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 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The baroreceptor-heart rate reflex in human is impaired 2 days after a myocardial infarction but it improves 10 days after the acute coronary event. This study investigated whether (1) the baroreceptor-heart rate reflex improvement takes the reflex back to normal, and (2) the cardiopulmonary reflex is affected by myocardial infarction. In subjects studied 8 to 11 days after a transmural anterior or inferior myocardial infarction the baroreceptor-heart rate reflex sensitivity (slope of the linear regression between negative neck chamber pressures and lengthenings in RR interval) was similar to that seen in control subjects (-6.2 +/- 0.8 vs -6.0 +/- 0.6 ms/mm Hg, mean +/- SEM) and did not change when reassessed 10 days later. In contrast, the cardiopulmonary reflex sensitivity (changes in forearm vascular resistance induced by changing central venous pressure through nonhypotensive lower body suction and leg raising) was markedly less in subjects studied 8 to 11 days after myocardial infarction than in control subjects; the reduction amounted to 58.1 +/- 8% (p less than 0.01). The cardiopulmonary reflex sensitivity greatly improved when reassessed 28 to 45 days later. Thus, the baroreflex is normal about 10 days after myocardial infarction. This condition markedly impairs the cardiopulmonary reflex, but the impairment is also transient.
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PMID:Cardiopulmonary receptor and arterial baroreceptor reflexes after acute myocardial infarction. 155 15

To determine the possible role of atrial natriuretic factor in right ventricular infarction, serial measurements of this hormone were performed in 21 patients with acute inferior myocardial infarction. All patients underwent enzymatic, electrocardiographic, echocardiographic and coronary arteriographic studies. Ten patients also had right heart hemodynamic measurements. Eight patients had evidence of an associated right ventricular infarction (Group I) and 13 patients did not (Group II). Enzymatically estimated infarct size, presence of left heart failure and arrhythmias were similar in both groups. Mean arterial pressure in Group I (72.1 +/- 4.4 mm Hg) was significantly lower (p = 0.02) than in Group II (89.5 +/- 4.6 mm Hg). Seven (88%) of the eight patients in Group I had elevated right atrial pressures and a higher incidence than Group II of prolonged hypotension (75%) and right ventricular dysfunction (75%) clinically and by echocardiography. Plasma atrial natriuretic factor levels (mean values +/- SEM in pg/ml) for days 1, 2, 3 and 7 after infarction were, respectively: 152 +/- 30, 165 +/- 48, 199 +/- 27 and 189 +/- 31 for Group I versus 55 +/- 9, 55 +/- 11, 61 +/- 13 and 77 +/- 20 for Group II. The difference between groups was significant for days 1 (p less than 0.05), 3 and 7 (p less than 0.01) and not significant for day 2 (p = 0.07). These findings show that atrial natriuretic factor elevation is part of the neurohumoral response to right ventricular infarction and are consistent with the hypothesis that atrial natriuretic factor may play a pathophysiologic role in the right ventricular infarct syndrome.
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PMID:Atrial natriuretic factor in patients with right ventricular infarction. 213 77

Reentrant ventricular tachycardia is dependent on an area of myofibers, embedded in scar tissue, which exhibit slow conduction. Late potentials recorded by signal-averaged electrocardiography appear to correspond to these zones of slow conduction and frequently are present in patients with VT. We hypothesized that elimination of inducible VT by catheter-mediated ablation of critical areas of slow conduction would alter late potentials. Four patients underwent catheter ablation in which radiofrequency current was delivered to zones of slow conduction exhibiting isolated mid-diastolic potentials that could not be dissociated from the tachycardia. The four patients had developed VT (cycle length 382 +/- 50 msec; mean +/- SEM) 13-180 months after inferior myocardial infarction. Late potentials were present in each patient before catheter ablation was attempted. Although VT was not inducible in any patient immediately after ablation, late potentials were still present in all four patients and there was no significant difference in the QRS duration (136.5 +/- 4.0 msec postablation; 135.7 +/- 4.5 msec preablation), root mean square voltage in the terminal 40 msec of the QRS (10.0 +/- 1.0 microV postablation; 5.9 +/- 0.4 microV preablation), or in the duration of the low amplitude signal (69.2 +/- 2.0 msec postablation; 62.7 +/- 3.4 msec preablation). At follow-up electrophysiology study performed 14 +/- 7 days after ablation, one of the four patients had inducible VT. In conclusion, late potentials persist even after successful radiofrequency catheter ablation and do not appear to be useful for predicting results of follow-up electrophysiology study.
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PMID:Late potentials are unaffected by radiofrequency catheter ablation in patients with ventricular tachycardia. 751

Ninety one consecutive survivors of a first acute myocardial infarction (MI) were studied prior to hospital discharge, in order to observe the relationship of signal-averaged electrocardiography (SAECG) to thrombolytic therapy, site of infarction and left ventricular function. Sixty six patients received thrombolytic agents and the remaining had conventional therapy. The overall incidence of abnormal SAECG was 27 percent and 16 percent with high-pass 40 Hz and 25 Hz filters respectively. The SAECG (40Hz) was abnormal in 12 of 25 patients (48%) who did not receive thrombolytic therapy and in 13 of 66 (20%) who were thrombolysed (p < 0.01). When patients were classified according to the site of myocardial infarction, 6 out of 10 patients (60%) with anterior MI who were not thrombolysed had abnormal SAECG as compared to 10 of 51(20%) who received this treatment (p < 0.01), with no significant difference among inferior myocardial infarction patients. The mean (+/- SEM) ejection fraction (EF%) of anterior myocardial infarction patients was 31 +/- 3 percent in those with abnormal SAECG when compared to 39 +/- 2 percent in patients with normal SAECG (p < 0.05). Similarly, in patients with inferior myocardial infarction, the mean EF among these respective groups was 41 +/- 2 and 47 +/- 2 percent (p < 0.05). The mean echocardiographic score, which reflected regional LV wall motion abnormality, was not different between patients with anterior infarction when the groups with abnormal and normal SAECG were compared (9.1 +/- 0.6 versus 6.4 +/- 0.4), but differed significantly between inferior infarction patients (5.8 +/- 0.7 versus 4.6 +/- 0.4 respectively; p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Signal-averaged electrocardiography in survivors of first acute myocardial infarction: a pre-hospital discharge study. 855 78