Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Awareness by medical practitioners of the need to keep their patients adequately informed of their conditions is of paramount importance in caring for those people who have had a myocardial infarction. This includes a realization that these people have questions to be answered at all stages of the illness, from the initial contact when in pain, throughout the hospital admission, and during rehabilitation.
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PMID:The coronary: "will I have another?". 49 31

In an effort to determine the usefulness of prodromata for predicting a myocardial infarction, a prospective analysis was made of 211 consecutive patients with chest pain who were admitted to the Stanford University Medical Center Coronary Care Unit. In their subsequent course, 91 patients had a myocardial infarction, 102 had a myocardial infarction ruled-out, and 18 had a noncardiac etiology for their chest pain. Prodromal chest pain in the previous six months had occurred in 65% of patients and unstable angina in 61%. Infarction versus noninfarction patient groups could not be identified on the basis of prodromal ill health, chest pain, unstable angina, typical versus atypical nature of the chest pain, or activity at the onset of pain. Complaints of preceding fatigue and increased perceived stress were common in both groups. Activity at the onset of the admission chest pain was strenuous in 15% of the infarction patients and 12% of the noninfarction patients. We conclude that prodromal symptoms are common in both infarction and noninfarction patients. Although chest pain probably remains the single most frequent identifier of a new cardiac event, it is common in noninfarction patients and cannot be used alone to predict infarction or death.
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PMID:Prodromal characteristics as indicators of cardiac events in patients hospitalized for chest pain. 49 4

Cardiogenic shock and severe left ventricular failure after acute myocardial infarction, refractory angina pectoris at rest either of new onset or superimposed on stable angina pectoris, or occurring in the post infarct (less than 2 weeks) period, and the suspicion of a slowly evolving infarction are the main indications for intra-aortic balloon pumping at the Thoraxcenter. 76 patients were treated with intra-aortic balloon pumping for cardiogenic shock after acute myocardial infarction and left ventricular failure, 42/76 (55%) could be weaned, 9 (12%) died within 3 months, 33 (43%) survived over 3 months, to date 29 are alive. 42 patients with refractory angina at rest were treated with intra-aortic balloon pumping. Pain relief was prompt in 41 (98%), who subsequently underwent coronary artery bypass grafting. Total myocardial infarction rate was 11% (5/42), total mortality rate was 7%. Perioperative myocardial infarction rate was 8% (4/42) and perioperative mortality was 7% (3/42). Pain relief was prompt in 14/17 patients (82%) with post infarct refractory angina. In 3 patients pain persisted despite intra-aortic balloon pumping, all sustained a myocardial infarction, 1 died, 2 other patients were excluded for surgery. 12 patients underwent coronary artery bypass grafting, none died, none developed acute myocardial infarction, 3 have mild stable angina. In 8 patients a slowly evolving myocardial infarction was suspected. Pain relief was prompt in 7/8 (88%) after institution of intra-aortic balloon pumping. Intra-aortic balloon pumping improves prognosis in cardiogenic shock after myocardial infarction, and abolishes refractory ischemic pain.
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PMID:Intra-aortic balloon pumping in coronary artery disease. 52 Sep 98

Twenty to sixty per cent of myocardial infarctions go unrecognized by patient and doctor, and there is no way to exactly predict these at the moment. But they have a much lower long-term mortality rate than do clinical infarctions. As a rule, a myocardial infarction will be preceded by pain and the sooner this is dealt with, the greater the salvage rate.
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PMID:The immediate care of threatening myocardial infarction in general practice. 53 66

We investigated the activity kinetics of CK-total and CK-MB in 83 patients with proven myocardial infarctions. Serial serum samples were taken at intervals of 2--6 h. The activity of isoenzym CK-MB was determined by means of the immunological inhibition method. CK-MB activity was determined in all patients. The mean peak activity of CK-MB was 65 U/l (range: 9-241 U/l). At the time of peak CK-MB activity the mean percentage CK-MB activity was 13.2% (range: 3.4--21.7%). The CK-MB activity reached its peak at 17.4 h (range: 3.0--32.5 h) after the onset of retrosternal pain. This is 1.4 h after peak CK-total activity. The mean disappearance rate constant for CK-MB (n = 31) was found to be 9.3 X 10(-4) U/min with a large individual variation. This value corresponds to a half life of 12.5 h (CK-total: 15.5 h). The determination of CK-MB activity is therefore only of diagnostic significance within 48 h of possible myocardial occurrence. Moreover, isoenzyme CK-MB is not found exclusively in myocardium. For this reason it is better to use the percentage CK-MB activity in the differential diagnosis of myocardial infarction. With 80% of the patients this value is greater than 6% within 36 h of proven myocardial infarction.
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PMID:[Studies of activity kinetic of isoenzyme CK-MB in serum after myocardial infarction (author's transl)]. 56 53

