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)

Intracoronary thrombus is regarded as a potentially important factor in the etiology of unstable angina, but the incidence of intracoronary thrombus in unstable angina has not been clearly defined. To determine the occurrence of intracoronary thrombus during ongoing angina pectoris, coronary angiography was performed during spontaneous ischemic attacks in 37 patients with prolonged rest angina. All patients exhibited significant (greater than 50%) stenoses of at least one major coronary artery. Of the 37 patients, 21 (57%) had intracoronary thrombus in major coronary arteries, whereas 14 (38%) had fixed narrowings without evidence of intracoronary thrombus and two exhibited coronary spasm. ST segment elevation was observed in 16 of 21 patients with thrombus and in all of the patients with coronary spasm, but all the patients with organic stable obstruction showed ST segment depression. Twenty of the 21 patients with thrombus improved after thrombolytic therapy with intracoronary injection of urokinase; obstructed arteries were reopened, or narrowings were attenuated, with relief of ischemic symptoms. In patients with fixed obstructions, the rate-pressure product during active symptoms was significantly higher than during an asymptomatic period, indicating that a transient increase in myocardial oxygen demand may contribute to the ischemic attack in these patients. A high incidence (71%) of recurrent symptoms was observed in patients with intracoronary thrombus even after successful thrombolysis, in contrast to a much lower incidence (36%) in those without intracoronary thrombus. Myocardial infarction within 4 weeks after catheterization was observed more frequently in patients with intracoronary thrombus (24%) than in those without thrombus (7%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The role of intracoronary thrombus in unstable angina: angiographic assessment and thrombolytic therapy during ongoing anginal attacks. 334 83

The emergency physician's disposition of patients with suspected myocardial ischemia is currently debated; some physicians believe that a subgroup of patients can be managed safely outside the coronary care unit. Clinical predictors are needed in assessing the patient with suspected myocardial ischemia to help identify this subgroup. Through a retrospective cohort study, we investigated the value of the initial emergency department ECG in discriminating between chest pain patients with low and high risk for immediately life-threatening complications. Two hundred eleven initially uncomplicated consecutive coronary care unit admissions with suspected unstable angina or myocardial infarction were studied. Patient outcome, including the incidence of myocardial infarction, complications, and mechanical and pharmacologic interventions, was reviewed. Immediately life-threatening complications included ventricular fibrillation, ventricular tachycardia, shock, 2 degrees and 3 degrees block, and death. Mechanical interventions included electrocardioversion or defibrillation, endotracheal intubation, intra-aortic balloon pump, Swan-Ganz catheter, or pacemaker insertion. Pressors, antiarrhythmics, and vasodilators were the reviewed pharmacologic interventions. A positive ECG was defined by the presence of ST elevation or depression, T wave inversion, left ventricular hypertrophy, left bundle branch block, paced rhythm, or new Q waves. All other ECG interpretations were considered negative. Patients were divided into two groups based on this initial emergency physician ECG interpretation and their complication incidences compared. Of the 211 patients, 96 had a positive ECG; 115 had negative ECGs. Patients with positive ECGs were older, had a greater history and concurrent incidence of myocardial infarction, and more complications and intensive interventions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The emergency department ECG and immediately life-threatening complications in initially uncomplicated suspected myocardial ischemia. 334 14

The aim of this study was to explore the capability of isosorbide dinitrate (ISDN) infusion to quench the 'hot phase' of unstable angina, a real cardiological emergency. Fifteen patients consecutively admitted to CCU because of angina at rest, with at least 4 ischaemic attacks per day, resistant to the usual therapy with oral and/or topical nitrates and calcium-antagonists, were included in the study. During ischaemia the electrocardiogram showed ST-segment elevation in 7 patients, ST-segment depression in 4, an alternation of ST-segment elevation and depression in 3 and pseudonormalization of a basally negative T wave in 1 patient. History of exertional angina with variable degrees of effort was reported in 6 patients and 9 had an old myocardial infarction. Coronary arteriography performed in 10 patients showed a significant stenosis of 1, 2 and 3 vessels in 5, 2 and 3 patients, respectively. ISDN infusion was started at 1.0 mg h-1, and was increased stepwise when persistence of ischaemic episodes had to be faced. The mean dosage infused was 3.5 mg h-1 (range 1.00-12). The mean duration of intravenous therapy was 8.3 days (range 2-25). Eleven of the 15 patients (73%) showed an effective decrease in the number of ischaemic episodes during ISDN infusion, as assessed by regression and variance analysis. After discharge (mean follow-up 59 months, range 2-96), 7 patients were free from ischaemic attacks, 3 underwent coronary by-pass surgery, 2 complained of some attacks and 3 died (2 because of sudden death three years after this study). In conclusion, ISDN infusion--individually tailored for dosage and duration--can be effective in 'cooling down' the storm of ischaemic episodes in unstable angina. An effective intravenous therapy with nitrates can represent, in some patients, a temporal remedy on the way to elective coronary bypass surgery and/or towards elective PTCA. Furthermore, in a sizeable number of patients with unstable angina, this approach can attain a complete abolishment of the ischaemic attacks.
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PMID:Cooling down unstable angina with high dosage of isosorbide dinitrate (ISDN) continuously infused. 340 12

