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 order to evaluate electrocardiographic changes in the diagnosis of the artery responsible for inferior myocardial infarction, a prospective study was performed on inferior and V2 ST segment deviation and its correlation using the arithmetic sum: II + V2, III + V2, and aVF + V2. A group of 66 patients with inferior acute myocardial infarction (AMI) was studied. A standard 12-leads electrocardiogram was performed within six hours of the onset of chest pain. Coronary arteriography was performed on each of the patients between one and twelve weeks after infarction. Right coronary artery (RCA) lesion was found in 46 patients, 27 at a proximal level and 19 at a distal level; in 20 patients the left circumflex coronary artery was affected. The isolated value of the magnitude of the inferior ST segment is not an efficient parameter for identifying the artery responsible for inferior AMI. In lead V2 all the patients with a lesion of the left circumflex artery showed ST segment depression > or = 1 mm (P < 0.001) and all those presenting ST segment elevation had stenosis of the proximal RCA. The most useful parameters for identifying the artery responsible for inferior AMI, with 100% specificity are: (1) for occlusion of the RCA, the arithmetic sum of ST segments: aVF + V2 > 0, with 86.9% sensitivity (P < 0.001); (2) for occlusion of the left circumflex artery III + V2 < 0, with 90% sensitivity (P < 0.001); and (3) for proximal occlusion of the RCA: aVF + V2 > or = 1, with 96.2% sensitivity (P < 0.001). No specific marker was observed for distal occlusion of the RCA. The value of the arithmetic sum of the ST segment: III + V2 between 0 and 0.9 was the most significant, with 94.7% sensitivity and 95.7% specificity (P < 0.001).
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PMID:Diagnostic value of the arithmetic sum of the ST segment of inferior and V2 leads, II + V2, III + V2 and aVF + V2 in identifying the artery responsible for inferior acute myocardial infarction. 748 9

Multivessel disease and decreased left ventricular ejection fraction (LVEF) are believed to be significant predictors of the outcome in patients with acute inferior myocardial infarction (AIMI). We attempted to determine new electrocardiographic (ECG) markers for detecting concomitant left anterior descending (LAD) disease and/or decreased left ventricular function in patients with AIMI. Eighty patients with AIMI were evaluated within 6 h of the onset of symptoms and grouped according to the presence (Group 1) or absence (Group 2) of concomitant LAD disease. All of the patients underwent coronary angiography and left ventriculography 4-6 weeks from the onset of their infarction. We studied the validity of two new ECG markers: S-T depression deeper in lead V5 than in V4 (S-T decreases V5 > V4) and negative U waves (NUs) > 0.5 mm (50 muV) in leads V4-6. The sensitivity and specificity of S-T decreases V5 > V4, NUs in V4-6, or both, in detecting concomitant LAD disease were 56% and 83%, 59% and 87%, and 35% and 98%, respectively. LAD lesions in patients who showed either of these new markers (74% of those with S-T decreases V5 > V4 and 80% of those with NUs in V4-6) were mostly in the proximal segments (AHA segments #6 or #7). Patients with either S-T decreases V5 > V4 or NUs in V4-6 tended to have asynergy in the anterolateral segment, while there was a strong correlation between the asynergy of the anterolateral and septal segments in patients who showed both ECG markers.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:New markers of remote ischemia in patients with evolving inferior myocardial infarction. 759 24

The significance of anterior ST segment depression (V1-V4) at the time of acute inferior myocardial infarction and exercise-induced anterior ST segment depression were studied in 30 patients. All patients carried out: two-dimensional echocardiography in the acute phase of myocardial infarction (Echo 1) and at predischarge (Echo 2); symptom-limited exercise test; coronary arteriography. According to ST segment changes, patients were divided into Group A (n = 15) with exercise-induced anterior ST segment depression and Group B (n = 15) with no ST segment depression during exercise. Group A showed a lower work physical capacity than Group B (6.8 +/- 3 METS and 9 +/- 2 METS, respectively). The wall motion index in Group A was 0.26 +/- 0.14 in the Echo 1 and 0.22 +/- 0.18 in the Echo 2 showing an improvement in wall motion abnormality; in Group B the same index was 0.35 +/- 0.19 in the Echo 1 and 0.34 +/- 0.18 in the Echo 2. Group A patients had a higher prevalence of multivessel disease compared with Group B patients and the right coronary artery was always involved. In conclusion, in inferior myocardial infarction the anterior ST segment depression, both in the acute phase and during the predischarge exercise test, reflects more extensive coronary disease and jeopardized myocardium.
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PMID:[Anterior ST segment depression in acute inferior myocardial infarct: significance of its reproducibility during early ergometric test]. 788 91

