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)

Comparison of the data of electrocardiographic diagnosis for determining the size of the necrotic and periinfarction zones in records from 35 precordial leads with the results of pathoanatomical study of the size of the focus of affection in 8 dead persons who had suffered from acute myocardial infarction showed the adequacy of the method for assessment of the state of the necrotic and periinfarction zones in patients with acute myocardial infarction by the sum elevation of the ST segment in anterior myocardial infarction and by the area of segment ST depression in inferoposterior myocardial infarction.
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PMID:[Comparison of electrocardiographic (35 leads) and pathologicoanatomic diagnostic data in determining the dimensions of necrotic and peri-infarct zones]. 67 26

9,10-Dihydro-10-(1-methyl-4-piperidylidene)-9-anthrol (danitracen, WA 335) is a substance with a stronger peripheral and partly central antiserotonin and antihistamine effect than cyproheptadine. In 5 different hospitals, WA 335 (3 X 1 mg/die) was investigated versus amitriptyline (3 X 50 mg/die) in a double-blind study in 116 depressive patients of different nosology. In the end of the investigation period (20 days), under WA 335 treatment 67.7% and under ami-riptyline treatment 66.7% of the patients showed an improvement of 50% = decrease in the Hamilton depression score. However, a decrease of 50% in the selfrating scale (von Zerssen) was only shown by 57% of the patients under WA 335 administration and 51% under amitriptyline administration. There were no significant differences seen as regards course and side effects of the two drugs. Like amitriptyline, WA 335 shows sedative properties at the beginning of therapy.
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PMID:[Comparison of the effects of the anthracene derivative danitracen (WA335-BS) and amitriptyline in depressive patients (author's transl)]. 78 11

To delineate the relative effects on left ventricular function of the site, extent and nature of the abnormal left ventricular segmental contraction (dyssynergy) and thereby determine the mechanism by which anterior myocardial infarction results in greater depression of left ventricular performance than does inferior infarction, 43 patients with remote myocardial infarction of similar extent (average 38 percent of left ventricular systolic perimeter) and associated hypokinesia or dyskinesia confined to either the anterior or inferior wall were compared; 10 additional patients were evaluated who exhibited generalized dyssynergy (72 percent of left ventricular perimeter). When the pattern of dyssynergy and extent of infarction were similar, the location alone of dyssynergy did not influence variables of left ventricular function. However paradoxical outward systolic movement (dyskinesia) of the anterior or inferior wall resulted in greater depression (P less than 0.05) of measures of left ventricular performance than did diminished inward systolic motion (hypokinesia) associated with infarction of similar extent and location. All measures of left ventricular performance were considerably more depressed (P less than 0.05) in the 10 patients with generalized dyssynergy than in the 43 patients with localized dyssynergy. Thus, the location of infarction is not a unique determinant of left ventricular performance. Instead, the size of infarction is the principal characteristic of dyssynergy that impairs left ventricular function; the severity of the pattern of dyssynergy is significant but of lesser importance. It is therefore concluded that the greater reduction of left ventricular function in anterior than in inferior myocardial is largely the result of the more extensive area of necrosis rather than of the location of the infarction.
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PMID:Pump dysfunction after myocardial infarction: importance of location, extent and pattern of abnormal left ventricular segmental contraction. 94 21

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

We presented two cases of acute coronary occlusion after successful percutaneous transluminal coronary angioplasty (PTCA) associated with a treadmill stress testing. Case 1: A 54-year-old man with effort angina was referred to our hospital for cardiac catheterization. At the time of cardiac catheterization, the proximal RCA had a 99% diameter narrowing, and the proximal LCX had a 90% diameter narrowing. PTCA was performed and both lesions were successfully dilated. Eight days after PTCA, he had a symptom-limited treadmill stress testing, using the Bruce protocol. The exercise was terminated at a peak heart rate of 173/min (103% of aged-predicted maximal heart rate), and at a maximal systolic blood pressure of 140 mmHg. A few minutes after the end of exercise, he developed a severe chest pain and ECG changes, which showed ST elevation in leads II, III, aVF and ST depression in leads V4-V6. Emergency coronary angiography disclosed an acute coronary occlusion of RCA at the site of PTCA. Emergency PTCA was performed and the lesion was successfully re-dilated. Case 2: A 68-year-old man was referred to our hospital for cardiac catheterization a month after subendocardial anterior myocardial infarction. At the time of cardiac catheterization, the proximal LAD have a 99% diameter narrowing. PTCA was performed and the lesion was successfully dilated. 18 days after PTCA, he had a symptom-limited treadmill stress testing, using the Bruce protocol. The exercise was terminated at a peak heart rate of 158/min (102% of aged-predicted maximal heart rate), and at a maximal systolic blood pressure of 218 mmHg. Ten minutes after the one of 218 mmHg.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Two cases of acute coronary occlusion after successful coronary angioplasty associated with a treadmill stress testing]. 221 90

