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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Variations in clinical noninvasive systolic pressure at the point of symptom-limited exercise on a treadmill were examined in six groups of subjects: 5,459 men and 749 women classified into three categories each. Among the men, 2,532 were asymptomatic healthy, 592 were hypertensive and 1,586 had clinical manifestations of coronary heart disease (that is, typical angina pectoris, prior myocardial infarction or sudden cardiac arrest with resuscitation). Among the women, 244, 158 and 347 were in the corresponding clinical categories. None had had cardiac surgery; all had follow-up status ascertained by periodic mail questionnaires. Reported deaths were reviewed and classified by three cardiologists; 140 deaths were attributed to coronary heart disease, 118 of them in the men classified as having coronary heart disease. The majority of maximal systolic blood pressure readings were reported to the nearest centimeter rather than millimeter of pressure. Retesting of 156 persons from 1 to 32 months later showed that pressure values agreed within 10 percent in two thirds, the overall mean difference was only 8.6 mm Hg and the correlation at maximal exercise was superior to that of the resting observations just before exercise. Hypertensive patients had a significantly greater body weight than normotensive persons. Among men, the lowest maximal systolic pressure was observed in the group with coronary heart disease; among women, the lowest mean pressure was found in the healthy group. Patients with coronary heart disease were slightly older, and only the women showed a significant correlation in maximal pressure with age. Only 5 percent of the variation in maximal systolic pressure in the patients with coronary heart disease was due to a shortened duration of exercise. Maximal systolic pressures correlated fairly well (r equals 0.46 to 0.68 for the various groups) with resting systolic pressure, and this relation was independent of the diagnosis of cardiovascular disease in both men and women. Relations between pressure and the number of stenotic coronary arteries and imparied ejection fraction at rest were examined in 22 men without and 182 men with coronary artery disease. Lower maximal systolic pressures were often associated with two or three vessel disease or reduced ejection fraction, or both. The prognostic value of maximal systolic pressure for subsequent death due to coronary heart disease was examined in the men with coronary heart disease. The annual rate of sudden cardiac death decreased from 97.9 per 1,000 men to 25.3 and 6.6 per 1,000 men as the range of maximal systolic pressure increased from less than 140 to 140 to 199 and to 200 mm Hg or more, respectively. Cardiomegaly, Q waves in the resting electrocardiogram and persistent postexertional S-T depression were more common in men with the lowest systolic pressure at maximal exercise.
Am J Cardiol 1977 May 26
PMID:Variations in and significance of systolic pressure during maximal exercise (treadmill) testing. 87 Nov 10

Twenty-one long-term survivors of out of hospital sudden cardiac death due to ventricular fibrillation underwent radionuclide angiography and myocardial imaging with thallium-201. In 13 patients images were obtained at rest and after maximal treadmill exercise; 11 of these 13 (85 percent) had an image defect in one or both studies. Eleven of the 21 patients (52 percent) had a defect in the image obtained at rest. The magnitude of myocardial image defects was typically great; some patients had an image abnormality without other clinical evidence (angina, S-T depression) of ischemia. The mean ejection fraction, assessed in 16 patients with radionuclide angiography, was 0.41 +/- 0.15 (standard deviation); in 5 of the 16 ejection fraction was normal (more than 0.50) and in 3 it was severely abnormal (less than 0.25). Thus, noninvasive radionuclide studies defined a broad spectrum of ischemic and ventriculographic abnormalities in survivors of sudden cardiac death. Further application of these noninvasive studies may identify those at high risk.
Am J Cardiol 1977 May 26
PMID:Myocardial imaging and radionuclide angiography in survivors of sudden cardiac death due to to ventricular fibrillation: preliminary report. 87 Nov 11

The electrocardiograms of 15 left atrial rhythm and sinusal rhythm patients are studied. The spontaneous occurrence of LAR and the possibility of return to SR by vagal stimulation manoeuvers are reported. The electrocardiographic modifications of the ectopic rhythm are shown and compared either with those of the coronary sinus rhythm or junctional A-V rhythm, or with those of the tracings recorded during atrial pacing. The intermittent occurrence of the LAR in the studied cases is theoretically ascribed to the awakening of an ectopic focus, localized in the left atrium, acting as a new pace-maker because of its excited activity or abnormal depression of the sinus.
G Ital Cardiol 1977
PMID:[Left atrial rhythm. Electrocardiographic study (author's transl)]. 87 97

