive infarcts of the internal carotid artery territory. The aim of our study was to analyze the clinical spectrum, the course, and the mechanism of these massive infarcts compared with the rare infarcts involving only the anterior choroidal artery territory. METHODS: Retrospective clinical examination and pathological study were performed in 35 patients with cerebral infarcts affecting at least the territory of the anterior choroidal artery. RESULTS: In no patient had the involvement of the anterior choroidal territory infarcts been recognized clinically, nor had the triad of clinical signs (hemiplegia, hemianesthesia, and hemianopsia) classically seen in infarcts restricted to this territory been found alone. Impairment of consciousness, cognitive disorders, or oculomotor palsies had been found in addition to one or more signs of the triad. This was probably related to the involvement of other territories (94%), especially the middle cerebral artery territory (68%) and the posterior cerebral artery territory (20%). The concomitant involvement of several territories was due most frequently to an occlusion of the internal carotid artery, which was found at autopsy in 74% of the patients. These occlusions were often associated with cardioembolism (54%). In contrast, artery-to-artery embolism (17%) and small-artery disease (6%) were seldom found. Only two cases of infarcts restricted to the anterior choroidal artery territory were observed. CONCLUSIONS: The involvement of the territory of the anterior choroidal artery in massive infarcts was due mainly to a cardioembolic occlusion of the internal carotid artery.     

Photodynamic therapy for early stage squamous cell carcinoma of the lung

We studied 9 patients with bilateral vertebral artery occlusion (BVAO). BVAO was confirmed using angiography in order to clarify its clinical feature, mechanism, and long term prognosis. Three patients showed bilateral intra-cranial occlusion, 3 bilateral extra-cranial occlusion, and 3 intra and extra-cranial occlusion. The basilar artery was fed by the posterior communicating artery in 8 out of 9 patients. In one of the 8, reconstitution of the thyrocervical artery was seen. We divided the patients into 4 groups according to MRI findings, as follows: Group 1 with no abnormal finding on MRI (N = 2); Group 2 with deep pontine infarcts and non-territorial small cerebellar infarcts (N = 2); Group 3 with extended pontine infarcts (N = 3); and Group 4 with cerebellar cortical artery infarcts, deep pontine infarcts, and non-territorial small cerebellar infarcts (N = 2). Transient episodes were seen in all patients, 8 patients out of 9 had vertigo/dizziness, 3 tinnitus, 2 diplopia, 2 headache, 2 numbness, and 1 hearing disturbance. These episodes preceded a final attack or complete stroke 2 days to 5 months, and those who had a longer period of episodes in the preceding term tended to have less severe deficits. Six of the patients had vertebro-basiler symptoms after being in the upright position, including all the patients in Groups 2 and 4, which had cerebellar border zone/terminal zone infarcts. These results indicate that the hemodynamic mechanism plays an important role in BVAO. The prognosis was not always grave. Four of the patients could walk independently, 2 could walk with a cane, and 3 were bed ridden (2 of which died). Long-term follow-up data (a mean of 5 years) were obtained in all patients. In the patients who could walk, one had asymptomatic cerebellar infarcts, and one had TIAs frequently. Patients with BVAO often also have TIAs and/or preceding episode and show cerebellar border zone/terminal zone infarcts. This research strongly suggests that hemodynamic mechanism might play an important role in BVAO, and that paying attention to border zone infarction in MRI and transient episodes can lead to earlier diagnosis and treatment.     

Second cancers following in situ carcinoma of the breast

Most reports of midbrain infarction have described clinicoanatomical correlations rather than associations and aetiologies. Thirty nine patients with midbrain infarction (9.4%) are described out of a series of 415 patients with vertebrobasilar ischaemic lesions in the New England Medical Center Posterior Circulation Registry. Patients were categorised according to the rostral-caudal extent of infarction. The "proximal" vertebrobasilar territory includes the medulla and posterior inferior cerebellar artery territory. The "middle" territory includes the pons and anterior inferior cerebellar artery territory. The "distal" territory includes the rostral midbrain, thalami, superior cerebellum, and medial temporal and occipital lobes. Midbrain infarction was accompanied by "proximal" territory infarcts in four patients, and by "middle" territory infarction in 19 patients. Thirteen patients had associated "distal" territory infarcts, three of whom had occipital or temporal lobe infarcts. Only three patients had isolated midbrain infarcts. Cardioembolism (n=11), in situ thrombosis (n=9), large artery to artery embolism (n=7), and intrinsic branch penetrator disease (n=5) were the most common aetiologies. Bilateral infarction and accompanying pontine infarction were associated with the most extensive vertebrobasilar occlusive disease. Midbrain infarction was 10-fold more likely to be accompanied by ischaemia of neighbouring structures than it was to occur in isolation. Recognition of the different patterns of infarction may act as a guide to the underlying aetiology and vascular lesions.     

