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)

Clinical presentation and course were studies in 45 consecutive patients (p)--39 males, 6 females with angiographically proven left main coronary artery stenosis (LMCA) > 50%. Mean age was 54.7 years. Three (6%) had no history of chest pain, 2 p (4%) had atypical chest pain, and the remaining (90%) had typical angina pectoris. 19 p (42%) had unstable angina, 20 p (44%) had suffered a myocardial infarction in the past. Outside an episode of chest pain most of the patients had an abnormal ECG with ST-T segment depression 2 mm or more in leads V3-6 and ST-T elevation in leads V1 and aVR. No significant differences were found when the abnormalities of the ST-T segment were compared to severity of LMCA obstruction. A symptom limited exercise test was performed in 17 (37%) p. It was abnormal in 13 p (29%). Thirty eight patients (85%) underwent bypass surgery and the mean number of bypass graft was 3.3. Seven patients were treated medically. In the surgical group four p (10.5%) died perioperatively. All of them had subtotal occlusion of LMCA, without significant lesions in the remaining coronary arteries, the ejection fraction (EF) was above 66%. Among thirty four living patients thirty have been asymptomatic. In the medically treated group 3 p (42%) died and only two of four survivors were asymptomatic at a mean follow-up 35.7 months. Left ventricle of all died patients were severely damaged (EF mean 28%), right coronary artery (RCA) was totally occluded and all had rythm disturbances. We conclude, that patients with significant LMCA stenosis had a good prognosis when treated surgically.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Constriction of the left main coronary artery. Early and long term treatment outcome]. 129 44

The author analyses the outcome and emotional repercussions of myocardial infarction in the patient, his or her partner, and of the medical team who manages the infarct (coronary care and cardiac rehabilitation). The adaptive value of certain psychological attitudes is emphasised, for example the denial of illness, and the poor prognosis associated not so much with "type A" behaviour reputed to cause coronary disease but more with post-infarction depression or even with a more stable tendency to hostility in the emotional control. Some of these psychological characteristics may explain the difficulties encountered in designing educative programmes or in poor therapeutic observance by patients despite being aware of the risks they run. These considerations led to therapeutic implication ranging from the strategy of communication with the coronary patient to specific relaxation techniques or with help, to the gestion of stress, to the judicious prescription of psychotropic agents.
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PMID:[Psychological aspects of short-term follow-up in myocardial infarction]. 130 46

Working capacity after myocardial infarction depends on the physical and cardiovascular status, psychological repercussions and conditions of work. The latter two are much more important than the first two factors. Cardiovascular functional status is readily assessed by the large number of available investigations which leave little unknown. Exercise stress testing during the second week is the most cost-efficient investigation, providing reliable and sufficiently quantifiable data about the possible sequellae of cardiac failure on effort, ischemia and arrhythmias: an idea of the patient's functional capacity and circulatory responses (athletic, hyperkinetic) may also be obtained allowing adjustment of treatment to improve exercise capacity which goes much further than the statistical hope of prolonging survival. However, it would be naive to think that a satisfactory exercise stress test guarantees the patients' capacity to return to work. Psychological and sociological factors are more important by far. The dominant trait of the post-infarction psychological syndrome must be identified (anxiety, depression, negation): the positive and negative influences of the family, social and professional environment must be evaluated. A good knowledge of the patient's working conditions is essential to go against a number of taboos hindering the return to work (stress, stairs, restaurant meals, etc...). Finally, the medico-legal relationship between the infarct and work should not be neglected: the management of myocardial infarction when an occupational disease must respect the legislative and judicial texts which do not always correspond with everyday clinical practice. There is a lack of structures for cardiac function testing for assessing physical aptitude: we suggest that in the context of the proposed hospital reforms, departmental heads should consider setting up such units which would have a specific task respecting the spirit of these reforms. Nevertheless, cardiologists should pay more attention to the convalescent phase of infarction. This is the time when many social catastrophes can be avoided.
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PMID:[Return to work after myocardial infarction: evaluation and decision]. 130 47

