Nonhemorrhagic Infarction Research Articles

The effect of postinfarction intramyocardial hemorrhage on transverse relaxation time.

1H NMR imaging has been used to define zones of myocardial infarction (MI), which appear as areas of relatively increased signal intensity (SI). However, zones of decreased SI have been observed within or around the areas of infarction in NMR images acquired at high magnetic fields. To determine the cause of these areas of reduced SI, ex vivo spin-echo 1H NMR imaging at 1.5 T was performed in eight dogs following 72 h of coronary artery occlusion. In all dogs, a zone of increased SI (122 +/- 7% compared to control myocardium; P less than 0.01) was observed in the territory of the occluded coronary artery. In seven of the dogs, additional zones were also seen, within or around the central zone of increased SI, which displayed SI that was reduced in comparison with the local enhanced intensity, but was similar to the intensity of normal myocardium (97 +/- 7% compared to control; P = NS). Gross inspection and histological assessment of sliced myocardium disclosed hemorrhage in these regions characterized by locally decreased NMR SI. Image-derived calculation of T2 in the various infarct regions revealed a significant shortening of T2 in the hemorrhagic infarct zones characterized by decreased SI, in comparison with the nonhemorrhagic infarct zones characterized by increased SI (59 +/- 7 ms vs 73 +/- 10 ms, P less than 0.05). No difference was found, however, between the observed T2's of hemorrhagic infarct and of control tissue (57 +/- 4 ms). Using a biexponential analysis of T2 from the hemorrhagic infarct zones, the intrinsic T2 of water protons affected by hemorrhage was determined to be 43 +/- 9 ms, significantly reduced in comparison with the values obtained with the standard monoexponential fit. The reduction in T2 in the hemorrhagic zone is consistent with the paramagnetic effects of deoxyhemoglobin associated with intramyocardial hemorrhage. Thus the apparent T2, measured in hemorrhagic infarct tissue, represents the result of an averaging effect of infarct and hemorrhage on T2 relaxation times. These observations improve our understanding of the changes in NMR SI within the infarcted regions, and may provide a noninvasive method for the detection and quantitative assessment of intramyocardial hemorrhage.

A prospective 1 year follow-up study with somatosensory potentials evoked by stimulation of the posterior tibial nerve in patients with supratentorial cerebral infarction

Somatosensory potentials evoked by stimulation of the posterior tibial nerve (tibial nerve SEPs) were studied in 40 patients with supratentorial non-haemorrhagic cerebral infarction and in 25 control subjects. SEPs were recorded twice in 39 patients and thrice in 35 patients. The first examination was carried out 4–19 days after the onset of the symptoms, the second examination 56–100 days after the stroke, and the third examination 348–393 days after the stroke. Increased side-to-side differences in the P57 and N75 peak latencies and absence of the P40 peak were the most frequent abnormal findings. The latency abnormalities were associated with involvement of the subcortical white matter of the rolandic region. The absence of the P40 peak was, in contrast, closely related to the extension of the infarcted area into the cortical gray matter of during the acute stage, 51% of patients had abnormal SEPs in the second examination and 43% of patients in the third examination. A nearly significant decrease was observed in the number of latency abnormalities, but the number of amplitude abnormalities, including absent responses, did not change during the 1 year follow-up period.

Stroke in pediatric acquired immunodeficiency syndrome

In a 4 1/2-year period, 4 of 68 children in a longitudinal study of neurological complications of human immunodeficiency virus (HIV) infection had clinical and/or neuroradiological evidence of stroke, yielding a clinical incidence of stroke in this population of 1.3% per year. During this period, 32 subjects died, and permission for autopsy was granted in 18 of the patients, including 3 of 4 who had clinical evidence of stroke. The prevalence of cerebrovascular pathological features in our consecutive autopsy series was higher than the clinical incidence. At autopsy cerebrovascular disease was documented in 6 (24%) of 25 children with HIV infection, including all 3 children who had clinical evidence of stroke. Four patients had intracerebral hemorrhages, 6 patients had nonhemorrhagic infarcts, and 3 had both. Hemorrhage was catastrophic in 1 child and clinically silent in 3 children, all of whom had immune thrombocytopenia. One child had an arteriopathy that affected meningocerebral arteries. In another child, the arteries of the circle of Willis were aneurysmally dilated. Two children had coexisting cardiomyopathy and subacute necrotizing encephalomyelopathy with vascular proliferation. These results suggest that stroke should be considered when children with HIV infection develop focal neurological signs.