The hemodynamic, coronary sinus blood flow and myocardial metabolic effects of 0.15 mg/kg body weight of intravenously administered propranolol were studied in 19 patients with coronary artery disease and 6 normal patients. Atrial pacing was performed in all patients and produced angina in 15 of the 19 patients with coronary artery disease. In these patients propranolol reduced heart rate from 78 to 69 beats/min, cardiac index from 3.0 to 2.6 liters/min per m2 and left ventricular stroke work index from 47 to 43 g-m/m2; it increased total peripheral resistance from 24 to 28 units and lactate extraction from 16.3 to 22.5%. There was no significant change in mean arterial pressure, left ventricular end-diastolic pressure, coronary sinus blood flow or myocardial oxygen consumption. During a second pacing stress propranolol produced clinical improvement in 9 of the 15 patients who experienced angina initially. The improvement was associated with less severe abnormalities in S-T depression and left ventricular end-diastolic pressure, increased lactate extraction and no significant change in coronary sinus blood flow or myocardial oxygen consumption. Thus, propranolol appears to be capable of modifying the anginal threshold as determined with atrial pacing, and the clinical response appears to be independent of global changes in coronary sinus blood flow and myocardial oxygen consumption.
Am J Cardiol 1977 Jul
PMID:Effects of propranolol on the hemodynamic, coronary sinus blood flow and myocardial metabolic response to atrial pacing. 87 19

A model of partial thickness ischemia has been developed using subendocardial S-T elevation without epicardial S-T elevation to detect partial thickness ischemia which is sufficient to cause subsequent necrosis. Subendocardial blood flow in this model (measured with radioactive microsphere techniques) may be reduced to 25 percent of normal (P less than 0.001) by coronary stenosis and tachycardia while subepicardial flow remains normal. Epicardial S-T depression seems to indicate reciprocally subendocardial S-T elevation as long as a layer of nonischemic epicardial muscle is present, but when ischemia becomes transmural, epicardial S-T elevation occurs. Regional pressure-flow relations were determined as distal coronary pressure was reduced at a constant aortic pressure, heart rate and cardiac output. These relations revealed remarkably effective autoregulation of epicardial blood flow concomitant with progressive subendocardial ischemia.
Am J Cardiol 1977 Sep
PMID:Significance of subendocardial S-T segment elevation caused by coronary stenosis in the dog. Epicardial S-T segment depression, local ischemia and subsequent necrosis. 90 35

Ergonovine maleate (Ergotrate) was given to 57 patients undergoing coronary arteriography for investigation of angina occurring at rest or without provocation when routine study showed normal arteries or insufficient occlusive disease to explain their symptoms. This provocative test induced coronary arterial spasm in 13 patients, 10 of whom had definite Prinzmetal's angina. The spasm was easily reversed with sublingually administered nitroglycerin. The spasm was occlusive or nearly occlusive in nine patients, and there was associated reproduction of the chest pain and S-T elevation similar to the spontaneous episodes. One patient with Prinzmetal's angina had S-T depression rather than elevation in association with the chest pain. The other three patients without Prinzmetal's angina had focal narrowing without coronary occlusion, reproduction of the chest pain or electrocardiographic changes. Of the 44 patients who did not demonstrate coronary spasm in response to ergonovine, 29 had normal coronary arteries and 15 had various degrees of atherosclerotic occlusive disease. We conclude that cautious administration of ergonovine maleate during coronary arteriography can be safely used to elicit coronary spasm in some patients who have insufficient fixed occlusive disease to explain their symptoms.
Am J Cardiol 1977 Oct
PMID:Provocation of coronary spasm with ergonovine maleate. New test with results in 57 patients undergoing coronary arteriography. 91 Jul 12

