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)

Two hundred patients (mean age 56 years, range 36 to 74) with unstable angina (chest pain at rest, associated with ST-T changes) underwent coronary angioplasty. In 65 patients with multivessel disease, only the "culprit" lesion was dilated. The initial success rate was 89.5% (179 of 200 patients). At least one major procedure-related complication occurred in 21 patients (10.5%): (death in 1, myocardial infarction in 16 and urgent surgery in 18). All patients were followed up for 2 years. Five patients died late; 8 had a late nonfatal myocardial infarction and 52 had recurrence of angina pectoris. The restenosis rate was 32% (51 of 158) in the patients with initial successful angioplasty who had repeat angiography. At the 2 year follow-up, after attempted coronary angioplasty in all 200 patients, the total incidence rate of death was 3% (one procedure related; five late deaths), of nonfatal myocardial infarction 12% (16 procedure related and 8 late after angioplasty), and 13% (26 patients) were still symptomatic although they had improved in functional class. Multivariate analysis showed that variables indicating an increased risk 1) for major procedure-related complications were: ST segment elevation, persistent negative T wave and stenosis greater than or equal to 65% (odds ratio 3.7, 3.7 and 3.3, respectively); 2) for angiographic restenosis were: presence of collateral vessels, ST segment depression, multivessel disease, left anterior descending coronary artery stenosis and history of recent onset of symptoms (odds ratio: 2.2, 2.0, 1.9, 1.9 and 0.54, respectively); and 3) for late coronary events (recurrence of angina, late myocardial infarction or late death) were: multivessel disease, total occluded vessel and ST segment elevation (odds ratio 3.7, 2.8 and 0.44, respectively). Thus, coronary angioplasty for unstable angina can be performed with a high initial success rate, but at an increased risk of major complications. The prognosis is favorable after initial successful coronary angioplasty.
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PMID:Coronary angioplasty for unstable angina: immediate and late results in 200 consecutive patients with identification of risk factors for unfavorable early and late outcome. 296 19

To assess the relations of electrocardiographic measures of ischemia with the development of adverse coronary events, 86 patients with stable coronary artery disease and positive exercise tests for myocardial ischemia underwent ambulatory monitoring of the electrocardiogram. Monitoring was performed after withdrawal of antianginal medications, and prospective follow-up was obtained on routine medical care as prescribed by physicians who were unaware of monitor results. Forty-nine patients (57%) had a total of 426 episodes of ST segment depression; only 60 episodes (14%) were associated with symptoms of angina or an equivalent. During a mean follow-up of 12.5 +/- 7.5 months, there were two cardiac deaths, four myocardial infarctions, four hospitalizations for unstable angina, and 11 revascularization procedures required for new or worsening symptoms in 15 patients. All but one of these events (a hospitalization for unstable angina) occurred in the group of patients with ST segment depression on monitoring (p = 0.003). In multivariate analysis controlling for age, sex, and clinical descriptions of angina, the presence of ischemia on ambulatory monitoring was a significant predictor of outcome, while exercise test characteristics were not. Therefore, ischemia detected by ambulatory monitoring was common in patients with stable symptoms of coronary artery disease, and its presence identified a high-risk group for the development of subsequent unfavorable outcomes while on routine medical therapies.
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PMID:Prognostic importance of myocardial ischemia detected by ambulatory monitoring in patients with stable coronary artery disease. 316 96

