Relevant bibliographies by topics / Infarcts

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  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
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Academic literature on the topic 'Infarcts'

Author: Grafiati
Published: 4 June 2021
Last updated: 25 April 2022

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Journal articles on the topic "Infarcts"

1

Han, Moon-Ku, Dong-Wha Kang, Byung-Woo Yoon, and Jae-Kyu Roh. "Vascular Territorial Classification and Etiologies of Acute MCA Infarct by Diffusion-Weighted MRI." Stroke 32, suppl_1 (January 2001): 346. http://dx.doi.org/10.1161/str.32.suppl_1.346-d.

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P42 Background and Purpose - The purpose of this study is to classify infarct subtypes of middle cerebral artery distribution (MCA) seen on diffusion-weighted MRI (DWI) and investigate infarct mechanisms and etiologies of MCA infarct subtypes. Method - We analysed 187 consecutive patients with acute MCA infarct who were studied by DWI/MRA within the first 4 days of stroke onset between 1997 and 1999, and stroke mechanism was determinedaccording to the criteria of the Trial of Org 10172 in Acute Stroke Treatment (TOAST). Infarct patterns from 128 patients except for lacunar infarcts (patients) were classified by the two types of multiple infarcts and large single infarcts: 2 types of multipleinfarcts; subcortical/cortical and cortical/cortical infarcts, 3 types of large single infarcts; subcortical, cortical and large infarcts including cortical and subcortical lesions Results -TOAST diagnostic subtypes were 78 large vessel strokes, 22 cardioembolic strokes, 59 lacune strokes, 4 other strokes, and 26strokes of unknown cause. We identified multiple infarcts (MI) in 41 patients: subcortical/cortical, 29 including 14 MCA disease (p=0.03); cortical/cortical, 7 including 6 ICA disease (p=0.005), and 87 large single infarcts (SI): subcortical, 32 including 13 MCA disease (p=0.02); cortical, 5 including 3 cardioembolism (p=0.03); large infarcts (cortical/subcortical), 50. There was no difference of etiologies among large infarcts (cortical/subcortical) in SI. Conclusion -MCA disease is the most important cause of subcortical and cortical multiple infarcts, and subcortical single infarcts. ICA disease is most frequent cause of cortical multiple infarcts and cardioembolism is more common cause in cortical single infarcts. We conclude that our classificationof MCA Infarct patterns using early DWI in acute ischemic stroke is useful to identify the causes of stroke according to subtypes and to consider the clinical decisions of etiologic investigations and to decide the early treatment modality in acute ischemic stroke.
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Kumar, Abhay, Robert Brown, Rajat Dhar, Tomoko Sampson, Colin P. Derdeyn, Christopher J. Moran, and Michael N. Diringer. "Early vs Delayed Cerebral Infarction After Aneurysm Repair After Subarachnoid Hemorrhage." Neurosurgery 73, no. 4 (June 19, 2013): 617–23. http://dx.doi.org/10.1227/neu.0000000000000057.

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Abstract BACKGROUND: Cerebral infarction is a major contributor to poor outcome after subarachnoid hemorrhage (SAH). Although usually considered a complication of delayed cerebral ischemia, infarcts may also occur early, in relation to initial brain injury or aneurysm-securing procedures. OBJECTIVE: We analyzed the relative frequency and volume of early vs delayed infarcts after SAH and their relationship to hospital outcome. METHODS: Retrospective review of consecutive patients admitted with aneurysmal SAH over 4 years who had follow-up brain imaging 7 days or later after admission. Imaging 24 to 48-hours after aneurysm-securing procedures was reviewed to classify infarcts seen on final imaging as early or delayed. Infarct volumes were measured by perimeter tracing and infarct burden calculated for each patient. RESULTS: Of 250 eligible patients, 205 had follow-up imaging; infarcts were present in 61 patients. Of these, 29 had early infarcts, 16 had delayed infarcts, and 5 had both early and delayed infarcts. Eleven patients with infarcts did not undergo postprocedure computed tomography; these were presumptively classified as having late infarcts. Early and delayed infarcts contributed equally to infarct burden. Early infarcts were associated with aneurysm clipping (odds ratio: 4.2, 95% confidence interval: 1.8-9.5 compared with coiling), whereas delayed infarcts were almost always seen in association with angiographic vasospasm (odds ratio: 3.3, 95% confidence interval: 1.5-7.3). Patients with early as well as late infarcts, especially those with infarct burden more than 30 cm3 had worse hospital discharge disposition. CONCLUSION: Early infarction occurs frequently after SAH and contributes as much as delayed cerebral ischemia to infarct burden and hospital outcome. Efforts to better understand and modify contributors to early infarction appear warranted.
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Skriver, E. B., and T. S. Olsen. "Repeated Computed Tomography in Lacunar Infarcts of the Brain." Acta Radiologica 30, no. 1 (January 1989): 1–6. http://dx.doi.org/10.1177/028418518903000101.

