Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0008031 (chest pain)
 17,248 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A radioimmunoassay was developed to measure serum levels of the B isoenzyme of creatine kinase(ATP: creatine N-phosphotransferase, EC 2.7.3.2) (CPK) in order to evaluate the time course and frequency of MB isoenzyme elevation in patients with acute myocardial infarction. The method can identify as little as 0.2 ng of the B portion of the CPK-MB isoenzyme, does not significantly crossreact with CPK-MM isoenzyme, and is not affected by storage of serum at --20 degrees CPK isoenzyme containing B subunits was detected in 48 out of 51 sera from normal adults; serum levels in these individuals ranged between 1.2 and 12.5 ng/ml [mean +/- SEM was 2.7 +/- 0.30 ng/ml]. The mean serum level of CPK-B isoenzyme in a pool of sera obtained from 100 normal subjects was 2.9 +/- 0.35 ng/ml; two patients with rhabdomyolysis that were studied had serum CPK-B isoenzyme levels of 2.5 and 3.5 ng/ml, respectively. In contrast, serum levels of the CPK-B isoenzyme were markedly elevated in sera from 18 patients with acute myocardial infarcts when obtained within 12 hr after hospital admission; the mean +/- SEM concentration was 56 +/- 7.8 ng/ml. We performed serial determinations on 14 patients with acute myocardial infarcts and demonstrated that maximal serum CPK-B levels occurred within the first 12 hr after admission and were lower thereafter. The serum concentration of B-containing CPK isoenzyme in 19 additional patients admitted with chest pain but without acute myocardial infarction was 3.4 +/- 0.50 ng/ml. Thus, radioimmunoassay measurement of CPK-B isoenzyme appears to be a useful and sensitive test for the detection of acute myocardial infarcts in patients.
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PMID:Radioimmunoassay of creatine kinase-B isoenzyme in human sera: results in patients with acute myocardial infarction. 26 11

Cardiac muscle death caused by coronary artery occlusion is a dynamic process that often takes hours or days. Emergency revascularization (saphenous vein bypass graft (SVBG) during acute myocardial infarction (MI) can interrupt myocardial necrosis, salvage ischemic myocardium and revascularize vessels with obstructive lesions not involved in the MI. In this report we describe a preliminary experimental study of 75 patients in which emergency SVBG was the therapy for acute MI. Group 1, 16 patients, required vasoactive medications and/or intraaortic balloon pumping to maintain their blood pressure preoperatively. There was one operative death and two late deaths. Group 2 consisted of 59 hemodynamically stable patients. There were no deaths. The average preop CPK in group 1 was 892 vs 504 in group 2 (p greater than 0.05). Surgical techniques were routine. The average time from the onset of chest pain that continued to surgery was 6.5 hours. Forty patients were restudied. Post- vs presurgical hemodynamics revealed ejection fraction increased by 34% (p greater than 0.05), left ventricular end-diastolic pressure reduced by 40% (p greater than 0.01). End-systolic and end-diastolic volume reduced by 30% (p greater than 0.05), and 15% (p greater than 0.01), and stroke volume improved 25% (p greater than 0.05). Operative mortality was 1.3% and late mortality 2.8%. These results suggest that cautious continued trial of emergency SVBG in patients with evolving MI is warranted.
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PMID:Emergency coronary artery revascularization: a possible therapy for acute myocardial infarction. 44 42

Sixty-eight patients of clinically diagnosed myocarditis, 0--15 years of age, were followed up and analyzed. Forty (58.8%) were males. The majority were older than 5 years. Clinical courses were rather mild, chronic and self-limiting at large. Only 1 case had a relation to chronic cariomyopathy. Exertional symptoms (chest pain, chest distress, syncope) were seen in 25 (36.8%). ECG changes were very common: the majority were nonspecific ST elevation, depression or both, mainly in leads II, III, V5 and V6. Positive Master' test, prolonged QTc, widened mean spatial QRS-T angle and various arrhythmias were also observed. Cardiac performance, estimated by echocardiogram and phono-mechanocardiogram was lowered in 41 (60.3%). Large IV sound and large A wave in apexcardiogram were also frequently found. All but 3 patients showed continuous elevation of serum enzymes, namely, LDH, LDH-1/LDH-2, CPK, CPK-MB, HBD and GOT. Etiological evidences were obtained by serological study in 11 cases (16.2%): 2 of Coxsackie B-1, 3 of Coxsackie B-2, 1 of Coxsackie B-4, 2 of mycoplasma pneumoniae, 1 of cytomegalovirus, 1 of ECHO-7 and 1 of rubella. We proposed a criteria for diagnosis of myocarditis as follows: (1) Exertional symptoms. (2) ECG findings. (3) Serum enzyme abnormality. (4) Lowered cardiac performance. (5) Cardiomegaly. (6) Changing character of all signs and symptoms.
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PMID:Clinical aspects of nonrheumatic myocarditis in children. 47 Jan 4