We prospectively evaluated 19 patients with prolonged chest pain not evolving to myocardial infarction and accompanied with reversible ST-T changes and tachycardia (heart rate greater than 100 beats/min) in order to correlate heart rate reduction with ischemic electrocardiographic (ECG) changes. Fourteen patients (74%) received previous long-term combined treatment with nifedipine and nitrates. Continuous ECG monitoring was carried out until heart rate reduction and at least one of the following occurred: (1) relief of pain or (2) resolution of ischemic ECG changes. the study protocol consisted of carotid massage in three patients (16%), intravenous propranolol in seven patients (37%), slow intravenous amiodarone infusion in two patients (10%), and intravenous verapamil in four patients (21%) with atrial fibrillation. In three patients (16%) we observed a spontaneous heart rate reduction on admission. Patients responded with heart rate reduction from a mean of 125 +/- 10.4 beats/min to 84 +/- 7.5 beats/min (p less than 0.005) and an ST segment shift of 4.3 +/- 2.13 mm to 0.89 +/- 0.74 mm (p less than 0.005) within a mean interval of 13.2 +/- 12.7 minutes. Fifteen (79%) had complete response and the other four (21%) had partial relief of pain. A significant direct correlation was observed for heart rate reduction and ST segment deviation (depression or elevation) (r = 0.7527 and 0.8739, respectively). These patients represent a unique subgroup of unstable angina, in which the mechanism responsible for ischemia is excessive increase in heart rate. Conventional vasodilator therapy may be deleterious, and heart rate reduction in mandatory.
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PMID:Unstable angina with tachycardia: clinical and therapeutic implications. 318 36

This study was undertaken to compare the relative values of the low level predischarge exercise test and the postdischarge (6 weeks) symptom-limited test in 518 consecutive patients admitted with an acute myocardial infarction. Of the patients who did not develop significant ST segment depression or angina during the predischarge test, the symptom-limited test also remained negative in 91.5 and 91.9% of the patients, respectively. Similar results were obtained with ST segment elevation and the systolic blood pressure response during the two exercise tests with only 2.1 and 11.4% changing from normal to abnormal, respectively. Discriminant function analysis was done to predict the occurrence of coronary events (unstable angina, reinfarction, cardiac failure, cardiac death) with use of the data from the exercise tests together with other clinical and investigational data. The jackknife method correctly classified 71.9 and 71.4% of the patients with the data from the predischarge exercise test and symptom-limited test, respectively. Combining the data from the two tests improved the overall predictive accuracy to only 75.0%. It is concluded that the routine performance of a symptom-limited test 6 to 8 weeks after infarction does not reveal any significant additional information in those patients who have undergone a predischarge low level exercise test. Thus the 6 to 8 week test should be restricted to selected patients after myocardial infarction.
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PMID:Exercise testing after myocardial infarction: relative values of the low level predischarge and the postdischarge exercise test. 280 96

The safety and efficacy of exercise electrocardiography and thallium scintigraphy early in the course of unstable angina pectoris were assessed 4.6 +/- 1.6 days after admission in 67 patients with unstable angina that stabilized after medical therapy. Coronary arteriography was performed in all patients 5.4 +/- 2.4 days after admission. There was no difference in clinical, exercise or scintigraphic variables between patients with stenoses less than 50% and patients with 1-vessel coronary artery disease (CAD) defined as a diameter stenosis greater than or equal to 50%. Patients with 3-vessel CAD had a significantly shorter exercise duration than patients with less than 50%-diameter narrowing (5.5 +/- 2.2 vs 8.3 +/- 3.3 minutes, respectively), lower exercise heart rate (119 +/- 20 vs 149 +/- 22 beats/min) and systolic blood pressure (156 +/- 29 vs 166 +/- 33 mm Hg), more frequent chest pain (76 vs 20%) and more pronounced ST depression (-1.48 +/- 1.37 vs -0.33 +/- 0.72 mm). In addition, thallium defect size on exercise was greater in the patients with 2-vessel CAD (159 +/- 132 degrees) and 3-vessel CAD (255 +/- 132 degrees) than in patients with no CAD (28 +/- 319 degrees) or 1-vessel CAD (73 +/- 78 degrees), p greater than or equal to 0.05. Multiple regression analysis demonstrated that thallium defect size was the best predictor of extent of CAD, with exercise heart rate and presence of chest pain during exercise also predictive of extent of CAD.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Usefulness of exercise electrocardiography and thallium scintigraphy in unstable angina pectoris in predicting the extent and severity of coronary artery disease. 319 77

