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)

From January 1, 1989 to September 30, 1990, 116 patients with acute myocardial infarction were hospitalized at the regional hospital of Langenthal. Of those 116 patients, 27 (23%) were treated with intravenous streptokinase; in 12 of them (44%) CPK reached its peak within 6 hours after starting lysis; all were admitted within 4 hours after the beginning of chest pain. Of the fibrinolyzed patients, 18 (67%) had arrhythmias which needed to be treated. In 10 of these 18 patients CPK reached its peak within 6 hours. Of the 89 patients not treated with streptokinase, 27 (30%) did not fulfill the entry criteria of the protocol, 16 (18%) had exclusion criteria, and 46 (52%) had exclusion criteria as well as absent inclusion criteria. In only 4 patients (4.5%) was lysis not possible because they entered hospital later than 6 hours after the beginning of pain, and 8 patients (9%) exceeded the upper age limit of 70 years. Of the 116 patients, 13 (11.2%) died; 12 were not treated with streptokinase. Our study shows that fibrinolytic treatment with streptokinase is a safe and effective therapy for patients with acute myocardial infarction and can easily be performed in a regional hospital.
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PMID:[Fibrinolysis in a regional hospital]. 173 14

Using the standard 12-lead electrocardiographic QRS scoring system modified by Nancy (1985), 99 ECGs of 52 patients with acute myocardial infarction were used for estimating myocardial infarct size (MIS). One point was designed to represent 3% of the left ventricle. Each patient had the first score of ECG at the day ranged from 7 to 12 and the second 25-32 days post acute chest pain except 5 cases died before the second scoring. The results showed that the averaged score was 6.7 +/- 3.1 points accumulated from all 99 ECGs and 11.0 points from 5 cases died. There was no statistic difference between the points value of the first scoring 6.4 +/- 2.9 vs second 6.5 +/- 2.7 points, nor between the points received from Q waves 4.0 +/- 1.5 vs 3.9 +/- 1.4 points in 47 patients. There was nevertheless strong correlation both between the total points of the first and second scoring, r = 0.85 (P less than 0.0005), and those between the points related to Q wave, r = 0.81 (P less than 0.005). Furthermore, early serial serum CPK changes were determined for evaluating MIS in 25 patients, the results were compared to the first and second scores respectively, the correlations were significant, r = 0.58, P less than 0.0025 and r = 0.47, P less than 0.01.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A study on standard 12-lead ECG QRS scoring system for estimating myocardial infarct size]. 181 89

Plasma cardiac myosin light chain I(CMLCI) was quantified by competitive enzyme-linked immunosorbent assay(ELISA) using a monoclonal antibody in 42 patients with confirmed acute myocardial infarction (AMI). In comparison to the value from healthy individuals, plasma CMLCI levels were significantly elevated in 40 patients. In 28 of the 42 patients (66.7%), two major peaks were observed on time activity curves. The early peak (CMLCIp1) began a rapid rising within 4-12 hours and peaked at a mean of 25 hours following the onset of chest pain. The CMLCIp1 appeared statistically higher and earlier in patients with early infarct-related artery recanalization (IRAR) than those without IRAR, which was assessed by CPK peaking time, continuous ST segment monitoring on 12 lead ECG and symptoms. Thus, CMLCIp1 might be influenced by early IRAR. The late peak (CMLCIp2), which was composed of another gradual increase of plasma CMLCI level, occurred at a mean of 142 hours after AMI and remained elevated for about 7-10 days. The magnitudes of CMLCIp2 were correlated with the infarct size estimated by LVEF and LVWMS on cineventriculography and QRS scores on ECG. In the rest 14 patients only one peak was observed. It was suggested that CMLCIp1 could provide an early diagnosis of AMI and might be influenced by early IRAR after thrombolysis, while CMLCIp2 was a good later marker of extent of myocardial necrosis.
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PMID:[Detection of cardiac myosin light chain I by monoclonal antibody in the patients with acute myocardial infarction]. 181 16