Stroke patterns of internal carotid artery dissection in 40 patients

BACKGROUND and PURPOSE: Internal carotid artery dissection (ICAD) is a frequent cause of ischemic stroke in young patients. Whether cerebral ischemia is of embolic or hemodynamic origin remains to be determined. Heparin is often administered in ICAD; however, a drug trial can hardly be conducted because of the low recurrence rate after the acute stage. Therefore, the best therapeutic approach should be determined on the basis of the presumed mechanism of cerebral ischemia. One way to approach the mechanism of stroke in ICAD is to determine stroke patterns. We postulated that most cortical and large subcortical infarcts (>/=15 mm) are of embolic origin and that small subcortical infarcts (<15 mm) and junctional infarcts are not. The aim of our study was to determine the stroke patterns in 40 consecutive patients with ICAD. METHODS: The patients (26 women and 14 men; mean age, 42.8 years) had a total of 65 ICADs. Seventeen patients were free of any vascular risk factor. CT scans, MRI scans, and angiographic features were analyzed by observers who were blinded to the clinical findings. RESULTS: We found 34 cortical infarcts, 25 large subcortical infarcts, 1 small subcortical infarct, and 5 junctional infarcts. CONCLUSIONS: Most infarcts related to ICAD are cortical infarcts or large subcortical infarcts; small subcortical infarcts and junctional infarcts are infrequent. Therefore, these findings suggest that most infarcts occurring in carotid artery dissection (CAD) are probably embolic rather than hemodynamic in origin. According to this presumed mechanism, anticoagulation seems a logical treatment at the early stage of CAD.     

Posterior distribution of infarcts in strokes related to cardiac operations

BACKGROUND: Stroke complicates cardiac surgical procedures in a substantial number of patients. The mechanism of stroke is predominantly embolic, although hypoperfusion may play a role. The aim of this study was to determine whether radiologic appearances in this population were consistent with an embolic cause. METHODS: We reviewed computed tomographic scans and medical records in 24 patients who suffered stroke after cardiac operation. Stroke was evident at 24 hours in 19 patients (79%). Infarcts were multiple in 16 and single in 3 patients (group 1). The remaining 5 patients suffered stroke beyond 24 hours and had single infarcts on computed tomographic scan (group 2). RESULTS: In group 1, 15 patients (79%) had bilateral cerebellar infarcts, 4 (74%) had posterior cerebral artery infarcts, 10 (53%) had posterior watershed infarcts, and 11 patients (58%) had middle cerebral artery branch infarcts. The mean number of vascular territories involved was 5.1 (range, 1 to 10). Mobile atheromatous plaque was present in the ascending aorta or arch in 5 of 9 patients (56%) in group 1. In group 2, stroke occurred in close association with atrial or ventricular fibrillation in 3 of 5 patients (60%). CONCLUSIONS: In patients with radiologic evidence of infarction, perioperative strokes after cardiac operation are typically multiple, and involve the posterior parts of the brain, consistent with atheroembolization. Delayed strokes may be attributable to cardiogenic embolism.     

Factors that influence the further survival of patients who survive for five years after the diagnosis of cancer in childhood or adolescence

Acute confusional states and agitated delirium are among the most common psychopathologic disorders in the elderly. However, they are rarely reported in the course of infarcts in the territory of the posterior cerebral artery. This study involving thirteen patients aged more than 65 years suggests that acute confusional states from posterior cerebral artery infarcts are less rare than usually thought, although the diagnosis may be difficult during the acute phase. The risk factors are no different from those observed for infarcts in other cortical areas, suggesting that this syndrome is due to structural damage of the brain rather than the other, usual causes of confusion in the elderly (intoxications, dysmetabolic diseases or dementia). The recognition of acute confusional states from posterior cerebral artery infarcts and its distinction from other causes of confusion is important in elderly patients because of the different diagnostic, prognostic and therapeutic implications involved.     