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This prospective and consecutive study of 74 patients with completed stroke elucidates occurrence, localization and evolution of lacunar infarcts on repeated CT examinations. Twenty patients had large infarcts (diameter >3 cm), 25 medium-sized infarcts (diameter ≥1.5 cm – ≤ 3 cm), and 16 had lacunar infarcts (diameter <1.5 cm). In 13 patients no infarct was seen. The lacunar infarcts were characterized by delayed appearance on CT, low incidence of fog effect, and infrequent presence of contrast enhancement. In 9 of the 16 patients (56%) the lacunar infarct could be identified on the first CT, performed approximately 3 days after the stroke. In 2 patients the infarct was first revealed on the second (2 weeks post stroke) and in 5 on the third CT (6 months post stroke). The delayed appearance might be due to a partial volume effect. Early development of fog effect may also be considered. As contrast enhancement was observed in only 8 per cent of the patients with lacunar infarcts on CT, and in 70 per cent of the entire group of patients in our series with ischemic infarcts, contrast enhancement seemed to be a function of lesion size.
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Pfeffer, J. M., M. A. Pfeffer, P. J. Fletcher, and E. Braunwald. "Progressive ventricular remodeling in rat with myocardial infarction." American Journal of Physiology-Heart and Circulatory Physiology 260, no. 5 (May 1, 1991): H1406—H1414. http://dx.doi.org/10.1152/ajpheart.1991.260.5.h1406.

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Ventricular dilatation may have important prognostic implications for the survival of patients with left ventricular (LV) dysfunction. To determine the manner and extent to which the left ventricle of the rat remodels and dilates after myocardial infarction, we obtained the passive pressure-volume relationships, chamber stiffness constants, and mass during both the early and late phases. In moderate and large infarcts as inflammation and edema developed, LV weight increased then progressively decreased as a thin scar formed, returning to normal values as a result of compensatory hypertrophy of the residual myocardium. LV dilatation occurred in all rats with infarcts but to different extents depending on infarct size and duration. In the early postinfarction phase, pressure-volume relationship was relatively unchanged in all infarct-size groups, except for significant rightward shift in low pressure range for rats with moderate and large infarcts and significant leftward shift in high pressure range for rats with small infarcts. During resolution of the inflammatory response, LV dilatation occurred in all infarct groups in relation to infarct size. As scar formation became complete, LV enlargement did not progress in rats with small infarcts but did so in rats with moderate and large infarcts. LV chamber stiffness remained within the range of normal values during the early phase in all rats with infarcts but decreased significantly during the late phase in rats with moderate and large infarcts in association with the extent of ventricular enlargement. Alterations in the volume-to-mass ratio (V/Vwt) were most marked in the late postinfarction phase, wherein both volume (increased) and mass (decreased, then increased) changed dramatically and V/Vwt progressively increased in rats with large infarcts.
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Nudo, R. J., and G. W. Milliken. "Reorganization of movement representations in primary motor cortex following focal ischemic infarcts in adult squirrel monkeys." Journal of Neurophysiology 75, no. 5 (May 1, 1996): 2144–49. http://dx.doi.org/10.1152/jn.1996.75.5.2144.

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1. Intracortical microstimulation (ICMS) techniques were used to derive detailed maps of distal forelimb movement representations in primary motor cortex (area 4) of adult squirrel monkeys before and a few months after a focal ischemic infarct. 2. Infarcts caused a marked but transient deficit in use of the contralateral hand, as evidenced by increased use of the ipsilateral hand, and reduced performance on a task requiring skilled digit use. 3. Infarcts resulted in a widespread reduction in the areal extent of digit representations adjacent to the lesion, and apparent increases in adjacent proximal representations. 4. We conclude that substantial functional reorganization occurs in primary motor cortex of adult primates following a focal ischemic infarct, but at least in the absence of postinfarct training, the movements formerly represented in the infarcted zone do not reappear in adjacent cortical regions.
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Fomovsky, Gregory M., and Jeffrey W. Holmes. "Evolution of scar structure, mechanics, and ventricular function after myocardial infarction in the rat." American Journal of Physiology-Heart and Circulatory Physiology 298, no. 1 (January 2010): H221—H228. http://dx.doi.org/10.1152/ajpheart.00495.2009.

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The mechanical properties of the healing scar are an important determinant of heart function following myocardial infarction. Yet the relationship between scar structure, scar mechanics, and ventricular function remains poorly understood, in part because no published study has tracked all of these factors simultaneously in any animal model. We therefore studied the temporal evolution of scar structure, scar mechanics, and left ventricular (LV) function in large anterior myocardial infarcts in rats. At 1, 2, 3, and 6 wk after left anterior descending coronary ligation, we examined LV function using sonomicrometry, infarct mechanical properties using biaxial mechanical testing, infarct structure using polarized light microscopy, and scar collagen content and cross-linking using biochemical assays. Healing infarcts in the rat were structurally and mechanically isotropic at all time points. Collagen content increased with time and was the primary determinant of scar mechanical properties. The presence of healing infarcts influenced systolic LV function through a rightward shift of the end-systolic pressure-volume relationship (ESPVR) that depended on infarct size, infarct collagen content, and LV dilation. We conclude that in sharp contrast to previous reports in large animal models, healing infarcts are structurally and mechanically isotropic in the standard rat model of myocardial infarction. On the basis of the regional strain patterns we observed in healing rat infarcts in this study and in healing pig infarcts in previous studies, we hypothesize that the local pattern of stretching determines collagen alignment in healing myocardial infarct scars.
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Mishra, Ajay Kumar, Vanjare Harshad Arvind, Divya Muliyil, Cijoy K. Kuriakose, Anu Anna George, Reka Karuppusami, Ronald Albert Benton Carey, Sunithi Mani, and Samuel George Hansdak. "Cerebrovascular injury in cryptococcal meningitis." International Journal of Stroke 13, no. 1 (April 19, 2017): 57–65. http://dx.doi.org/10.1177/1747493017706240.