Because the Na+ pump is considered to modulate the contractile force development by the cardiac muscle and depressed cardiac pump function is the hallmark of congestive heart failure, we characterized the sarcolemmal Na(+)-K(+)-ATPase activity in failing rat hearts after myocardial infarction. For this purpose, the left ventricular coronary artery was ligated, and hearts were examined 4, 8, and 16 wk later; sham-operated animals served as controls. Hemodynamic assessment revealed the presence of abnormal cardiac function at 4, 8, and 16 wk. Although accumulation of ascites in the abdominal cavity was present in experimental animals at 4 wk, other clinical signs of congestive heart failure in experimental rats including lung congestion and cardiac dilatation were evident 8 and 16 wk after induction of myocardial infarction. The depression in Na(+)-K(+)-ATPase activity in purified sarcolemmal membrane from the uninfarcted experimental left ventricle at 8 wk was associated with depressed Vmax without any changes in the affinities for Mg-ATP, Na+, and K+ or the pH optimum for the enzyme. The Kd values of both the high- and low-affinity binding sites for [3H]ouabain, which is believed to interact with Na(+)-K(+)-ATPase, were increased; however, no change in the density of either class of ouabain binding site was evident. The depression of Na(+)-K(+)-ATPase activity in failing hearts at 16 wk of myocardial infarction was not different from that observed at 8 wk but the enzyme activity was not altered at 4 wk of coronary occlusion. These data support the view that depression of Na(+)-K(+)-ATPase activity may serve as an adaptive mechanism during the development of congestive heart failure.
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PMID:Sarcolemmal Na(+)-K(+)-ATPase activity in congestive heart failure due to myocardial infarction. 131 80

Because Na(+)-Ca2+ exchange and Ca2+ pump are thought to play a role in sarcolemmal Ca2+ movements, we examined the Na(+)-dependent Ca(2+)-uptake and ATP-dependent Ca(2+)-uptake activities in failing heart after myocardial infarction in rats. The left coronary artery was ligated, and the viable left ventricle was used 4, 8, and 16 wk later; sham-operated animals served as controls. Increased left ventricular diastolic pressure and decreased positive and negative change in pressure over time were observed in experimental animals at 4, 8, and 16 wk; these changes were associated with accumulation of fluid in the abdominal cavity. The sarcolemmal Na(+)-dependent Ca2+ uptake was depressed in 4-, 8-, and 16-wk experimental hearts. The decrease in sarcolemmal Na(+)-dependent Ca2+ uptake in failing hearts was seen when the activity was assayed either as a function of time or Ca2+ concentration; a depression of maximal velocity without any change in activity constant for Ca2+ was observed. No alteration in the Ca2+ pump (ATP-dependent Ca2+ accumulation and Ca(2+)-stimulated adenosinetriphosphatase) activities was evident in the 4-, 8-, and 16-wk experimental groups. These data suggest that changes in the Na(+)-dependent Ca2+ handling by the sarcolemmal membrane may be associated with contractile abnormalities in this model of congestive heart failure.
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PMID:Sarcolemmal calcium transport in congestive heart failure due to myocardial infarction in rats. 131 26

Developed for the treatment of migraine, sumatriptan is an agonist of 5-hydroxytryptamine-1-receptors. Though a pressure sensation is a common complaint, significant ECG changes have not been reported after subcutaneous administration of sumatriptan. A case history is given where angina pectoris after sumatriptan self-administration was experienced on two occasions by a 61-year old man with a history of minor myocardial infarction--without post-infarction angina--two years previously. The angina after sumatriptan was accompanied on both occasions by significant ST-segment depression on ECG-monitoring. An extracranial vasoconstrictor action of sumatriptan in patients with ischaemic heart disease is suggested.
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PMID:[Angina pectoris after sumatriptan (Imigran)]. 133 86

To evaluate the prognostic and clinical significance of silent myocardial ischemia (SMI), we examined cardiac events in 160 patients with old myocardial infarction who underwent ambulatory Holter monitoring, treadmill exercise testing and coronary angiography. Using the Cox's proportional hazard regression model and the survival curves with the Kaplan-Meier method, we identified the predictors of cardiac events. The incidence of cardiac events for all the patients during the 44-month follow-up period was 18%. The significant predictors of unfavorable outcomes were severe coronary lesions and SMI. The incidence of SMI was 38%. The cardiac event rate in patients with SMI was higher than in those without SMI (32 vs 9%, p < 0.05). The most frequent cardiac event in patients with SMI was reinfarction, and the significant predictors of cardiac events for these SMI patients were lower ejection fraction and maximum ST depression on Holter monitoring. In conclusion, SMI proved to be a significant predictor of unfavorable outcome in patients with old myocardial infarction. It was, therefore, suggested that revascularization (PTCA/CABG) should be used as early as possible in patients with SMI whether anginal symptoms are present or not.
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PMID:[Silent myocardial ischemia in myocardial infarction patients: its prognostic significance]. 133 98