Computerized nuclear morphometry of hepatocellular carcinoma and its relation to proliferative activity

Acute infarcts of the anterior inferior cerebellar artery (AICA) are unusual. We report 15 cases of AICA infarcts and their correlation with the topography of the lesion by brain MRI. During 2 years we prospectively identified 7 cases of AICA infarcts among 770 acute strokes (0.9% of the acute strokes seen in our department). We studied these cases and also another 8 that we found retrospectively. Most patients (8/15) had a unilateral affectation of both middle cerebellar peduncle (MCP) and inferior lateral pontine area (ILP), in these cases the main symptoms were vertigo, ataxia, peripheral facial palsy and hypoacusia. Two other patients had isolated MCP infarcts and were characterized by peripheral vertigo and ataxia, without hypoacusia or facial palsy. Another 2 patients had isolated ILP territory infarct characterized by vertigo, left peripheral facial palsy without hypoacusia and mild or no ataxia. One patient had a Gasperini syndrome. Finally 3 patients had bilateral AICA infarcts due to basilar thrombosis. The etiology was atherosclerosis in 9 patients, lacunar due to hypertension in 1, cardiac embolism in 1, migraine in 1 and unknown in 3. Among the 15 patients only 2 died, both with AICA plus infarcts. In the remaining patients a follow-up during a mean of 31 months (3 months to 12 years) showed no recurrences.     

T2-weighted hyperintense MRI lesions in the pons in patients with atherosclerosis. Amsterdam Vascular Medicine Group

BACKGROUND AND PURPOSE: Pontine hyperintense lesions (PHL) on T2-weighted MRI have been recognized recently. Histopathological findings resemble periventricular leukoaraiosis, and a vascular etiology has been suggested. We studied the frequency and the associated factors of PHL in patients with symptomatic atherosclerosis. METHODS: Two independent observers assessed brain MRIs in a prospective cohort of patients with symptomatic atherosclerosis. Only patients in whom both observers scored PHL on T2- and proton density-weighted images, but not on T1-weighted images, were considered to have the lesion. RESULTS: We studied 229 patients 31% presenting with ischemic stroke, 31% with myocardial infarction, and 38% with peripheral artery disease. Both observers scored PHL in 23% of all patients. Patients with PHL were significantly older and had more lacunar infarcts and periventricular leukoaraiosis than patients without PHL. There were more women, more hypercholesterolemic and diabetic patients, and more cortical infarcts on MRI (P = NS). After logistic regression the presence of leukoaraiosis (odds ratio, 2.4; 95% confidence interval, 1.6 to 3.4) and lacunar infarcts (odds ratio, 2.2, 95% confidence interval, 1.5 to 3.1) remained independently associated with PHL. PHL was more common in patients with ischemic strokes (39%) than in patients with myocardial infarctions (11%) or peripheral artery disease (19%) (P < .001). CONCLUSIONS: We found that PHL on T2- and proton density-weighted MR images are often found in patients with symptomatic atherosclerosis. The association with periventricular leukoaraiosis and lacunar infarcts suggests that PHL is a variant of leukoaraiosis, with possibly the same pathophysiology. The clinical symptoms and consequences of PHL, however, are not yet clear.     

Myocardial color scan with 43K in ischemic heart disease

The value of myocardial scanning with 43K was assessed in 64 consecutive patients undergoing coronary arteriography, and in five young volunteers. Myocardial scans at rest detected only 16 of the 35 transmural infarcts documented on electrocardiograms, 11 of 11 anterior infarcts and five of 24 in other sites. Myocardial scans were obtained immediately after a graded exercise test in the five normal volunteers, in nine patients with normal coronary arteriograms and in 25 patients with atherosclerotic narrowing greater than 75% involving the left anterior descending artery, with or without disease of other coronary vessels. All patients with normal coronary arteriograms had normal myocardial scans. A regional perfusion deficit was observed after exercise in all six patients with single vessel disease, but in only 11 of the 19 patients with disease involving two or three vessels. Although the technique was specific, it lacked sensitivity, due mostly to poor resolution and the location of the disease.     