A consecutive series of 205 myocardial scans, performed with 99mTc-labeled phosphates, in 185 patients with acute chest pain, were independently evaluated by comparing myocardial concentration intensity of the tracer to that in bone, and by rating this intensity by a six-category rating scale, which imply five criterion levels for calling an image "positive". The optimal criterion level was determined for each day of evolution of illness, as the one in which a shift to a more lax criterion level produces a bigger increment in false-positive results than in True-positive results, and in which a shift to a stricter criterion level causes a greater decrease in true positive results than in false-negative results. In all instances, the optimal criterion level was that with a moderate (2+) myocardial tracer concentration, lower than rib uptake, but with a focal pattern of myocardial distribution of the tracer (2F). By using this optimal criterion level, our results agree with the general consensus in that the procedure's usefullness is restricted to the first five days of evolution of illness. However, our daily statistical analysis showed that the best period to obtain the maximal diagnostic efficiency lies between the third and fourth days after the onset of acute chest pain. A negative result during this period, in patients with ECG and CPK serum concentration compatible with acute myocardial infarction, should be considered of prognostic significance, since it may translate a defficient colateral coronary circulation.
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PMID:[Evaluation of radioactive phosphate scintillography in relation to time elapsed after acute myocardial infarct]. 48 69

1. One hundred consecutive patients admitted with ischemic chest pain to the Emergency Department of Vancouver General Hospital were studied. The diagnosis was based on clinical assessment, EKG changes and the total CPK and LDH activities. However, unknown to the clinician. CPK and LDH isozyme determinations were also carried out and their possible impact on the diagnosis and management of the patients was evaluated retrospectively. In 37 patients with definitive myocardial infarction by all the above mentioned criteria the isozyme dterminations were of no further help. Similarly, the isozyme analysis was of no value in 22 patients with negative findings. In 26 patients with normal or unchanged EKG but elevations in either LPK or LDH, the isozymes were not absolutely necessary for the diagnosis but would have been highly reassuring to the clinician. 2. In the remaining 15 patients, the isozyme analysis would have enabled the clinician to make diagnosis of myocardial damage in 12 and rule out myocardial infarction in 3.
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PMID:Study of the value of CPK and LDH isoenzyme determinations in the differential diagnosis of ischemic chest pain. 73 46

Episodes of chest pain are not common in patients undergoing cardiac catheterization. The diagnostic implications of this symptom may be complicated by the occasional appearance of electrocardiographic changes mimicking those seen in acute myocardial infarction, and by the frequent elevation of conventionally measured serum enzymes. Exclusion of infarction is particularly important when coronary revascularization is contemplated. Since the MB CPK isoenzyme is relatively specific to myocardium, we assayed CPK isoenzymes in plasma samples from 184 patients undergoing cardiac catheterization to determine whether CPK elevations accompanying catheterization can be distinguished from those associated with myocardial infarction. Samples were obtained every 2 hr for 24 hr, and CPK isoenzymes quantified by a kinetic fluorometric method. Total plasma CPK increased in all patients (mean peak 0.238 +/- 0.042 (SD) IU/ml) but MB CPK remained normal in 181 patients (less than 0.005 IU/ml). In three remaining patients, MB CPK was elevated and myocardial infarction was confirmed by 99mTc (SN) pyrophosphate scan. Twelve patients after catheterization, in whom no intramuscular premedication was given, exhibited only minimal elevation of total plasma CPK. In contrast, 100 control patients with acute myocardial infarction exhibited peak total CPK activity averaging 0.833 +/- 0.037 (SD), and MB CPK was elevated in all cases (0.078 +/- 0.027 (SD) IU/ml). Thus, CPK elevations after catheterization reflect release of enzyme from noncardiac sources rather than from injured myocardium. Furthermore, increased plasma MB CPK activity may be considered a reliable index of myocardial infarction in patients undergoing cardiac catheterization.
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PMID:Determination of the origin of elevated plasma CPK after cardiac catheterization. 100 Jun 20