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Background Cryptococcal meningitis continues to be one of the common causes of chronic central nervous system infection worldwide. Individuals with cryptococcal meningitis can occasionally present with small vessel vasculitis causing infarcts primarily in the basal ganglia, internal capsule, and thalamus. Literature regarding patterns of cerebrovascular injury among patients with cryptococcal meningitis is scanty, and outcome following these vascular involvements is unknown. Aim To study the clinical profile, imaging findings, and details of vascular territory involved among patients admitted with cryptococcal meningitis and central nervous system infarct in a tertiary care center from India. And to compare the outcomes of patients of cryptococcal meningitis with or without central nervous system infarcts in terms of mortality and morbidity, Methodology A total of 151 patients with microbiologically proven cryptococcal meningitis over a time span of 11 years were retrospectively enrolled into the study. Of these, 66 patients met the inclusion criteria of having appropriate imaging of the brain. The presence of infarct in the imaging was analyzed by two independent radiologists. Patterns of central nervous system involvement and types of vascular injury were ascertained based on radiological parameters. Clinical parameters and outcomes of patients with and without infarcts were compared. Results Twenty (13%) of these patients had evidence of central nervous system infarcts on imaging. The mean age of patients with and without infarcts was 41 years and 38 years, respectively. Male predominance was present among both the groups. The presence of fever, neck stiffness, positive blood culture, and hydrocephalus in central nervous system imaging was similar among patients with or without infarct. Longer duration of illness, low sensorium at the time of presentation, low Glasgow Coma Scale score, presence of meningeal inflammation, cryptococcomas, and basal exudates in imaging were higher in patients with infarct. All the infarcts were of the lacunar type. Sixty percent of the cerebrovascular infarcts were acute in nature, 50% of these being multiple. Unilateral infarcts were seen in 70% of the patients. The most common site of infarct was the basal ganglia, others being distributed over the thalamus, frontal, temporal, parieto-occipital regions in the descending order. The presence of neurovascular involvement in the form of infarcts to the risk of morbidity and mortality had an odds ratio of 9.1 and 2.6, respectively. Conclusion Neurovascular involvement in chronic cryptococcal meningitis is a rare entity. These tend to present as multiple lacunar infarcts. Mortality and morbidity associated with these patients is higher when compared to patients who do not have infarcts. This result suggests that vascular injury plays a role in predicting outcome of patients with cryptococcal meningitis. Future studies are needed to understand the mechanism by which vascular events (infarcts) occur and result in poor outcome.
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Ospel, Johanna M., Petra Cimflova, Martha Marko, Arnuv Mayank, Moiz Hafeez, Mohammed A. Almekhlafi, Michael D. Hill, Andrew M. Demchuk, Bijoy K. Menon, and Mayank Goyal. "Prevalence and Outcomes of Medium Vessel Occlusions With Discrepant Infarct Patterns." Stroke 51, no. 9 (September 2020): 2817–24. http://dx.doi.org/10.1161/strokeaha.120.030041.

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Background and Purpose: The prognosis of medium vessel occlusions (MeVOs), that is, M2/3 middle cerebral artery, A2/3 anterior cerebral artery, and P2/3 posterior cerebral artery occlusions, is generally better compared with large vessel occlusions, since brain ischemia is less extensive. However, in some MeVO patients, infarcts are seen outside the territory of the occluded vessel (MeVO with discrepant infarcts). This study aims to determine the prevalence and clinical impact of discrepant infarct patterns in acute ischemic stroke due to MeVO. Methods: We pooled data of MeVO patients from INTERRSeCT (Identifying New Approaches to Optimize Thrombus Characterization for Predicting Early Recanalization and Reperfusion With IV Alteplase and Other Treatments Using Serial CT Angiography) and PRove-IT (Precise and Rapid Assessment of Collaterals Using Multi-Phase CTA in the Triage of Patients With Acute Ischemic Stroke for IA Therapy)—2 prospective cohort studies of patients with acute ischemic stroke. The combination of occlusion location on baseline computed tomography angiography and infarct location on follow-up computed tomography/magnetic resonance imaging was used to identify MeVOs with discrepant infarct patterns. Two definitions for discrepant infarcts were applied; one was more restrictive and purely based on infarct patterns of the basal ganglia, whereas the second one took cortical infarct patterns into account. Clinical outcomes of patients with versus without discrepant infarcts were summarized using descriptive statistics. Logistic regression was performed to obtain adjusted effect size estimates for the association of discrepant infarcts and good outcome, defined as a modified Rankin Scale score of 0 to 2, and excellent outcome (modified Rankin Scale score 0–1). Results: Two hundred sixty-two patients with MeVO were included in the analysis. The prevalence of discrepant infarcts was 39.7% (definition 1) and 21.0% (definition 2). Patients with discrepant infarcts were less likely to achieve good outcome (definition 1: adjusted odds ratio, 0.48 [95% CI, 0.25–0.91]; definition 2: adjusted odds ratio, 0.47 [95% CI, 0.22–0.99]). When definition 1 was applied, patients with discrepant infarcts were also less likely to achieve excellent outcome (definition 1: adjusted odds ratio, 0.55 [95% CI, 0.31–0.99]; definition 2: adjusted odds ratio, 0.62 [95% CI, 0.31–1.25]). Conclusions: MeVO patients with discrepant infarcts are common, and they are associated with more severe deficits and poor outcomes.
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Cauley, Keith A., Gino J. Mongelluzzo, and Samuel W. Fielden. "Automated Estimation of Acute Infarct Volume from Noncontrast Head CT Using Image Intensity Inhomogeneity Correction." International Journal of Biomedical Imaging 2019 (August 21, 2019): 1–8. http://dx.doi.org/10.1155/2019/1720270.

