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)

Identification of patients with angina but normal coronary arteriograms (syndrome X) using noninvasive means would be desirable. The ability of four established exercise electrocardiographic methods to identify angina patients with and without coronary artery disease was compared with that of a method based on a combination of the above (combined method). A treadmill score, a multivariate method, the ST segment recovery loop, the ST/heart rate adjustment, and the combined method were applied to 112 patients who had typical exertional angina and positive exercise tests (greater than 1 mm ST segment depression); 90 had documented coronary artery disease and 22 had syndrome X. The combined method and the treadmill score had a significantly higher diagnostic accuracy (both 81%, as 91 of the 112 patients were correctly identified by both methods) than the multivariate (66%) and ST segment recovery loop (64%) methods (p less than 0.05). The ST/heart rate adjustment had a lower sensitivity for syndrome X than any other method (1 of 22). Thus methods that involve the assessment of both ST and non ST segment variables have greater accuracy in separating syndrome X and coronary artery disease patients than methods relying more heavily on ST segment changes.
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PMID:A combination of electrocardiographic methods represents a further step toward the noninvasive identification of patients with syndrome X. 134 74

The dose-effect relation and duration of action of 10 mg, 20 mg, 40 mg, and 80 mg ridazolol on ischemic ST-segment depression in exercise-ECG were determined in a randomized, double-blind, acute, cross-over study of 15 patients with confirmed coronary artery disease and reproducible ST-segment depression. Maximal reduction of ST-segment depression in comparison to placebo during constant exercise was 0.16 vs. 0.25 mm (n.s.) after 10 mg, 0.09 vs. 0.25 mm (p less than 0.01) after 20 mg, 0.11 vs. 0.25 mm (p less than 0.01) after 40 mg, and 0.07 vs. 0.25 mm (p less than 0.01) after 80 mg ridazolol. A remarkable reduction of ST-segment depression under placebo was seen in the third and fifth hours after application. Systolic blood pressure under exercise was reduced significantly after 80 mg ridazolol (145 vs. 176 mm Hg; (p less than 0.05) over a period of 5 h. Heart-rate was reduced significantly after 80 mg ridazolol (102 vs. 131/min; p less than 0.05) for 5 h. Rate-pressure product after 20 mg (174 vs. 234 mm Hg/min; p less than 0.01), 40 mg (169 vs. 234 mm Hg/min; p less than 0.01), and 80 mg (153 vs. 234 mm Hg/min; p less than 0.01) ridazolol was reduced significantly over 3 to 5 h. 20, 40 and 80 mg ridazolol show a good antianginal and antihypertensive efficacy. Blood pressure and heart-rate under exercise were significantly reduced over 5 h. In contrast, improvement of ST-segment depression only lasted 1 h. Ridazolol was well tolerated.
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PMID:[Duration of the effect and dose-response relationship of ridazolol in patients with coronary heart disease]. 135 33

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

There is no established treatment specifically aimed at protecting or restoring cardiac energy metabolism, which is greatly impaired by ischaemia. Even after reperfusion, myocardial content of ATP remains low for more than 72 h. Long-term post-ischaemic dysfunction and irreversibility of ischaemic damage have been associated with low ATP content. Evidence that the pentose sugar ribose stimulates ATP synthesis and improves cardiac function led us to test the possibility that ribose increases tolerance to myocardial ischaemia in patients with coronary artery disease (CAD). 20 men with documented severe CAD underwent two symptom-limited treadmill exercise tests on 2 consecutive days; we postulated that the ischaemia induced might bring about changes in ATP metabolism lasting for several days. Patients whose baseline tests showed reproducibility were randomly allocated 3 days of treatment with placebo or ribose 60 g daily in four doses by mouth. Exercise testing was repeated after treatment on day 5. At that time mean (95% confidence interval) treadmill walking time until 1 mm ST-segment depression was significantly greater in the ribose than in the placebo group (276 [220-331] vs 223 [188-259] s; p = 0.002). The groups did not differ significantly in time to moderate angina. In the ribose-treated group the changes from baseline to day 5 in both time to ST depression and time to moderate angina were significant (p less than 0.005), but these changes were not significant in the placebo group. In patients with CAD, administration of ribose by mouth for 3 days improved the heart's tolerance to ischaemia. The presumed effects on cardiac energy metabolism offer new possibilities for adjunctive medical treatment of myocardial ischaemia.
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PMID:Effects of ribose on exercise-induced ischaemia in stable coronary artery disease. 135 76