Non q wave myocardial infarction has been attributed to occlusion of a vessel with no ECG representation, early reperfusion of the occluded artery or occlusion of a vessel with generous collateral flow. The coronary arteriography of 84 patients with non Q wave myocardial infarction performed at 16 + 17 (SD) days after infarction was analyzed. Main left lesion was found in 6 (17%), single vessel disease in 30 (36%), two vessel disease in 18 (24%) and 3 vessel disease in 16 (19%). The "culprit" vessel had a critical residual lesion in 38 patients (45%): 22 affected the left anterior descending artery, 10 the circumflex, and 5 the right coronary artery. No residual lesion was found in 10 patients (12%). An occluded artery was found in 32 patients (38%): circumflex in 20, right coronary artery in 9 and left anterior descending in 3 (p < 0.01). Significant collateral flow to the occluded vessel was present in 41% of cases. The ST segment was analyzed in 82 patients. Depression of ST was found in 29 (35%), elevation in 22 (27%), negative T waves in 17 (21%) and minimal alterations in 17%. There was no correlation between ST levels and coronary occlusion of the culprit artery. Depression of ST was more commonly (p < 0.01) associated with severe coronary artery disease (main left or 3 vessel disease), which may be related to the poorer prognosis in these cases.
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PMID:[Angiographic findings in non-Q wave infarction and their relation to ST-T changes]. 134 94

Exercise testing has been shown to be predictive for future cardiac events in patients with established diagnosis of coronary heart disease. Exercise test parameters associated with poor prognosis may be unreliable if patient is receiving beta adrenergic agents. The purpose of this study was: 1) to compare the results of exercise testing performed before and during beta blocking therapy, and 2) to determine the role of beta blockers in the prognostic significance of the ST-segment response recorded during exercise testing. The study population consisted of 518 patients (mean age 52 +/- 7 years) with coronary heart disease. The diagnosis was based on the presence of one of the following three criteria: 1) typical history and significant ST-segment depression on resting or exercise electrocardiogram, 2) history of myocardial infarction, 3) significant coronary angiographic abnormalities. In all patients symptom-limited exercise test was performed before and two weeks after the onset of beta blocker therapy. The data from the first and second tests were estimated for significance of differences between the mean values with following results: maximal heart rate--135 +/- 21 and 123 +/- 19 bpm (p less than 0.001), maximal work load achieved--98 +/- 43 and 109 +/- 44 W (p less than 0.001), maximal systolic blood pressure--171 +/- 28 and 163 +/- 26 mmHg (p less than 0.001). Occurrence of characteristic ST-segment depression was more frequent during the first than during the second test (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effect of beta adrenergic blocking drugs on the prognostic value of ST-segment depression during exercise electrocardiogram testing]. 135 45

On exercise testing after an episode of unstable coronary artery disease (CAD; unstable angina or non-Q-wave myocardial infarction), a proportion of patients show ST-segment depression, indicating myocardial ischaemia, but do not report concomitant symptoms of angina. Treatment of such "silent" ischaemia aims mainly to reduce the risk of subsequent cardiac events. We have studied the effect of low-dose aspirin in patients with myocardial ischaemia defined at the predischarge test as silent (though patients might have had symptomatic ischaemia at other times) or symptomatic. 740 men with unstable CAD aged 70 years or less underwent symptom-limited exercise testing before hospital discharge; 144 showed ST depression without pain and 230 ST depression with simultaneous chest pain. Of the silent ischaemia group, 67 were randomly assigned placebo and 77 aspirin (75 mg daily); the corresponding numbers in the symptomatic group were 125 and 105. Angina symptoms were less common in the silent than in the symptomatic ischaemia group both before inclusion and during follow-up, and a greater proportion of the silent ischaemia group were included because of myocardial infarction. In both ischaemia groups aspirin treatment reduced the risk of subsequent myocardial infarction or death by 3 months' follow-up (silent 4% of aspirin-treated vs 21% of placebo-treated patients, p = 0.004; symptomatic 9% vs 18%, p = 0.05); at 12 months' follow-up a significant benefit of aspirin was still apparent in the silent ischaemia group (9% vs 28%, p = 0.005) but not in the symptomatic group (13% vs 22%, p = 0.109). Low-dose aspirin reduced the risk of subsequent myocardial infarction at least as well in silent as in symptomatic myocardial ischaemia. Since improvement of outlook is the main treatment objective in symptom-free patients, aspirin should be a mainstay of their treatment.
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PMID:Prevention of serious cardiac events by low-dose aspirin in patients with silent myocardial ischaemia. The Research Group on Instability in Coronary Artery Disease in Southeast Sweden. 135 74


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