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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The sensory function of the upper limbs was examined in 18 subjects who had a myocardial infarction without a well-defined episode of chest pain. The cutaneous pain threshold was significantly higher than in normals. The ischaemia of the upper limbs induced patterns of sensations different from the normals, with onset of pain and of autonomic and coenaesthesic disturbances. These modifications of the sensory function are the same as observed in subjects with a previous painful infarction, but are quite different from those observed in patients with angina pectoris.
Pain 1976 Sep
PMID:Myocardial infarction without pain. A study of the sensory function of the upper limbs. 80 Feb 52

Two randomized series of 60 cases of myocardial infarction or menace syndrome have been treated at the acute stage, one by Heparin alone, the other by the combination Urokinase-Heparin. The average dosage was 300 mg Heparin in the first series, of 2,700,000 CTA units of Urokinase combined with 240 mg of Heparin in the second series. After the first 24 hours, equal heparinization was performed in both series up to the third week. Significantly different results were obtained in the two series. They favour Urokinase and concern: -- the disappearance time of pain, -- the course of the arrhythmias and of cardiac failure, -- the regression or limitation of the necrosis q waves and the lesion areas on the electrocardiogram. Finally the 30th-day overall mortality was 13% in the Heparin series and 3% in the myocardial infarction on the way of constitution, or which have done so for less than 24 hours.
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PMID:[Treatment by urokinase of myocardial infarction and threatened infarction. Randomised study of 120 cases]. 81 98

We studied the effects of coronary artery spasm on perfusion of the microvasculature in a patient with Prinzmetal's angina. Intracoronary injections of 99mTc and 131I-labelled macroaggregated human serum albumin were performed (1) at rest, (2) during spontaneous angina, (3) after the administration of nitroglycerin and (4) during pacing-induced spasm and the resultant scans compared. The resting scan was normal. Pain and spasm were associated with a perfusion defect that was localized to the anterior and inferior walls of the left ventricle. The localization of the perfusion defect corresponded with angiographically demonstrated spasm involving left anterior descending and distal circumflex coronary arteries. A subsequent myocardial infarction was localized by 43K scanning to the same perfusion area. Metabolic and parasympathetic stimulation studies were performed but were inconclusive. The patient's recurrent pains were ultimately controlled with large oral doses of isosorbide dinitrate.
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PMID:Prinzmetal's angina with coronary artery spasm. Angiographic, pharmacologic, metabolic and radionuclide perfusion studies. 82 56

Among 90 patients admitted to hospital with a diagnosis of first myocardial infarction consistent significant associations were found between pain duration, increase in concentration of serum glutamic oxaloacetic transminase (SGOT), maximum temperature and type of infarct (transmural or nontransmural). This suggests that infarct size may be associated with pain duration, increase in SGOT concentration and maximum temperature, and that patients with transmural infarcts have larger infarcts than those with nontransmural infarcts. A higher incidence of premonitory pain -- in particular, premonitory rest pain -- was noted in patients with transmural infarcts, who also had a significantly higher leukocyte count than patients with nontransmural infarcts. Pain intensity was also found to be associated directly with increase in SGOT concentration. However, because intergroup differences were not significant consistently, the association between infarct size, premonitory pain, pain intensity and leukocytosis is less certain. If the association between pain duration and infarct size is confirmed, a simple means would be available for the early recognition of the patient with a large infarct and adverse prognosis who would benefit from prompt therapeutic measures to reduce infarct size.
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PMID:Chest pain in the early recognition of large infarcts. 83 18

Six new cases of acute myocardial infarction with normal coronary arteriogram are presented and supplemented by 19 collected cases (group I). These are compared with 16 cases of myocardial infarction caused by occlusive coronary artery disease in a comparable population (group ii). The following significant differences between the two groups are established: patients in group I were younger (27.5 years vs 33.7 years, P less than 0.005); at least one risk factor was present in all patients in group II, but in only 40% of group I (P less than 0.0001). effort angina preceded the attack in ten patients of group II, but in none of group I (P less than 0.0001). The attack was unheralded in 24 of the 25 patients in group I, but was preceded by prodromes in 11 of 16 in group II (P less than 0.0001). Attacks of pain following myocardial infarction occurred in five patients of group 2 and II of group II) (P less than 0.001). Results are discussed in the light of the nature of myocardial infarction in group I. No support is found for the coronary spasm theory. The most likely mechanism for development of myocardial infarction in group I is thought to be a thromboembolic "accident." This accident is not necessarily related to atherosclerotic coronary disease and is presumed to be benign in nature.
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PMID:The nature and clinical features of myocardial infarction with normal coronary arteriogram. 83 99

