Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serial monitoring of the serum isoenzyme patterns of creatine phosphokinase (CPK) and lactate dehydrogenase (LDH) in patients suspected of acute myocardial infarction has become a highly sensitive and specific diagnostic method. The predictable evolution of isoenzyme patterns following infarction permits diagnosis and recognition of early stages, recovery stages and extension of infarction in the individual. Usual therapeutic and resuscitative manipulations do not interfere with evaluation of patients with angina or following cardiopulmonary arrest without infarction. Despite significant elevations of serum enzyme levels following general and cardiac operative procedures, the occurrence of myocardial necrosis in the surgical population can be recognized by detection of the specific CPK-MB isoenzyme.
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PMID:Diagnosis of myocardial infarction by serum isoenzyme analysis. 32 44

Eight patients with severe peripheral vascular atherosclerosis scheduled for abdominal aortic surgery were investigated to detect coexisting coronary artery disease. None of the patients had a history of angina pectoris or previous myocardial infarction. Preoperative computerised thallium-201 dipyridamole myocardial scintigraphy was abnormal in all patients, showing either myocardial scar tissue and/or ischaemia with redistribution and/or low washout. In all but one patient, the serum level of creatin kinase was elevated during the first postoperative days. In two patients, the serum concentrations of aspartate aminotransferase and lactate dehydrogenase were elevated. None of the patients showed clinical or electrocardiographical signs of acute myocardial infarction. Thallium-201 dipyridamole myocardial imaging is a new noninvasive method for detection of ischaemic heart disease in patients with severe peripheral atherosclerosis who are unable to perform a bicycle exercise test. The new programme for determination of regional washout appeared to be very precise and may be especially applicable in the case of low washout values.
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PMID:Thallium-201 myocardial scintigraphy during dipyridamole-induced coronary hyperaemia. First experiences with a new regional washout programme. 321 87

Male patients with effort angina were studied before (n = 7), 1 week, and 1 and 6 months (n = 6) after coronary artery bypass grafting (CABG) with 2 to 7 grafts. The test battery included graded exercise, which was performed until unbearable leg exertion or chest pain, or both, was present. Onsets of blood lactate accumulation, anginal pain, leg exertion and dyspnea were interpolated for either the lactate concentration 2 mmol X 1-1 or the ratings 2 on the Borg subjective intensity scale. Onsets of blood lactate accumulation and symptom-limited exercise capacity before surgery amounted to 58 and 100 W, respectively. The corresponding figures 6 months later were the same for onset of blood lactate accumulation, whereas symptom-limited exercise capacity had increased by 58%. Blood lactate was the same at rest and mild exercise (congruent to onset of blood lactate accumulation) but more than doubled at symptom-limited exercise capacity (peak blood lactate concentration). Muscle fiber typing showed a low figure for the slow twitch fiber proportion (35%), which was unchanged after 6 months. Fast twitch subtype C was elevated before (7%) but disappeared after surgery, and fast twitch subtype A percent increased correspondingly. The major muscle biochemical changes were in the glycogenolytic pathway and the lactate dehydrogenase enzyme system, which appeared to increase in a quantitative manner, but with an unchanged relative lactate dehydrogenase isozyme pattern. The increased symptom-limited exercise capacity was related to the increased glycogenolytic activity and peak blood lactate (i.e., increased "anaerobic power"). Whether the causative explanation was the relief from chest pain, i.e., a psychophysiologic feature or the biochemical changes that took place in the muscle could only be speculated on.
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PMID:Onset of blood lactate accumulation exercise capacity, skeletal muscle fibers and metabolism before and after coronary artery bypass grafting. 326 32

