Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Occlusion of the rodent middle cerebral artery by embolism, using an intraluminal filament, produces behavioral alterations which resemble many symptoms associated with stroke. This model has been used to examine treatment interventions for the disease, however, variable success rate in completely blocking the middle cerebral artery may present inconclusive interpretation of the data. To detect successful occlusion of the middle cerebral artery, we demonstrate here sensitive and reliable behavioral parameters including the elevated body swing test, the postural tail-hang test, the spontaneous rotational test, and the forelimb akinesia test. These assays provide a criterion for identifying animals with incomplete occlusion which could promote host-related spontaneous recovery and might confound true effects of experimental therapies on ischemia-induced dysfunctions. From a practical standpoint, the early reliable identification of partial cerebral ischemia aids in immediate and efficient adjustments of the surgical procedure to create a complete and stable ischemia stroke animal model.
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PMID:Early assessment of motor dysfunctions aids in successful occlusion of the middle cerebral artery. 985 69

The purpose of this study was to compare 2 different techniques--dobutamine-atropine stress echocardiography (DSE) and dual-isotope simultaneous acquisition (technetium-99-m-tetrofosmin/fluorine 18-fluorodeoxyglucose) single-photon emission computed tomography (DISA-SPECT)--for assessment of viable myocardium. One hundred ten patients (mean age 55 +/- 9 years) with left ventricular (LV) dysfunction (mean LV ejection fraction 27 +/- 13%) underwent both DISA-SPECT and DSE. A 16-segment scoring model was adopted for both techniques. Four types of wall motion during DSE were assessed: (1) biphasic, improvement at low dose (10 microg/kg/min) with worsening at high dose; (2) worsening, deterioration without initial improvement; (3) sustained, persistent or late improvement; and (4) no change. Viability criteria were biphasic, worsening, and sustained improvement with DSE. Viability criteria with DISA-SPECT were normal perfusion and metabolism (normal), concordantly mildly reduced perfusion and metabolism (subendocardial scar), or severely reduced perfusion and increased metabolism (mismatch). Myocardium was considered nonviable with DSE in case of unchanged wall motion, or moderate reduction or absence in both technetium-99m-tetrofosmin perfusion and fluorodeoxyglucose uptake with DISA-SPECT. Of 1,756 of 1,760 analyzable LV segments, 1,373 (78%) had severe wall motion abnormalities at baseline (severe hypokinesia, akinesia, or dyskinesia). Of these abnormal segments, 282 (21%) were considered viable during DSE (63 [5%] with biphasic response, 47 [3%] with ischemia, and 172 [13%]) with sustained improvement, whereas 1,091 (79%) were considered nonviable. With DISA-SPECT, 396 (29%) segments were considered viable (312 [23%] with matched perfusion/metabolism and 84 [6%] with mismatch), whereas 977 segments (71%) were considered nonviable. Both techniques showed agreement for viability in 201 segments and 896 were concordantly classified as nonviable. Disagreement was present in 276 segments of which 195 (71%) were nonviable with DSE and viable with DISA-SPECT. Overall agreement between the 2 techniques was 81% (kappa 0.46) in a subgroup of patients with an ejection fraction <25% 78% (kappa 0.39). Thus, DSE and DISA-SPECT show good agreement for assessing viable myocardium not influenced by resting ejection fraction. DSE underestimated the amount of viable tissue compared with DISA-SPECT.
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PMID:Dobutamine stress echocardiography and technetium-99m-tetrofosmin/fluorine 18-fluorodeoxyglucose single-photon emission computed tomography and influence of resting ejection fraction to assess myocardial viability in patients with severe left ventricular dysfunction and healed myocardial infarction. 1042 27

In patients with a previous myocardial infarction, controversy exists regarding the significance of postexercise ST-segment elevation in the infarct-related leads. Although usually admitted to be a sign of left ventricular dysfunction or myocardial aneurysm, other studies however have related this finding to transient myocardial ischemia and to the presence of jeopardized but viable myocardium in the infarct area. The aim of the present study was to assess the significance of postexercise ST-segment elevation in Q-wave leads as a marker of transmural ischemia or left ventricular dysfunction in 36 consecutive patients, 16 with exercise-induced ST-segment elevation in infarct-related leads. Patients were evaluated by treadmill exercise testing, coronary angiography and ventriculography, thallium-201 tomographic scintigraphy and radionuclide ventriculography within 3 months of the first myocardial infarction. Sixteen patients (group I) had exercise-induced ST segment elevation and 20 (group II) postexercise inversion, no change or pseudonormalization of the T wave in infarct-related leads. The study showed no difference in infarct-related artery, vessel disease or luminal diameter stenosis in groups I and II. The overall agreement between ST shifts and myocardial perfusion in the infarct area was 30.56% with a kappa coefficient of -0.33 (p = NS). The overall agreement between ST shifts and wall motion abnormalities was 69.44% with a kappa coefficient of 0.39 (p < 0.01), stress-induced ST-segment elevation being associated with severe wall contractile disorders in 85% of the patients. In conclusion stress-induced ST-segment elevation in Q wave leads, although not a marker of wall motion abnormalities, is associated with akinesia or dyskinesia of the left ventricular wall.
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PMID:Role of myocardial ischemia and left ventricular wall motion abnormalities as contributory factors in the genesis of exercise-induced ST-segment elevation in Q-wave myocardial infarction. 1054 77