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Identification of early ischemic changes (EIC) on noncontrast head CT scans performed within the first few hours of stroke onset may have important implications for subsequent treatment, though early stroke is poorly delimited on these studies. Lack of sharp lesion boundary delineation in early infarcts precludes manual volume measures, as well as measures using edge-detection or region-filling algorithms. We wished to test a hypothesis that image intensity inhomogeneity correction may provide a sensitive method for identifying the subtle regional hypodensity which is characteristic of early ischemic infarcts. A digital image analysis algorithm was developed using image intensity inhomogeneity correction (IIC) and intensity thresholding. Two different IIC algorithms (FSL and ITK) were compared. The method was evaluated using simulated infarcts and clinical cases. For synthetic infarcts, measured infarct volumes demonstrated strong correlation to the true lesion volume (for 20% decreased density “infarcts,” Pearson r = 0.998 for both algorithms); both algorithms demonstrated improved accuracy with increasing lesion size and decreasing lesion density. In clinical cases (41 acute infarcts in 30 patients), calculated infarct volumes using FSL IIC correlated with the ASPECTS scores (Pearson r = 0.680) and the admission NIHSS (Pearson r = 0.544). Calculated infarct volumes were highly correlated with the clinical decision to treat with IV-tPA. Image intensity inhomogeneity correction, when applied to noncontrast head CT, provides a tool for image analysis to aid in detection of EIC, as well as to evaluate and guide improvements in scan quality for optimal detection of EIC.
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Ganesh, A., JM Ospel, AT Wilson, M. Goyal, M. Tymianski, and MD Hill. "P.083 Early and 30-day clinical and neuropsychological effects of iatrogenic brain infarcts in the ENACT randomized-controlled trial." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 48, s3 (November 2021): S43. http://dx.doi.org/10.1017/cjn.2021.362.

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Background: Small brain infarcts are often seen on diffusion-weighted MRI(DWI) following surgical/endovascular procedures. Little is known about their clinical effects. We examined the association of iatrogenic infarcts with outcomes in the ENACT(Evaluating Neuroprotection in Aneurysm Coiling Therapy) trial of nerinetide in endovascular aneurysm repair. Methods: In this post-hoc analysis, we used multi-variable models to evaluate the association of presence/number of DWI iatrogenic infarcts with NIHSS(National Institutes of Health Stroke Scale), mRS(modified Rankin Scale), and cognitive/neuropsychological scores(30-minute battery) at 1-4 and 30-days post-procedure. We also related infarct number to a Z-score-derived composite outcome score(quantile regression). Results: Among 185 patients(median age:56,IQR:50-64), 124(67.0%) had iatrogenic infarcts(median:4,IQR:2-10.5). Nerinetide resulted in fewer infarcts. Patients with infarcts had lower Mini-Mental State Exam(MMSE) scores at 2-4 days(median:28 vs 29, adjusted-coefficient[acoef] per additional infarct:-1.11,95%CI:-1.88 to -0.34,p=0.005). Infarct number was associated with worse day-1 NIHSS(aOR for NIHSS≥1:1.07,1.02-1.12,p=0.009), day 2-4 mRS(adjusted common odds-ratio[aOR]:1.05,1.01-1.09,p=0.005) and MMSE(acoef:-0.07,-0.13 to -0.003,p=0.040), 30-day mRS(aOR:1.04,1.01-1.07,p=0.016) and Hopkins Verbal Learning Test scores(acoef:-0.21,-0.39 to -0.03,p=0.020), as well as worse composite scores at 1-4 and 30-days(acoef:-0.09,-0.15 to -0.03,p=0.006). Conclusions: Iatrogenic infarcts were associated with subtle differences in post-procedural(1-4 days) and 30-day outcomes in this middle-aged cohort. Future studies should use batteries of similar/greater granularity to validate optimal measures for short- versus long-term manifestations.
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Dissertations / Theses on the topic "Infarcts"

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Low, Wee Chuang Roger. "Molecular pathology of cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) and hereditary multi-infarct dementia." Thesis, University of Newcastle Upon Tyne, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.417546.

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Grau, Olivares Marta. "Neuropsychological and structural brain correlates of lacunar infarcts." Doctoral thesis, Universitat de Barcelona, 2008. http://hdl.handle.net/10803/2714.

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L’infart cerebral és la segona causa de mort, així com d’incapacitació a nivell mundial (Di Carlo et al.,2000), essent responsable de múltiples seqüeles físiques i cognitives, incloent la demència. L’infart cerebral es caracteritza per una simptomatologia neurològica focal i sobtada en consonància amb la localització topogràfica de la lesió cerebral, un cop s’han exclòs altres possibles causes. La demència vascular (DV) històricament s’ha basat en el model de demència multi-infart (Erkinjuntti et al.,2002), tot i que cada vegada hi ha una major evidència de que diferents patologies vasculars (malaltia vascular subcortical de petit vas o infarts llacunars), així com infarts corticals, poden contribuir a desenvolupar-la (Hachinski et al.,1974; Esiri et al.,1997; Rockwood et al.,1999; Erkinjuntti et al.,1999; Pohjasvaara et al.,2000; Ballard et al.,2000). L’objectiu d’aquesta recerca és l’estudi del perfil neuropsicològic i dels dèficits cognitius associats a la malaltia vascular cerebral de petit vas (infarts llacunars i lesions de la substància blanca), així com l’evolució d’aquests pacients després de 2 anys d’haver patit l’event vascular. Aquest tema mereix especial interès perque la malaltia vascular subcortical de petit vas és una de les causes més comunes de demència vascular (DV), i el fet de poder conèixer el seu estat prodròmic i poder previndre els principals factors de risc, ens podrien fer possible el desenvolupament d’estratègies preventives. Aquesta àrea d’estudi també mereix atenció perque s’han fet molts estudis sobre l’evolució i les seqüeles cognitives en els infarts isquèmics de gran vas, però no hi ha gaire evidència sobre l’efecte d’un primer ILL i l’evolució a llarg terme d’aquests pacients. Finalment, no hi ha estudis a la literatura sobre el perfil neuropsicològic de les diferents síndromes llacunars (segons Miller-Fisher) i la seva evolució a llarg terme.
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Luijckx, Gert-Jan Reinier. "Lacunar brain infarcts a clinical and pathogenetical study /." Maastricht : Maastricht : Universitaire Pers Maastricht ; University Library, Maastricht University [Host], 1995. http://arno.unimaas.nl/show.cgi?fid=7285.

