Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

The prevalence rate of exercise- S-T segment elevation of 0.1 mV or greater in symptomatic patients is 3.0 to 6.5 percent in most studies. S-T segment elevation is associated with a more severe degree of myocardial ischemia than depression and frequently implies a high grade coronary stenosis in the vessel that supplies the site of ischemia. Leads V4 to V6 and bipolar lead CM5 have been found to be relatively insensitive in detecting exercise-induced S-T segment elevation. The pathogenesis of S-T segment elevation is different in three clinical patient subsets reviewed. In patients afer infarction, the largest of the three subgroups, exercise-induced S-T segment elevation usually appears in leads with Q waves, is more common after anterior myocardial infarction and implies underlying akinetic of dyskinetic wall motion. Of patients with variant angina, 10 to 30 percent have during exercise S-T segment elevation that is most likely provoked by coronary arterial spasm. The natural history of variant angina is cyclic, and clinical observations and laboratory findings are dependent on particular phases in the disease process and treatment. Finally, 0.2 to 1.7 percent of symptomatic patients without infarction or variant angina have exercise-induced S-T segment elevation. Although most of the latter have fixed high grade coronary arterial stenoses at angiography, the exact pathogenetic mechanism of S-T segment shift in this patient group is not yet fully understood.
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PMID:S-T segment elevation and coronary spasm in response to exercise. 701 17

Serial ECGs of 16 patients with repetitive attacks of spontaneous angina in the CCU were studied from admission to the hospital to the follow-up phase at the cardiac clinic. Transient repolarization ECG changes occurring during unprovoked angina included ST-segment elevation and ST-segment depression, alterations of T-wave amplitude and polarity, and pseudonormalization of previously inverted T-waves. In addition, QRS complexes were altered transiently during chest pain. Such changes comprised augmentation or reduction of amplitude of R and S waves, widening of QRS complexes and a merging of R waves with the elevated ST-segments. Occasionally the ECG during attacks of angina did not show any change. During asymptomatic periods, between attacks of spontaneous angina, the ECG either returned to baseline, or displayed minor ST-segment shifts, and/or T-wave alterations of varying durations. However, such changes became either persistent or were replaced in the late course of hospitalization by ECG alterations diagnostic of transmural or nontransmural myocardial infarction. Twelve patients suffered an acute myocardial infarction. Four patients died within one month of admission. During follow-up of the 12 surviving patients in the cardiac clinic, amelioration of T-wave changes was noted in the ECGs of patients who remained asymptomatic, but new ischemic alterations were seen in the ECG of patients who had recurrent angina, or were readmitted to the hospital for evaluation. Increase in the amplitude of R-waves, disappearance of Q-waves, or reduction of Q-wave depth were noted at follow-up, in comparison with the discharge ECG, in some patients who had suffered primarily an anterior myocardial infarction.
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PMID:Spontaneous angina in the coronary care unit. 2. Electrocardiographic changes during and after chest pain. 710 53

In a pilot study, 32 patients with mixed states of anxiety, depression, somatization and panic received amitriptyline for 4 weeks, the dose ranging from 50 to 300 mg/day. Steady-state plasma levels of the drug and activity of platelet monoamine oxidase were measured after 4 weeks. Clinical change was rated, using the SCL-90. Amitriptyline produced a small but significant inhibition of platelet monoamine oxidase activity (range 1.4--82%). A significant positive correlation was noted between MAO inhibition and improvement on somatization, and psychological and panic-phobic components of anxiety, but not for depression. No significant correlations were observed between improvement and combined or separate ami- + nortriptyline plasma levels.
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PMID:MAO inhibition and control of anxiety following amitriptyline therapy. A pilot study. 723 72

We have examined the relation between electrocardiographic ST elevation during treadmill exercise (greater than or equal to 1 mm, using the conventional 12 leads), the severity of coronary artery disease, and left ventricular wall motion abnormalities in 680 patients. They were divided into three groups: (1) 218 patients with clinically significant coronary artery disease, (2) 178 patients with clinically significant coronary artery disease, and (3) 284 patients with clinically significant coronary artery disease and previous myocardial infarction. ST elevation during exercise (predominantly in lead V2) was seen in two patients (1%) in group 1, three patients (2%) in group 2, and 147 patients (52%) in group 3. Coronary artery disease (number of vessels involved and severity of stenoses) was comparable in groups 2 and 3. All the patients in group 1 showed a normal left ventricular contraction pattern; 64% of the patients in group 2 showed wall motion abnormalities (predominantly hypokinesia) and 95% of group 3 (mainly akinesia, dyskinesia, or aneurysm). A strongly positive correlation was seen between the ST elevation and left ventricular dysfunction in patients belonging to group 3. The overall sensitivity and the specificity of the stress test in detecting wall motion abnormalities was 55% and 100% respectively. The sensitivity increased with deterioration in left ventricular function, reaching 81% and 90% in patients with dyskinesia and aneurysm, respectively. Maximal ST elevation (greater than or equal to 3 mm) was confined to the patients with dyskinesia or aneurysm. The incidence of ST elevation during exercise was also related to the location of previous infarction, showing a positive response in 85% of patients with anterior myocardial infarction and in only 33% with inferior myocardial infarction. We conclude that ST segment elevation during exercise in patients with previous myocardial infarction is a sensitive and a specific indicator of advanced left ventricular asynergy. The ST segment response during exercise in patients with previous infarction and with angiographically demonstrated myocardial asynergy appears to be a continuous spectrum. A normal ST segment response or elevation alone usually signifies involvement of only one vessel supplying the infarcted myocardium, ST elevation with concomitant ST depression indicates additional coronary artery disease, and ST depression alone indicates overwhelming myocardial ischaemia resulting from multiple vessel disease. The employment of multiple leads is essential to obtain this information.
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PMID:Clinical significance of exercise-induced ST segment elevation. Correlative angiographic study in patients with ischaemic heart disease. 727 18