Demonstration of ischaemic left ventricular dysfunction in the absence of chest pain should provide important confirmation of silent myocardial ischaemia in patients with asymptomatic ST segment changes. For this purpose, a new portable scintillation probe (VEST) similar to a miniaturized nuclear stethoscope combined with a Holter ECG was evaluated. After standard equilibrium radionuclide angiocardiography with technetium-99m labelled red blood cells, the VEST was positioned under gamma-camera control and data were recorded from 1-12 h in 61 unselected patients. Ejection fraction (LVEF), relative changes in volumes, heart rate and ST segment changes were determined. Reproducibility of LVEF at rest (r = 0.91; variability 3.8 +/- 3%, N = 19) and during exercise (r = 0.98; variability 3.2 +/- 2%, N = 19) was good. In 15 asymptomatic exercise tests four different patterns of LVEF and ST segment responses were identified: (1) decrease in LVEF followed by significant ST depression (five times); (2) ST depression followed by decrease in LVEF (three times); (3) decrease in LVEF without significant ST changes (three times); and (4) ST depression without significant LVEF change (four times). In this still small series, patterns (1) to (3) corresponded to patients with documented coronary artery disease, which was not the case for pattern (4). For detection of silent ischaemia at rest, a decrease in LVEF of greater than 5% lasting for greater than 1 min was defined as ischaemic LV dysfunction. Using this definition, four spontaneous episodes of silent LV dysfunction could be demonstrated in two of three CCU patients with unstable angina during 160-680 min of data recordings without simultaneous ST changes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ambulatory scintigraphic assessment of transient changes in left ventricular function: a new method for detection of silent myocardial ischaemia. 324 66

Despite the widespread use of the exercise stress test in diagnosing asymptomatic myocardial ischemia, exercise radionuclide imaging remains useful for detecting silent ischemia in numerous patient populations, including those who are totally asymptomatic, those who have chronic stable angina, those who have recovered from an episode of unstable angina or an uncomplicated myocardial infarction, and those who have undergone angioplasty or received thrombolytic therapy. Studies show that thallium scintigraphy is more sensitive than exercise electrocardiography in detecting ischemia, i.e., in part, because perfusion defects occur more frequently than ST depression and before angina in the ischemic cascade. Thallium-201 scintigraphy can be performed to differentiate a true- from a false-positive exercise electrocardiographic test in patients with exercise-induced ST depression and no angina. The development of technetium-labeled isonitriles may improve the accuracy of myocardial perfusion imaging.
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PMID:Myocardial perfusion imaging for detection of silent myocardial ischemia. 328 20

ACBGS is indicated in patients with stable angina who have left main coronary artery disease; three-vessel disease; three or four of the clinical variables set forth in the Veterans Administration Cooperative Study; obstruction in proximal third of left anterior descending coronary artery as part of two- or three-vessel disease; and two- or three-vessel disease and exercise-induced ischemic ST-segment depression greater than or equal to 1.5 mm. ACBGS may increase survival in patients with limited exercise capacity. Finally, ACBGS may be indicated to increase the quality of life in patients with disabling angina that is refractory to medical treatment. Patients with unstable angina who have an inadequate response to intensive medical therapy should have emergency ACBGS. Indications for elective ACBGS in patients with unstable angina who respond adequately to medical therapy are the same as those for stable angina. Patients with rupture of the ventricular septum, acute severe mitral regurgitation, and cardiogenic shock with vessels suitable for ACBGS should have urgent ACBGS after acute myocardial infarction. Patients with postinfarction angina after the first few days following acute myocardial infarction, especially non-Q-wave infarction, should be considered for ACBGS. Indications for elective ACBGS in postinfarction patients are the same as those in stable angina. Patients with coronary artery disease, especially those with a significant amount of ischemic myocardium, who must undergo cardiac surgery for valvular heart disease or for congenital heart disease should probably have ACBGS performed at the time of surgery.
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PMID:Indications for coronary artery bypass graft surgery. 331 16

