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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Concurrent viral infection and myocarditis presumably indicate viral myocarditis. The electrocardiographic and pathologic changes developing during acute infection may, however, result from changes not produced by the infection itself, eg, fever, tachycardia, ischemia, potassium depletion, vitamin deficiencies, drugs. This qualification should be remembered in the evaluation of all alleged virus myocarditis. Viral infection seems to prefer the very young. Its localization in the heart is favored by general or local hypoxia, perhaps thus explaining a predilection for the subendocardium. It may be influenced by the strain of the organism or by the hormonal or immunologic state of the host. Intrauterine infection of the fetus with rubella, mumps, and perhaps coxsackievirus can induce congenital cardiac defects. The role of virus infection in precipitating acute myocardial infarction deserves further study. The value of treatment, including steroids, nonsteroidal immunosuppressive agents, and "antiviral" agents is not yet established.
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PMID:Virus myocarditis: a critique of the literature from clinical, electrocardiographic, and pathologic standpoints. 46 41

Eight dogs with severe neurologic signs, including seizures, had polioencephalomalacia of the pyriform cortex, Ammon's horn and deep structures in the temporal lobe. The polioencephalomalacia was considered to be a consequence of canine distemper virus infection based on clinical signs, typical inclusions, the demonstration of viral antigens in the lesions and of characteristic paramyxovirus nucleocapsids by electron microscopy. Little evidence for neuronal destruction by direct viral activity was found. Selective nerve cell necrosis was attributed to ischemia (vascular lesions and seizure induced consumptive anoxia) and immune mechanisms. The selective involvement of the rhinencephalic structures was thought to be related to the mode of entry and spread of the virus.
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PMID:Polioencephalomalacia associated with canine distemper virus infection. 50 90

Episodes of graft dysfunction are frequently observed after liver transplantation and can be due to different causes requiring specific therapy. In this study the usefulness and reliability of liver transplant aspiration cytology (TAC) for differential diagnosis of liver graft dysfunction is assessed. Out of more than 1500 TACs performed, 292 TACs, taken during episodes of liver dysfunction due to retrospectively defined causes, were analyzed. Immune activation and parenchymal damage in the aspirates were determined cytologically. In 63 episodes of acute rejection, marked immune activation was present in aspirate but not in blood, with varying degrees of hepatocyte damage and cholestasis. No or only minimal immune activation was observed in 86 cases of toxic, ischemic, or septic liver damage, but considerable parenchymal damage and cholestasis were observed. In 3 cases of hepatitis slight-to-moderate immune activation with large granular lymphocytes was found in the aspirate, while 17 cases of viral infection presented with slight-to-moderate immune activation in aspirate and blood. After successful treatment the cytologic patterns normalized, except when the cause of liver dysfunction persisted. Moreover, typical patterns of parenchymal changes were found for preservation damage of the liver (n = 108), fatty degeneration (n = 3), obstructive cholestasis (n = 5), and acute arterial ischemia (n = 2). One case of moderate subcapsular hematoma was the only complication observed (less than 0.1%). Thus, liver TAC is an easy, safe, and clinically useful method for differential diagnosis of liver graft dysfunction. In particular, differentiation between acute rejection and nonimmunologic causes of dysfunction is very reliable, but hepatitis and viral infections also present distinctive patterns in liver TAC.
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PMID:Differentiation of liver graft dysfunction by transplant aspiration cytology. 201 31

To elucidate the heart involvement associated with influenza virus infection, the authors studied the hearts of influenza A/PR/8/34 virus-inoculated ICR mice by light and electron microscopy, cardiac catheterization, virus assay, and indirect immunofluorescence. Light microscopy showed small necrotic foci with inflammatory cell infiltration spreading in the myocardium on days 3 to 7 and evidence of healing by day 9 after inoculation. Electron microscopy demonstrated that necrotic cell debris was phagocytosed by macrophages, and that degenerating cardiocytes, macrophages, and lymphocytes were often in close contact, suggesting immunologic interactions, and that platelet thrombi were present in some capillaries on days 3 to 5. Both systolic and diastolic functions of the left ventricle (LV) were impaired on days 3 to 9 and recovered almost to normal by day 14. The virus could be isolated from the heart on days 3 to 7. Immunofluorescent preparations showed virus antigens in the vascular walls and cardiocytes until day 7. These results suggest that the acute cardiac injury was related to cytotoxic immunologic interactions, virus-induced cytolysis and, at least in part, to ischemia due to intracapillary thrombosis. Compared with coxsackie B3 myocarditis in mice, the influenza myocarditis was mild in degree and short in duration, but the influenza infection is a most common and repetitive disease in humans. The clinical implications of this animal model with myocarditis are discussed.
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PMID:Experimental influenza A virus myocarditis in mice. Light and electron microscopic, virologic, and hemodynamic study. 215 29