Correlation of tibial nerve SEPs with the development of seizures in patients with supratentorial cerebral infarcts

In 40 patients with supratentorial non-haemorrhagic cerebral infarct, the findings in the tibial nerve SEPs recorded during the acute stage correlated significantly with the development of seizures during a 1 year follow-up period. Abnormality in the side-to-side difference of the P40-N48 amplitude was the finding with the highest correlation with the development of seizures: 87.5% of the patients were classified correctly as to the risk of seizures.

Placental hypoechoic-anechoic areas and infarction: sonographic-pathologic correlation.

High-resolution ultrasound (US) and pathologic analysis were used to define the relationship between placental hypoechoic-anechoic areas, frequently seen in the third trimester, and the clinically significant entity of placental infarction. Placentas were obtained from three groups of patients: those prospectively demonstrating one or more placental hypoechoic-anechoic areas greater than or equal to 1 cm in diameter on third-trimester sonograms (n = 14), those with risk factors for vascular disease (n = 12), and control patients without risk factors (n = 16). Pathologic analysis demonstrated significantly more infarcts in patients with risk factors than in control patients (17 vs three, P = .047). Of a total of 22 infarcts from all three groups, 19 (86%) were isoechoic to viable placenta and therefore not detected with US. The three infarcts identified with US contained hypoechoic or anechoic foci of fibrin or hemorrhage. Of 26 placental hypoechoic-anechoic areas 23 (88%) were decidual septal cysts or intervillous thrombosis without infarction. The authors conclude that nonhemorrhagic placental infarction cannot be identified with ex utero US and, by inference, that prenatal US is probably insensitive for detection of placental infarction.

Cardiac morphologic findings in patients with acute myocardial infarction treated with recombinant tissue plasminogen activator

The hearts of 52 patients (aged 61 ± 11 years, 34 men) who participated in the Thrombolysis in Myocardial Infarction (TIMI) Study and died from 5 hours to 260 days (median 2.7 days) after onset of chest pain were studied. One heart became available at cardiac transplantation. Of the 52 patients, 38 received recombinant tissue plasminogen activator (rt-PA) not followed by percutaneous transluminal coronary angioplasty (PTCA) or coronary artery bypass grafting (CABG). Eight had PTCA, and 6 had CABG. The infarcts were hemorrhagic by gross inspection (with histologic confirmation) in 23 patients, nonhemorrhagic in 20, not visible grossly in 2 and, in 7, there was no myocardial necrosis by either gross or histologic examination. Comparisons between the 23 patients with hemorrhagic infarcts and the 20 patients with nonhemorrhagic infarcts showed: (1) similar frequencies of myocardial rupture (left ventricular free wall or ventricular septum) [6 (26%) of 23 vs 5 (25%) of 20], cardiogenic shock [10 (43%) of 23 vs 9 (47%) of 19], and fatal hemorrhage [2 (9%) of 23 vs 2 (10%) of 20]; (2) similar percents of necrotic portions of left ventricular wall among patients surviving >18 hours from onset of chest pain (26 ± 11 vs 23 ± 11%) with the hemorrhage confined to areas of necrotic myocardium in all cases; (3) similar frequencies of thrombi in the infant-related arteries [7 (32%) vs 7 (37%)], but all thrombi in patients with hemorrhagic infarcts were nonocclusive, and all thrombi in those with nonhemorrhagic infarcts were occlusive (p = 0.0002); (4) similar degrees of luminal cross-sectional area narrowing over all 5-mm segments of the 4 major (left main, left anterior descending, left circumflex and right) epicardial coronary arteries in 27 patients receiving rt-PA alone between patients with hemorrhagic and nonhemorrhagic infarcts; (5) similar numbers of patients in whom the infarct-related artery was narrowed >75% in cross-sectional area at some point by plaque [21 (95%) of 22 vs 16 (84%) of 19], and similar mean percent reduction in crosssectional area by plaque of the infarct-related arteries calculated by planimetry (67 ± 10 vs 68 ± 9%); (6) similar frequencies of plaque rupture [11 (55%) of 20 vs 12 (75%) of 16] and similar frequencies of hemorrhage into a plaque [13 (65%) of 20 vs 13 (81%) of 16] in patients without PTCA; (7) fewer right ventricular infarcts in patients with hemorrhagkic infarcts (2 of 10 posterior hemorrhagic infarcts vs 6 of 9 posterior nonhemorrhagic infarcts); (8) similar percents of plaque with pultaceous debris (13 ± 11 vs 18 ± 9%), calcific deposits (14 ± 12 vs 20 ± 14%) and acellular fibrous tissue (49 ± 14 vs 53 ± 11%). Thus, hemorrhage occurs frequently in the infarcts of patients who receive rt-PA. Hemorrhage into an infarct does not appear to extend the infarct, and patients with hemorrhagic (vs nonhemorrhagic) infarcts have no greater frequency of myocardial rupture or cardiogenic shock, and no significant differences in coronary luminal narrowing, plaque rupture or plaque composition. However, those with hemorrhagic infarcts had only nonocclusive thrombi and fewer right ventricular infarcts.

