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)

Reproducibility of myocardial ischemia induced by atrial pacing (P) was investigated in 25 patients (pts) without previous anterior myocardial infarction and showing a positive exercise stress test. The second period of atrial pacing (P2) was exerted 20 minutes after the first (P1). During P2, a reduction in the parameters reflecting myocardial oxygen requirements (maximal left ventricular pressure, dp/dt max, TTI*HR values) was noted, while the signs of ischemia were less pronounced (ST depression decreasing from 2.3 +/- 1 mm to 1.6 +/- 1.0 mm; % of lactate extraction (%L) decreasing from - 6.4 +/- 25.5 to + 8.5 +/- 19.2; p less than 0.5). The 25 pts were divided into 2 groups according to the ejection fraction (EF greater than .55 16 pts Gr.F+; EF less than .55 9 pts Gr.F-). The distribution of coronary lesions was the same for the 2 groups. During P1 GR.F+ registered a negative % L as opposed to Gr.F-. During P2, the difference in the % L between the 2 groups was also significant (2.6 +/- 19.9% F+ vs 18.9 +/- 14.3% F-; p less than .05). Collateral circulation had no effect upon the results, neither for P1 or P2. This study shows that a second period of atrial pacing, 20 minutes after the first, induced lesser ischemia than the first period of atrial pacing. This phenomenon could explain the paradoxical improvement observed in certain patients after a first episode of angina. These results have implications as regards the necessity of double blind studies compared to placebo when using this technique in the evaluation of the effects of anti-ischemic drugs.
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PMID:[Reproducibility of myocardial ischemia induced by atrial stimulation]. 314 36

To clarify the mechanism of stress-induced ST segment elevation in patients with previous anterior myocardial infarction, we examined myocardial lactate metabolism during atrial pacing in 32 patients with previous anterior myocardial infarction (MI group) and 11 control subjects (control group). In the MI group, atrial pacing resulted in new or additional ST segment elevation in leads with Q waves in 15 patients (ST elevation group), ST segment depression in 7 (ST depression group), but induced no appreciable ST segment changes in the remaining 10 patients (ST unchanged group). In all patients, the ST segment changes were identical to the results of exercise stress testing which was carried out prior to the atrial pacing. Lactate extraction ratio increased moderately during the atrial pacing in the control group (p less than 0.01). Although marked reduction of the myocardial lactate extraction ratio was noted in the ST depression group (p less than 0.05), no significant change in the ratio was evoked in the ST elevation group or the ST unchanged group during atrial pacing. Left ventricular end-diastolic pressure (LVEDP) increased markedly in the ST depression group during atrial pacing, but the elevation was less evident in the other groups. The ST elevation group demonstrated the lowest left ventricular ejection fraction and the severest degree of left ventricular asynergy. Thus, the present study indicates that aggravated left ventricular asynergy in the infarcted area and associated left ventricular dysfunction, rather than peri-infarction zone ischemia is a possible mechanism of stress-induced ST segment elevation in leads with Q waves following previous anterior myocardial infarction.
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PMID:Clinical significance of stress-induced ST segment elevation in patients with previous anterior myocardial infarction. Analysis of lactate metabolism with atrial pacing. 317 72

In order to evaluate the diagnostic value of exercise-induced Q wave changes and its relationship with the extent of coronary involvement and presence and location of a previous myocardial infarction, we examined the stress electrocardiograms of 188 consecutive patients with chest pain. Coronary arteriography shoved single vessel disease (SV) in 28 patients and multivessel disease (MV) in 130 patients; a previous myocardial infarction was present in 64 patients. The Q wave amplitude was measured as average of ten values in CM5 at rest and at peak exercise; a Delta-Q less than 0, i.e. reduction or no change of Q wave at peak exercise, was considered a positive response for coronary artery disease. The Delta-Q criterion shoved a significantly better sensitivity than ST depression, as a whole, but this improvement was nullified when patients with anterior myocardial infarction were excluded; as well specificity of Delta-Q although better than ST, did not allow a significant improvement for the diagnostic value of stress test. We also evaluated the diagnostic accuracy for multivessel coronary artery disease of both criteria positive was 78% whereas the negative predictive value of both criteria negative was 91%. We concluded that the exercise-induced Delta-Q less than 0 is a good indicator of coronary artery disease, although not superior to ST depression; the negativity of both criteria seems to be highly reliable for the exclusion of multivessel coronary artery disease.
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PMID:[Diagnostic value of changes in the Q wave induced by exertion]. 343 97