Bilateral caudate head infarcts

We reported a 67-year-old woman with bilateral caudate head infarcts. She developed sudden mutism followed by abulia. She was admitted to our hospital 2 months after ictus for further examination. She showed prominent abulia and was inactive, slow and apathetic. Spontaneous activity and speech, immediate response to queries, spontaneous word recall and attention and persistence to complex programs were disturbed. Apparent motor disturbance, gait disturbance, motor aphasia, apraxia and remote memory disturbance were not identified. She seemed to be depressed but not sad. Brain CT and MRI revealed bilateral caudate head hemorrhagic infarcts including bilateral anterior internal capsules, in which the left lesion was more extensive than right one and involved the part of the left putamen. These infarct locations were thought to be supplied by the area around the medial striate artery including Heubner's arteries and the A1 perforator. Digital subtraction angiography showed asymptomatic right internal carotid artery occlusion. She bad had hypertension, diabetes mellitus and atrial fibrillation and also had a left atrium with a large diameter. The infarcts were thought to be caused by cardioembolic occlusion to the distal portion of the left internal carotid artery. Although some variations of vasculature at the anterior communicating artery might contribute to bilateral medial striate artery infarcts, we could not demonstrate such abnormalities by angiography. Bilateral caudate head infarcts involving the anterior internal capsule may cause prominent abulia. The patient did not improve by drug and rehabilitation therapy and died suddenly a year after discharge.     

Simple uniformity and penetration phantoms for the quality assurance of ultrasound scanners

Noncontrast computed tomographic scans (CT scans) may show a hyperdense basilar artery before a brainstem infarct is visualized. This early sign should assist clinicians in confirming the diagnosis of basilar artery thrombosis. In a review of admission records of 750 patients with acute cerebrovascular disease from July 1991 to June 1993, at Saint Louis University Hospital, 20 patients were identified with clinical signs of nonlacunar, vertebrobasilar distribution infarction. Eight of these had pontomesencephalic ischemia. Their neuroimaging studies and medical records were evaluated. Four patients with acute clinical signs of pontomesencephalic infarction were found to have a hyperdense basilar artery on CT scans. The scans of 2 patients were excluded because of dolichoectasia; in the other 2 patients, the basilar artery appeared normal on the CT scan. The hyperdense basilar artery was detected within the early hours of neurological symptoms and often was the only detectable abnormality on the scan. In 3 patients extensive brainstem infarcts subsequently developed and they died. Basilar artery thrombosis was confirmed by pathological study in all these patients. In the fourth patient basilar artery occlusion and a large pontine infarct were evident by magnetic resonance imaging and angiography. A hyperdense basilar artery is a common feature on CT scans of patients presenting with an early clinical diagnosis of thrombosis. Untreated, the hyperintense basilar artery often portends a poor prognosis. Its ready recognition should guide further interventional studies and treatment.     

Use of changes in ST segment elevation for prediction of infarct artery recanalization in acute myocardial infarction