Myocardial contraction behaves heterogeneously, being greater in subendocardial than in subepicardial layers. Similarly, during acute myocardial ischemia or infarction, the subendocardium is the first myocardial layer to suffer. Conventional two-dimensional echocardiography cannot distinguish the transmural extension of myocardial ischemia or infarction, showing akinesia also when only the subendocardium is affected. Novel ultrasonographic techniques (like tissue characterization with integrated backscatter or Doppler tissue imaging) and nuclear magnetic resonance tagging can investigate myocardial contraction in different transmural layers and distinguish subendocardial from transmural ischemia or infarction. With the advent of thrombolysis and primary angioplasty in the acute phase of myocardial infarction a correct diagnosis of the extension of myocardial necrosis cannot ignore its transmural wavefront development. The salvage of the subepicardial layer does not give direct information on overall myocardial thickening but is one of the major determinants of overall left ventricular dysfunction and size. Although it is still necessary to investigate this phenomenon, new ultrasonographic techniques give us important information and more opportunities to appropriate diagnosis and future treatment of cardiac patients.
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PMID:Transmural heterogeneity of myocardial contraction and ischemia. Diagnosis and clinical implications. 1080 84

This study sought to examine the effects of graded dobutamine infusion on QT dispersion early after acute myocardial infarction (AMI) and to investigate the relation of dobutamine-induced changes in QT dispersion to wall motion responses. Seventy-eight patients with a first AMI underwent dobutamine-atropine stress echocardiography 5 +/- 2 days after admission. Contractile reserve was identified in 45 patients and ischemic myocardium in 40. Sixteen patients had persistent akinesia. The best cut-off value of QT dispersion on the baseline electrocardiogram for predicting myocardial viability was 65 ms (sensitivity and specificity of 68%). Dobutamine infusion increased QT dispersion only in patients with viable myocardium (61 +/- 18 to 83 +/- 19 ms, p = 0.003) and/or ischemia (72 +/- 16 to 112 +/- 25 ms, p < 0.0001). No change was observed in patients with persistent akinesia (84 +/- 10 to 87 +/- 15 ms, p = NS). QT dispersion increased by 22 +/- 12 ms with administration of low-dose dobutamine in patients who had viable myocardium and by 47 +/- 21 ms with administration of low- to high-dose dobutamine in patients with ischemic myocardium. An increase in QT dispersion of > or = 20 ms from at rest to low-dose dobutamine infusion was associated with myocardial viability with a sensitivity of 78% and a specificity of 79%, whereas an increase in QT dispersion of > or = 10 ms from low- to high-dose dobutamine infusion predicted ischemic myocardium with a sensitivity of 85% and a specificity of 82%. In conclusion, (1) low QT dispersion on the baseline electrocardiogram is determined by the presence of viable myocardium, (2) a dobutamine-induced increase in QT dispersion is associated with viable and jeopardized myocardium, and (3) unchanged QT dispersion during dobutamine stress is a simple marker of extensive necrosis.
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PMID:Significance of dobutamine-induced changes in QT dispersion early after acute myocardial infarction. 1170 85

A case of parkinsonian syndrome caused by normal pressure hydrocephalus (NPH) accompanied by cauda equina neurinoma is reported. A 69-year-old woman presented with typical symptoms of parkinsonism, including akinesia, resting and postual tremor, and cog-wheel rigidity. CT scan of the brain revealed dilatation of ventricles, but she did not present dementia and urinary incontinence that are common symptoms in NPH. Her cerebrospinal fluid (CSF) pressure was normal, and her protein level was high at 2,970 mg/dl. An electroencephalogram (EEG) showed diffuse slow waves. An IMP-SPECT images of the brain showed diffuse reduction of radioisotope uptake. Levodopa was not effective in treating her parkinsonism. Removal of the tumor caused dramatic improvement in her parkinsonism. Her CSF protein level was normalized and EEG and SPECT images were improved after the operation. However, ventricular size on brain CT showed no change. It was considered that the causal mechanism of NPH was due to high protein levels in the CSF. The parkinsonism in this case was caused by dysfunction of the circuits linking the cortex, basal ganglia, and thalamus associated with metabolic disorder due to periventricular ischemia. Typical parkinsonism caused by NPH associated with spinal cord tumor has not been reported. When we examine a patient with parkinsonian syndrome caused by NPH, we should check the CSF protein level. And if that level is high, the possibility of spinal cord tumor should be considered.
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PMID:[A case of parkinsonian syndrome caused by normal pressure hydrocephalus accompanied by the cauda equina neurinoma]. 1242 62