In order to investigate the clinical significance of exercise-induced ST changes in patients with prior myocardial infarction, we performed an exercise tolerance test using bicycle ergometer, coronary arteriography and left ventriculography in 77 patients with prior myocardial infarction and compared exercise-induced ST changes with coronary arteriographic and left ventriculographic findings. At end-point time in the exercise test, we observed abnormal ST elevation in 36 patients (46.7%), ST depression in 11 (14.3%) and no significant ST changes in the remaining 30 (39.0%). After exercise, 29 out of 48 patients (60.4%) with prior anterior myocardial infarction had significant ST elevation, 9 (18.8%) had ST depression, and 10 patients (20.8%) had no significant ST changes. Of the 29 patients with exercise-induced ST elevation, 26 (89.6%) had no significant coronary lesion or simply had single vessel disease, and 6 of 9 patients with ST depression (66.7%) had multiple vessel disease. Furthermore, 18 of 29 patients with exercise-induced ST elevation (62.1%) had dyskinesis, 8 (27.6%) had akinesis and only 3 (10.3%) had hypokinesis. ON the other hand, only 2 of 9 patients with exercise-induced ST depression (22.2%) had dyskinesis, 5 had akinesis, and 2 had hypokinesis. Only 7 out of 29 patients (24.1%) with prior inferior myocardial infarction had ST elevation, 2 (6.9%) had ST depression, and no significant ST changes were observed in the remaining 20 (69.0%). No significant correlation was obtained between exercise-induced ST changes and coronary arteriographic and left ventriculographic findings. These findings strongly suggest that exercise-induced ST elevation is commonly observed in patients with anterior myocardial infarction and correlated with the severity of abnormal left ventricular wall movement, and ST depression is related with the extent of coronary artery lesion.
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PMID:Clinical significance of exercise-induced ST changes in patients with prior myocardial infarction: comparison of electrocardiographic and angiographic findings. 729 92

The hemodynamic monitoring of acute myocardial infarctions has been carried out in patients less than 75 y.o. who showed: a) extensive anterior myocardial infarction; b) inferior myocardial infarction and ST segment depression of the anterior chest leads; c) acute myocardial infarction and cardiac failure. The hemodynamic measurement were carried out at the 12 hours (mean) from the beginning of chest pain on 65 patients who suffered the first myocardial infarction and were protracted to 60 hours (mean). The hemodynamic findings were classified according to the relationship between the stroke work index of the left ventricle (LVSWI) and the mean pulmonary artery pressure (MPAP) as following: normals: 6 pts; hypovolemia: 15 pts; reduced compliance: 2 pts; mild LV failure: 19 pts; severe LV failure or shock: 23 pts. 35 pts have carried out a complete rehabilitation programme has shown an inverse linear relationship to the MPAP of the first recording in CCU. The incidence of death was 29% one year after the myocardial infarction and showed a significant relationship to the hemodynamic findings. The LVSWI resulted more sensitive than MPAP; 90% of patients who showed a LVSWI less than 20 gmb/m2 died.
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PMID:[Correlations among the haemodynamic effects in acute myocardial infarction. Function evaluation and prognosis 12 months later (author's transl)]. 732 21