Lissencephaly is a brain malformation manifested by a smooth cerebral surface and caused by incomplete neuronal migration. Clinical sequellae include minor craniofacial changes (bitemporal hollowing, small jaw), severe mental retardation, and other neurological abnormalities. Patients with classical or type I lissencephaly and its sequellae but no other significant anomalies are classified as having isolated lissencephaly sequence. Possible causes of isolated lissencephaly sequence include ischemia or viral infection during the time of neuronal migration, microdeletion within the Miller-Dieker syndrome critical region in chromosome band 17p13.3, and Mendelian inheritance. The last is based on a report of a single family with three affected children in 1933. We report four patients with isolated lissencephaly sequence from two unrelated families who provide further support for autosomal (or possibly X-linked) recessive inheritance. In the first family, three brothers were affected. In the second, the parents are first cousins.
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PMID:Isolated lissencephaly: report of four patients from two unrelated families. 229 40

The degree of participation and regional specificity of virus infection in relation to atraumatic acute peripheral facial palsy was studied, placing particular emphasis on change in the CF titre of varicella zoster virus (VZV), herpes simplex virus (HSV) and adenovirus (adeno). The subjects of the study were 91 patients with Hunt's syndrome and 396 patients with Bell's palsy treated at 17 institutions all over Japan in the period between April 1985 and November 1986. Among the cases of Hunt's syndrome, the positive conversion rate of CF antibody titre of VZV was 81%. In Bell's palsy cases, virus participation was detectable in 8% with VZV, 4% with HSV and 4% with adeno. With regard to the age distribution, Bell's palsy cases with possible virus involvement tended to be observed in younger patients than those without that possibility. As to regional specificity, the incidence of Bell's palsy with possible virus involvement tended to be higher in densely populated areas. With regard to the main cause of acute peripheral facial palsy, virus infection has been implicated, as well as insufficient blood circulation (ischemia). Even in cases of acute peripheral facial palsy, in which herpes zoster oticus is not observed, the participation of varicella zoster virus (VZV) as a cause of paralysis has been pointed out in some cases (zoster sine herpete). Furthermore, it is known that the serum antibody titres of various viruses such as herpes simplex virus (HSV) change significantly in some cases of Bell's palsy (2, 5-13).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Viral infections in acute peripheral facial paralysis. Nationwide analysis centering on CF. 284 57

A 26-year-old male shortly after an acute respiratory disease was affected by a thrombophlebitis of the left leg. After a few days he had two syncopal attacks. Later on, a myocardial ischemia was diagnosed. Subsequently the patient began to complain of a bilateral claudication of the calves; after an attack of fever, the ischemia of the lower limbs worsened with recurring pain at rest. At the same time, in absence of any symptom, a myocardial ischemia occurred again and the presence of a thrombus was observed in the right atrium. After surgical removal of it, the ischemic troubles of the lower limbs once again began to worsen with the occurrence of bilateral gangrene of the feet. An amputation of both the legs was promptly performed at the level of the thighs. The histological examination of the arteries of the amputated legs showed segmental arteritis with partially recanalized thrombi of the popliteal, left femoral and tibioperoneal arteries. In the meantime, the titres for Coxsackie virus B2 and B6 were found slightly increased. One month later, the left radial pulse disappeared for a few days. The histopathological findings may relate this arteritis to a form of Buerger's disease even if a systemic thromboangiitis obliterans is not commonly accepted. In case that the acute respiratory infection represented the true onset of the sickness, it seems conceivable that the hypothesis of a viral infection gave raise to arteritis with morphological features recalling those of Buerger's disease.
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PMID:An uncommon systemic arteritis--a case report. 286 78