Recent investigations of SMI occurring during daily life have advanced our understanding of the pathophysiology of myocardial ischemia. These contributions have directed our attention away from "chest pain" alone and physical exertion as the central provoking factor toward transient myocardial ischemia and its broader triggers and consequences. Transient myocardial ischemic episodes, the majority of which are silent, are found in a subset of patients with any clinical manifestations of CAD (eg, stable angina, unstable angina, myocardial infarction, and sudden death), as well as in those patients with CAD who are and have been totally asymptomatic. These episodes are an independent predictor of increased risk for future cardiac events. Most medical therapy and revascularization therapies have the potential to prevent or relieve these silent episodes; however, we do not yet know which method is superior in reducing SMI episodes or preventing future cardiac events. Furthermore, the benefit of reducing SMI versus the cost and potential morbidity of these chosen therapies is not known. At least three trials are now underway to examine some of these concerns (Table 2). Focus on pain relief alone does not appear to be an adequate approach to alter outcome in patients with CAD and may prove insufficient to control SMI. Until these issues are resolved, we believe a conservative approach to the management of patients with CAD is warranted. Documentation of ischemia (painful or painless) is essential. Three general principles should be kept in mind. First, the presence of detectable ischemia is of central importance. This information should be used in the overall risk assessment of the patient. Second, the level of concern or aggressiveness of treatment should be based on the risk associated with the ischemic abnormalities documented (Table 3). The exercise stress test is the most useful to begin this process. The detection of ischemic-type ST-segment depression, either silent or painful, at a low workload (eg, less than or equal to 120 beats per minute or less than or equal to 6.5 metabolic equivalents [METS]) implies high risk for adverse outcome. Likewise, these ST-segment changes occurring in leads that reflect multiple coronary artery distribution, of greater than 2 mm in magnitude and persisting for greater than 6 minutes, are all markers for high risk. Thallium redistribution defects occurring at low work loads, in multiple areas, associated with increased lung uptake and enlargement of the cardiac pool all imply high risk.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Treatment strategies for daily life silent myocardial ischemia: a correlation with potential pathogenic mechanisms. 135 7

The effects of 5 and 10 mg of amlodipine and of placebo were compared in 21 patients with stable angina pectoris and multivessel coronary artery disease. The blind comparison was performed by means of bicycle ergometry and stress echocardiography using esophageal stimulation of the left heart atrium. All patients subsequently received placebo, amlodipine 5 mg and 10 mg for 2 weeks. In bicycle ergometry both doses of amlodipine in comparison with placebo significantly lowered the ST segment depression in lead V5 and prolonged the time to onset of angina. The exercise duration was significantly prolonged only after 10 mg of amlodipine. In stress echocardiography 10 mg of amlodipine significantly improved ejection fraction and reduced wall motion score during stimulation and increased peak velocity of relaxation of left ventricular posterior wall at rest and immediately after stimulation. In the patients with left ventricular end-diastolic pressure < or = 20 mmHg, amlodipine reduced the ratio of peak transmitral flow velocity in atrial contraction to that in early diastole (A/E) at rest and shortened deceleration time at rest and immediately after stimulation. Amlodipine in patients with stable angina pectoris significantly improved the exercise tolerance and the function of the left ventricle in a dose-dependent way. Amlodipine was well tolerated.
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PMID:Amlodipine in patients with stable angina pectoris treated with nitrates and beta-blockers. The influence on exercise tolerance, systolic and diastolic functions of the left ventricle. 135 30

In patients ranked ASA 1, laryngoscopy and intubation lead to an average increase in blood pressure of 40 to 50%, and a 20% increase in heart rate. These changes, which are greatest one minute after intubation, last for 5 to 10 min. They are due to sympathetic and adrenal stimulation, which may also result in some arrhythmias. About half the patient with coronary artery disease experience episodes of myocardial ischaemia during intubation when no specific prevention is undertaken. Among the different means available for this, narcotics seem to have a reliable and constant effect, but they may be responsible for postoperative respiratory depression. The protective effect of fentanyl starts at 2 micrograms.kg-1, and is at a maximum at 8 micrograms.kg-1. Lidocaine is the drug used most. Recent studies have questioned its efficacy. In clinical practice, it is particularly effective in preventing the pressor response to tracheal intubation, whatever its route of administration (intravenous or intratracheal), but not the increase in heart rate. Beta blockers with bradycardic, antihypertensive, antiarrhythmic and antiischaemic properties, have been advocated. As opposed to lidocaine, these agents are more effective in preventing the changes in heart rate than the pressor response. Because of their depressor effect on the myocardium, their place still remains to be defined, especially in the cardiac risk patient. Short-acting beta blockers should be preferred. Nitroglycerin is specifically indicated in coronary artery disease. Other agents, such as clonidine or calcium blockers, seem to be less effective or less convenient in preventing the haemodynamic alterations. In clinical practice, prevention will first rely on a sufficient dose of narcotics. In some cases, nitroglycerin or beta blockers may be used so as to decrease the doses of narcotics, without altering their efficacy; however, the risk of hypotension should be constantly borne in mind. If preventing measures have not been taken, short-acting antihypertensive agents (beta blockers, calcium blockers) should be used in patients who develop major hypertension during laryngoscopy and intubation.
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PMID:[Consequences and prevention methods of hemodynamic changes during laryngoscopy and intratracheal intubation]. 135 16