BACKGROUND: The role of the ECG in evaluating reperfusion status after thrombolytic treatment in acute myocardial infarction is not clear. Dramatic ST segment changes have been observed during recanalization of an infarct-related artery, but ST criteria have not been definitively established for prediction of coronary artery patency. Differences in ST segment changes in relation to infarct localization have not been evaluated, and further investigation is required into reciprocal ST depression, which provides information independent from ST elevation. Therefore, the aim of this study was to evaluate how early changes in ST segment elevations and depressions predict vessel patency after fibrinolysis for patients with anterior and inferior/lateral infarcts. METHODS AND RESULTS: Two hundred patients with a Pardee wave in the ECG and chest pain of less than 6 h duration were given thrombolytic treatment. The result of the therapy was assessed simultaneously with coronary angiography. Patients were divided into two groups: I (50 patients) without recanalization (TIMI grade 0, 1 or 2), and II (150 patients) with successful recanalization (TIMI grade 3). Before and after therapy, analysis of the 12 lead ECG included maximum ST elevation measurement (H1, H2 respectively), the sum of ST elevations (sigma H1, sigma H2), the sum of ST segment depressions (sigma h1, sigma h2), and the ratios of ST segment changes (R1 = H2:H1, R2 = sigma H2:sigma H1, R3 = sigma h2:sigma h1). The mean interval from the first to the second ECG was 3.5 +/- 1 h. Successive values of R1 and R2 were examined to find that which best distinguished between the two groups. The best values for prediction of reperfusion were: (1) For anterior wall infarct [table: see text] (2) For inferior and lateral infarct [table: see text] In 13 patients with a complete right or left bundle branch block in the first or second ECG, the result of treatment was predicted in 11 patients using criteria for factor R1 and in 12 patients using criteria for R2. Analysis of ST segment depressions revealed a significant correlation between normalization of ST segment depressions and elevations (R3 vs R1: r = 0.60, P < 0.05; R3 vs R2 r = 0.59, P < 0.05). Multivariate discriminant analysis showed an independent value of R3 for discrimination between the two groups, but only in patients with inferior/lateral infarcts. The overall accuracy of the common algorithm in predicting reperfusion was significantly better in patients with inferior/lateral infarcts (Chi2 test, P = 0.0078). When separate algorithms were used, there was no significant difference between patients with anterior or inferior/lateral infarcts because of the significant improvement in prediction of reperfusion in patients with anterior infarcts (McNemar's test: P = 0.041). CONCLUSIONS: We conclude that analysis of ST segments on the standard 12-lead ECG offers valuable help in the early identification of successful recanalization of infarct-related arteries after thrombolytic therapy in patients with acute myocardial infarction. Use of the ratio of ST segment normalization according to the separate criteria for anterior and inferior/lateral infarcts gives the test a high sensitivity and specificity, even in the presence of interventricular conduction disturbances.     

A surgical approach to coexistent coronary and carotid artery disease

OBJECTIVE: To assess the early results of combined coronary artery bypass graft surgery and carotid endarterectomy. DESIGN: Retrospective and ongoing analysis of patients who underwent combined coronary artery bypass graft surgery and carotid endarterectomy. SETTING: Cardiothoracic unit in a London teaching hospital. PATIENTS: From June 1987 to March 1995, 64 patients were identified. They were patients who were scheduled to have coronary artery bypass graft surgery or required urgent coronary revascularisation and who were found to have significant coexistent carotid disease. (Unilateral carotid stenosis > 70%, bilateral carotid stenosis > 50%, or unilateral carotid stenosis > 50% with contralateral occlusion.) INTERVENTIONS: Both procedures were performed during one anaesthesia: the carotid endarterectomy was performed first without cardiopulmonary bypass. After completion of carotid endarterectomy, coronary artery bypass graft surgery was performed. MAIN OUTCOME MEASURES: The incidence of stroke, transient ischaemic attack, and myocardial infarction in the early postoperative period was analysed. RESULTS: Myocardial revascularisation was successful in all 64 patients. There were no perioperative infarcts. In three patients (4.7%) a new neurological deficit developed postoperatively: two recovered fully before hospital discharge. CONCLUSIONS: Combined coronary artery bypass graft surgery and carotid endarterectomy were performed safely and with good results.     

Sarcoma in association with bone infarcts. Report of five cases

Sarcoma associated with bone infarct is rare, and only 41 well-documented cases have been published. We describe five additional patients, three women and two men, aged 39 to 57 years. The tumors involved the femur (three patients), tibia (one patient), and humerus (one patient). In three patients, the infarcts were idiopathic. Radiologic evidence of malignancy was found in all patients, and bone infarcts were suspected in four. Four of the patients had malignant fibrous histiocytoma and one an osteosarcoma. Histologically, bone infarcts were seen in all patients, but in three they were mostly replaced by tumor. Portions of intact infarcts were seen adjacent to the tumor, indicating that they had preceded the development of the sarcoma. No hypercellular or atypical reparative tissue was found in the infarcted bones or in three additional uncomplicated infarcts studied from the same patients. The pathogenesis of sarcoma arising in bone infarct is unknown. The prognosis is poor; four of our five patients died within 2 years.     