Systemic thrombolysis is an effective therapy for acute myocardial infarction, since it restores coronary flow and contributes to preserve left ventricular function. We analyze our experience with intravenous thrombolytic therapy in 45 cases with acute myocardial infarction treated within 6 hours of onset of symptoms. 28 patients had anterior and 17 inferior myocardial infarction. We treated 38 patients with streptokinase 1 to 1.5 million units infused during a 30 to 60 minute period and 7 patients with tissue plasminogen activator factor, 100 mg infused during 2 hours. Regression of chest pain and ST segment elevation and early CPK peaking (less than 4 hours) were utilized as criteria for reperfusion. Accordingly 29 patients (64%) met these criteria. Coronary angiogram was performed within 7 days in 38 patients. It disclosed a patent coronary artery in the infarcted area in 28 cases (74%). Transient hypotension with thrombolytic therapy was observed in 17 patients (38%) and bleeding complications in 3 cases (7%). Two patients (4%) died early after therapeutic failure. In summary we have confirmed that intravenous thrombolytic therapy is safe and effective in the early period of myocardial infarction and that is associated with a high incidence of clinical and angiographic reperfusion.
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PMID:[Early systemic thrombolysis in acute myocardial infarction: clinical and angiographic results]. 182 39

Observations made in animal models of reperfusion in acute myocardial infarction have shown that early reperfusion results in myocardial salvage. But the relation between the time of reperfusion and myocardial salvage is not clear in human patients. If earlier reperfusion provides smaller infarct size, reperfusion therapy initiated in the first 1 hour should be the most beneficial. In this study, we compared the results of therapy initiated in the first 1 hour (group A, n = 19) with treatment started 1 to 24 hours after the onset of chest pain (group B, n = 652). The infarct location, development of collateral vessels, number of diseased vessels and reperfusion rate of thrombolysis in the two groups didn't differ. There was a statistically insignificant trend towards total occlusion of the infarct artery in group A (89.5% vs 69.7%, p less than 0.1). Peak CPK and changes in left ventricular ejection fraction (delta EF) were assessed in patients with total occlusion of the left anterior descending artery and successful reperfusion (n = 8 in group A, n = 120 in group B). There was no difference in peak CPK (3281 +/- 2192Iu/l vs 3490 +/- 1811Iu/l) and delta EF (6.3 +/- 17.1% vs 5.8 +/- 11.9%). These findings suggest that there is no relation between the time of reperfusion and myocardial salvage in human patients.
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PMID:[A clinical study of the relation between time to reperfusion and infarct size]. 202 76

In order to determine whether acute myocardial infarction (AMI) presents a circadian periodicity in its occurrence, the onset of AMI, evaluated by onset of clinical symptoms and pain, has been analysed in 520 patients with AMI. The definitive criteria of AMI were: typical chest pain, electrocardiographic findings, and plasma CPK-MB elevation. All cases of AMI were divided into subgroups according to sex (males = 369, females = 151), age (less than 60 years old = 254, more than 60 years old = 266), type of AMI (Q wave AMI = 407, non Q wave AMI = 113), previous pharmacological treatment (no treated = 373, treated = 147), history of arterial blood hypertension (normotensive = 403, hypertensive = 117). Cases of Q and non Q wave AMI were also subdivided according to treatment and hypertensive conditions. All AMI occurred outside hospital; silent AMI and reinfarctions were excluded by analyses. The data have been analysed by chronograms and by means of "single cosinor" method, both for total cases, and for each subgroup of AMI. The results show a diurnal variation in AMI occurrence regarding the whole group, with a peak from 4:00 am to noon and with a secondary small no-significant peak in the late evening, and the minimum in the afternoon. Rhythmometric analysis demonstrates a significant circadian rhythm (p less than 0.001) with acrophase at 7:52 am (from 6:08 am to 9:36 am). A statistically-significant circadian rhythm is demonstrated in each subgroup, except in hypertensive patients. Acrophases of males and females, and of patients aged over or under 60 years do not differ from that of the whole group, and between them (p greater than 0.05). The peak of non Q wave AMI occurs at 4:44 am, while the peak of Q wave AMI at 10:08 am: this difference is significant (p less than 0.001). There is also a significant difference between the acrophases of AMI in the treated and untreated groups (p less than 0.01), as well as between normotensive and hypertensive subjects (p less than 0.001). The previous treatment seems able to anticipate the maximum occurrence of AMI in the whole group and in the group of Q wave AMI. These results are very similar to previous observations and confirm the greater morning occurrence of AMI. The present data are discussed in respect with the literature observations, and the possible pathophysiological mechanisms that contribute and conditionate the morning increase and the different peaks in subgroups of AMI patients are discussed.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Differentiated circadian chrono-risk of acute myocardial infarct]. 224 25