Cerebral infarctions and transiet neurologic deficits associated with acquired immunodeficiency syndrome

purpose: Little information is available concerning the clinical importance of cerebral infarction in patients with acquired immunodeficiency syndrome (AIDS). The purpose of this retrospective study was two-fold: (1) to determine the frequency and clinical characteristics of cerebral infarction and transient neurologic deficits (TNDs) among patients with AIDS; and (2) to identify specific patient subgroups at risk for such complications and whether there were underlying associated diseases requiring specific therapy. patients and methods: Neurology inpatient and consult service records, neuropathology reports, and the University of California, San Francisco, AIDS computerized registry were used in identifying study cases. Information on demographic background, associated clinical diagnoses, presenting neurologic symptoms and signs, laboratory results, pathologic findings, and clinical follow-up was obtained from each patient's medical record. results: Twenty-five patients with AIDS (mean age, 38) having clinical or pathologic findings suggestive of focal cerebral ischemia or infarction were identified. Ten patients had non-hemorrhagic cerebral infarctions, 13 had acute TNDs, and two had both. Cerebral infarction was associated with central nervous system (CNS) infections (cryptococcus, four; tuberculosis, one; zoster vasculitis, one) and cardiogenic embolism (one). TNDs were associated with toxoplasmosis (four), cerebral infarction (two), cryptococcal meningitis (one), vasculitis (one), and CNS Kaposi's sarcoma (one). A presumptive cause was absent in five cases of cerebral infarction and eight of TND. All five patients with pathologically proven macroscopic cerebral infarcts were diagnosed clinically before death. conclusions: We conclude the following: (1) AIDS patients, especially given their young age, appear to be at increased risk for cerebral infarction and TND. (2) Cerebral infarction and TND may be the initial presentation of AIDS. (3) TND and cerebral infarction often signify treatable CNS infection among ADIS patients. (4) The causes of AIDS-related cerebral infarction and TND are unknown in many cases.

Etiology, prognosis, and hemostatic function after cerebral infarction in young adults.

We retrospectively evaluated 66 patients younger than 40 years of age who presented with acute nonhemorrhagic cerebral infarction (n = 63) or transient ischemic attacks (n = 3) to determine the possible etiology and long-term outcome at a mean follow-up interval of 3 years after initial presentation. A probable cause for the stroke was identified in 24 patients (36%); this group included one woman with a history of recurrent spontaneous abortions and a positive test for the presence of the lupus anticoagulant. We performed detailed hemostatic investigations at follow-up in 38 (90%) of the remaining 42 patients in whom the cause of the stroke was unknown or uncertain; results of the basic hemostatic screening tests (including that for fibrinogen) were uniformly normal. All 38 patients demonstrated a normal fibrinolytic response as measured by tissue plasminogen activator release to a standard venous occlusion stress test; concentration of the inhibitor of tissue plasminogen activator was not increased. No abnormalities in the concentrations of the inhibitory proteins C or S or antithrombin III were identified, and none of the 38 patients had evidence of a lupus anticoagulant. Neurologic recovery was complete or the residual disability mild in 46 of 59 (78%) patients. Overall prognosis was excellent and independent of whether a precipitating factor for the stroke could be identified.