The significance of inferior ST segment changes was studied in 23 patients with acute anterior myocardial infarction by the distribution of the left anterior descending artery (LAD) after percutaneous transluminal coronary recanalization. In 9 patients (Group A) LAD supplied the anterior wall of the left ventricle up to or including the apex but did not reach the inferior wall; in 8 patients (Group B) it continued beyond the apex onto the inferior wall of the left ventricle with well developed collateral circulation; in 6 patients (Group C) it continued beyond the apex onto the inferior wall of the left ventricle with less-developed or no collateral circulation. Thallium-201 scintigraphy and contrast left ventriculography showed that inferior myocardial ischemia was significantly more prominent in Group C than Group A. These results were consistent with coronary anatomy. Inferior ST segment was significantly more depressed in Group A with no concomitant inferior wall ischemia, than in Group C with concomitant inferior wall ischemia (maximal inferior ST segment change: -1.7 +/- 1.1; 0.8 +/- 1.7 mm, respectively; p less than 0.02). In Group A inferior ST segment was depressed in all 6 patients with lateral ST segment elevation, but it was depressed in only one of 3 patients with no lateral ST segment change. Lateral ST segment elevation tended to cause inferior ST segment depression. This study indicates that the inferior ST segment changes in patients with acute anterior myocardial infarction depend on concomitant ischemia of the inferior wall of the left ventricle by the distribution of LAD and the lateral ST segment changes.
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PMID:[Significance of inferior ST segment changes in acute anterior myocardial infarction--relationship between the distribution of left anterior descending artery and concomitant ischemia of the inferior wall]. 240 71

A double-blind, 3-phase, cross-over, placebo-controlled trial of the pain-relieving effect of amitriptyline and carbamazepine was carried out in 15 patients with central post-stroke pain (CPSP) but without signs of depression. Treatment was given, in randomized order, for periods of 4 weeks, separated by 1 week wash-out. The final doses were 75 and 800 mg/day, respectively, for amitriptyline and carbamazepine. The treatment effects were assessed by daily ratings of pain intensity on a 10-step verbal scale and at the end of each treatment period by a global rating of the analgesic effect on a 5-step verbal scale. For the assessment of depression the Comprehensive Psychopathological Rating Scale (CPRS) was used. Amitriptyline produced a statistically significant reduction of pain when compared to placebo. According to the global rating, 10 of the 15 patients were responders to this drug. The effect could already be noticed during the second treatment week and it appeared to be correlated to the plasma concentration, since the median total ami- and nortriptyline concentrations were 497 and 247 nmol/l, respectively, for responders and non-responders. The early onset, together with the fact that the patients were not depressed, nor did they obtain reduced scores on ratings of depressive symptoms and signs, provides strong support for the conclusion that the pain relief was not caused by an antidepressive effect. Five of the 14 patients treated with carbamazepine reported some pain relief, but the effect did not reach statistical significance when compared to placebo. No correlation was found between effect and plasma concentration. In general, the patients tolerated the planned final dose of amitriptyline well. No final dose reduction was necessary. Carbamazepine caused more side effects and the final dose had to be reduced in 4 patients. However, only 1 patient had to be taken off medication, on day 25, due to drug interaction.
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PMID:Central post-stroke pain--a controlled trial of amitriptyline and carbamazepine. 246 30

