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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The submaximal treadmill exercise test is a valuable noninvasive tool for the diagnosis of overt or latent coronary artery disease (CAD). When submaximal heart rates of 80% to 90% of the predicted maximal rates are attained and when ST-segment depression of at least 1 mm is taken as a criterion of ischemia, testing by any of the various exercise protocols with continuous ECG monitoring affords reasonable specificity and sensitivity. The objectives of testing are to (1) diagnose and determine the severity of CAD, (2) assess functional capacity, (3) observe the natural history of disease, (4) evaluate the effects of medical and surgical treatment, and (5) evaluate responses to physical conditioning or to programs directed toward prevention of CAD. Proper precautions and safety standards minimize the risk of exercise testing.
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PMID:Submaximal treadmill exercise testing of patients with coronary artery disease. 85 49

Six men, clinically diagnosed as having coronary heart disease, had postexertional ventricular fibrillation after maximal exercise testing. The common featureof their treadmill performance was "exertional hypotension," that is, a decrease or a limited increase (10 mm Hg) in systolic blood pressure. All six men were successfully resuscitated with electircal defibrillation. The major indication for electrocardiographic monitoring is the detection of major ventricular arrhythmias and changes in QRS-ST-T of acute myocardial infarction or severe ischemia, all of which are urgent indications for stopping exertion. Close supervision both during and after exercise testing is essential, particularly in men with severe coronary artery disease; monitoring of changes in systolic pressure during and shortly after exercise testing is as important as searching for changes in the -S-T segment.
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PMID:Exertional hypotension and postexertional ventricular fibrillation in stress testing. 86 Jun 95

Because of their potential role in the pathogenesis of sudden death, cardiac arrhythmias in patients with coronary artery disease have become the subject of increasing concern and investigation. A series of studies on the problem of ventricular ectopy as it relates to the entire spectrum of sudden death in coronary disease were carried out utilizing continuous portable electrocardiographic monitoring systems. Evaluation of arrthymias during the entire 3 week in-hospital period after acute myocardial infarction in 83 patients revealed that absence of premature ventricular contractions, including their serious forms (multifocal, paired, R on T phenomenon, frequency 5/min or greater) and ventricular tachycardia in the coronary care unit did not exclude their high incidence rate (premature ventricular contractions 30 percent, serious forms 41 percent, ventricular tachycardia 6 percent) in the late hospital phase. Because late hospital serious forms of ventricular ectopy correlated with arterial hypoxia and elevated left ventricular filling pressure in the coronary care unit and with persistent S-T abnormalities, the extent of left ventricular dysfunction and ischemia with acute myocardial infarction appeared precursors to these arrhythmias. Study of ventricular ectopy in the late hospital phase of acute myocardial infarction indicated that ventricular ectopy and particularly its serious forms and prognostic significance relative to subsequent sudden death after discharge; the extent of predischarge S-T segment alterations was greater in subjects who died suddenly than in survivors, suggesting that persistent ischemia or segmental dyssynergy, or both, predisposed to lethal arrhythmias. Among 86 patients with chronic coronary disease documented by catheterizerization, 87 percent had ventricular ectopy and 62 percent serious ventricular arrhythmias, in contrast to 34 percent and 9 percent, respectively in normal subjects; frequency of serious forms of ventricular ectopy was related to extent of coronary atherosclerosis. Correlation of standard electrocardiograms with continuous Holter electrocardiograms in 101 patients with chronic coronary disease over 24 months revealed that the former modality was insensitive in arrhythmia detection; patients free of ventricular ectopy by serial standard electrocardiograms had a 62 percent incidence rate of serious forms of ventricular ectopy and 6 percent ventricular tachycardia on portable continuous monitoring. Additional studies of patients with chronic coronary disease showed that assessment of both the type of ventricular ectopy and the setting in which it occurs provides the most meaningful characterization of risk of sudden death. These systematic series of observations identify premature ventricular ectopic beats as important and separate risk factors in coronary disease...
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PMID:Identification of sudden death risk factors in acute and chronic coronary artery disease. 87 Nov 8