The effect of thiamine deficiency on the structure and physiology of the rat forebrain

Dietary thiamine deficiency, enhanced by pyrithiamine administration in adult rats, produces overt lesions in the brain that are especially prominent in the thalamus. The present study was undertaken to determine whether the thalamic lesions could be correlated with alterations in the physiological properties of neurons in the thalamus and somatosensory cortex. The regimen for experimentally inducing thiamine deficiency produced large lesions in the thalamus of every case; the lesions included most, if not all, of the neurons in the intralaminar thalamic nuclei. The extent of the lesion in the intralaminar thalamus was highly correlated with the loss of bilaterally synchronous spontaneous activity in the cerebral cortex. This correlation was seen in animals analyzed as early as 1-18 hr after the appearance of opisthotonus, the crisis state of thiamine deficiency, and as late as 2-9 weeks of recovery following thiamine replacement therapy. The loss of bilateral synchronous bursting neuronal activity following intralaminar thalamic lesions is consistent with the proposed role of the intralaminar thalamus as a pacemaker for rhythmic cortical activity (Armstrong-James et al., Exp. Brain Res., 1985; Fox and Armstrong-James, Exp. Brain Res. 63: 505-518, 1986). The location and size of the central lesions within the thalamus suggest that the observed neuronal loss could result from a nonhemorrhagic infarction in the ventromedial branches of the superior cerebellar arteries. Experimental thiamine deficiency also produced alterations in the receptive field properties of the somatosensory cortex neurons in all animals examined. Changes in cortical receptive field properties were correlated with the destruction of sensory relay neurons in the thalamic ventrobasal complex. The loss of the central lateral thalamic input to the cortex and the loss of somatosensory relay neurons in the ventrobasal thalamus in experimental thiamine deficiency produce alterations in cortical function which may contribute to deficits in memory and cognition analogous to those which characterize Korsakoff's psychosis in humans.

Angiography of nonhemorrhagic cerebral infarction in young adults.

The radiographic examinations and hospital records of 93 young adult patients (15-45 years of age) with nonhemorrhagic cerebral infarction evaluated at our institution during the past 9 years were reviewed. The angiographic examinations were abnormal in 76% of patients. The most common abnormalities were embolic disease and atherothrombotic disease. Forty-seven patients underwent angiography within 7 days of their event. There were no major neurologic or systemic complications related to early angiography. We believe that angiography performed early in the course of the illness is a high-yield, safe procedure that may significantly alter the management of acute stroke in young adults.

Status of the myocardium and infarct-related coronary artery in 19 necropsy patients with acute recanalization using pharmacologic (streptokinase, r-tissue plasminogen activator), mechanical (percutaneous transluminal coronary angioplasty) or combined types of reperfusion therapy

In acute myocardial infarction, myocardial salvage is dependent on rapid restoration of blood flow. Pharmacologic (streptokinase, recombinant tissue-type plasminogen activator), mechanical (percutaneous transluminal coronary angioplasty, guide wire perforation) or combined forms of reperfusion therapy can accomplish this goal, but their effects on infarcted myocardium and vessel occlusion site have not been compared at necropsy. The heart of 19 necropsy patients who had received various forms of acute reperfusion therapy was studied: 14 had pharmacologic or combined forms of reperfusion therapy (13 streptokinase and 1 tissue-type plasminogen activator, including 4 with combined balloon angioplasty) and 5 had had purely mechanical (balloon angioplasty) reperfusion therapy. Reperfusion was initially clinically successful in all 19 patients with the average time from onset of symptoms to reperfusion being 3.7 hours. Necropsy observations separated the 19 patients into distinct subgroups based on changes in the myocardium and infarct-related coronary arteries. Of the 19 patients, 14 (74%) had hemorrhagic myocardial infarction and they all received pharmacologic or combined forms of reperfusion therapy. The remaining five patients (26%) had nonhemorrhagic (anemic) infarction and were treated with balloon angioplasty therapy alone. Increased luminal cross-sectional area was present in 8 of 9 patients with acute balloon angioplasty but severe coronary atherosclerotic plaque remained in 9 of 10 patients without acute balloon angioplasty. Severe hemorrhage surrounded angioplasty sites in all four patients who also received streptokinase or tissue-type plasminogen activator. Severe bleeding at the angioplasty site compromised the dilated coronary lumen in one patient. No patient with angioplasty alone had intraplaque bleeding. Thus, acute coronary balloon angioplasty reperfusion therapy alone appears to avoid the potentially adverse effects of myocardial and intraplaque hemorrhage while simultaneously increasing luminal cross-sectional area at the site of acute occlusion.