Values for total lactate dehydrogenase (LD, EC 1.1.1.27) activity in serum, LD isoenzymes 1 and 2, and the LD 1:2 ratio in 25 patients with unstable angina were compared with the same variables in 25 patients whose angina was stable 24, 48, and 72 h after admission. Mean total LD activity and mean LD-2 activity were found to be within the normal range, both in the unstable angina and stable angina groups of patients. In the unstable angina group the mean LD-1 was significantly higher (p less than 0.01) than in the stable angina group at each time studied. The mean LD 1:2 ratio was also significantly different (p less than 0.001) between the two groups of patients. In the unstable angina group of patients the ratio was increased (0.85, SD 0.09), as in patients with acute myocardial infarction, whereas in the stable angina group of patients the ratio was normal (0.60, SD 0.06). We conclude that a high LD 1:2 ratio, even in the presence of normal total LD activity, may indicate myocardial damage in some patients with unstable angina and could therefore help in the clinical and functional evaluation of patients with unstable angina.
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PMID:Lactate dehydrogenase isoenzymes in serum during unstable angina. 373 54

Platelet number and mean platelet volume (MPV) were measured in 100 patients with acute chest pain, 41 with acute myocardial infarction (AMI), 33 with angina pectoris (AP) and 26 with non-coronary event (NCE), and compared with 21 controls. We found no significant difference in platelet count on admission in the patient groups, but it was lower compared with controls. There were no significant differences in MPV between the patient groups nor between patients and controls. Thirty patients with AMI were followed for 10 days and showed an initial 12% fall in platelet count followed by a 36% increase. Initially there was an increase in MPV (2%) followed by a fall (8%). The fall in platelet count and increase in MPV correlated with infarct size (maximum activity of lactate dehydrogenase (LDH)) and might reflect consumption of platelets. The precise role of platelets in the process of infarction is still unknown.
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PMID:Platelet number and volume during myocardial infarction in relation to infarct size. 381 27

In 585 patients with a first myocardial infarction the enzymatically estimated infarct size was related to the clinical course during a 2-year follow-up. Infarct size was estimated from maximum heat-stable lactate dehydrogenase activity. A higher maximum serum activity was associated with a higher mortality rate, more treatment with diuretics, digitalis and antiarrhythmics and a lower frequency of return to work. Patients with smaller infarcts according to maximum serum activity, however, had a higher incidence of angina pectoris and a higher reinfarction rate. We conclude that although there is a strong association between serum enzyme activity and mortality during a 2-year follow-up, the relation with morbidity appears to be more complex.
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PMID:Relationship between serum enzyme activity in acute myocardial infarction and morbidity during a 2-year follow-up. 395 84

Angina pectoris may occur in the presence of normal major coronary vessels (NCA) in 10-20 per cent of patients investigated by coronary arteriography. Whilst hypertrophic cardiomyopathy, mitral valve prolapse and hyperthyroidism are excluded by routine investigation, in the remainder coronary vasospasm may be demonstrated. An organic basis for angina may not always be found. In order to document the pathophysiological basis for angina pectoris with NCA we have investigated patients using atrial pacing stress with measurement of coronary sinus blood flow and lactate metabolism, together with myocardial biopsy to determine biochemical and histopathological abnormalities. These have been correlated with localised coronary vasospasm induced by ergometrine (E). Thallium scintigraphy has also been used to detect the myocardial changes. Fifteen patients were investigated: 5 of 15 patients developed abnormal lactate metabolism on atrial pacing (change greater than 0.8 mg per cent in A/V lactate difference) and all had greater than 50 per cent coronary luman reduction after E. In 10 of 15 patients no lactate change occurred and in 7 no significant response to E was seen. However, significantly lower myocardial enzyme activities were found in the first group (lactate dehydrogenase p less than 0.01, malate dehydrogenase p less than 0.05, alpha hydroxy-butyrate dehydrogenase p less than 0.02). The change in myocardial enzyme activities in angina with NCA may indicate a metabolic basis for angina in those patients who develop both abnormal lactate metabolism on pacing and coronary vasospasm after ergometrine. The enzyme activities and histological changes in angina with NCA are similar to these in dilated cardiomyopathy.
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PMID:The pathophysiology of angina pectoris with normal coronary arteriograms. Histopathological and metabolic correlations with coronary vasospasm. 640 44