The significance of inferior ST segment changes during acute anterior myocardial infarction was studied in 60 patients with acute anterior infarction who had angiographic visualization of the entire distribution of the left anterior descending artery after thrombolytic therapy with streptokinase. In 34 patients (Group 1) this artery supplied the anterior wall of the left ventricle up to or including the apex but did not reach the inferior wall; in 16 patients (Group 2) it continued beyond the apex onto the inferior wall of the left ventricle; and in 10 patients with prior inferior infarction (Group 3) it partially supplied the inferior wall of the left ventricle through collateral channels to an occluded right or dominant circumflex coronary artery. Consistent with this anatomy, evidence of inferior wall ischemia was significantly more frequent in Groups 2 and 3 than in Group 1 by thallium-201 scintigraphy (91 versus 7%) and by contrast left ventriculography (91 versus 13%). There was no difference in the magnitude of precordial ST segment elevation among the three groups but the inferior ST segment depression was significantly smaller in Groups 2 and 3 with concomitant inferior wall ischemia than in Group 1 (aVF: -0.5 +/- 0.7; -0.5 +/- 1.0; -1.8 +/- 0.8 mm, respectively; p less than 0.001) with 10 of the 26 patients in Groups 2 and 3 having an elevated or isoelectric ST segment in aVF compared with none of the 34 patients in Group 1 (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Inferior ST segment changes during acute anterior myocardial infarction: a marker of the presence or absence of concomitant inferior wall ischemia. 362 58

Many factors have been found to influence the magnitude of ST-segment depression in the exercise electrocardiogram. We investigated whether R-wave amplitude is a significant factor. We studied the exercise electrocardiogram of 20 patients with angiographically documented coronary artery disease, including greater than or equal to 70% stenosis of the left anterior descending artery, who had an ischemic response to exercise but no previous anterior myocardial infarction. Precordial leads V1-6 were taken into account. When all 120 leads were measured, those with ST-segment depression greater than or equal to 2.0mm at peak exercise had a mean resting R-wave amplitude of 19.03 +/- 5.81mm; those with ST-segment depression 2.0-1.0mm, R 11.42 +/- 5.99mm; and those with ST-segment depression less than 1.0mm, R 5.9 +/- 5.21mm (p less than 0.001 between groups). When the R-wave amplitude was correlated with the ST-segment depression in each precordial lead, the correlation was 1.0. In leads V1-6, when 67 tracings with ST-segment depression greater than 0.5mm were measured, the correlation was 0.537 (p less than 0.001). In each precordial lead the t values of R-wave differences correlated very strongly (r less than 0.883) with the differences in ST-segment depression. We conclude that precordial R-wave amplitude significantly influences the magnitude of ST-segment depression.
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PMID:The influence of R-wave amplitude on the degree of ST-segment depression in exercise electrocardiography in the individual patient. 381 19

We initiated a retrospective study to determine whether ST segment depression seen in inferior leads (II, III, and aVF) during acute anterior myocardial infarction (MI) is a reciprocal change or an independent sign of ischemia of additional myocardium. We selected 20 patients with anterior MI and attempted to compare findings of subsequent cardiac catheterization and the clinical course of 14 patients with ST segment depression (group A) and six without ST segment depression (group B). Patients in group A had a higher prevalence of right coronary artery disease (13 vs 0, P less than .01), multivessel disease (14 vs two, P less than .01), inferior wall motion abnormalities (seven vs 0, P less than .01), and ejection fraction of less than .50 (ten vs two, P greater than .05) than those in group B. A greater number of patients in group A had serious in-hospital and follow-up complications (12 vs two, P less than .05). We conclude that ST depression in leads II, III and aVF during acute anterior MI is not "reciprocal change" but a high-risk indicator.
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PMID:ST segment depression in acute anterior myocardial infarction. 400 99

In a consecutive series of 56 patients with acute myocardial infarction, ST segment depression and elevation in the electrocardiographic limb leads I, II, and III were summated for each patient before and immediately after intracoronary streptokinase infusion and the results compared with the angiographic findings. Forty three patients had angiographically confirmed reperfusion of an initially occluded vessel and showed a significant decrease in summated ST shift. The ST segment changes in the limb leads virtually returned to normal in all 43 patients, and in most, inverted T waves developed. Thrombolysis was unsuccessful in 10 patients, and the infarct related coronary artery was already patent in three. When these two groups are combined, all 13 patients without reperfusion showed no significant change in summated ST segment shift. During percutaneous transluminal angioplasty inflation of the balloon in the vessel that was previously occluded simulated reocclusion and was followed by new ST elevation if the artery supplied viable myocardium. In a further consecutive study of 54 patients with anterior myocardial infarction, the precordial R waves and Q waves were studied over the four to six months following infarction using a standardised 48 electrode mapping system. All patients underwent a repeat angiogram after four to six months. In 36 patients the infarct related vessel was patent. They showed a significant mean increase in summated precordial R wave amplitude and a reduction in the mean number of precordial leads without R waves. In 18 patients with unsuccessful thrombolysis or reocclusion there was a further reduction in mean summated R wave amplitude and an increased number of precordial leads not showing R waves. Precordial R wave mapping seems to be a valuable non-invasive method of assessing the salvage of myocardium after reperfusion and the damage caused by reocclusion. Loss of R waves in the acute phase of myocardial infarction does not necessarily mean an irreversibly damaged myocardium.
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PMID:Myocardial infarction and thrombolysis. Electrocardiographic short term and long term results using precordial mapping. 401 17