This study assessed the prognostic significance of ischemic changes during daily activity as recorded by ambulatory electrocardiographic monitoring in a group of 224 low-risk postinfarction patients. Of the 224 patients studied, 74 (33%) had transient ischemic episodes on Holter monitoring. During the 28 months of follow-up the frequency of cardiac events (cardiac death, reinfarction, hospitalization for unstable angina, balloon angioplasty or coronary bypass surgery) was 51% among those with ischemic episodes on Holter monitoring, compared with 12% in those without such changes (p less than 0.0001). The 74 patients with positive results in their exercise tests and Holter monitoring had a 51% event rate, compared with 20% among the 44 patients with a positive exercise test result but negative Holter results (p less than 0.001). The event rate in those without ischemic changes either on the exercise test or on Holter was only 8.5%. Among patients with good (greater than 40%) or reduced (less than 40%) left ventricular ejection fraction, those with transient ST depression on Holter had a significantly higher cardiac event rate compared with those without it. A similar event rate was found in patients with only silent, only symptomatic and with silent and symptomatic ischemic episodes.
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PMID:Prognostic significance of ischemic episodes in patients with previous myocardial infarction. 342 Nov 61

Regional myocardial utilization of glucose can be assessed non-invasively in man with the sugar analogue F18-2-fluoro-2-deoxyglucose (FDG) and positron emission tomography (PET). The preliminary observations made in patients with different clinical forms of ischaemic heart disease using FDG and PET are reported. In patients with stable angina pectoris at rest, regional myocardial glucose utilization was comparable to that in normal volunteers whilst an increased utilization of glucose was found in the recovery from exercise-induced ischaemia in the regions that showed an abnormal perfusion during the stress test. These metabolic changes persisted in the recovery phase when all the parameters that were altered during the exercise, including myocardial perfusion, had normalized. In patients with unstable angina, characterized by repeated episodes of spontaneous ST depression, myocardial glucose utilization was regionally or globally increased already at rest in the absence of symptoms or signs of ischaemia at the time of study and most often without evident perfusion abnormalities. In patients with a recent infarction, two different patterns of glucose utilization in the infarcted area have been described: a concordant decrease of myocardial perfusion and glucose utilization; a disproportionately increased glucose utilization relative to perfusion interpreted as an index of the presence of ischaemic, but still viable myocardium.
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PMID:Myocardial glucose utilization in ischaemic heart disease: preliminary results with F18-fluorodeoxyglucose and positron emission tomography. 349 37

Thirty patients (28 males and 2 females) aged 46-68 years with established chronic stable angina were studied in a placebo-controlled double-blind crossover trial to examine the efficacy of oral ticlopidine (an antiplatelet agent) 250 mg twice daily. The baseline mean +/- SEM exercise time of 7.5 +/- 0.5 min rose to 8.1 +/- 0.6 min after 2 weeks of placebo run-in, 8.8 +/- 0.7 min after 4 weeks of double-blind placebo, and to 9.2 +/- 0.6 min with ticlopidine therapy; none of these changes achieved statistical significance. Similarly, time to the development of 1 mm ST-segment depression, maximal ST-segment depression, heart rate, and rate-pressure product failed to show any statistically significant changes during ticlopidine therapy. Ambulatory electrocardiographic monitoring showed that the mean number of episodes of ST-segment depression greater than 1 mm remained unaltered during ticlopidine therapy. Four patients (3 during placebo, 1 during ticlopidine) stopped treatment prematurely because of unstable angina and two because of adverse effects. Our data suggest that ticlopidine has no significant effect on objective indices of myocardial ischemia in patients with chronic stable angina, that placebo has no effect on the objective indices of myocardial ischemia derived from exercise testing and ambulatory electrocardiographic monitoring, and that exercise testing and ambulatory electrocardiographic monitoring in patients with chronic stable angina pectoris are reproducible.
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PMID:Are anti-platelet drugs of value in the management of patients with chronic stable angina? A study with ticlopidine. 353 37

Ambulatory electrocardiographic (ECG) monitoring of ischemia in patients with coronary artery disease (CAD) provides a new technique for the assessment of ischemic activity and the evaluation of therapies outside of the hospital. Numerous studies have demonstrated that the majority of patients with CAD have episodes of symptomatic and asymptomatic ST segment depression during routine daily activities. Rubidium-82 positron-emission tomographic studies have provided evidence for decreased myocardial perfusion during these episodes of ST segment depression. The prognostic importance of asymptomatic ischemia has been shown in patients with unstable angina to be a marker for early unfavorable cardiac events. Preliminary results suggest a poorer outcome for those patients with chronic stable angina who show episodes of ischemia as well. Ambulatory monitoring studies suggest that total ischemic activity may be underestimated by conventional testing. Whether all ischemic activity detected by ambulatory monitoring requires treatment awaits further study.
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PMID:Characteristics and significance of ischemia detected by ambulatory electrocardiographic monitoring. 355 18

