Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Anthracyclines, found to be efficacious in the treatment of a broad spectrum of pediatric malignancies, are cardiotoxic and may lead to heart failure even a long time after successful treatment of cancer. It is thought that subtle abnormalities can progress to the more permanent myocardial disease, resulting in cardiomyopathy which may progress to congestive heart failure. There are some precipitating factors leading to the sudden onset of cardiac symptoms such as increase in afterload or preload. We describe a young patient with congestive heart failure treated with doxorubicin (cumulative mean dose 420 mg/m2) in infancy because of pelvic sarcoma in whom the appearance of symptoms was related to pulmonary embolism. Four years before hospital admission, the patient presented echocardiographic abnormalities such as left ventricular fractional shortening and thickness reduction and he was treated with ACE-inhibitors. The myocardial ischemia, which is present in pulmonary embolism, probably worsened the left ventricular systolic function and caused congestive heart failure.
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PMID:[Biventricular heart failure in patient treated with anthracycline in childhood: myocardial dysfunction is not always the cause]. 1518 68

Anthracyclines, found to be efficacious in the treatment of a broad spectrum of pediatric malignancies, are cardiotoxic and may lead to heart failure even a long time after successful treatment of cancer. It is thought that subtle abnormalities can progress to the more permanent myocardial disease, resulting in cardiomyopathy which may progress to congestive heart failure. There are some precipitating factors leading to the sudden onset of cardiac symptoms such as increase in afterload or preload. We describe a young patient with congestive heart failure treated with doxorubicin (cumulative mean dose 420 mg/m2) in infancy because of pelvic sarcoma in whom the appearance of symptoms was related to pulmonary embolism. Four years before hospital admission, the patient presented echocardiographic abnormalities such as left ventricular fractional shortening and thickness reduction and he was treated with ACE-inhibitors. The myocardial ischemia, which is present in pulmonary embolism, probably worsened the left ventricular systolic function and caused congestive heart failure.
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PMID:[Heart failure in a subject treated with anthracyclines in childhood: myocardial dysfunction is not always the only reason of it]. 1534 97

The authors examined 1,615 workers exposed to dioxins in trichlorophenol production in Midland, Michigan, to determine if there were increased mortality rates from exposure. Historical dioxin levels were estimated by a serum survey of workers. Vital status was followed from 1942 to 2003, and cause-specific death rates and trends with exposure were evaluated. All cancers combined (standardized mortality ratio (SMR) = 1.0, 95% confidence interval (CI): 0.8, 1.1), lung cancers (SMR = 0.7, 95% CI: 0.5, 0.9), and nonmalignant respiratory disease (SMR = 0.8, 95% CI: 0.6, 1.0) were at or below expected levels. Observed deaths for leukemia (SMR = 1.9, 95% CI: 1.0, 3.2), non-Hodgkin lymphoma (SMR = 1.3, 95% CI: 0.6, 2.5), diabetes (SMR = 1.1, 95% CI: 0.6, 1.8), and ischemic heart disease (SMR = 1.1, 95% CI: 0.9, 1.2) were slightly greater than expected. No trend was observed with exposure for these causes of death. However, for 4 deaths of soft tissue sarcoma (SMR = 4.1, 95% CI: 1.1, 10.5), the mortality rates increased with exposure. The small number of deaths and the uncertainty in both diagnosis and nosology coding make interpretation of this finding tenuous. With the exception of soft tissue sarcoma, the authors found little evidence of increased disease risk from exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin.
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PMID:Mortality rates among trichlorophenol workers with exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin. 1999 29

We present a unique case of cardiac pseudopyogenic granuloma in a 61-year-old man that underwent orthotopic heart transplantation for end-stage ischemic heart disease. The lesion was an incidental pathological finding in the allograft removed for chronic graft vascular disease. This lesion is attributed to the minor trauma of the biopsy in the right side of the heart following cardiac transplantation. The cardiac right side can be considered the venous side of the heart; therefore, we consider the lesion a mimicker of an intravenous pyogenic granuloma. Pseudopyogenic granuloma may represent organization of a mural thrombus which formed secondary to biopsy procedure(s). The lesion must be distinguished from bacillary angiomatosis, Karposi sarcoma, and other neoplasms that may present an intravascular type of growth.
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PMID:Cardiac pseudopyogenic granuloma: a type of vascular hyperplasia in the transplanted heart mimicking pyogenic granuloma. 2598 88

The therapeutic goal for peripheral arterial disease and ischemic heart disease is to increase blood flow to ischemic areas caused by hemodynamic stenosis. Vascular surgery is a viable option in selected cases, but for patients without indications for surgery such as progression to rest pain, critical limb ischemia, or major disruptions to life or work, there are few possibilities for mitigating their disease. Cell therapy via monocyte-enhanced perfusion through the stimulation of collateral formation is one of a few non-invasive options. Our group examines arteriogenesis after monocyte transplantation into mice using the hindlimb ischemia model. Previously, we have demonstrated improvement in hindlimb perfusion using tetanus-stimulated syngeneic monocyte transplantation. In addition to the effects on the collateral formation, tumor growth could be affected by this therapy as well. To investigate these effects, we use a basement membrane-like matrix mouse model by injecting the extracellular matrix of the Engelbreth-Holm-Swarm sarcoma into the flank of the mouse, after occlusion of the femoral artery. After the artificial tumor studies, we use intravital microscopy to study in vivo tumor-angiogenesis and monocyte homing within collateral arteries. Previous studies have described the histological examination of animal models, which presupposes subsequent analysis to post-mortem artifacts. Our approach visualizes monocyte homing to areas of collateralization in real time sequences, is easy to perform, and investigates the process of arteriogenesis and tumor angiogenesis in vivo.
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PMID:Intravital Microscopy of Monocyte Homing and Tumor-Related Angiogenesis in a Murine Model of Peripheral Arterial Disease. 2887 19