With the inception of continuous ECG monitoring with high-fidelity reproduction of the ST-segment, silent myocardial ischemia has been regarded with increasing importance in the detection and management of coronary artery disease. With the aid of a variety of invasive and noninvasive methods, the validity of ST-segment depression as indicative of myocardial ischemia, even in the absence of symptoms, has been adequately documented. In completely asymptomatic subjects with positive evidence of silent ischemia in the exercise ECG or Holter monitoring, the risk of developing a future manifestation of coronary artery disease may be up to ten-fold higher than in individuals with negative tests In patients with established coronary artery disease, concomitant use of continuous ECG monitoring and exercise testing, methods which complement each other rather than being mutually exclusive, a substantial number of patients with otherwise typical angina pectoris may be found to have silent ischemic episodes. An adequate differentiation between those with symptomatic and those who are asymptomatic based on characterization with respect to age, sex, hypertension, coronary anatomy, etc., has not been successful. Patients with silent ischemia during exercise may also exhibit more episodes of silent ischemia during daily activities and up to 75% of ischemic episodes may be asymptomatic. In general, however, silent ischemia during exercise appears more common than silent ischemia only during daily activities. In the latter case, since there is usually no increase in heart rate, the pathophysiology is regarded as dissimilar from that associated with exercise-induced ischemia. While the presence of silent ischemia appears quite common in patients after acute myocardial infarction, its occurrence, to date, has not been confirmed to carry additional risk, whereas in unstable angina, the association of silent ischemia is indicative of a higher probability of subsequent cardiac events.
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PMID:Silent myocardial ischemia: diagnosis, clinical significance and management. 331 17

Regardless of the factor assumed responsible for precipitation of myocardial ischemia - varying from coronary occlusion in acute myocardial infarction to increased oxygen demand in exertional angina pectoris and reduced myocardial oxygen supply due to plaque rupture or changes in vasomotor tone in unstable angina - its incurrence may or may not be associated with pain. In the vast majority of cases, silent myocardial ischemia is observed in patients with established symptomatic coronary artery disease. Interindividual comparisons have not enabled reliable differentiation between those with painful and those with silent ischemia based on the anatomic extent of coronary artery disease, left ventricular function or previous myocardial infarction. Similarly, functional parameters such as exercise capacity, exercise duration, time to onset of ST-segment depression during exercise as well as heart rate and blood pressure both at rest and during exercise have failed to reveal differences between the symptomatic and the asymptomatic patients. Intraindividual differences have also been noted, but not consistently corroborated, and postulated as responsible for the fact that ischemia in a given patient alternates in its presence with and without pain. Since most patients with silent ischemia either have, or at some time in the past have experienced, painful ischemia, the integrity of the appropriate nervous system function can be assumed to be intact and neurocardiologic factors seem most likely to account for apparent discrepancies in pain perception. Prior to precipitation of pain, myocardial ischemia must elicit an adequate stimulus. According to some investigators, the adequate stimulus is that associated with a duration of the ischemic episode of at least three minutes and with increase in left ventricular filling pressure of more than 7 mm Hg. This threshold, consequently, represents a prerequisite but not invariably sufficient criteria for the occurrence of pain. The next step in the sequence of pain is generation of an action potential, that is, transduction by means of chemical or mechanical stimuli. During this process, a latency of 20 to 40 seconds is incurred such that the appearance of pain usually has its onset after derangement of relaxation and contraction, increased filling pressure and the observation of ECG changes. Through conduction, the information is forwarded to the central nervous system after coding of the details with regard to intensity. The intensity, in turn, is determined by the number of receptors (free nerve endings) in the field activated by the ischemic event.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Pathophysiology of painful and silent myocardial ischemia]. 332 3


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