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Schmiedel, Janet, Georg Gahn, Rüdiger von Kummer, and Heinz Reichmann. "Cerebral Vasculitis with Multiple Infarcts Caused by Lyme Disease." Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-135328.

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Schmiedel, Janet, Georg Gahn, Rüdiger von Kummer, and Heinz Reichmann. "Cerebral Vasculitis with Multiple Infarcts Caused by Lyme Disease." Karger, 2004. https://tud.qucosa.de/id/qucosa%3A27639.

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Marchbank, Gavin Clyde. "Posterior cerebral artery (PCA) infarcts and dreaming : a neuropsychological study." Master's thesis, University of Cape Town, 2013. http://hdl.handle.net/11427/14091.

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Recent case reports have shown that global loss of dreaming can result from medial occipitotemporal lesions. These findings have cast doubt on Solms's reformulation of Charcot-Wilbrand Syndrome (CWS) into two distinct disorders of dreaming, and caused substantial confusion in dream research as far as the neurological correlates of dreaming are concerned. This study attempted to confirm these case reports and determine whether there were any characteristics unique to the lesions among patients who had lost the ability to dream following damage to medial occipito-temporal cortex. Nine participants (three non-dreamers and six dreamers) who had suffered non-hemorrhagic infarction in the territory of the posterior cerebral artery were recruited in this study. Case histories and neuroradiological data were used to compare the lesion sites of non-dreamers with dreamers. It was confirmed that complete loss of dreaming could result from lesions in medial occipito-temporal cortex. It was found that non-dreamers always suffered bilateral cortical damage as opposed to dreamers who all suffered unilateral damage. The lesions in the non-dreamers tended to be more posterior than the dreamers. It was further speculated that concomitant damage to the thalamus or parietal areas played a role in the causation of heteromodal loss of dreaming. The implications of these findings were discussed in relation to CWS, Solms's dream system, and dream-function research. Finally, future directions were considered.
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Likens, Jacob Andrew. "The Pathophysiology of Chronic Stroke Infarcts| What Happens After Brain Tissue Dies?" Thesis, The University of Arizona, 2018. http://pqdtopen.proquest.com/#viewpdf?dispub=10813111.

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A stroke can occur when blood flow to a specific area of the brain is interrupted. There has been extensive research in both animal models and humans that has characterized the pathophysiology of the first few weeks following stroke. However, there has been far less research into the chronic stage of infarction. This is an important area for research because more than 10 million individuals worldwide suffer a stroke each year. Approximately one-third of these survivors develop dementia in the first year after their stroke. The cause behind this dementia is currently unclear, and there are no neuro-protective drugs that can improve recovery and provide cognitive protection in the chronic time period. Therefore, the chronic stage of stroke recovery is a promising target for future therapeutics for stroke-related dementia and, as will be shown later in the paper, Alzheimer’s disease as there are likely to be neurodegenerative processes that proceed for months following stroke. The goal of this thesis is to provide a review of what is currently known about the pathophysiology of chronic stroke infarcts (an area of brain tissue that has necrotized due to a blockage in an artery in the brain causing a lack of oxygen), explain why so little is known, and how we can learn more, and provide potential mechanistic links between the response to dead brain tissue and the development of dementia.

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J?NCK, Fernanda. "A intoxica??o de bovinos por Pteridium (aquilinum) arachnoideum em Santa Catarina e a identifica??o das bact?rias envolvidas nos infartos do quadro agudo." Universidade Federal Rural do Rio de Janeiro, 2014. https://tede.ufrrj.br/jspui/handle/jspui/2306.