Changes in hemodynamics and plasma norepinephrine levels during supine bicycle exercise after myocardial infarction were measured to investigate the mechanism of exercise-induced ST-segment elevation. Seventy-eight patients were divided into groups which showed either ST elevation (STE), ST depression (STD), or no ST changes (STU). Most of the STE group had anterior myocardial infarction (90.6%) and single-vessel disease (76.7%). The STE group achieved a significantly higher workload (119.5 +/- 4.0 watts, mean +/- SEM) than the STD group (82.3 +/- 2.8, p < 0.01). Heart rate and cardiac output at maximal workload were significantly higher in the STE group (136.6 +/- 3.4 beats/min, 7.44 +/- 0.28 l/min/m2) than in the STD group (110.0 +/- 3.9, 4.83 +/- 0.36, p < 0.01). Pulmonary artery pressures were less elevated in STE than STD patients. Plasma norepinephrine levels increased significantly at maximal workload in STE patients, as compared to the other groups. In conclusion, the STE group achieved a higher exercise level associated with augmented sympathetic activity, which may be a possible mechanism of exercise-induced ST elevation after myocardial infarction.
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PMID:Exercise-induced ST-segment elevation and hemodynamic responses one month after myocardial infarction. 796 97

The purpose of this study was to examine the relationship between the presence or absence of ST segment depression in inferior leads (II, III, and aVF) and ST segment elevation in lateral (I and aVL) or left precordial (V5 and V6) leads with the amount and location of myocardium at risk for infarction in patients with acute anterior myocardial infarction. Forty-three patients with anterior infarctions were injected with technetium 99m-sestamibi when they were first seen and underwent tomographic imaging to measure the amount and location of myocardium at risk. Patients with inferior ST depression (n = 10) compared with those without ST depression (n = 33) had perfusion defects that extended significantly further into the lateral wall (47 degrees vs 20 degrees, p = 0.04) and larger anterior injury vectors (6.47 vs 4.92, p = 0.008). There was no significant association with the percentage of myocardium at risk, disease of the right coronary artery, the presence of an inferior perfusion defect, or the size of the inferior injury vector. Among the patients with ST elevation in lateral leads (n = 16) compared with those without (n = 27), there was a significantly more lateral defect border (47 degrees vs 25 degrees, p = 0.007) and a larger anterior injury vector (6.07 vs 4.81, p = 0.01). There was no significant correlation with the percentage of myocardium at risk. A significant relationship could not be demonstrated between the presence of ST elevation in the left precordial leads and any measure of the amount or location of myocardium at risk. These data support the theory that inferior ST depression in patients with transmural anterior ischemia is a "reciprocal" finding and does not represent inferior ischemia. The presence of inferior ST depression or lateral ST elevation is associated with a more lateral perfusion defect. Neither of these ECG findings is associated with the amount of myocardium at risk for infarction.
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PMID:The relationship of inferior ST depression, lateral ST elevation, and left precordial ST elevation to myocardium at risk in acute anterior myocardial infarction. 836 5

To determine whether or not ST segment deviation on admission electrocardiograms can identify patients with anterior acute myocardial infarction due to proximal left anterior descending artery occlusion, the magnitude and location of ST segment elevation or depression were compared between patients with proximal left anterior descending artery occlusion (group A, n = 47) and those with distal left anterior descending artery occlusion (group B, n = 59). ST segment depression in each of the inferior leads was significantly greater in group A than in group B. The incidence of ST segment depression > or = 1 mm in each of the inferior leads (II; 81% vs 27%, III; 85% vs 54%, aVF; 87% vs 47%, P < 0.01) was significantly higher in group A than in group B. In addition, the incidence of ST segment depression > or = 1 mm in all of the inferior leads was significantly greater in group A than in group B (77% vs 22%, P < 0.01). In group A, maximal ST segment elevation was more frequent in lead V2 alone (43% vs 14%, P < 0.01). Group A had greater ST segment elevation in lead aVL than group B, and the incidence of ST segment elevation > or = 1 mm in lead aVL was significantly higher in group A than in group B (66% vs 47%, P < 0.05). ST segment depression > or = 1 mm in all of the inferior leads was most valuable for identifying group A patients (77% sensitivity and 78% specificity). In contrast, the maximal ST segment elevation in lead V2 alone or ST segment elevation > or = 1 mm in lead aVL had a low diagnostic value (43% sensitivity and 86% specificity, 66% sensitivity and 53% specificity, respectively). In conclusion, this study indicates that analysis of ST segment deviation in the inferior leads is useful for identifying patients with acute anterior myocardial infarction due to proximal left anterior descending occlusion.
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PMID:Inferior ST segment depression as a useful marker for identifying proximal left anterior descending artery occlusion during acute anterior myocardial infarction. 868 9

To elucidate which clinical features produce U-wave inversion, 339 patients with severe narrowing of the left anterior descending artery were evaluated. In patients with anterior myocardial infarction, extensive coronary artery disease and protected left anterior descending arterial territory are essential in the development of U-wave inversion, whereas electrocardiographic changes at rest in addition to anterior lead ST depression, rather than coronary anatomy, are important in those without anterior myocardial infarction.
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PMID:Clinical and electrocardiographic profiles producing exercise-induced U-wave inversion in patients with severe narrowing of the left anterior descending coronary artery. 929 96


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