24-hour ambulatory monitoring of the ST segment in patients with angina has shown that ST segment depression may be accompanied by angina pectoris, but it occurs equally often without any symptoms. Approximately half of all episodes of ST segment depression are accompanied by chest pain. Doubt has been expressed as to the significance of ST segment changes that occur in the absence of chest pain, but haemodynamic studies and nuclear imaging have shown that such changes are accompanied by alterations in left ventricular filling pressure. Ambulatory pulmonary artery monitoring has also shown that silent ST segment depression is accompanied by a significant increase in pulmonary artery diastolic pressure, and this does not differ from painful episodes of ST segment depression. Studies using ambulatory monitoring have shown that antianginal drugs are capable of reducing the frequency of ST segment depression accompanied by pain. We have recently performed studies investigating the use of antianginal medications; i.e. beta-blocking drugs with and without sympathomimetic activity, alpha-beta-blocking drugs, calcium antagonists and nitrates in the treatment of both painful and painless ST segment depression. These studies have shown that the effect of these drugs on painless episodes is similar to their effect on painful episodes of myocardial ischaemia. Although the prognostic implications of silent ischaemia and the importance of these therapeutic findings are unknown, it is well known that approximately one-quarter of all myocardial infarctions occur without chest pain. Moreover, recent investigations in unstable angina show that silent myocardial ischaemia is an important predictor of future coronary events.
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PMID:Should we treat silent ischaemic? 362 15

The occurrence of silent ischemia in various ischemic myocardial syndromes has attracted increasing attention. In unstable angina hemodynamic monitoring has suggested that the symptomatic and silent episodes of ischemia do not differ significantly. In two discrete studies we determined the characteristics and prognostic significance of silent ischemic episodes in unstable angina. In one study with 41 patients, there were 781 episodes of ischemia in Holter recordings: 392 (50%) with ST-segment depression, 242 (31%) with ST-elevation, 45 (6%) with ST-elevation and depression in different leads, 70 (9%) with pseudonormalization of T waves and 32 (4%) with T wave augmentation. Ventricular arrhythmias were associated with 18% of the episodes. The mean duration of ischemia was 14 minutes (range 30 seconds to almost twelve hours), the majority being less than five minutes. Only 154 (20%) of the 781 episodes of ischemia were associated with pain. Conversely, 77 episodes of chest pain were not associated with electrocardiographic changes. Analysis of the temporal sequence of heart rate during the development of ischemia (analysed in 415 episodes) showed that in only 43 (10%) the heart rate at the beginning of ischemia was significantly (exceeding 6 beats/minute) greater than that at five minutes (baseline) preceding the onset of ischemia. At the peak of ischemia, the mean heart rate increase was 10% and returned to baseline at the end of the ischemic episode. The data indicate that 80% of ischemic episodes in unstable angina are silent and over 90% are not triggered by increases in heart rate indicating that increased oxygen demand is an uncommon cause of ischemia in unstable angina.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Characterization of silent ischemia in patients with unstable angina: prognostic and therapeutic implications. 367 65

The relations between reciprocal ST segment depression in the electrocardiogram and infarct size and 10 year prognosis were studied in 315 patients who survived for at least 28 days after a first anterior or inferior myocardial infarction. ST depression was more common in inferior infarcts (72%) than in anterior (37%) ones. It occurred more frequently in complicated infarcts and in the presence of considerable ST elevation. Patients experiencing second or third degree heart block were significantly more likely to show reciprocal changes. The rise in peak cardiac enzyme concentration was higher in patients showing ST depression. In patients with ST depression, peak creatine kinase concentration was 46% higher, aspartate aminotransferase was 39% higher, and lactate dehydrogenase 29% higher after correction for site and complications. A discriminant function analysis selected infarct site, peak aspartate aminotransferase, and magnitude of ST elevation as predictors of the occurrence of ST depression. Age, severity, and smoking status did not significantly improve discrimination. Despite larger increases in peak enzyme concentrations patients with ST depression had marginally fewer subsequent episodes of unstable angina or fatal or non-fatal infarction and a marginally lower 10 year death rate. Neither difference was statistically significant. ST depression occurring early in the acute phase of myocardial infarction is likely to be a reflection of electrophysiological changes taking place at the site of the infarct that is manifested in the contralateral surface of the heart. Other causes, however, such as transient ischaemia at the site of the reciprocal changes or extension of the infarct to contiguous areas cannot be excluded in all cases.
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PMID:The aetiology and prognostic implications of reciprocal electrocardiographic changes in acute myocardial infarction. 370 82


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