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Pteridium (aquilinum) arachnoideum is a cosmopolitan plant, responsible for heavy losses in cattle for heavy losses in almost all Brazil. This plant causes three clinical pictures: an acute disease, characterized by hemorrhages and fever, and two chronic diseases characterized by bladder tumors and carcinomas of the superior digestive tract. In Santa Catarina, in a retrospective study, the acute poisoning is the form that prevailed. Most of the cases ocurred in the autumn and the main clinical signs observed were fever and faeces with blood. The macroscopic lesions were widespread hemorrhages and infarcts mainly in lung, liver, intestine and lymphnodes, which were characterized by necrosis associated with groups of basophylic bact?ria, sometimes with formation of bubbles of gas. In the bone marrow there was rarefaction or absence of hematopoietic tissue. The experimental reproduction of the disease was realized in four cattle, two vaccinated against clostridioses and two not vaccinated. These cattle received doses of 20, 20, 14 and 10g/kg/day, and they died after 82, 94, 46 and 76 days, when they had ingested 149, 180, 71 and 75% of the plant in relation to their weight. The course of the clinical signs was 5, 4, 1 and 5 days, and at post-mortem examination the lesions found were hemorrhages of varied degrees and locations. Liver infarcts were found in bovines 2, 3 and 4, and in the intestine in all the cattle. The histological lesions were characterized by rarefaction and absence of hematopoietic tissue in the bone marrow, necrosis and bacterial aggregates in the liver, lung, intestine and lymphnodes. Histopathology did not reveal inflammatory reaction and if present the intensity was slight. Samples of organs with infarcts collected at necropsy, in the spontaneous and experimental intoxication, sown in Tarozzi medium, produced gas. Five samples caused death in mice after inoculation of the medium. At necropsy the carcasses had putrid smell, the subcutaneous tissue was red and there was edema and red liquid in the abdominal cavity. Two mice that were sacrificed presented inflammatory reaction in the place of the application, characterized by areas of adherence of the skin to the subcutaneous tissue and presence of abscesso, and four presented putrid smell at necropsy. The impression of of the liver capsula of the mice that died or got sick, revealed small Gram positive rods. Histopathology of the mice that died, revealed in the skeletal musculature of the thighs edema between the fibers with necrosis and eosinofilia of fibers and great amount of small basophylic rods, associated with slight inflammatory mononuclear infiltration and hemorrhage. In the skin also inflammatory filtrate was observed, with edema in the derma and great amount of small basophylics rods. The rest of the mice were sacrificed and no alterations were found. The identification by Chain reaction of Polimerase (PCR) of the liver of the mice that had died, in Tarozzi medium, resulted in Clostridium septicum.
Pteridium (aquilinum) arachnoideum ? planta cosmopolita, respons?vel por perdas vultuosas na cria??o de bovinos em quase todas as regi?es do Brasil. Esta planta ? respons?vel por causar tr?s quadros cl?nicos: um quadro agudo, caracterizado por hemorragias e febre, e dois quadros cr?nicos caracterizados por tumores de bexiga e do trato digest?rio superior. Em Santa Catarina, em estudo retrospectivo, a intoxica??o aguda ? a forma que prevaleceu sobre as demais. A maioria dos casos ocorreu no outono e os principais sinais cl?nicos observados foram febre e fezes com sangue. As les?es macrosc?picas encontradas foram hemorragias generalizadas e infartos principalmente em pulm?o, f?gado, intestino e linfonodo, os quais se caracterizavam por necrose associada a agregados bacterianos bas?filos, em alguns casos com forma??o de bolhas de g?s. Na medula ?ssea havia rarefa??o ou aus?ncia do tecido hematopo?tico. A reprodu??o experimental da doen?a foi realizada em quatro bovinos, dois vacinados contra clostridioses e dois n?o vacinados. Estes receberam doses de 20, 20, 14 e 10g/kg/dia de Pteridium (aquilinum) arachnoideum, e morreram com 82, 94, 46 dias e 76 dias, quando tinham ingerido 149, 180, 71 e 75% de planta em rela??o ao peso vivo. A evolu??o dos sinais cl?nicos foi de 5, 4, 1 e 5 dias, e, ? necropsia, as les?es consistiram de hemorragias em variados graus e localiza??es. Infartos de f?gado foram encontrados nos Bovinos 2, 3 e 4 e no intestino em todos os bovinos. As les?es histol?gicas se caracterizaram por rarefa??o e aus?ncia de tecido hematopo?tico na medula ?ssea, necrose e agregados bacterianos no f?gado, pulm?o, intestino e linfonodo. As les?es histol?gicas n?o revelaram rea??o inflamat?ria e quando presente, a intensidade era leve. Amostras de ?rg?os com infartos coletadas de necropsias nas intoxica??es espont?nea e experimental foram semeadas no meio de cultivo de Tarozzi e produziram g?s. Cinco amostras causaram a morte dos camundongos ap?s inocula??o do meio. ? necropsia desses camundongos verificou-se carca?as com cheiro p?trido, tecido subcut?neo avermelhado e com edema e l?quido avermelhado na cavidade abdominal. Dois camundongos que foram eutanasiados apresentaram rea??o inflamat?ria no local da aplica??o, caracterizada por ?reas de ader?ncia da pele com o tecido subcut?neo e abscessos; quatro exalavam cheiro p?trido na hora da realiza??o da necropsia. A impress?o da c?psula do f?gado dos camundongos que morreram e que ficaram doentes, revelou bastonetes Gram-positivos. ? histologia dos camundongos que morreram verificou-se na musculatura esquel?tica da regi?o da coxa, edema e hemorragia entre as fibras, necrose e eosinofilia de fibras e grande quantidade de bastonetes bas?filos, associado a infiltrado inflamat?rio mononuclear leve e hemorragia. Na pele tamb?m verificou-se, infiltrado inflamat?rio, com edema na derme e grande quantidade de bastonetes bas?filos. Os demais camundongos foram eutanasiados e n?o tiveram altera??es. A identifica??o por Rea??o em Cadeia de Polimerase (PCR) do meio de Tarozzi do f?gado dos camundongos que morreram foi detectado Clostridium septicum.
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Boon, Arthur Edwin. "Cardiac and vascular riskfactors in stroke the role of cardiac valve calcification and silent brain infarcts /." Maastricht : Maastricht : Rijksuniversiteit Limburg ; University Library, Maastricht University [Host], 1996. http://arno.unimaas.nl/show.cgi?fid=7392.

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Munro, N. A. R. "The control of saccadic and smooth pursuit eye movements in patients with lesions of the central nervous system." Thesis, University of Oxford, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.319050.