Twenty-seven patients with suspected acute myocardial infarction were studied by precordial scanning after intravenous administration of 99mTc-gluchoheptonate 2-48 hr after the onset of chest pain. Fifteen of the patients had clinically documented acute myocardial infarctions. Twelve of these 15 (80%) had areas of distinctly increased tracer uptake in the region of the heart. The three infarctions not identified by scan had peak serum CPK values of less than 300. In seven patients without infarction, no distinct areas of increased tracer uptake were found in the region of the heart. Five patients could not be classified as to whether infarction had or had not occurred. Three had abnormal scans, the significance of which is uncertain. Infarct size was estimated from the area of increased 99mTc-glucoheptonate concentration on scan and compared to peak serum CPK values. A linear correlation with a correlation coefficient of 0.77 was found. Technetium-99-m-glucoheptonate scanning was useful for the identification and size estimation of moderate- to large-size transmural and nontransmural acute myocardial infaractions.
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PMID:Detection and size estimation of acute myocardial infarction using 99Tc-glucoheptonate. 118 77

Short-term results of aggressive surgical management were compared with results of medical management in forty-three patients with preinfarction angina admitted to the coronary-care unit (CCU) over an 18 month period. These patients were selected from 1,609 consecutive admissions to the CCU because they met strict criteria for preinfarction angina: severe chest pain at rest, ST-segment elevation or depression during pain which subsided rapidly after cessation of pain, and normal serum enzymes (CPK, SGOT, and LDH). Twenty-three patients had coronary angiography, done with operating room and pump standby. One patient, who had total occlusion of the left main coronary artery, died during the study. Twenty-one of the remaining patients were considered surgical candidates, and were treated immediately after angiography with 1 to 3 vein bypass grafts. There was one late postoperative death and, of the 20 survivors, 2 had ECG evidence of acute myocardial infarction and one had mild angina at time of discharge. In contrast, of the 21 patients treated medically, 13 sustained acute MI, resulting in 8 instances of congestive heart failure and 4 cases of ventricular fibrillation. Four patients died in cardiogenic shock. With the use of rigid criteria, a small subgroup of patients with variant angina at high risk of developing AMI has been identified and categorized as having preinfarction angina. Our experience suggests that aggressive surgery immediately following coronary angiography offers a lower incidence of MI, morbidity, and death than does medical management.
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PMID:Management of preinfarction angina. Evaluation and comparison of medical versus surgical therapy in 43 patients. 124 46

The aim of this prospective study was to assess the prognostic and most suitable management of AMI in elderly patients (age > or = 75 years). From September 1988 to August 1991, 129 such patients (pts) were evaluated: 35 (27%) were admitted to CCU because of arrhythmias or severe hemodynamic complications; 94 (73%) were addressed, according to bed availability, to CCU (55 pts) or Cardiology Ward (39 pts), where all patients underwent continuous ECG monitoring for at least 72 hours. Age, gender, history of previous angina or myocardial infarction, presence of chest pain or ECG ischemia on admission, site and extent of AMI, delay on admission, CPK-MB peak, recurrent angina, arrhythmias, heart failure, emotional disorders, hospital mortality and length of hospital stay were compared. Our results show that elderly patients who suffered from complicated AMI were at high risk for death and severe in-hospital complications. No significant prognostic differences were observed between the two groups with uncomplicated AMI. Thus hospitalization in the Cardiology Ward seems to be valuable, safe and well tolerated in our population of elderly patients with AMI, and without initial complications.
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PMID:[Management and prognosis of acute myocardial infarct in advanced age: comparison of the cardiac intensive care unit and the cardiology ward]. 129 24

We report a case of unstable angina in an active phase of polymyositis. A 51 year-old man was admitted with a diagnosis of polymyositis and unstable angina with ST elevation on prolonged rest chest pain. Rest anginal attack which had been refractory to conventional antianginal medications was controlled by high dose of glucocorticosteroid. Electrocardiography revealed multifocal premature ventricular contraction. Since silent ischemia on exercise persisted, percutaneous transluminal coronary angioplasty (PTCA) was performed on a stenotic lesion in the left anterior descending artery. Since there was recurrent anginal attack, re-PTCA was carried out at the same site. He was discharged in a good condition. This case is considered to be associated with cardiac involvement of polymyositis because of ventricular arrhythmia, persistent increased serum levels of CPK-MB, and the marked benefits of corticosteroid against unstable angina. In addition, clinical manifestations, coronary arteriographic findings, and increased plasma levels of thrombin-antithrombin III complex suggest that cardiac involvement in polymyositis accelerates intracoronary thrombus formation and/or coronary spasm.
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PMID:[A case of unstable angina pectoris associated with an active phase of polymyositis]. 158 49


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