The in-hospital course of 500 consecutive patients treated with coronary angioplasty for acute myocardial infarction was reviewed in relation to their clinical and angiographic presentation and angioplasty outcome to determine which patients benefit most from successful angioplasty in this setting. Patient age was 56 +/- 11 years (mean +/- SD) and 78% were men; 46% had anterior myocardial infarction, 49% received concomitant intravenous thrombolytic therapy, left ventricular ejection fraction was 47 +/- 11% and median time to angioplasty was 4.7 h (range 1 to 24). Angioplasty was successful in 78% of patients and partially successful in 7% of patients; the overall in-hospital mortality rate was 10.2%. Multivariate analysis found six independent correlates (p less than 0.05) of in-hospital mortality: left ventricular ejection fraction less than or equal to 30%, lack of postangioplasty infarct artery patency, age greater than 65 years, recurrent ischemia after successful angioplasty, emergency bypass surgery and arterial pressure on admission to the catheterization laboratory less than 100 mm Hg. After consideration of these predictors of survival in multivariate analyses, angioplasty success still was independently correlated with improved in-hospital survival for patients with cardiogenic shock (p = 0.002) and anterior myocardial infarction (p = 0.007). A trend toward an independent beneficial effect of successful angioplasty on survival was also noted in patients with inferior wall infarction and precordial ST segment depression (p = 0.063) and for all patients who were hypotensive on admission to the catheterization laboratory, regardless of the infarct site (p = 0.057).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Implications for patient triage from survival and left ventricular functional recovery analyses in 500 patients treated with coronary angioplasty for acute myocardial infarction. 252 54

To elucidate the clinical significance of the exercise-induced negative U-wave (NU) in patients with anterior myocardial infarction, we compared the angiographic and scintigraphic findings in 15 patients with and 20 patients without NU, and obtained the following results: 1) On coronary angiography, all patients in the NU (+) group showed over 90% stenosis or total occlusion of the left anterior descending coronary artery (LAD). In the latter cases moderate to abundant collaterals were visualized on the anterior wall. In contrast, such a tendency was not observed in the NU (-) group. 2) Segments composed of viable myocardium (estimated by preservation of contraction at rest and T1-201 redistribution after exercise) numbered 30 of 45 segments (67%) in the NU (+) group, and 13 of 60 segments (22%) in the NU (-) group. Segments composed of lost myocardium (estimated by loss of contraction at rest and persistent defect in T1-201 uptake) numbered 7 of 45 segments (16%) in the NU (+) group, and 38 of 60 segments (63%) in the NU (-) group. 3) Exercise-induced NU was frequently observed on R-wave preserved leads with ST depression, but was also observed over abnormal Q waves, ST elevation and in isolation in some instances. 4) In 3 patients, preexisting exercise-induced NU was no longer observed and a transient stress-induced T1-201 defect disappeared after successful LAD revascularization. In conclusion, exercise-induced NU on precordial leads in patients with anterior myocardial infarction may be a sign suggesting the presence of jeopardized, but still salvageable, myocardium in the infarcted area.
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PMID:Clinical significance of exercise-induced negative U-waves in patients with anterior myocardial infarction. 272 36

The results of exercise electrocardiography were studied in a random sample of 317 subjects with clinical suspicion of coronary artery disease. In 278 patients with coronary artery disease the rate of false negative tests was 18% with and 12% without previous myocardial infarction. If ST elevation was considered a negative response, the corresponding values were 25% and 13%, respectively, p less than 0.01. The greatest prevalence of negative tests was seen after anterior myocardial infarction: 27% or 42% when ST elevation was not included into positive responses. The sensitivity of exercise-induced ST depression for the presence of multivessel disease was lower after anterior infarction (67%) than in other patients with previous infarction (86%), p less than 0.01. The corresponding specificities were 71% and 22%, respectively, p less than 0.005. If ST elevation was included into positive responses these differences were abolished. In subjects without myocardial infarction the sensitivity was 89% and specificity 43%. Digitalized patients had somewhat higher sensitivity in the exercise electrocardiogram than those without digoxin, 90% vs. 81% (p less than 0.05), but the difference was not seen with exclusion of ST elevation. The specificity was not influenced by digitalis. beta-blockade had no effect on the sensitivity or specificity, but the prevalence of postexercise ST evolution was lower with (11%) than without (30%) beta-blockade. The prevalence of slowly ascending ST depression was reduced by three factors: the presence of digitalis in patients without previous myocardial infarction, infarction itself, and the extent of coronary artery disease. We conclude that exercise electrocardiography has only a limited value in prediction of multivessel disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Studies on ergometer exercise testing. II. Effect of previous myocardial infarction, digoxin, and beta-blockade on exercise electrocardiography. 287 94


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