To evaluate whether elevated arterial free fatty acids (FFA) increase myocardial oxygen demand and ischemia, 15 fasting patients with coronary artery disease underwent a standardized atrial pacing test before (PTI) and during (PT2) heparin infusion. The patients were monitored for clinical and electrocardiographic (ECG) manifestations of ischemia. Myocardial extraction of lactate, inorganic phosphate, oxygen and FFA was measured before and during each PT. The control arterial FFA was 0.65 +/- 0.03 micromole/ml and rose to 1.83 +/- 0.16 micromole/ml during heparin influsion. Myocardial oxygen extraction at rest and during PT was not affected by the increase in arterial FFA. Seven patients asymptomatic during PT1 did not develop ischaemic manifestations during PT2. In eight patients with angina during both PTs, increased arterial FFA concentration did not modify the severity of anginal pain, the amount of ST-segment depression and the myocardial balance of lactate or inorganic phosphate. Elevation of arterial FFA by heparin neither increased myocardial oxygen extraction at rest or during pacing nor accentuated ischemic manifestations during PT.
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PMID:Effect of increased free fatty acids on myocardial oxygen extraction and angina threshold during atrial pacing. 87 27

In order to improve the value of exercise tests for the detection of coronary artery disease (CAD) a system for on-line computer processing of the Frank lead exercise ECG was developed. Data were analyzed from 95 patients with CAD and 129 ostensibly healthy men. All subjects had a normal ECG at rest. Visual ECG interpretation during exercise yielded a sensitivity of 50% and a specificity of 95%. A large number of QRS and ST measurements were compared by discriminant function analysis in a group of 86 normal subjects and 52 patients (designated training group). Best results were obtained with a combination of two ST amplitudes from lead X: sensitivity, 85%, specificity, 90%. This was confirmed in a test group of 43 patients and 43 normal subjects. The results of the discriminant function were expressed as the likelihood ratio for an abnormal or normal ST segment at a given heart rate, a figure which provides a quantitative assessment of the degree of exercise-induces ischemia. This is a more realistic approach than classification into normal or abnormal since persons with and without CAD fall along the same continuous spectrum.
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PMID:Estimation of the probability of exercise-induced ischemia by quantitative ECG analysis. 90 81

The possible relationship between the cardiac volume, as determined radiologically in the supine position in 119 patients with angiographically proven coronary artery disease, and the results of ergometry and balloon catheterization was investigated. There was no relationship between the heart size on the one side and the maximum exercise tolerance and the maximum cardiac output on the other, except for the fact, that these parameters tended to decrease with increasing heart size. This was especially true in patients with angina. The maximum cardiac output of patients with angina was always below the value of patients without angina but comparable heart size. Reduced cardiac output under exercise (exertional cardiac insufficiency) was present in 50% of patients with enlarged hearts but already in 22% of patients with heart volumes in the lower range of normal. The diastolic pulmonary artery pressure, determined under exercise, was the only parameter with a significant relationship to the heart size: The larger the heart size, the higher the diastolic pulmonary artery pressure. On the other hand: the diastolic pulmonary artery pressure at rest was abnormal with significant frequency only, when the heart was enlarged. Our data suggest, that the hemodynamics are determined by 2 factors: Myocardial scarring secondary to infarction and coronary insufficiency (ischemia). Of these two factors only the former influences cardiac size. Therefore, determination of the heart volume helps evaluating the respective role of these two factors in individual cases.
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PMID:[Heart size and left ventricular function in coronary artery disease: I. Heart size, exercise tolerance, cardiac output and filling pressures (author's transl)]. 92 89