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Books on the topic "Infarcts"

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Zülch, Klaus-Joachim, ed. The Cerebral Infarct. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70765-0.

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Infarctus parmi les piétons. Moncton, N.B: Éditions Perce-Neige, 2000.

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Třešňák, Vlastimil. Infarkt. Praha: Edice Expedice, 1985.

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Plachtinská, Ida. Infarkt. Žilina: Knižné centrum, 1997.

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Schmutzler, Horst, Wolfgang Rutsch, and Frank Christopher Dougherty, eds. Limitation of Infarct Size. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-73585-1.

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Števček, Ján. Fenomenológia infarktu. Bratislava: Slovenský spisovatel̕, 1994.

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Kame, Miroslav Robert. Infarkt svetla. Bratislava: Vydavatel̕stvo Spolku slovenských spisovatel̕ov, 2001.

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Akʹov, Vasil. Infarkt: Roman. Sofii͡a︡: Bŭlgarski pisatel, 1988.

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Halhuber, Carola. El infarto. León: Everest, 1998.

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Halhuber, Carola. El infarto. León: Everest, 1998.

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Book chapters on the topic "Infarcts"

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Oliver, Rupert, and Richard Perry. "Bihemispheric Infarcts." In Stroke Medicine, 151–55. London: Springer London, 2015. http://dx.doi.org/10.1007/978-1-4471-6705-1_24.

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Mull, Michael, and Armin Thron. "Spinal Infarcts." In Magnetic Resonance Imaging in Ischemic Stroke, 251–67. Berlin, Heidelberg: Springer Berlin Heidelberg, 2006. http://dx.doi.org/10.1007/3-540-27738-2_17.

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Hendrikse, Jeroen. "Silent Infarcts." In This is Our Brain, 22–23. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-4148-8_6.

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Jelliffe, Roger W. "The Infarcts." In Fundamentals of Electrocardiography, 90–111. New York, NY: Springer New York, 1990. http://dx.doi.org/10.1007/978-1-4613-8972-9_4.

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Ferro, JosÉ M. "Territorial and Embolic Infarcts." In Magnetic Resonance Imaging in Ischemic Stroke, 209–23. Berlin, Heidelberg: Springer Berlin Heidelberg, 2006. http://dx.doi.org/10.1007/3-540-27738-2_14.

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Amici, Serena. "Thalamic Infarcts and Hemorrhages." In Frontiers of Neurology and Neuroscience, 132–36. Basel: KARGER, 2012. http://dx.doi.org/10.1159/000333611.

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Pellizzaro Venti, Michele, Maurizio Paciaroni, and Valeria Caso. "Caudate Infarcts and Hemorrhages." In Frontiers of Neurology and Neuroscience, 137–40. Basel: KARGER, 2012. http://dx.doi.org/10.1159/000333616.

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Moncayo, Jorge. "Midbrain Infarcts and Hemorrhages." In Frontiers of Neurology and Neuroscience, 158–61. Basel: KARGER, 2012. http://dx.doi.org/10.1159/000333630.

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Moncayo, Jorge. "Pontine Infarcts and Hemorrhages." In Frontiers of Neurology and Neuroscience, 162–65. Basel: KARGER, 2012. http://dx.doi.org/10.1159/000333631.

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Balucani, Clotilde, and Kristian Barlinn. "Medullary Infarcts and Hemorrhages." In Frontiers of Neurology and Neuroscience, 166–70. Basel: KARGER, 2012. http://dx.doi.org/10.1159/000333632.

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Conference papers on the topic "Infarcts"

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Fomovsky, Gregory M., and Jeffrey W. Holmes. "Evolution of Scar Mechanical Properties During Myocardial Infarct Healing in Rat." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176422.

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The mechanics of healing myocardial infarcts are an important determinant of post-infarction left ventricular (LV) function and remodeling. Large animal infarct models are well studied; healing infarct scars have been shown to be mechanically and structurally anisotropic [1], and this anisotropy may help preserve LV function during some stages of healing [2]. At the same time, it has been suggested that the rat model of myocardial infarction is more similar to humans in the range of infarct sizes and observed LV dysfunction [3]. However, in the rat model, infarct mechanics and their effect on the overall LV function have not been described so far.
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Fomovsky, Gregory M., and Jeffrey W. Holmes. "Collagen Fiber Structure Correlates With Mechanical Environment in Healing Myocardial Infarcts." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206767.

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Mechanics of healing myocardial infarcts are an important determinant of ventricular function. Large collagen fibers are the major contributors to the mechanical properties of healing scar. It has been suggested that an anisotropic structure, as observed in healing pig scars, may help preserve ventricular function, and that the alignment of collagen fibers could be guided by the regional mechanical environment in the infarct — in pig scars the alignment of collagen fibers was in the direction of greatest stretch [1]. By contrast, in the standard rat model of infarction we found that scars are structurally and mechanically isotropic at all time points in healing [2].
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Richardson, William J., and Jeffrey W. Holmes. "Do Infarcts Really Expand or Compact? Relationship Between Changing Material Properties and Apparent Infarct Remodeling." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14411.

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Myocardial infarction (MI) is a leading cause of mortality and morbidity with over 600,000 new Americans suffering an MI each year [1]. Following infarction, damaged muscle is gradually replaced by collagenous scar tissue, while undamaged (remote) myocytes remodel due to altered load. Remodeling of both the infarcted and remote myocardium are important determinants of cardiac function and the risk of progression to heart failure.
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O'Corragain, O. A., D. Sacher, T. A. Ho, H. Zhao, G. J. Criner, and P. Rali. "Pulmonary Infarcts in Pulmonary Embolism - Does It Matter?" In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a3725.