Exercise thallium-201 imaging using single-photon emission computed tomography (SPECT) was evaluated in 154 patients with angiographically documented coronary artery disease (CAD) and in 25 normal subjects. Of the 154 patients with CAD, 134 (87%) had abnormal thallium images. By contrast, only 77 (50%) patients had ischemic ST-segment depression (p < 0.001). Among 25 normal subjects, 20 had normal exercise SPECT images. The specificity of exercise SPECT imaging (80% or 20/25) in excluding patients with CAD was not significantly higher than that of exercise electrocardiography (76% or 19/25). For the detection of individual vessel involvement by analysis of territories of perfusion abnormalities, the sensitivity and specificity of exercise SPECT were 72% and 96% for the left anterior descending, 78% and 85% for the right coronary, and 47% and 98% for the left circumflex artery. Ninety (group 1) of the 154 patients with CAD achieved adequate exercise end points (ischemic ST-segment depression or > 85% of maximal predicted heart rate) and 64 (group 2) did not. Exercise SPECT showed significantly more perfusion abnormalities in group 1 than in group 2 (96% vs 75%, p < 0.001). We conclude that: (1) exercise SPECT thallium imaging is more sensitive than exercise electrocardiography for detecting patients with CAD; (2) the sensitivity of the test is affected by the level of exercise; and (3) it is valuable in the identification of individual vessel involvement.
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PMID:Exercise thallium-201 tomographic scintigraphy in the diagnosis of coronary artery disease: emphasis on the effect of exercise level. 136 12

In order to examine the possible role of coronary artery spasm in the pathogenesis of unstable angina, provocative testing for coronary spasm was performed in 43 patients with unstable angina who had 0- or 1-vessel disease. Coronary spasm was induced in 20 (65%) of 31 patients by hyperventilation testing (ST increases in 18, ST decreases in 2). Anginal attacks with either ST-segment elevation or ST-segment depression in patients without a significant organic stenosis were induced in 23 (55%) of 42 patients during treadmill exercise testing. Coronary artery spasm, showing severe (> or = 90%) vasoconstriction with angina and/or ischemic electrocardiographic ST-segment deviation, was also documented angiographically in 42 (98%) of 43 patients following intracoronary injection of acetylcholine. We conclude that dynamic coronary obstruction plays an important role in the genesis of attacks in patients with unstable angina who had 0- or 1-vessel organic coronary artery disease.
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PMID:Pathogenesis of unstable angina with 0- or 1-vessel disease. Important role of coronary artery spasm. 136 32

A number of studies have addressed the response to calcium antagonists, used alone or combined with other therapy, in patients with silent myocardial ischemia (SMI). Nifedipine, the first calcium antagonist to be studied, was shown to be superior to pindolol in patients with effort angina. Although both nifedipine and diltiazem significantly reduced episodes of ST depression, compared with placebo, in patients with stable effort angina, the addition of nifedipine to diltiazem removed the beneficial effect of diltiazem in another study. Studies have shown a reduced incidence of ischemic episodes during nicardipine treatment in patients with ambulatory ischemia, predominantly SMI, and rest angina due to coronary artery spasm. Other workers similarly reported that verapamil was superior to both placebo and propranolol in reducing painful and painless ischemia in patients with angina at rest. It has been demonstrated that, compared with placebo, nifedipine reduced ischemic episodes by 50% and also markedly reduced total ischemic time in totally asymptomatic men with coronary artery disease and SMI. It was suggested that the well-documented increase in SMI occurring between 0600 and 1200 h was reduced, but not eliminated, by nifedipine. Diltiazem may also attenuate the circadian variation in SMI. Nifedipine has been shown to be particularly effective in SMI when combined with a beta-blocker. This has been substantiated in a large group of patients; both drugs reduced the number of episodes of SMI when used as monotherapy, and the combination decreased the incidence by 95%. These findings collectively indicate that calcium antagonists are effective in reducing or preventing SMI.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical effects of calcium antagonists in silent ischemia. 136 8


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