Myocardial infarction is considered the prime cause of death among adult diabetic patients. In a great number of cases, during myocardial infarction the patients don't feel pain or it is atypical. Diagnosis can be neglected, and mortality increases. In search of an explanation for the absence of pain in these patients, the authors studied the autonomic nerve fibers of the heart muscle with argentic and combined techniques, looking for lesions in the sympathetic or parasympathetic nerve fibers that conduct pain. In the five cases of painless myocardial infarction studied, the nerve fibers showed typical lesions of diabetic neuropathy: beaded thickenings, spindle-shaped thickenings, fragmentation of fibers, and diminution of the number of fibers in the nerves. The patients in the control group (five diabetics with painful infarction, five diabetics with infarction, five nondiabetics with painful infarction, and five nondiabetics without infarction) had no lesions. These facts led us to assume that the absence of pain in diabetics with myocardial infarction could be due to a lesion of the afferent nerves that conduct pain.
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PMID:Autonomic neuropathy and painless myocardial infarction in diabetic patients. Histologic evidence of their relationship. 59 Jun 38

The current series represents the total experience of one institution that has treated concurrently a large number of patients with medical or surgical therapy. As previously reported, surgery offers a greater chance for pain relief but no obvious protection from future myocardial infarction. Patients with single artery disease show no difference in survival or future myocardial infarction rate whether treated medically or surgically. Improvement in survival following surgery, determined by univariate analysis of clinical descriptors, in several subsets of patients in the present series has not been confirmed when multivariate analysis techniques are used. If surgical mortality can be further lowered there may well be subsets of patients with coronary artery disease who will outsurvive similar medically treated patients. The current and future natural history of coronary artery disease, whether treated medically or surgically, is not settled by this or any other series because both forms of therapy are rapidly changing and no current series meets valid statistical criticisms. We are in a state of evaluation concerning not only therapeutic approaches, but also the development of suitable statistical methods for determining the efficacy of various forms of therapy. Only by continual modification of therapeutic approaches and the statistical tools to measure their effectiveness can we approach confident conclusions.
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PMID:The natural history of coronary artery disease: an update on surgical and medical management. 61 18

Seventy-five patients who had chest pain but no history or ECG evidence of myocardial infarction (MI) underwent myocardial-stress perfusion scintigraphy (MSPS) with thallium-201, treadmill-stress testing (TST), and coronary cineangiography (CA). The sensitivities of MSPS and TST for coronary stenosis greater than or equal to 75% were 68% and 71%, respectively; their specificities were 97% and 79%, respectively (0.1 greater than p greater than 0.05). When the character of a patient's chest pain is considered, Bayesian analysis leads to the following conclusions: (a) MSPS can be useful in pre-CA screening of patients with chest pain but no MI if their pain is thought to be of uncertain or nonischemic origin: (b) the sensitivity of Tl-201 MSPS is not sufficient for pre-CA screening of patients without MI who have typical or atypical angina pectoris; (c) the sensitivity of MSPS would have to be approximately 95% in order for the test to be useful in pre-CA screening of patients who have atypical angina pectoris; (d) MSPS may be superior to TST in these applications; and (e) it is not clear that there is any advantage in combining MSPS and TST into a single screening test rather than using MSPS alone.
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PMID:The predictive value of myocardial perfusion scintigraphy after stress in patients without previous myocardial infarction. 63 1

Although many patients with coronary artery disease (CAD) have a positive exercise test without pain, the frequency and significance of this "silent" ischemia is unclear. Therefore, we studied 122 consecutive clinically stable patients with angiographically defined CAD (greater than 75 per cent luminal stenosis) and a positive exercise test. Seventy-eight patients had pain or anginal equivalent during or after a positive exercise test; 44 did not, including 32 (26 per cent) with no symptoms at all. Patients were evaluated as to age, sex, prior myocardial infarction, congestive failure, hypertension, diabetes mellitus, and digoxin or propranolol therapy--in addition to anginal symptoms before, during, or after the exercise itself. Extent of CAD, presence of collaterals, and left ventricular ejection fraction were also determined. All exercise tests were evaluated for evidence of ST-T abnormalities or prior infarction on the control ECG as well as peak heart rate during exercise and post-exercise degree of ST segment depression. There were no significant differences between patients with and without exercise-induced pain in regard to any of the clinical and angiographic features noted above, demonstrating that "silent" myocardial ischemia during or after exercise testing is not uncommon and is not readily attributable to any obvious clinical or catheterization findings. Further studies are necessary to determine if patients with evidence of "silent" myocardial ischemia are especially prone to sudden death.
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PMID:"Silent" myocardial ischemia during and after exercise testing in patients with coronary artery disease. 63 80

When a patient's coronary arteries are anatomically normal, variant angina probably results from transient spasm that narrows and occludes a coronary artery; medical treatment is usually advised. But this distinctive type of pain can also occur in conjunction with atherosclerotic disease, in which case bypass surgery may prove highly effective in relieving symptoms and averting the risk of myocardial infarction.
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PMID:Management of variant angina and coronary spasm. 64 Jun 33


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