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Pabón, P., V. Vicente, I. Alberca, C. Martin Luengo, and A. Lopez Borrasca. "EFFECT OF DDAVP ON MYOCARDIAL INFARCT SIZE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644127.

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Infarct size, estimated by electrocardiographic changes (the QRS Scoring System, developed by Wagner et al, Circulation 65,342, 1982) and enzymatic analysis (creatinine kinase, CK) was studied in 45 patients with no history of previous infarcts. 25 received an intravenous dose of DDAVP (0.3 ug/kg) and 20 received a placebo solution (saline). The time between the onset of symptoms and DDVAP administration was less than 12 hours. The results showed no significant differences between the two groups in maximal or acumulative activity of creatinine kinase (CKr) or the QRS score peak. However, in patients with a mean evolution time of less than 1 hour, the CK peak was significantly lower in the DDAVP group than in the placebo group (p<0.05). Furthermore the percent of maximal increase in the QRS score was lower in the DDAVP group than in the patients receiving the placebo (p=0.1). On admission, the fibrinolytic activity of euglobulin fractions (measured by fibrin plates) was higher in the patients in both groups than in a group of healthy subjects (n=40). Also, DDAVP significantly increased fibrinolyric activity whereas no changes were found in patients receiving the placebo. The mean CKr value was lower in patients with an increase in fibrinolysis than in those who showed no changes in it. Finally, in the DDAVP group the QRS score peak was strongly dependent on the initial QRS score and, regarding this, our results suggest that small infarcts on admission may represent a potential indication for DDAVP therapy.
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Uchiyama, Yoshikazu, Ryujiro Yokoyama, Hiromichi Ando, Takahiko Asano, Hiroki Kato, Hiroyasu Yamakawa, Haruki Yamakawa, et al. "Improvement of Automated Detection Method of Lacunar Infarcts in Brain MR Images." In 2007 29th Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2007. http://dx.doi.org/10.1109/iembs.2007.4352611.

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Tanaka, H., A. Shiino, T. Tateyama, X. H. Han, X. Wei, and Y. W. Chen. "Construction of Probabilistic Atlas and Its Application to Detection of Lacunar Infarcts." In 2015 International Conference on Artificial Intelligence and Industrial Engineering. Paris, France: Atlantis Press, 2015. http://dx.doi.org/10.2991/aiie-15.2015.93.

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Teddy Weiss, A., David G. Fine, David Applebaum, Sima Welber, Dan Sapoznikov, Chaim Lotan, Morris Mosseri, Yonathan Hasin, and Meryyn S. Gotsman. "PREHOSPITAL CORONARY THROMBOLYSIS: A NEW STRATEGY IN ACUTE MYOCARDIAL INFARCTION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642979.

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Thirty-four patients with acute myocardial infarction were treated prospectively using a new strategy of pre-hospital intravenous streptokinase given by a physician-operated mobile intensive care unit. Prehospital treated patients who had experienced no previous myocardial infarction were compared to a similar group treated with streptokinase in-hospital. All patients underwent cardiac catheterization on day 6.Patients receiving streptokinase in the pre-hospital phase of acute myocardial infarction had smaller infarcts and better residual myocardial function than the group given streptokinase in-hospital in terms of peak creatine phosphokinase (900 v.1298 IU, p=0.023), ejection fraction (62 v. 55%, p=0,004), computer-derived dysfunction index (427 v. 727, p=0.003), and electrocardiographic QRS score (4.1 v. 6.4, p=0.001). The only difference between these groups at baseline was the duration of pain prior to initiation of streptokinase therapy (1.0 ± 0.4 hours vs. 1.9 ± 0.9 hours). There were no major complications related to pre-hospital administration of streptokinase.Pre-hospital stretokinase infusion is feasible, safe and practical. It reduces ischemia time because treatment is not delayed until hospital arrival and therapy limits infarct size. Thrombolytic therapy for acute myocardial infarction can be initiated at home and should not be limited to hospitalized patients.
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Luo, Jianwen, Kana Fujikura, and Elisa E. Konofagou. "Detection of murine infarcts using myocardial elastography at both high temporal and spatial resolution." In Conference Proceedings. Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2006. http://dx.doi.org/10.1109/iembs.2006.4397711.

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Luo, Jianwen, Kana Fujikura, and Elisa E. Konofagou. "Detection of murine infarcts using myocardial elastography at both high temporal and spatial resolution." In Conference Proceedings. Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2006. http://dx.doi.org/10.1109/iembs.2006.259868.

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Reports on the topic "Infarcts"

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Arboix, Adrià, Paula Escarcena, Mireia Bernal, Joan Massons, Laura Díez, Enric Vergés, María José Sánchez López, and Luís García-Eroles. Perfil Clínico Diferencial entre los Infartos Lacunares y los Infartos Cerebrales Aterotrombóticos. Buenos Aires: siicsalud.com, September 2018. http://dx.doi.org/10.21840/siic/157220.

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Sahún Español, Álvaro. Más allá del infarto de miocardio: curando el corazón. Sociedad Española de Bioquímica y Biología Molecular (SEBBM), May 2016. http://dx.doi.org/10.18567/sebbmdiv_rpc.2016.05.1.

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Zaidel, E. Diferente abordaje del infarto de miocardio en el entorno de la salud pública o privada. Buenos Aires: siicsalud.com, April 2015. http://dx.doi.org/10.21840/siic/145112.

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