Noninvasive myocardial imaging with potassium-43 and rubidium-81 has been used successfully to identify areas of infarction and exercise-induced ischemia as regions of decreased radioactivity. The image defects observed are believed to be due to a decreased radionuclide uptake in regions of myocardial scar or to heterogeneous myocardial accumulation of tracer as a result of regional ischemia. Of 27 patients with left bundle branch block studied with noninvasive imaging at rest and during exercise, 25 manifested at rest reduced radioactivity in the region of the interventricular septum. This pattern is similar to that seen in patients with anteroseptal myocardial infarction. Sixteen of the 27 patients underwent diagnostic coronary arteriography and left ventriculography. Only five of these patients had evidence of either previous infarction or significant obstructive coronary artery disease as assessed with clinical or angiographic criteria, or both. Although the image defect was routinely demonstrated at rest in patients with left bundle branch block, this defect was generally normalized or less distinct with exercise in patients with no anatomic heart disease. In contrast, a larger, more distinct or new image defect with exercise correctly identified the presence of significant obstructive coronary artery disease in patients with left bundle branch block. In the clinical application of noninvasive myocardial imaging, these image defects observed at rest can lead to the false pasitive radionuclide interpretation of anteroseptal myocardial infarction.
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PMID:Noninvasive myocardial imaging with potassium-43 and rubidium-81 in patients with left bundle branch block. 97 Mar 29

A morphologic study of the small (50 to 200 micron) intramyocardial coronary arteries was performed. The cases chosen for study were selected from a relatively young group of patients without clinical evidence of alcoholic cardiomyopathy or pathologic evidence of large coronary artery disease, in order to evaluate alterations in the small vessels which could possibly be attributed to the chronic alcoholic state. Five basic vascular abnormalities were described. The most common alteration found in all nine cases was vascular wall edema (48 per cent), followed by perivascular fibrosis (42 per cent), vascular sclerosis (36 per cent), subendothelial humps (13 per cent), and vascular wall inflammation (11 per cent). The significance and pathogenesis of these changes were discussed. Primary endothelial cell damage was proposed as a common pathogenic mechanism for all five types of vascular abnormality. It was suggested that following endothelial damage, fluid and macromolecules penetrate into the vessel wall or into the perivascular space where, by incompletely understood processes, they induce vascular wall myocytes to produce collagen, elastin, and basement membrane-like substances. Evidence supporting this mechanism was derived from the common observation of vascular wall edema, from the occasional presence of erythrocytes and leukocytes within the vessel wall, and from experimental data in the literature. Several possible etiologic agents were implicated in the pathogenesis of endothelial and vessel wall injury. These included alcohol itself, acetaldehyde, biogenic amines, and magnesium deficiency. It is probable, however, that there are multiple etiologic factors which affect the small cardiac vessels of the chronic alcoholic. Finally, the proposal was advanced that the nonspecific pathology of the myocardium in chronic alcoholism may be a result of ischemia secondary to disease of the small intramyocardial coronary ateries.
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PMID:Intramyocardial small-vessel disease in chronic alcoholism. 98 32

Actively contracting segments, preoperatively akinetic, were found in 8 of 63 patients, evaluated 6-12 months after aortocoronary surgery by coronary angiography. Ejection fraction was increased from 48.1% (S.D. 15.7) to 68.3% (S.D. 11.4). These patients are characterized by two simple clinical parameters: 1. All patients had angina pectoris at rest or at minimum exercise except for one; 2. preoperatively, there was a discrepancy between severe ventriculographic and discreet Ecg findings. These findings prove that myocardial function in coronary artery disease can be impaired at rest by ischemia, without clinical signs of coronary insufficiency, such as angina pectoris. Even severe impairment of left ventricular function is no contraindication for coronary artery surgery, if caused by reversible myocardial ischemia.
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PMID:[Function improvement in levography following aortocoronary bypass]. 108 30

Sudden death, known since antiquity, is almost always due to cardiovascular disorder, but not exclusively to coronary artery disease. It is postulated that two processes, action of pre-existing risk factors (enlarged heart, abnormal conduction, extra systoles, ischemia) and new, untoward events (acute infarction or ischemia) culminate in the catastrophic event. Sudden death is apparently most likely during waking hours; sleep is a lesser risk. Which subjects are at greatest risk and which circumstances are most dangerous remain unknown and are important topics for further investigation.
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PMID:Time, place, event of sudden death. 110 45


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