Fifty-eight of 220 consecutive patients had exercise-induced ST depression in some or all precordial leads 3 to 12 months after a first inferior myocardial infarction. All 58 patients underwent thallium-201 exercise testing, 2-dimensional echocardiography and coronary angiography. ST depression was confined to leads V1-4 in 22 patients (group A); thallium-201 exercise testing showed reversible anterior perfusion defects and left anterior descending coronary artery disease in 11 of the 22 patients (50%). None of the other 11 with negative thallium-201 exercise test results had significant left anterior descending narrowing, and the anterior ST depression could be explained by asynergy of the posterior wall found on 2-dimensional echocardiography in 10. ST depression appeared in leads V5-6 in 22 patients (group B); reversible anterior perfusion defects and left anterior descending disease was demonstrated in 18 patients (82%). In the other 4 patients posterior wall asynergy was demonstrated. ST depression was seen from leads V1-6 in 14 patients (group C); reversible anterior perfusion defects were seen in 6 patients (43%), 5 of whom had significant left anterior descending disease. Among the other 8 patients without reversible anterior perfusion defects, posterior wall asynergy was found in 6.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Correlation of exercise-induced ST depression in precordial electrocardiographic leads after inferior wall acute myocardial infarction with thallium-201 stress scintigraphy, coronary angiography and two-dimensional echocardiography. 785 47

To determine the cause of precordial ST depression in acute inferior myocardial infarction, we evaluated the relationship between precordial ST deviation and ventricular involvement. Forty-nine patients who were admitted to the hospital with an acute inferior myocardial infarction, and 60 patients who were treated with elective angioplasty to the right coronary artery, were analyzed. All patients had single vessel disease and were divided into 2 groups (A and B) according to the site of the lesion. Patients in group A had a lesion proximal to the largest right ventricular branch, while in group B the lesion was distal to that branch. There were no differences in inferior ST elevation between the 2 groups, but precordial ST segments were more depressed in group B than in group A. A significant correlation was observed between inferior and precordial ST deviation in group B, but not in group A. These results were similar in patients with myocardial infarction and in those treated by angioplasty. These results suggest that precordial ST depression in an evolving inferior infarction is due to reciprocal ST deviation which reflects inferoposterior involvement. In addition, when inferior infarction is accompanied by right ventricular involvement the precordial ST depression is lessened.
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PMID:Influence of right ventricular ischemia on precordial ST depression during right coronary artery occlusion. 835 98

In the submitted study the authors evaluate the relationship of the clinical course in patients with inferior myocardial infarction (AIM) in relation to the electrocardiographic (ECG) finding in standard and dextro-lateral leads. In a group of 96 patients (mean age 65 +/- 10 years, 66 men and 30 women) according to the ECG 38 had an isolated inferior AIM (group 1), 28 had signs of extension of the inferior AIM to the posterior wall of the left ventricle (group 2) and 30 patients in group 3 had an extension of the inferior AIM to the right ventricle, i.e. an infarction of the right ventricle. All three groups differed significantly as regards the extent of the AIM according to creatine kinase values (7.1 +/- 4.4 and 18.2 +/- 7.2 resp. and 24.8 +/- 11.6 resp.), as regards mortality (0 and 14% and 37% resp.). In group 2, contrary to the other groups, the significantly most frequent complication was pulmonary oedema (36%) and ventricular tachycardia (30%) and in group 3 the significantly most frequent complication was cardiogenic shock (30%) and advanced atrioventricular block (50%). The cause of death in these patients with infarctions of the right ventricle was cardiogenic shock (n = 6), cardiac rupture (n = 3) and electromechanical dissociation (n = 2). A total of 29 (30%) patients with inferior AIM were treated by temporary pacing: in group 1 21%, in group 2 14% and in group 3 57%. The prognosis of these patients was favourable in groups 1 and 2 (1 of 12 patients died) while in group 3 with infarctions of the right ventricle 9 of 17 patients died (p < or = 0.001). The authors found moreover that patients with precordial depression of the ST segment and inferior AIM have, as compared with patients without this depression, significantly higher creatine kinase values (12.5 +/- 5.5 vs. 5.2 +/- 1.3 mu kat; p < or = 0.001) and a higher general incidence of complications. Patients with inferior AIM are thus a non-homogeneous group from which we can differentiate, based on standard ECG examination and by recording right-sided thoracic leads, patients with an increased risk and start specific treatment in time.
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PMID:[Clinical picture of various types of inferior myocardial infarcts. Clinico-electrocardiographic study]. 837 61

