Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In patients with myocardial infarction (MI) the presence or absence of lesions in vessels other than the one which perfuses the infarcted area, has implications regarding coronary bypass surgery, long term anticoagulant therapy, work capacity and prognosis. We investigated whether involvement of a 2nd or 3rd vessels as demonstrated by coronary angiography can be predicted on the basis of angina pectoris and/or ischemic ST-segment depression during exercise. Inferior myocardial infarction (IMI, n = 146) Severe lesions (greater than or equal to 75%) of a 2nd or 3rd vessel were found in 61.7% of patients with IMI, who developed angina pectoris and ischemic ST-segment depression, in 18.6% of patients with ST-segment depression only, in 9.1% of patients with angina pectoris only and in 3.4% with neither angina pectoris nor ST-segment depression. Anteroseptal infarction (ASI, n = 116) Severe lesions (greater than or equal to 75%) of a 2nd or 3rd vessel were found in 30.2% of patients with ASI, who developed Angina pectoris and ischemic ST-segment depression; in 26.6% of patients with ST-segment depression only, in 20.0% of patients with angina pectoris only and in 3.0% of the patients with neither angina pectoris nor ST-segment depression. The clinical implications of the results are discussed.
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PMID:[Stress tests and coronary angiography in chronic myocardial infarct]. 122 60

The effect of different glutamate-receptor antagonists on the induction of cortical spreading depression of Leao and of cortical anoxic membrane depolarization were investigated in the anaesthetized rat. Spreading depression (SD), elicited by mechanical stimulation of the cortical surface, was inhibited by the non-competitive N-methyl-D-aspartate (NMDA)-receptor blocker, (+-)-5-methyl-10,11-dihydro-5H-dibenzo(a,d)-cyclo-hepten-5,10-imi ne maleate (dizocilpine or MK-801), (0.30 mumol kg-1 (0.10 mg kg-1)), and the competitive NMDA-receptor antagonists; cis-4-phosphonomethyl-2-piperidine carboxylate (CGS 19755), (3.36 mumol kg-1 (0.75 mg kg-1)), D-(E)-2-amino-4-methyl-5-phosphono-3-pentenoic acid (CGP 40116), (1.20 mumol kg-1 (0.25 mg kg-1)) and its carboxylester CGP 43487, (6.30 mumol kg-1 (1.50 mg kg-1)). The alpha-amino-3-hydroxy-5-methyl-4-isoxazolepripriate (AMPA)-receptor blocker, 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo(F) quinoxaline (NBQX), administered as an intravenous dose of 29.76 and 89.29 mumol kg-1 (10 & 30 mg kg-1), which is sufficient to block seizures and protect against ischaemic brain damage, did not inhibit spreading depression. None of the drugs utilized inhibited the anoxic membrane depolarization. The data demonstrate that NMDA-receptor activation is essential for the initiation and propagation of spreading depression, while activation of AMPA-receptors is not obligatory. The observed initiation and propagation of SD, during AMPA-receptor blockade, suggest that activation of voltage-operated ion channels may contribute to release the magnesium block of the NMDA-receptor operated channel and to the initiation of SD.
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PMID:NMDA-receptor blockers but not NBQX, an AMPA-receptor antagonist, inhibit spreading depression in the rat brain. 128 83

Study on 108 patients of acute myocardial infarction has shown the incidence of reciprocal ST depression in ECG in 58.3% patients. Those showing reciprocal changes had higher (65.0% Vs 15.5%) incidence of complication such as dysrhythmias, conduction disorders. hypotension, left ventricular failure or CCF which was more conspicuous in inferior myocardial infarction. There was higher incidence of complications (74.4% vs 18.7%) whenever ST depression was 2 mm or more (P < 0.001) and there was steep rise in complications whenever the ST depression persisted for 2 days and beyond.
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PMID:Prognostic significance of reciprocal changes in acute myocardial infarction. 130 28

Large-scale, randomized clinical trials have produced over the last few years a wide consensus about the role of thrombolysis in the treatment of acute myocardial infarction (AMI). It has been estimated from the trials with broader inclusion criteria that about 40% of the patients admitted to coronary care units with AMI are eligible for fibrinolytic therapy and can benefit from it. On the other hand, drug utilization data suggest that only a fraction of eligible patients actually receive thrombolysis. A reason for this dissociation between knowledge and practice lies in the widespread assumption that thrombolysis is inefficacious in particular population subsets, as well as in the setting of a number of contraindications based on controversial evidence. Age per se does not represent a contraindication to thrombolysis, which could display a lifesaving potential two or three times that estimated for the general population of patients with AMI. Although it has been shown that the sooner thrombolytic treatment is provided after the onset of symptoms the more effective it is, the available evidence seems to indicate that the effect could well extend up to 12 h from the onset of symptoms. Patients with an inferior myocardial infarction should also receive thrombolytic treatment on the basis of the results of a meta-analysis carried out on 12,000 patients. Very misleading recommendations for practice can be produced by adjusting the main results so as to conveniently allow for subgroup findings, regardless of their degree of epidemiologic, biologic, and pathophysiologic consistency. For all categories of patients included in the population trials (with the exception of those with ST depression), thrombolysis should be considered a recommended treatment. From an epidemiologic perspective, the extension of the benefits of thrombolytic therapy to all AMI patients for whom the drug is not clearly contraindicated is a goal of primary importance.
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PMID:GISSI update. Which patients with myocardial infarction should receive thrombolysis? 153 50