In vitro experiments employing the polarographic technique of in-rush currents have demonstrated that adrenalin and noradrenaline in concentrations approaching those found in blood of myocardial infarction patients during the early days of the disease inhibit the tissue respiration of the cardiac muscle by 10--50%. A 10-minute intensive pain stimulation was found to inhibit the aerobic processes in the myocardium by 20--24%. Hypercatecholaminemia observed in the acute period of myocardial infarction is suggested to play an important role in the pathogenesis of cardiac insufficiency during myocardial infarction, since it causes histotoxic hypoxia of the intact portions of the cardiac muscle. The importance of eliminating the pain syndrome in patients with myocardial infarction and angina pectoris is emphasized.
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PMID:[Effect of exogenous catecholamines and pain action on the tissue respiration of the myocardium]. 85 43

In order to investigate the relation between the release of creatine kinase (CK) in acute myocardial infarction and the evolution of infarction, the appearance functions of CK (release of CK from the heart into the circulation) were calculated by the modified method of Sobel and associates from the serial determinations of serum CK activity in 50 patients with acute myocardial infarction. The relation of the time between the onset of infarction and the peak value of the appearance function to the duration of the evolution of abnormal Q waves in 14 patients with inferior infarction and to the duration of pain in all patients was investigated. The duration of CK release from the heart averaged 37-2+/-2-4 hours and correlated well with the total CK released (R=0.665) which represents the infarct size. The mean per cent of the total CK eventually released by the time of maximum sigmaQ (sum of the amplitude of Q wave in leads II, III, and aVF) was 80-0+/-6-4 per cent and that of CK released while pain persisted was 72-0+/-3-9 per cent. These results strongly suggest that the appearance function of CK reflects the evolution of myocardial infarction.
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PMID:Evaluation of evolution of myocardial infarction by serial determinations of serum creatine kinase activity. 86 Oct 91

Forty-six patients admitted with acute coronary insufficiency are reviewed. All were investigated by coronary angiography; 4 had normal coronary arteries and are included in this study; the remainder had a distribution of coronary artery disease similar to other angina patients. The clinical and angiographic findings, management, and subsequent course of the other 42 patients are presented. Fourteen patients (33%) in whom rest pain persisted after 48 hours underwent emergency coronary angiography, with 3 deaths; of the surviving 11 who had acute saphenous vein bypass grafting, 2 died at operation and 3 had perioperative myocardial infarctions. Seventeen patients (41%) who initially improved required surgery within 6 months because of symptoms. Eleven patients (26%) were not operated on. It is concluded that acute coronary insufficiency is best managed initially by intensive medical therapy but a high proportion will require surgery later because of disabling angina. Early investigation and surgery are associated with a high mortality and incidence of myocardial infarction. Survivors of surgery are symptomatically improved and there is a low incidence of late infarction and death.
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PMID:Acute coronary insufficiency. Review of 46 patients. 86 73

Three patients with clinical diagnosis of myocardial infarction are described, whose cardiograms are characterized by a transitory positivation of the negative T-waves. The confrontation of those changes with the clinical picture reveals that the transitory positivation of the T-wave coincides with the clinical and paraclinical signs of intensification of the myocardial hypoxia (pain, collapse, enzyme positivation). The possible electrophysiological mechanisms are discussed that could explain the transitory positivation of the negative T-waves, as a manifestation of the intensified ischemia.
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PMID:[Atypical hypoxic changes in the T wave]. 89 10

The instable angina pectoris belongs to the prodromes of an acute transmural my ocardial infarction, to which we refer every fresh angina pectoris, increase and prolongation of the anginous pain after stress and the appearance of pain in rest. Retrospectively we established the instable angina pectoris in 45% of the cases of a transmural myocardial infarction. Prospectively the syndrome of the instable angina pectoris was followed by a transmural myocardial infarction in 18%. In 14% of the cases with instable angina pectoris without provable transmural myocardial infarction a sudden heart death took place. In the discussion the author deals with questions of the not clarifyed pathogenesis and therapy. The instable angina pectoris is, indeed, an important clinical syndrome, but from the point of view of the short-time prognosis in our opinion it has not the presumed significance for the development of the transmural myocardial infarction and the sudden heart death.
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PMID:[Instable angina pectoris and the pre-infarct condition]. 90 97


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