Isolated junctional S-T depression induced during treadmill exercise testing was correlated with coronary arteriographic findings in 230 patients. Of 75 patients with junctional depression of less than 1.5 mm, 10 had 50% or greater stenosis of at least one major coronary artery and 2 patients (3%) had multivessel disease. Of 42 with junctional depression of 1.5 mm or more and a rapid upsloping S-T segment, 23 had 50% or greater coronary stenosis and 12 of these had multivessel disease. Of 35 with an upsloping pattern (junctional depression of more than 2 mm, upsloping S-T segment depressed 2 mm or more, 0.08 second after the J point), 33 (94%) had 50% or greater coronary stenosis compared with 46 (96%) and 30 (97%) with 2 mm or more junctional depression ahd a horizontal or downsloping S-T segment. In conclusion, multivessel disease is rare with isolated exercise-induced junctional depression of less than 1.5 mm but common when the J point is depressed 1.5 mm or more. Junctional depression of more than 2 mm is associated with the same incidence of coronary disease when the S-T segment is slowly ascending (upsloping pattern) as when it is horizontal.
Am J Cardiol 1977 Oct
PMID:Significance of exercise-induced junctional S-T depression in evaluation of coronary artery disease. 91 Jul 13

A 40 year old man with far advanced coronary heart disease consistently experienced pain and exhibited marked S-T segment depression after 44 crossings during a Master two-step test. When the number of times traversed was miscounted so that he exercised less, the pain occurred at the precise count of 44 and he showed the same marked degree of S-T depression. However, when the count was accurate, he had neither pain nor S-T segment deviation at the reduced exercise level. The possible basis for verbal conditioning provoking angina pectoris is explored.
Am J Cardiol 1977 Oct
PMID:Verbal conditioning of angina pectoris during exercise testing. 91 Jul 28

To delineate the relative effects on left ventricular function of the site, extent and nature of the abnormal left ventricular segmental contraction (dyssynergy) and thereby determine the mechanism by which anterior myocardial infarction results in greater depression of left ventricular performance than does inferior infarction, 43 patients with remote myocardial infarction of similar extent (average 38 percent of left ventricular systolic perimeter) and associated hypokinesia or dyskinesia confined to either the anterior or inferior wall were compared; 10 additional patients were evaluated who exhibited generalized dyssynergy (72 percent of left ventricular perimeter). When the pattern of dyssynergy and extent of infarction were similar, the location alone of dyssynergy did not influence variables of left ventricular function. However paradoxical outward systolic movement (dyskinesia) of the anterior or inferior wall resulted in greater depression (P less than 0.05) of measures of left ventricular performance than did diminished inward systolic motion (hypokinesia) associated with infarction of similar extent and location. All measures of left ventricular performance were considerably more depressed (P less than 0.05) in the 10 patients with generalized dyssynergy than in the 43 patients with localized dyssynergy. Thus, the location of infarction is not a unique determinant of left ventricular performance. Instead, the size of infarction is the principal characteristic of dyssynergy that impairs left ventricular function; the severity of the pattern of dyssynergy is significant but of lesser importance. It is therefore concluded that the greater reduction of left ventricular function in anterior than in inferior myocardial is largely the result of the more extensive area of necrosis rather than of the location of the infarction.
Am J Cardiol 1976 Mar 04
PMID:Pump dysfunction after myocardial infarction: importance of location, extent and pattern of abnormal left ventricular segmental contraction. 94 21

Several electrophysiological aspects of the effects of procainamide were analyzed, using a method which allows direct study in man. The following electrophysiological parameters were determined under normal conditions in pace-maker carriers: myocardial stimulation threshold (M.S.T.), above-normal excitability phase (A.N.P.), effective refractory period (E.R.P.), pre-automatic pause (P.A.P.) and frequency of spontaneous rhythm (S.R.). After i.v. somministration of 10 mg/kg of procainamide in six subjects, and of 20 mg/kg in one, the modifications resulting from the examined parameters were analyzed. They showed that procainamide determines the constant elevation of the M.S.T., the shortening of duration of the A.N.P., lengthening of the E.R.P. and depression of the ventricular, but the superventricular automatism. Hypotheses on the electrophysiological mechanism of the observed effects are analyzed, and some clinico-electrophysiopathological correlations are traced, which help in the understanding of the anti-arrhythmic activity of procainamide.
G Ital Cardiol
PMID:[Study of several electrophysiological effects of procainamide in man (author's transl)]. 101 Feb 15


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