MRI and MR angiography of vertebral artery dissection

A review of 4,500 angiograms yielded 11 patients with dissection of the vertebral arteries who had MRI and (in 4 patients) MR angiography (MRA) in the acute phase of stroke. One patient with incidental discovery at arteriography of asymptomatic vertebral artery dissection and two patients with acute strokes with MRI and MRA findings consistent with vertebral artery dissection were included. Dissection occurred after neck trauma or chiropractic manipulation in 4 patients and was spontaneous in 10. Dissection involved the extracranial vertebral artery in 9 patients, the extra-intracranial junction in 1, and the intracranial artery in 4. MRI demonstrated infarcts in the brain stem, cerebellum, thalamus or temporo-occipital regions in 7 patients with extra- or extra-intracranial dissections and a solitary lateral medullary infarct in 4 patients (3 with intracranial and 1 with extra-intracranial dissection). In 2 patients no brain abnormality related to vertebral artery dissection was found and in one MRI did not show subarachnoid haemorrhage revealed by CT. Intramural dissecting haematoma appeared as crescentic or rounded high signal on T1-weighted images in 10 patients examined 3-20 days after the onset of symptoms. The abnormal vessel stood out in the low signal cerebrospinal fluid in intracranial dissections, whereas it was more difficult to detect in extracranial dissections because of the intermediate-to-high signal of the normal perivascular structures and slow flow proximal and distal to the dissection. In two patients examined within 36 h of the onset, mural thickening was of intermediate signal intensity on T1-weighted images and high signal on spin-density and T2-weighted images. MRA showed abrupt stenosis in 2 patients and disappearance of flow signal at and distal to the dissection in 5. Follow-up arteriography, MRI or MRA showed findings consistent with occlusion of the dissected vessel in 6 of 8 patients.     

Thrombolytic therapy in acute occlusion of the intracranial internal carotid artery bifurcation

PURPOSE: To evaluate efficacy and clinical benefit of early thrombolytic therapy in intracranial internal carotid artery occlusion. METHODS: Thirty-two patients (mean age, 56 years) with acute intracranial internal carotid artery occlusion were studied clinically and with CT and angiography before and after thrombolytic therapy with intravenous alteplase (n = 16), superselective intraarterial alteplase (n = 8), and superselective intraarterial urokinase (n = 8). RESULTS: Initial CT showed a large parenchymal hypodensity in 11 (34%) patients, a small hypodensity in 15 (47%) patients, and no hypodensity in 6 (19%) patients. Recanalization after thrombolytic therapy was observed in 4 patients (12.5% in each treatment group). Follow-up CT showed six hemorrhagic infarcts and four parenchymal hematomas unrelated to recanalization, alteplase, or urokinase administration, but commonly associated with intraarterial treatment. Clinical outcome was fatal in 53%, poor in 31%, and moderate or good in 16% of the patients. Outcome was equal in different treatment groups and closely linked to both the quality of leptomeningeal collaterals and the extent of parenchymal hypodensity on the first CT. CONCLUSION: Because intravenous or intraarterial treatment with alteplase or urokinase fails to recanalize the vascular obstruction, it does not improve the prognosis of intracranial internal carotid artery occlusion over that of the natural course. Improved results may be possible with novel recanalization techniques.     

Clinical features of anterior inferior cerebellar artery territory infarcts--a study of ten patients

Clinical features of the anterior inferior cerebellar artery (AICA) territory infarcts were investigated in ten patients, ranging in age from 38 to 76 years. In all patients, there were MR images of infarction located in the area supplied by the AICA. The lesion was on the left side in 6 patients and right side in 4. The lesion of brain stem including the middle cerebellar peduncle was found in 7 patients and that extended to the cerebellum was in 3 patients. The main ipsilateral neurological signs were the VII and VIII cranial nerves palsy and cerebellar ataxia. The V and VI cranial nerves palsy. Horner's syndrome, and dysphagia were also present. The main contralateral sign was superficial sensory disturbance, but no hemiplegia. The underlying pathology included chiefly hyperlipidemia, hypertension, and diabetes mellitus. Cerebral angiography was performed in 8 patients, most of which was observed severe arteriosclerosis suggesting poor hemodynamics in the vertebral and basilar arteries. The prognosis was relatively good, but the VII, VIII, and V cranial nerves palsy and contralateral superficial sensory disturbance remained as the sequelae. As mentioned above, there were various neurological findings and MR images in AICA territory infarcts. Especially there were some patients whose lesion extended to the upper medulla and neurological findings were similar to the Wallenberg syndrome. It is important that one investigates not only axial slices but also coronal slices of MR image to estimate the extension of AICA territory infarct.     