To investigate the significance of precordial ST-segment depression in acute inferior myocardial infarction, we compared the Gensini score of coronary artery stenosis between 2 groups of patients with and without precordial ST-segment depression. Group I consisted of 28 patients who showed ST-segment depression on admission (greater than or equal to 1 mm in V2-V6) and Group II (n = 16) those without ST-segment depression (less than 1 mm). The Gensini score of the coronary arteries (56 +/- 29 vs. 28 +/- 18; p less than 0.001), the partial score of the infarction-related artery (29 +/- 16 vs. 17 +/- 11; p less than 0.01) and of the infarction-nonrelated artery (27 +/- 24 vs. 11 +/- 12; p less than 0.02) were significantly higher in Group I than in Group II. The Killip score (greater than or equal to II) (34% vs. 6%; p less than 0.05), frequency of arrhythmias (75% vs. 38%; p less than 0.02) and peak CK value (3,676 +/- 2,290 vs. 1,818 +/- 1,153 IU/L; p less than 0.005) were higher in Group I than in Group II. Four patients in Group I died following admission, while no patient died in Group II (N.S.). Autopsy findings from the 4 Group I patients revealed fresh extensive inferior infarction and healed diffuse subendocardial infarction which could not be predicted from electrocardiograms. All patients who survived the acute stage performed treadmill exercise testing and 22 patients underwent exercise thallium-201 single photon emission computer tomography (SPECT). On treadmill exercise test, there was no significant difference between the 2 groups in the frequency of angina pectoris and ST-segment depression. On SPECT, the perfusion defect area under 55% of maximum uptake at the redistribution phase was 45.8 +/- 19.6 cm2 in Group I (n = 14) and 34.7 +/- 21.3 cm2 in Group II (n = 8; N.S.). In conclusion, precordial ST-segment depression in acute inferior myocardial infarction suggested advanced atherosclerosis in both the infarction-related and nonrelated coronary arteries, indicating a larger infarct size.
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PMID:Higher Gensini score of coronary arteries in acute inferior myocardial infarction with precordial ST-segment depression. 157 78

ST segment change in procordial leads was analysed in 58 patients with acute inferior myocardial infarction (IMI). ST segment depression in V2 lead was negatively correlated with ST segment elevation in a VF lead in patients with IMI. ST segment depression in V2 lead was not observed when IMI was accompanied by right ventricular infarction. It indicates that ST segment depression in procordial leads was the reciprocal change of ST segment elevation in inferior leads. The direction and amplitude of ST segment shift in procordial leads may be affected by the presence of right ventricular infarction (RVI). The ratio of ST V2/ST aVF less than 0.5 may suggest a diagnosis of IMI with accompanying RVI.
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PMID:[An analysis of ST segment shift in procordial leads in patients with acute inferior myocardiac infarction with and without right ventricular infarction]. 175 55

Assessments of the significance of precordial ST segment depression in acute inferior myocardial infarction (AIMI) have yielded conflicting results. Among 92 AIMI patients admitted within 6 hrs after the onset, 65 showed ST depression, and the remaining 27 showed no ST depression. These depressions were present in all of V1-4 (right type; 17), V2-5 (middle type; 10), V3-6 (left type; 13) and V1-6 (broad type; 25). The clinical severity was Forrester subset I in the majority (89%) of patients without ST change, while complications were prevalent in patients with ST depression, especially in the right type (44% were Forrester subset II-IV). Peak CK was 2,150 +/- 399 U/L in patients without ST depression, but it was elevated to 3,172 +/- 811 in patients with ST depression, especially in the right type (4,506 +/- 499). Wall motion evaluated by echocardiography and QRS scores on ECG also revealed greater abnormality in patients with ST change. The initial right coronary angiogram on admission revealed complete occlusion in 76% of these patients with ST depression of whom all of the right type had completely occluded artery. Abnormal motion of the anterior wall, which suggests remote ischemia associated with AIMI was proved neither by left ventriculography nor echocardiography. Hospital mortality in patients with ST depression (9.2%) was as twice as high as that in those without ST depression (4.6%). We concluded that ST depression in patients with acute inferior infarction may not be indicative of remote ischemia but manifests as a mirror image of a large infarction with a complicated clinical course.
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PMID:[Clinical characteristics of precordial ST-segment depression in acute inferior myocardial infarction]. 184 9