The purpose of this study was to evaluate the detectability of stress-induced ischemic lesion in patients with previous myocardial infarction using single photon emission computed tomography (SPECT) producing thallium-201 (T1-201) myocardial perfusion imagings (MPI). Seventy patients underwent stress SPECT by symptom-limited graded bicycle ergometer exercise using a dual-headed rotating gamma camera (Toshiba GCA70A) equipped with a computer system (GMS90). After intravenous administration of 2.5 mCi of T1-201, stress SPECT data at 10 minutes and delayed SPECT data at 3 hours after the injection were collected in the 64 X 64 matrix form covering 360 degrees directions by camera sweep of 180 degrees in 6 minutes, which were immediately followed by conventional planar imagings (PL). Transaxial tomographic image reconstruction was performed by convolution method using a Shepp-Logan's filter. Thereafter, sagittal and coronal tomographic images were reconstructed for about 2 minutes. Image interpretation was assessed visually. The results were as follows: Sensitivity and specificity in detecting the affected vessel with more than 75% stenosis by segmental analysis of myocardial images were higher by SPECT than by PL (LAD 89% and 65%, LCX 68% and 56%, RCA 89% and 76% in sensitivity and LAD 94% and LCX 75%, 92% and 94%, RCA 81% and 59% in specificity, respectively). Sensitivity in detecting both single (82%) and multivessel disease (76%) was fairly high. Detectability of stress-induced ischemia (i.e. occurrence of a new defect in patients with previous myocardial infarction and ST-segment depression in ECG) was significantly higher in SPECT (67%) than in PL (39%, p less than 0.005) and in ECG (39%, p less than 0.005). A perfusion defect in the extensive anterior wall, marked left ventricular dilatation and the widening of the angle toward the apex composed of septal and anterolateral walls in transaxial images were the findings characteristic of anterior myocardial infarction with severe dyskinesis. We conclude that stress SPECT is a useful noninvasive technique for the documentation of the number of vessels affected and severe wall motion abnormality of the LV and for the detection of stress-induced ischemia in previous myocardial infarction.
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PMID:[Detectability of stress-induced ischemic lesion in previous myocardial infarction using 201T1 myocardial single photon emission computed tomography]. 633 58

This study was performed to determine whether inferior ST segment depression during early stages of acute transmural anterior myocardial infarction identifies patients with multivessel coronary artery disease and additional inferior ischemia. Coronary and left ventricular angiography were performed within 3.4 months in 33 patients with acute transmural anterior infarction. Initial electrocardiograms, 2 to 5 hours after onset of chest pain, revealed significant ST segment depression (greater than or equal to 0.1 mV) in at least two of leads II, III and a VF in 15 patients (45%) (group B); in 18 patients (group A) this finding was absent. Compared with group A, patients in group B had greater anterior ST elevation (1.2 versus 0.7 mV, p less than 0.025); higher serum peak creatine kinase (2,475 versus 1,147 IU/liter, p less than 0.005); higher Killip scores (2.1 versus 1.3, p less than 0.001); more in-hospital complications (60 versus 17%, p less than 0.05); lower mean left ventricular ejection fraction (34 versus 55%, p less than 0.001); more frequent regional left ventricular dysfunction in anterolateral (91 versus 44%, p less than 0.05), posterolateral (36 versus 0%, p less than 0.05) and inferior (100 versus 6%, p less than 0.005) regions; greater wall motion abnormality scores (10.0 versus 5.5, p less than 0.005); higher frequency of concomitant left circumflex or right coronary artery disease, or both (80 versus 28%, p less than 0.01); more frequent postinfarction angina (100 versus 39%, p less than 0.001) and lower New York Heart Association functional classification scores (1.7 versus 2.4, p less than 0.05) at 6 month follow-up. The time course of inferior ST depression differed from that of anterior ST elevation. Thus, inferior ST depression was maximal in the first 48 hours and decreased (p less than 0.05) thereafter. In contrast, ST elevation in leads V1 to V6 and I appeared to decrease (p = NS) between days 4 and 7. However, inferior ST depression "mirrored" ST elevation in lead aVL, which also decreased (p less than 0.05) after 48 hours. Thus, inferior ST depression during anterior infarction is associated with more extensive infarction, greater morbidity and higher frequency of multivessel coronary disease. Such inferior ST depression might reflect not only "reciprocal change," but also ischemia in adjacent lateral and remote inferior regions.
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PMID:Inferior ST segment depression during acute anterior myocardial infarction: clinical and angiographic correlations. 647 Mar 25

A retrospective study was conducted on 488 patients admitted in our rehabilitation center after a recent acute myocardial infarction. Purpose of the study was to assess the incidence and prognostic value of exertional hypotension in these patients. Of 488 patients admitted to the study 33 (6%) were found to have exertional hypotension; 14 patients had an inferior myocardial infarction, 18 patients had an anterior myocardial infarction, 3 patients had a history of previous myocardial infarction. In the follow-up period (28.3 +/- 13.2 months) the worse prognosis (death or pulmonary oedema) was associated with the presence during exercise of hypotension, ST segment elevation in leads were Q waves were present and no ST depression in other leads. In conclusion, recent anterior myocardial infarctions associated with hypotension and ST segment elevation during exercise appear to be at risk for future cardiac events.
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PMID:Exertional hypotension after myocardial infarction. 650 Feb 24


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