Pulmonary infarcts can mimic pulmonary metastases from renal cancer

PURPOSE: Spontaneous regression of pulmonary metastases from renal cell carcinoma is a rare but well documented event. We present 2 recent cases that were radiographically consistent with pulmonary metastases from renal cell carcinoma but were pathologically shown to be pulmonary infarcts with no evidence of metastatic cells. Stable pulmonary infarcts can be misconstrued as metastatic disease in patients with renal cell carcinoma while resolving pulmonary infarcts may represent a subpopulation of patients with apparent spontaneous regression. Clinical implications of these findings are discussed. MATERIALS AND METHODS: Clinical and pathological data from 2 patients with large primary renal tumors, venous thrombi and lung masses were reviewed. Data from these cases, as well as pertinent urological and pathological literature, are presented. RESULTS: Although preoperative assessment was consistent with stage IV renal cell carcinoma, pathological examination of the lung masses in these patients showed no evidence of tumor cells. CONCLUSIONS: Pulmonary infarcts may mimic resolving or stable pulmonary metastasis in patients with renal cell carcinoma. Accurate clinical staging is crucial for the prognosis and treatment of renal cell carcinoma. Mistaking pulmonary infarcts for metastatic lesions can lead to inaccurate prognoses and inappropriate treatment.     

Consequences of intramyocardial arterial lesions in aortic valvular stenosis

Proliferative lesions, which included collagen deposition, developed with age in intramyocardial arteries of 27 patients with aortic stenosis and matched controls. Those with the most extensive intramyocardial artery lesions developed massive subendocardial infarcts during surgery. Using histologic quantitation, the percent of intramyocardial arteries with lesions in a patient was correlated with decreases in the amount of muscle in arterioles between the subepicardial and subendocardial zones of the left ventricle. The mean decrease in arteriolar muscle was 43% in patients with aortic stenosis and 19% in controls. Blood pressures correlate with the amount of muscle in arterioles, so subendocardial perfusing pressures were presumably low in those with aortic stenosis. Patients with the greatest decrease in arteriolar muscle across the myocardium had the most impaired left ventricular function, i.e., highest end diastolic pressures, lowest ejection fractions, and lowest mean fiber shortening rates.     

Comparison of hypertensive and non-hypertensive lacunar infarcts

INTRODUCTION: Arterial hypertension and hypohyalinosis of the arterias perforantes are said to be the commonest cause of lacunar infarcts, although other etiological factors and anatomo-pathological lesions are described more and more frequently. We designed a study to compare the clinical topographic and prognostic characteristics of patients with hypertensive and non-hypertensive lacunar infarcts. MATERIAL AND METHODS: We selected 51 patients with lacunar infarcts: in 23 (45%) arterial hypertension was the only etiological factor recognized. In 28 (55%) other risk factors (16 diabetes mellitus, 17 cardiopathy, 8 hyperlipemia, 13 cigarette smoking and 11 alcoholism) were seen. We evaluated the form of presentation, the type of infarct and whether this was associated with headache. The degree of defect was determined on admission using the Canadian scale. The size of the infarct was measured on CT or RM, using whichever measurement was greater. The evolution of the condition was determined on the Canadian scale and the index of Barthel after three months. RESULTS: Age and sex distribution was similar to both groups. Motor hemiparesia was the commonest lacunar syndrome and the distribution was similar. There was no difference in form of onset, association with headache or neurological defect between the hypertensive and non-hypertensive lacunar infarcts. The topographical distribution, the presentation of single or multiple lesions, the size of the infarcts and the prognosis were similar in both groups. CONCLUSIONS: Lacunar infarcts, whether hypertensive or not, show no differences regarding clinical, neuro-radiological or evolutionary characteristics.