Cerebral infarction with a single oral dose of phenylpropanolamine

Phenylpropanolamine (PPA), a synthetic sympathomimetic that is structurally similar to amphetamine, is avallable over the counter in anorectics, nasal congestants, and cold preparations. Its prolonged use or overuse has been associated with seizures, intracerebral hemorrhage, neuropsychiatric symptoms, and nonhemorrhagic cerebral infarction. We report the case of a young woman who suffered a cerebral infarction after taking a single oral dose of PPA.

Diagnostic neuroimaging in stroke. The complementary roles of referring physician and neuroradiologist.

The number and sophistication of neuroimaging methods for identifying location, size, type, and causes of stroke or stroke-like syndromes have expanded rapidly. In acute stroke, computed tomography is used to distinguish between nonhemorrhagic and hemorrhagic infarction and to eliminate several potential alternative diagnoses. Cerebral angiography can identify surgically treatable lesions in patients experiencing transient ischemic attacks and thus aid in preventing stroke. The superb sensitivity of magnetic resonance imaging has opened new vistas in the ongoing investigation of multiinfarct dementia and small infarcts in neurologically "noneloquent" regions of the brain. The more complete the referring physician's clinical and neurologic workup, the more able is the neuroradiologist to structure and coordinate the safest, fastest, and most cost-effective plan of neuroimaging to diagnose a patient's neurologic problem.

Nonhemorrhagic cerebral infarction in young adults.

We evaluated 144 patients (81 males and 63 females) aged 15 to 45 years who had nonhemorrhagic cerebral infarction. Atherosclerotic cerebral infarction was diagnosed in 38 patients. Potential cardiac causes of cerebral embolism were found in 33 patients. Only three events could be attributed to mitral valve prolapse. Hematologically related disorders were diagnosed in 21 patients, while 38 patients had nonatherosclerotic vasculopathies. Young patients with cerebral infarction are a heterogeneous group. A potential cause can be found in most patients. We found more than 40 possible etiologies among our patients. Mitral valve prolapse apparently is not a common cause of cerebral infarction among young adults. Cerebral infarction should not be ascribed to oral contraceptives or migraine until other possible causes have been eliminated.

Echocardiographic evaluation of young adults with nonhemorrhagic cerebral infarction.

We reviewed echocardiographic findings in patients aged 15 to 45 years with acute nonhemorrhagic cerebral infarction (NHCI). Among 132 patients with NHCI, 96 (72.7%) had M-mode and two-dimensional echocardiography, including contrast echocardiography with intravenous saline injection when clinically indicated. Echocardiograms were abnormal in 33 patients. Of these, 7 had other conditions that could cause NHCI. Echocardiography corroborated the clinical diagnosis of a cardiogenic source for cerebral infarction in 17 others. The other 9 had no other clues for cardiovascular disease. Potential etiologies of NHCI diagnosed by echocardiography in these 9 cases included: paradoxical embolism, 5 patients; right atrial myxoma, 1; rheumatic mitral valve vegetation, 1; myxomatous mitral valve (marantic endocarditis at postmortem), 1; and left atrial enlargement associated with decreased left ventricular function, 1. Routine echocardiography frequently conveys useful information in patients under age 45 with NHCI. In young patients with cerebral embolism of unknown etiology if routine M-mode and two dimensional echocardiographic studies are normal, contrast echocardiographic studies should be performed to rule out intracardiac shunts and the possibility of paradoxical cerebral embolism.

Stroke in a patient with hemolytic-uremic syndrome with a good outcome

We report a child with HUS complicated by stupor, hemiparesis, expressive aphasia and focal seizures. CAT scan of the brain demonstrated 2 large cerebral non-hemorrhagic infarcts. Despite the severe neurological involvement the child eventually made a good recovery.

Computerized tomographic findings in cardiogenic cerebral embolism

The CT scan findings in 50 patients with cardiogenic cerebral emboli are reviewed. In 38 cases there was CT evidence of a nonhemorrhagic infarct and in 12 cases there were findings consistent with a hemorrhagic infarct. There was a single infarct in 40 cases and more than one lesion in 10 cases. In 6 of 9 cases in which the patients showed delayed neurological deterioration, repeat CT showed an increase in mass effect (4 cases) or hemorrhagic transformation of the infarct (2 cases).