To study the predictive value of silent ischemia, a total of 132 patients with first transmural myocardial infarction were examined, 69 had anterior and 63 had inferior myocardial infarction. On days 8-12 of onset of the disease, all the patients underwent loading two-dimensional echocardiography along with transesophageal pacing, as well as polyposition coronary angiography. According to the echocardiographic findings, 3 groups of patients were identified: 1) 34 (25.8%) with painful ischemia; 2) 37 (28.0%) with silent ischemia; 3) 61 (46.2%) with a negative test. Ischemic alterations were more frequently seen in inferior (73%) than in anterior (36.2%) myocardial infarction. The patients with painful ischemia showed a lower threshold of ischemia occurrence, more severe and prolonged ST segment depression, and greater extent of an asynergic area than did the patients with silent ischemia. A 1-5-year (mean 2.4) follow-up revealed that in terms of the risk for postinfarction angina, recurrent myocardial infarction and fatal outcomes, patients with silent ischemia represent an intermediate group between those with painful ischemia and those who have a negative load test.
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PMID:[Prognostic significance of post-infarction "silent" ischemia]. 192 Nov 27

To determine the ability of initial ST segment elevation and depression to predict infarct size limitation by thrombolytic therapy, data were analyzed in 721 patients with acute myocardial infarction who were admitted to a randomized, placebo-controlled study of intravenous recombinant tissue-type plasminogen activator. Patients with QRS duration of 120 msec or more or with previous history of myocardial infarction were excluded, leaving 322 in the treatment and 333 in the placebo group. Cumulative 72-hour release of alpha-hydroxybutyrate dehydrogenase and global ejection fraction as well as left ventricular wall motion derived from angiography were used as independent measures of infarct size. Electrocardiograms obtained at admission, 6 hours after start of therapy, and before discharge were analyzed. All ST measurements were made by hand at the J point and 60 msec after the J point. Patients with high ST segment elevation at admission (i.e., sum of ST elevation at 60 msec after the J point was 20 mm or more) had significantly larger infarction and higher hospital mortality when compared with those with lower (less than 20 mm) ST elevation. Reciprocal ST segment depression also showed a linear relation with infarct size and mortality, independent from ST elevation, both in anterior and inferior myocardial infarction. The sum of deviations measured at the J point and 60 msec after the J point differed significantly, especially in anterior myocardial infarction at admission (mean, 16 +/- 9 versus 23 +/- 11 mm). The prognostic value of one measurement was not, however, superior over the other. Treatment with recombinant tissue-type plasminogen activator was most effective in those with large ST deviations at admission, but patients with anterior infarction and smaller ST shifts also appeared to benefit from therapy. Results in individual patients were variable, and the overall correlation of initial ST shifts with enzymatic infarct size was rather low. In conclusion, the present study shows that the magnitude of initial ST elevation and also of reciprocal ST depression in the admission electrocardiogram is valuable for the management and assessment of thrombolytic therapy in patients with acute myocardial infarction.
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PMID:Significance of initial ST segment elevation and depression for the management of thrombolytic therapy in acute myocardial infarction. European Cooperative Study Group for Recombinant Tissue-Type Plasminogen Activator. 211 63

The impact of associated precordial ST segment depression in inferior myocardial infarction on angiographic and clinical outcomes after thrombolytic therapy and selective coronary angioplasty was studied in 583 patients with acute myocardial infarction. Anterior infarction (Group I), inferior infarction with precordial ST segment depression (Group II) and inferior infarction without precordial ST segment depression (Group III) were present in 289, 135 and 159 patients, respectively. Precordial ST segment depression was more frequent in circumflex than right coronary infarct-related arteries (44 [71%] of 62 versus 91 [40%] of 230; p = 0.000). Although acute patency rates were not statistically different, there was a trend toward different patency rates at day 7 (Group I 88%, Group II 84%, Group III 80%; p = 0.089) partly because of insignificantly higher reocclusion rates in inferior infarction without precordial ST segment depression (Group I 11%, Group II 10%, Group III 18%, p = 0.104). Infarct zone regional wall motion (standard deviations/chord) in inferior infarction was lower with precordial ST segment depression, both acutely (Group I -2.8 +/- 0.9, Group II -2.5 +/- 1.2, Group III 2.0 +/- 1.1; p = 0.000) and at day 7 (Group I -2.2 +/- 1.1, Group II -2.3 +/- 1.1, Group III -1.9 +/- 1.3; p = 0.011). Precordial ST segment depression was associated with a lower ejection fraction in inferior infarction both acutely (Group I 47 +/- 11%, Group II 53 +/- 11%, Group III 58 +/- 9%; p = 0.000) and at day 7 (Group I 49 +/- 12%, Group II 53 +/- 10%, Group III 58 +/- 8%; p = 0.000). Complication rates tended to be higher in inferior infarction when precordial ST segment depression was present. Mortality rates for Groups I, II and III were 8%, 6% and 5%, respectively. These results suggest that precordial ST segment depression in inferior infarction predicts a worse ventriculographic and clinical outcome despite reperfusion therapy.
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PMID:Precordial ST segment depression predicts a worse prognosis in inferior infarction despite reperfusion therapy. The Thrombolysis and Angioplasty in Myocardial Infarction (TAMI) Study Group. 212 3


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