As well as pheochromocytoma, in which it has been established that an excess of circulating catecholamines is responsible for the development of catecholamine-induced acute myopathy, some rare cases have been reported of a similar cardiac incident following intense emotional stress. In this study, the case has been examined of a 56-year old female with no history of cardiovascular disorder who presented with intense, nitro-resistant prolonged chest pain mimicking an acute coronary syndrome immediately following a situation involving major psychological stress. The admission electrocardiogram revealed a sharp decrease in R-wave amplitude in the right chest leads associated with an extended QT interval, and secondarily with subepicardiac ischemia in the lower leads. However, a few days after admission the electrical signs and septo-apical akinesia that had initially been observed by echocardiography completely disappeared. The clinical examination ruled out a diagnosis of myocardial necrosis, acute myocarditis, or pheochromocytoma. Moreover, no direct evidence of coronary spasm was found. The outcome was positive, with complete reversibility of all clinical signs and no organic sequelae. It is considered that this was probably a case of catecholaminergic acute cardiomyopathy triggered by intense emotional stress, a rare occurrence that should nevertheless be systematically taken into account in cases with similar clinical signs.
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PMID:[Myocardial pseudo-infarction: "stress"-associated catecholamine-induced acute cardiomyopathy or coronary spasm?]. 1255 32

Anagrelide is a phosphodiesterase III inhibitor utilized in the treatment of essential thrombocythemia. Anagrelide can be responsible for positive inotropic and chonotropic activity of the cardiovascular system. Moreover, it can induce vasospam directly on the epicardial coronary arteries. In the literature, it is well reported that this inhibitor can determine serious cardiovascular side effects, including congestive heart failure, arrhythmia and acute coronary syndrome. We describe the case of a 75-year-old woman who developed a mid-ventricular Takotsubo syndrome while on anagrelide therapy. Takotsubo cardiomyopathy, also known as left ventricular ballooning syndrome, is characterized by a reversible ventricular contractile dysfunction with akinesis and expansion of apical segments and hyperkinesis of the basal segments. Recently, atypical cases with akinesia and dilation of mid-ventricular segment and hypercontraction of the apical segments, also called mid-ventricular and inverted Takotsubo syndrome, have been described. Even though the pathogenesis of Takotsubo syndrome is poorly understood, several mechanisms have been proposed, including catecholamine-induced myocardial stunning, and ischemia-mediated stunning due to multivessel epicardial or microvascular spasm. We think that in our case, the adverse response of anagrelide therapy was determined, by accumulated dosage of the drug, through an intensive inotropic stimulation and a sympathetic hyperactivation in a vulnerable myocardium. To our knowledge, this is one of the first reports of an association between anagrelide therapy and Takotsubo cardiomyopathy.
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PMID:Atypical Takotsubo syndrome during anagrelide therapy. 1939 76

A low-dose cardiac CT examination for preoperative assessment of coronary artery disease and mitral valve annulus dimensions in 79-year-old female with mitral valve regurgitation, consisting of a prospectively ECG-triggered high-pitch first-pass perfusion scan under adenosine stress and a sequential scan at rest enabled the diagnosis of occlusion of the right coronary artery and high-grade stenosis of the left circumflex artery, reversible perfusion defects of the inferoseptal and inferolateral walls and a persistent inferior wall perfusion defect associated with inferior wall thinning and akinesia. All findings were confirmed with catheter coronary angiography and cardiac magnetic resonance imaging. Because of the diagnosis of peri-infarct ischemia, the patient underwent aortocoronary bypass grafting in addition to mitral valve reconstruction. CT allowed for comprehensive preoperative assessment of cardiac morphology, function, and perfusion at a low cumulative radiation dose of 4.3 mSv.
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PMID:Evaluation of cardiac morphology, function, and perfusion at low radiation dose before mitral valve surgery. 2151 59

A 75-year-old man with a 120-bpm tachycardia and typical atrial flutter was admitted. Echocardiography showed a dilated left ventricle with anterior and apical wall akinesia. Tachycardia was terminated with cavotricuspid isthmus ablation. Multiple imaging findings revealed a woven coronary artery anomaly (WCAA) in the left anterior descending artery. Stress myocardial perfusion imaging was performed after ablation in the sinus rhythm and revealed stress-induced ischemia and a fixed low uptake in the WCAA territory. WCAA is generally regarded as a benign condition; however, compromised blood flow within the anomaly, caused by tachycardia-related diastolic shortening, may induce ischemia.
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PMID:Chronic Ischemia Induced by Woven Coronary Artery Anomaly with Typical Atrial Flutter: Insights from Multiple Imaging Devices. 2632 44


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