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)

We herein report the cases of two patients with bilateral symmetrical pallidal lesions mimicking hypoxic encephalopathy following severe anemia associated with gastrointestinal hemorrhage despite a lack of carbon monoxide intoxication. Although severe anemia can theoretically result in anemic hypoxia, vulnerable pallidal lesions have rarely been described in anemic patients. Interestingly, both patients shared common conditions associated with atherosclerosis, including heavy smoking, hypertension, type 2 diabetes mellitus and a history of coronary artery bypass grafting for ischemic heart disease. Anemic hypoxia may cause pallidal involvement in atherosclerotic patients with multiple risk factors.
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PMID:Bilateral symmetrical pallidal lesions following severe anemia associated with gastrointestinal hemorrhage: report of two cases. 2385 98

Cerebrogenic ECG abnormalities, especially prominent T wave inversions and prolongation of the QT(U) interval, are well-described. Brady- and tachyarrhythmias, including polymorphic VT, have been also described in the setting of neurologic injury. We report an unusual case of a 22-year-old man who presented with idiopathic acute encephalopathy. His hospital course was complicated by persistent fevers, along with refractory seizures treated with propofol. Serial ECG findings included marked ventricular repolarization prolongation with bursts of torsade de pointes, diffuse ST elevations simulating extensive myocardial ischemia or infarction, as well as a Brugada-like pattern. To our knowledge, this case is the first reported with the combination of such findings in a patient with a catastrophic neurologic syndrome.
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PMID:Catastrophic neurologic syndrome with dramatic ECG changes. 2397 89

Mitochondria play an important role in energy production for the cell. The proper function of a myocardial cell largely depends on the functional capacity of the mitochondria. Therefore it is necessary to establish a novel and reliable method for a non-invasive assessment of mitochondrial function and metabolism in humans. Although originally designed for evaluating myocardial perfusion, (99m)Tc-MIBI can be also used to evaluate cardiac mitochondrial function. In a clinical study on ischemic heart disease, reverse redistribution of (99m)Tc-MIBI was evident after direct percutaneous transluminal coronary angioplasty. The presence of increased washout of (99m)Tc-MIBI was associated with the infarct-related artery and preserved left ventricular function. In non-ischemic cardiomyopathy, an increased washout rate of (99m)Tc-MIBI, which correlated inversely with left ventricular ejection fraction, was observed in patients with congestive heart failure. Increased (99m)Tc-MIBI washout was also observed in mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS) and in doxorubicin-induced cardiomyopathy. Noninvasive assessment of cardiac mitochondrial function could be greatly beneficial in monitoring possible cardiotoxic drug use and in the evaluation of cardiac damage in clinical medicine.
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PMID:Evaluation of Cardiac Mitochondrial Function by a Nuclear Imaging Technique using Technetium-99m-MIBI Uptake Kinetics. 2740 41

We present a case of simultaneous cardiotoxicity and stroke-like neurotoxicity in a patient treated with FOLFOX, a 5-Fluorouracil (5-FU)-containing chemotherapy regimen. Within hours of FOLFOX infusion, the patient began to exhibit signs and symptoms of myocardial ischemia and stroke mimic. Coronary vasoconstriction and vasospasm is a known mechanism of 5-FU-induced cardiotoxicity. 5-FU-induced neurotoxicity commonly presents as encephalopathy and is likely attributable to the accumulation of ammonia, a product of 5-FU metabolism. However, our patient presented with focal neurological signs and normal levels of ammonia. This suggests that 5-FU-induced vasospasm in the coronary arteries and cerebral vasculature is a likely cause of the simultaneous cardiac and neurological events we report here which have not been reported previously. Recognition of these toxicities as complications of 5-FU chemotherapy is crucial for the proper diagnosis and treatment of patients.
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PMID:Simultaneous Cardiotoxicity and Neurotoxicity Associated with 5-fluorouracil Containing Chemotherapy: A Case Report and Literature Review. 3214 85


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