Neurologic sequelae of cardiac catheterization

Neurologic complications are a known and at times tragic consequence of cardiac catheterization. During a four-year period, 1,362 procedures were performed at our institution on children less than 15 years of age. Eighteen children, without prior nervous system disease, developed neurologic sequelae within 24 hours of cardiac catheterization (1.3%). Three presented with seizures only, ten with neurologic deficits, and five with both focal seizures and stroke. Computerized tomography scans (16 patients) demonstrated areas of nonhemorrhagic infarction in all but one. The 18 patients were studied retrospectively for possible factors contributing to the neurologic complications. They were matched to controls by age, cardiac lesion, and catheterization technique. Data examined included catheterization duration and approach, contrast agent, precatheterization urine specific gravity, pre- and postcatheterization hematocrit, blood loss, and intracatheterization events. Catheter and catheter sheath clots were noted in both patient groups. The neurologic complication group had 7/18 intracatheterization neurologic events versus only one in the controls and the change in hematocrit was greater in the complication group (t = 2.89, p less than 0.01). Due to this study's results and to prevent possible thromboembolic events, a heparinization protocol was instituted and patients were prospectively observed for neurologic complications. No neurologic complications have occurred over three years since the institution of this protocol.

Monocular pattern-shift visual evoked potentials in hemispheric strokes

Monocular pattern-shift visual evoked potentials were obtained in (i) 33 patients with unilateral non-hemorrhagic hemispheric infarction (age 50–79 years; 23 males, 10 females), (ii) 21 age- and sex-matched patient controls (control group or CGI) with no remote or recent stroke, normal neurological examination and similar incidence of diabetes mellitus, hypertension and heart disease, and (iii) 21 age- and sex-matched healthy elderly community volunteers (CGII). Subjects with history of glaucoma, cataracts, other media opacities or symptomatic retinal lesions were not considered or included in any of the 3 study groups. In addition, all subjects in each of the 3 groups had a normal ocular and fundoscopic examination. The mean interocular P100 latency difference in the stroke group was significantly greater than that in CGI or II ( P < 0.01). The mean interocular P100 amplitude ratio (small P100/large P100) in the stroke subjects was significantly different from that of CGI or II ( P < 0.02). The mean P100 latency on ocular stimulation ipsilateral to the side of infarction was significantly longer than that of either left or right ocular stimulation in CGI or II ( P < 0.01). The mean P100 latency on ocular stimulation contralateral to the side of infarction was similarly but less significantly longer than that on left or right ocular stimulation in CGI or II ( P < 0.05). Evidence of anterior visual pathway dysfunction was thus elicited in the stroke population using the technique.

Clinical Features of the Hemorrhagic Cerebral Infarction

Among 199 cases with cerebral infarction 23 cases ( 11.6%) developed hemorrhagic infarction on repeated computerized tomography (CT) scans. The hemorrhagic pattern was classified into 3 groups according to the CT findings; massive type (12 cases), partial type (6 cases), and scattered type (6 cases). Massive type hemorrhagic infarction was accompanied by cerebral swelling and mass effect and was observed, as a rule, within 4 days from clinical onset of the infarction, although there were a couple of exceptional cases, who developed hemorrhage over 2 weeks after the onset. Scattered type hemorrhagic infarction did not show mass effect and was always found after more than 8 days from the onset and no clinical evidence of symptomatic deterioration was encountered. Partial type hemorrhagic infarction appeared from within 4 days to 3 weeks after the onset. Mass effect was exceptional and symptomatic change was infrequent. Overall mortality of the non-hemorrhagic infarction was 15.3%, whereas it was 13% with hemorrhagic infarction, and the mass effect was the principal cause of mortality. Cardiac diseases were found to be the main risk factor in developing hemorrhagic infarction, while hypertension and diabetes mellitus did not appear to be significantly related to hemorrhagic changes of the cerebral infarction. Aspirin and other anticoagulant medication showed no significance either in this study. It is suggested that the causes of hemorrhage are different in massive type and partial or scattered type hemorrhagic cerebral infarctions.