General patterns of tissue injury are recognized as characteristic for certain groups of viruses and certain types of host/virus interactions. Acute viral infections, limited in time and space, tend to be accompanied by florid but brief virus replication cycles in tissues and lesions or signs of disease are largely attributable to the cytolytic effects of the virus on host cells. Chronic or persistent viral diseases tend to have low (or difficult to detect) levels of infectious virus on tissues and the lesions tend to be dominated by inflammation, antiviral immune responses and/or host tissue proliferation. At the cellular level, 3 general categories of response to viral infection are recognized: acute cellular swelling with eventual cytolysis, persistent infection, and transformation (neoplastic) infection. Acute cellular swelling may be accompanied by syncytial giant cell formation and/or viral inclusion bodies. Cells persistently infected with viruses though morphologically normal, are increasingly recognized as functionally deficient and may eventually display degenerative change. Transformation to neoplastic growth can be both benign or malignant in cellular expression. In vivo, the initial neutrophilic inflammatory response to virus-induced cellular necrosis is transient and is rapidly superseded by virus-specific inflammation mediated by both humoral and cellular factors and supplemented by the numerous inflammation amplification pathways. Vasculitis, a common but frequently unappreciated event, may produce nonspecific tissue damage via hemorrhage and ischemia in addition to providing a mechanism for egress of inflammatory factors into the areas of virus-induced cellular damage. During the healing phase, repair by substitution (e.g., fibrosis and scarring) or by proliferation of uninfected replacement cells may dominate sites of viral infection.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Immunity, viral pathology and assessment of immune dysfunction in virology and toxicology. 357 74

Infection and rejection remain the greatest threats to the survival of pulmonary allograft recipients. Furthermore, a relationship may exist between these events, because the occurrence of one may predispose to the other. By using multivariate analysis for repeated events, we analyzed the risk factors for bacterial, fungal, and viral infection, grade II or greater acute rejection, and death among 239 lung transplant recipients who received 250 allografts between January 1988 and September 1993. A total of 90 deaths, 491 episodes of acute rejection, and 542 infectious episodes occurred during a follow-up of 6 to 71 months. The hazard or risk patterns of death, infection, and rejection each followed an extremely high risk during the first 100 days after transplantation, a second modest risk period at 800 to 1200 days, and a lower constant risk. Infection and graft failure manifested by diffuse alveolar damage were the major causes of early death (< 100 days), whereas infection and chronic rejection were primary causes of later death after pulmonary transplantation. By multivariate analysis, cytomegalovirus mismatching risk for primary infection was the most significant risk factor for death, rejection, and infection. Absence of cytomegalovirus prophylaxis was also a risk factor for early and late death and late infection. Survival of recipients who received cytomegalovirus prophylaxis was significantly improved. Immunosuppression based on cyclosporine versus FK 506 was a risk factor for late death and late infection. Graft failure manifested by diffuse alveolar damage/adult respiratory distress syndrome was a significant risk for death late after transplantation. These data suggest the following: (1) The hazard for death, infection, and rejection after pulmonary transplantation appears biphasic; (2) lower survival is associated with ischemia-reperfusion lung injury represented by diffuse alveolar damage/adult respiratory distress syndrome; (3) cytomegalovirus mismatch, absence of cytomegalovirus prophylaxis, and development of cytomegalovirus disease are significant threats for death, rejection, and infection after pulmonary transplantation; (4) prevention of cytomegalovirus disease should improve survival by decreasing the prevalence of infection and rejection.
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PMID:Analysis of time-dependent risks for infection, rejection, and death after pulmonary transplantation. 781 7

Sinus nodes of five symptomatic patients with the long QT syndrome were surgically excised and followed by permanent electronic pacing as part of a new surgical treatment. We examined those sinus nodes by light and electron microscopy with tissue that was promptly fixed at the time of surgery. All five sinus nodes were similarly abnormal. By light microscopy we found distinctive focal fibrosis, some degenerating myocytes and neural elements, and numerous narrowed small vessels. Except in the nerves there was no evidence of inflammation. In electron micrographs the mitochondria within nodal myocytes were abnormally abundant, remarkably pleomorphic, and smaller than those in normal human sinus nodal cells. The ultrastructural features of the degenerated nodal cells were typical of apoptosis, characterized by the absence of inflammation, well-preserved mitochondria, the presence of apoptotic bodies, phagocytosis of these cells by neighboring myocytes, and especially in smooth muscle cells of arterioles, nuclear chromatin margination and nucleolar disintegration. Apoptotic degeneration of nodal myocytes was stochastic, with adjacent cells appearing unaffected. Focal ischemia caused by narrowed vessels may be a contributory factor, and the nerves may harbor some viral infection, but for the nodal myocytes the abnormality appears to be primarily apoptosis, sometimes called programmed cell death. Both the typically episodic clinical features and the terminal event in fatal cases of the long QT syndrome may be due to apoptosis.
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PMID:Apoptosis and pleomorphic micromitochondriosis in the sinus nodes surgically excised from five patients with the long QT syndrome. 840 7


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