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)

ST elevation in right chest leads during evolving inferior myocardial infarction indicates right ventricular involvement. Theoretically, such changes may be due to reversible or irreversible myocardial ischemia. Whether similar ST elevations can be recorded in patients with myocardial ischemia without infarction is unknown. To clarify this, right chest leads V3R to V7R were recorded during percutaneous transluminal coronary angioplasty in 43 patients who had a total of 45 arteries dilated. Balloon occlusion of the right coronary artery caused transient ST elevation, whereas closure of the left anterior descending coronary artery or the left circumflex artery was associated with transient ST depression. These findings were 100% discriminative in leads V5R and V6R. Furthermore, ST elevation greater than or equal to 1 mm in one or more of leads V4R to V7R was seen only when the right coronary artery was occluded. Thus transient myocardial ischemia without infarction may cause ST elevation in the right chest leads and ST elevation greater than or equal to 1 mm in one or more leads V4R to V7R is seen exclusively with occlusion of the right coronary artery.
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PMID:ST deviation in right chest leads V3R to V7R during percutaneous transluminal coronary angioplasty. 230 94

The electrocardiogram is the graphic representation against time of the difference in potential between points of the body caused by the current field of the heart. To examine the origin of this current field, a method of transforming body surface electrocardiographic data to the epicardial surface has been developed. The computed epicardial current density distributions in 219 patients with acute inferior myocardial infarction showed that, in 89% of patients, the current flow out of the heart during the ST segment came from two regions, not only from the infarction region but also from a region over the great vessels. This findings suggests that current flows from the ischemic region, through the low-resistance pathway provided by the intracavity blood, out the great vessels, and back to the epicardium. A similar pathway has been hypothesized when ischemia caused endocardial ST elevation, such as during a stress test or with unstable angina. To test this hypothesis, a group of patients with ST depression on the 12-lead electrocardiogram, not associated with ST elevation, was examined with body surface mapping. Ninety-four percent of patients had epicardial current density distributions that showed a region of current flow out of the heart and over the great vessels that was consistent with this hypothesis. This could explain the poor localization of coronary artery disease by electrocardiographic techniques when there is ST depression on the body surface.
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PMID:Importance of the great vessels in the genesis of the electrocardiogram. 186 Jan 91

Exercise electrocardiography with or without thallium-201 scintigraphy was performed (pre-hospital discharge) in 66 asymptomatic survivors of a first inferior myocardial infarction (IMI). Although coronary angiography revealed an 82% incidence of multivessel coronary artery disease (MV-CAD) in the total cohort, the sensitivity of exercise ECG for MV-CAD in the group with absent anterior ST-depression in the acute phase was low (11%). In contrast the presence of acute phase anterior ST-segment depression improved the yield for MV-CAD to 55%. Forty-six patients agreed to a symptom-limited exercise ECG plus/minus thallium imaging at 8-10 weeks post IMI. The sensitivity of detecting MV-CAD improved by 15% in patients with no acute phase anterior ST-segment depression and 16% in patients with acute phase anterior ST-segment depression. At each exercise protocol, thallium improved the sensitivity of exercise in detecting ischemia in the noninfarct zone. It is concluded that following IMI, a high percentage of asymptomatic patients whose acute phase ECG showed anterior ST-segment depression will have MV-CAD detected by heart-rate limited and, more so, by symptom-limited exercise ECG. The detection rate will double in patients with no anterior ST-segment depression if exercise testing is delayed until 8-10 weeks post IMI.
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PMID:Timing of stress testing in an asymptomatic survivor of inferior myocardial infarction. 233 45

To investigate the clinical significance of exercise-induced ST changes, we performed exercise body surface mapping (87 leads) in 52 patients (one-vessel disease [1 VD] n = 12, multivessel disease [MVD] n = 40) with previous inferior myocardial infarction (MI). ST isointegral maps were constructed and the locations of ST changes were compared with the findings of exercise thallium-201 (TI-201) myocardial scanning. Exercise-induced ST elevation was observed in 14 patients (27%) on the lower chest and on the back, corresponding to the infarcted area. Exercise-induced ST depression was observed more frequently in the MVD group (n = 30, 75%) than in the 1VD group (n = 2, 17%). Seventeen (77%) of 22 patients with ST depression had thallium-201 redistribution. There was a significant association between ST depression and TI-201 redistribution (chi2 = 13.1, p less than 0.001), but no association between ST depression and ST elevation. The body surface distribution of ST depression was shifted upward and rightward compared with its appearance in angina pectoris without MI. These findings suggest that exercise-induced ST depression reflects myocardial ischemia in patients with previous inferior MI.
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PMID:The clinical significance of exercise-induced ST segment changes in patients with previous inferior myocardial infarction. 238 91