In a substantial percentage of patients with acute myocardial infarction, especially in those with inferior wall involvement, no ST elevation is detected on the electrocardiogram. In many of them, ST depression is found in leads oriented to remote segments of the heart. The importance of those reciprocal changes for early diagnosis of acute inferior myocardial infarction in patients without ST elevation has not been stressed. In order to find the prevalence of reciprocal ST depression, we evaluated the admission electrocardiograms of 107 consecutive patients with evolving first acute inferior myocardial infarction. Ninety-three patients had ST elevation of at least 0.1 mV in at least one of the inferior leads: II, III or aVF (group A) and in 14 patients ST displacement did not reach 0.1 mV in any of these leads (group B). In both groups, reciprocal ST depression occurred more frequently in aVL than in any other lead. Only three patients had no ST depression in aVL. In eight patients (7.5%) ST depression in aVL was the sole early electrocardiographic sign of the inferior infarction. aVL is the only lead that is facing the superior part of the left ventricle and thus is the only lead that is truly opponent to the inferior wall. It seems that ST depression in aVL, by contrast to that in the precordial leads, is found in the majority of patients with evolving inferior wall myocardial infarction and is not influenced by extension of the infarction to the right ventricle or to the posterior wall.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:ST segment depression in a VL: a sensitive marker for acute inferior myocardial infarction. 843 89

To examine the diagnostic significance of precordial ST segment depression in Q wave inferior myocardial infarction, 157 consecutive patients were examined carefully by means of auscultation, ECG, and two-dimensional echocardiography. Precordial ST segment depression was transient (lasting < 72 hours from the onset of myocardial infarction) in 63 patients and persistent (> or = 72 hours) in 40. Twenty-eight patients with persistent, 19 patients with transient, and 14 patients without precordial ST segment depression had advanced asynergy (akinesia or dyskinesia) in the posterior segments, whereas 13 patients with persistent, six with transient, and six without precordial ST segment depression had pericardial rub. Patients with persistent precordial ST segment depression had a significantly higher incidence of severe wall motion abnormality (p < 0.01) and inflammation (p < 0.05) of the posterior wall than the other two groups. In 5 of 40 patients with persistent ST segment depression, pericardial rub was detected in the absence of advanced asynergy in the posterior segments. Although not highly sensitive, persistent precordial ST segment depression appeared to be a fairly specific indicator (specificity 92%) of concomitant posterior involvement with severe wall motion abnormality, inflammation, or both.
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PMID:Precordial ST segment depression in patients with Q wave inferior myocardial infarction: role of infarction-associated pericarditis. 843 95

Coronary spasm was observed in two sisters. Neither of them had significant atheromatous stenosis in the coronary arteries. The 41-year-old elder sister presented with resting morning angina. The stress electrocardiogram showed marked depression of the ST-segment in precordial leads. Diffuse vasospasm in the left anterior descending artery was induced by the intracoronary administration of acetylcholine. The 38-year-old younger sister suffered from acute inferior myocardial infarction after taking methylergonovine following an abortion. Emergent coronary angiography disclosed a thrombus in the proximal right coronary artery which was dissolved with intracoronary administration of urokinase. There was no residual stenosis in the culprit vessel. Although the sisters do have risk factors for coronary spasm, an inherited factor may contribute to the mechanism of the spasm.
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PMID:Coronary spasm in two sisters. 851 Mar 17

To determine the role of the sinus node artery and the clinical course in postmyocardial infarction sinus node dysfunction, 27 patients with acute inferior myocardial infarction and single-vessel coronary artery disease were studied. In 13 patients (group 1) the infarct-related coronary artery was occluded proximally and in 14 (group 2) distally to the site of origin of the sinus node artery. At electrophysiology, performed 10 +/- 3 days from the acute event, basal and intrinsic heart rate were lower in group 1 compared to group 2 patients (54 +/- 4.8 vs. 69 +/- 7 beats/min, p = 0.001, and 66 +/- 7 vs. 76 +/- 8 beats/min, p = 0.006, respectively) while basal and intrinsic corrected sinus node recovery times were prolonged in group 1 compared to group 2 patients (585 +/- 49.3 vs. 324 +/- 61.3 ms, p = 0.0001, and 601 +/- 39.1 vs. 335 +/- 73 ms, p = 0.0001). During a 6-month follow-up no episodes of dizziness, syncope or angina were reported. Moreover, at the end of follow-up resting heart rate (70 +/- 11 vs. 73 +/- 7 beats/min, nonsignificant), maximal exercise heart rate (166 +/- 19 vs. 170 +/- 23 beats/min, nonsignificant), and exercise time (491 +/- 120 vs. 480 +/- 155 s, nonsignificant) were similar between the two groups and no exercise-induced ischemic ST segment depression was observed. Sinus node dysfunction in patients with inferior myocardial infarction and one-vessel disease is related to the occlusion of the infarct-related coronary artery proximal to the site of origin of the sinus node artery and is not associated with increased cardiovascular morbidity in the first 6 months from the acute event.
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PMID:Sinus node dysfunction in acute inferior myocardial infarction. Role of sinus node artery and clinical course in patients with one-vessel coronary artery disease. 909 18


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