The mortality and morbidity of 150 young (less than 45 years) survivors of myocardial infarction was studied prospectively over a 10-year period. Thirty-seven deaths (36 due to coronary artery disease) occurred from one month to 10 years after myocardial infarction and the cumulative 10-year mortality was 27 per cent compared with 5 per cent in the general population. High initial lactate dehydrogenase levels and continued cigarette smoking after infarction were associated with a poor long-term survival. Angina was present at some time during follow-up in 60 per cent of patients. Severe limitation of exercise tolerance was present in 18 per cent, and 16 per cent had radiological evidence of cardiomegaly. Left ventricular failure occurred in 13 patients and carried a very poor prognosis. Unemployment in 95 men who survived 10 years was 32 per cent, half of whom had never returned to work following infarction, compared with a regional value of 7 per cent. We have shown that there is a prolonged and persistent mortality and morbidity in young survivors of myocardial infarction with a high level of male unemployment. Careful rehabilitation should reduce the economic loss to the community together with persuasive advice against cigarette smoking.
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PMID:The mortality and morbidity of young survivors of myocardial infarction. 714 16

We have studied 135 subjects of whom 100 were normal individuals; 10 with diagnosis of acute myocardial infarction (AMI); 10 with angina pectoris; 10 undergoing cardiac catheterism; 5 who underwent open heart surgery. To verify the radioimmunoassay usefulness of CPK cardiac isoenzyme (CK-RIA), of lactate dehydrogenase [LDH (H4)], of myoglobin (MG) in the diagnosis of ischemic disease, we have determined for serum samples: LDH (H4) by radioimmunoassay and HBDH by biochemical assay; CK by biochemical assay; CK-MB by biochemical and radioimmunological assay; MG by radioimmunoassay. The results indicate MG as a sensitive marker for the diagnosis of AMI. In fact serial serum determinations in patients with AMI showed myoglobin levels in 60% of the cases within 1 h after the onset of pain. The CK-RIA is the most sensitive test to evaluate infarct size and LDH (H4) conditioned by the amount of intracellular lactate is an useful test to evaluate myocardial anoxia.
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PMID:[Critical analysis of the radioimmunological methods of determining creatine kinase isoenzyme MB (CK-MB), myoglobin (MG) and of LDH (H4) in ischemic cardiopathy]. 724 91

SQ 32,926 and SQ 32,547, two dihydropyrimidine calcium channel blockers, were characterized as potent inhibitors of depolarization-induced contractions of isolated smooth muscle preparations. In rat aorta, the IC50 values were 5.5 nM for SQ 32,547 and 8.1 nM for SQ 32,926, values which compare favorably with that of 2.9 nM for nifedipine. The dihydropyrimidines were also tested in a model of stable angina: pacing-induced ischemia in dogs. Both SQ 32,547 and SQ 32,926 reduced the ST-segment elevation observed in vehicle-treated animals. No significant changes in hemodynamic status were detected, suggesting that a reduction in cardiac work secondary to afterload reduction was probably not a major contributor to the protective effects. Neither was increased coronary blood flow important for the antiischemic outcome because no significant effects of the dihydropyrimidines were observed on ischemic regional blood flow. SQ 32,547 was also studied in globally ischemic, isolated rat hearts. In this model, SQ 32,547 was protective because it significantly reduced contracture formation and lactate dehydrogenase (LDH) release. Washing out the effect of SQ 32,547 in isolated hearts and smooth muscles was difficult, presumably due to its lipophilicity. In the smooth muscle preparations, the effects of both nifedipine and SQ 32,926 were much more easily washed out. As with other calcium channel blockers, increasing the antiischemic effects of SQ 32,547 was associated with a higher cost in terms of cardiac function. In summary, the two novel dihydropyrimidines, SQ 32,547 and SQ 32,926 showed antiischemic properties in animal models.
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PMID:Pharmacologic profile of the dihydropyrimidine calcium channel blockers SQ 32,547 and SQ 32,926 [correction of SQ 32,946]. 747 54


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