In order to evaluate the incidence and prognostic significance of anterior precordial ST segment depression (decreases ST) in acute inferior myocardial infarction (MI), 158 patients with inferior MI were selected. In 90 patients (56.9%) an anterior decreases ST was associated with inferior lesion wave (group A), and in 68 patients (43.1%) only an ecg pattern of inferior myocardial infarction (group B) was present. No significant statistical differences were observed in mortality (group A 10% vs group B 10.2%), in compliances (group A 54.4% vs group B 47.0%) and in higher peak serum ck-levels (group A 83.3% vs group B 69.1%) in two groups during hospitalization period. In conclusion the anterior decreases ST during inferior MI should not be considered a negative prognostic sign. These favourable results are probably related to stringent criteria for ecg diagnosis of inferior myocardial infarction used and to exclusion of all patients with non contemporary evolution of anterior decreases ST and inferior lesion wave.
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PMID:[Incidence and prognostic significance of anterior precordial ST segment depression in acute inferior myocardial infarct]. 260 72

To determine whether precordial ST segment depression during acute inferior myocardial infarction indicates posterolateral wall ischemia, anatomical predominance of coronary circulation was examined by coronary angiography and evaluated in 43 patients who experienced first acute inferior myocardial infarction. Among patients who underwent intracoronary thrombolysis within six hours from the onset of symptoms, the infarct-related artery was the right coronary artery (RCA) in 35. In addition, their early 12-lead electrocardiographic features were compared with those in eight patients having the infarct-related left circumflex coronary artery (group Cx). Thirty-five patients with RCA obstruction were categorized in four groups: Four patients with left predominant type (group L), 10 with balanced type (group B), five with right super-predominant type (group SR), and 16 with right intermediate type (group RI). Seventeen of the 21 patients in groups SR and RI demonstrated precordial ST segment depression, whereas it was present in only six of the 14 patients in groups L and B (p less than 0.05). Of the 29 patients in groups SR, Cx and RI, total ST segment depression in leads V1 through V4 (sigma ST) was greater in the 14 patients in groups L and B (p less than 0.05) than in other groups. Furthermore, in these 29, all patients in groups SR and Cx had greater sigma ST than did the patients in group RI (p less than 0.05). There was no significant difference in sigma ST between groups SR and Cx. Precordial ST segment depression did not correlate with concomitant disease of the left anterior descending artery and was not a mirror image of ST segment elevation in inferior leads. On thallium-201 scintigraphy, additional perfusion defects of the posterolateral wall were present in all eight patients in group Cx and in ten of the 21 patients in groups SR and RI. Thus, precordial ST segment depression during acute inferior myocardial infarction seemed to be affected by the pattern of coronary circulation. It was concluded that this ST depression represents more extensive involvement of the posterolateral wall in patients with right predominant coronary circulation as well as in those with left circumflex artery obstruction.
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PMID:[Precordial ST segment depression in acute inferior myocardial infarction: the importance of posterolateral wall infarction]. 263 23

Thirty-three patients with acute inferior myocardial infarction (MI), who were treated with intravenous streptokinase, were studied by serial 12-lead ECGs for 48 hours to determine the relationship between early changes in the sum of elevations above the baseline 40 ms after the end of the QRS complex in leads II, III and AFV (SumST), the sum of amplitude of R waves in leads II, III and AVF, the sum of the Q waves in leads II, III and AVF, the sum of ST-segment depression in leads V1-V4 as measured from the baseline to 80 ms after the J point (SumST (V1-V4] and the patency of the infarct-related artery at angiography after MI. Patients with patent arteries had a faster rate of decline in the SumST during the first 2.5 hours; reached the steady state earlier; had a more pronounced decrease in the SumST at 1.25 hours; a larger percentage drop in SumR at 4.5 hours and a more pronounced SumST (V1-V4) early on but resolution times similar to that of patients with closed arteries. Several ECG indices may indicate reperfusion of the infarct-related artery in patients with inferior MI.
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PMID:Quantitative ECG changes and patency of infarct-related arteries after intravenous streptokinase. 271 68

It was hypothesized that in acute inferior wall myocardial infarction, an additional ischemic area in the subendocardium of the noninfarcting territory would produce a selective current dipole between the infarcting and ischemic regions. A resistance network model to calculate epicardial potentials from body surface electrocardiographic potentials was developed and used to examine the hypothesis in 219 patients with acute inferior myocardial infarction. In the learning set of 110 patients, two characteristic dipole patterns were observed, each associated with a high mortality rate in the ensuing 15 months when compared with that in the remaining patients. In the test set of 109 patients, a double-blind analysis of the patterns showed that the 34 patients with a dipole pattern had a collective mortality rate of 35% at 15 months compared with a 15 month rate of 5% in the remaining patients. In the total group of 219 patients, the magnitude of ST segment elevation and both the magnitude and integral of the area voltage of ST depression on the epicardium were significantly correlated with the mortality rate (p less than 0.0002 for all variables against death at 15 months). This study strongly suggests that ST depression due to ischemia can be differentiated from ST depression secondary to the ST elevation in acute inferior infarction by the examination of epicardial potential distributions.
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PMID:Derived epicardial potentials differentiate ischemic ST depression from ST depression secondary to ST elevation in acute inferior myocardial infarction in humans. 276 19

We investigated the mechanisms of exercise-induced precordial ST depression in prior inferior myocardial infarction in single vessel disease, and attempted to differentiate ST depression in single vessel from multivessel disease. Subjects were categorized as; Group I (n = 18), with inferior myocardial infarction and single vessel disease without (n = 11; Ia) and with (n = 7; Ib) exercise-induced precordial ST depression and group II (n = 10), inferior myocardial infarction with multivessel disease. The subjects were examined using 12-lead exercise ECG, stress T1-201 myocardial imaging and stress radionuclide ventriculography. Compared to group Ia, exercise-induced precordial ST depression in group Ib was associated with extensive infarction extending into the inferoseptal left ventricular wall by T1-201 myocardial imaging. Worsening of septal wall motion was also more frequently observed on stress radionuclide ventriculography. For detecting multivessel disease in prior inferior myocardial infarction, exercise ECG and radionuclide ventriculography had poor specificity and predictive value compared to stress T1-201 myocardial imaging. We conclude that exercise-induced precordial ST depression observed in patients with prior inferior myocardial infarction due to single vessel disease reflects a peri-infarction ischemia in the inferoseptal wall of the left ventricle. Great caution is necessary when predicting multivessel disease in prior inferior myocardial infarction using exercise ECG. Stress T1-201 myocardial imaging is the most accurate diagnostic means for this purpose.
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PMID:[Exercise-induced precordial ST depression in patients with prior inferior myocardial infarction with single vessel disease]. 281 51

Somatostatin (SRIF) (6 nmol) given intracisternally (i.c.) into the alpha-chloralose anaesthetized rat has recently been shown to cause apnoea with a latency of 5-10 minutes (Kalia et al. 1984a). The apnoea produced by SRIF is very rapid, irreversible and leads to the death of the animal. In view of the existence of SRIF nerve cell bodies and terminals in medullary respiratory nuclei such as the ventral and ventrolateral subnuclei of the nucleus of the tractus solitarius (nTS) (Kalia et al. 1984b, Johanson et al. 1984), we have proposed the existence of somatostatinergic mechanisms in the respiratory nuclei of the medulla oblongata involved in mediating apnoeic conditions (Kalia et al. 1984a). In the present study, we have analysed whether the SRIF induced apnoea could be counteracted by a previous i.c. administration of the highly selective alpha 2-adreno-receptor blocking agent RX 781094 (2-(2-(I,4 benzodioxanyl]2-imi-dazoline HCl) (Doxey et al. 1983), or an opiate receptor blocking agent such as naloxone. Thus, both alpha 2-adrenoreceptor agonists and opiates induce respiratory depression, and opiates in high doses cause apnoea (Bolme et al. 1974, Hassen et al. 1982, Sitsen et al. 1982). In addition, catecholamine (CA) and enkephalin immuno-reactive nerve terminal networks exist in high densities within the nucleus tractus solitarius (nTS) of the medulla oblongata and may therefore interact with somatostatin nerve terminals in regulation of respiratory activity (Kalia et al. 1984b).
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PMID:Somatostatin induced apnoea: prevention by central and peripheral administration of the opiate receptor blocking agent naloxone. 286 86


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