Effects of reperfusion by intra-coronary thrombolysis (ICT) or percutaneous transluminal coronary angioplasty (PTCA) on the myocardial imaging using 111In-labeled antimyosin monoclonal antibody Fab (In-AM) were studied. Reperfusion by ICT or PTCA was done in 16 patients (reperfusion group) and recanalization was seen in 14. Positive images were obtained in 28 of 30 patients (93%) with acute myocardial infarction (onset to imaging: 9.9 +/- 9.8 days). Among the reperfusion group, one patient in whom PTCA was done early after the onset of chest pain and CPK did not elevate showed no significant uptake of radioactivity at cardiac region, while other 15 patients with elevation of CPK demonstrated positive images. Planar images (anterior, left anterior oblique 45 degrees, left lateral) were divided into 15 segments and infarct size (antimyosin-segment) was determined by sum of positive segments on each image. There were no significance between the infarct size in the reperfusion group (7.2 +/- 2.9) and that in the non-reperfusion group (6.9 +/- 3.4). Intensity of the accumulation of radioactivity in each image was classified into 5 grades by comparison with uptake of the liver (antimyosin-score). Reperfusion group demonstrated high intensity compared with non-reperfusion group (2.6 +/- 0.7 vs. 2.0 +/- 0.4; p less than 0.05). Thus, In-AM imaging may be influenced by coronary blood flow, which should be taken into consideration in the interpretation of In-AM imaging.
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PMID:[Clinical trial of 111In-antimyosin antibody imaging: (4). Effect of reperfusion in acute myocardial infarction]. 234 82

Sixteen out of 293 (5.4%) procedures for percutaneous transluminal coronary angioplasty, performed between 1985 and 1988, were complicated by acute closure and required emergency revascularization surgery. The injured vessel was the left anterior descending artery in 14 cases and the right coronary artery in 2 cases. All patients had persistent chest pain associated with ST-segment elevation in 14 cases and ST-segment depression in 2 cases. Two patients developed cardiogenic shock and were in cardiac arrest at the beginning of operation; one of these died immediately after the operation. Thus the overall mortality rate was 6.2%. Enzyme evidence of myocardial infarction (CPK-MB greater than 40 UI/I) occurred postoperatively in 8 patients (50%), but only the 6 patients (37.5%) with electrocardiographic evidence of myocardial necrosis (new Q-waves or loss of R-wave voltage) showed akinesis of the myocardium perfused by the occluded vessel at the echocardiographic examination performed two weeks after the operation. The occurrence of myocardial infarction was correlated with the degree of preoperative ischemia and hemodynamic deterioration. A collateral flow was present in 3 cases and none of these showed evidence of myocardial necrosis after the operation. Our results show that emergency bypass surgery for failed coronary angioplasty is less satisfactory than elective surgery, and has a higher mortality and myocardial infarction rate. Thus, the risk of emergency operation for complicated dilation must be considered when selecting of candidates for coronary angioplasty.
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PMID:[Results of emergency aortocoronary bypass in complicated coronary angioplasty]. 252 74

Medical data of 181 patients, affected by confirmed acute myocardial infarction, were reviewed to evaluate the initial clinical, electrographic and radiological data, and the first CPK test. Eleven patients went to the emergency department without chest pain (6.1%). The percentage of patients with oppressive chest pain was 73%, being of thoracic localization in 86.4%, 20%. Related to effort; 47.1% referred; and 92.9% of more than 30 mins. duration. 35.3% had normal blood pressure. Only 5 patients (2.8%) had normal EKG, the S-T segment elevation being the most frequent alteration (71.3%). 89.5% of patients had sinusal rhythms; 20.4% were bradycardic. 58.6% had normal levels of CPK at the first test. We concluded that EKG is the most important test in diagnosing acute myocardial infarction; it being very rarely normal. The clinical data are coadjuvant, while isolated initial CPK had not value.
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PMID:[The evaluation of the diagnostic usefulness of the clinical picture, electrocardiography and enzymes in the initial presentation of an acute myocardial infarct]. 256 18

A 66-year-old woman, who had had bronchial asthma, was admitted to our hospital because she suffered from fever, productive cough, wheezing, dyspnea, and chest pressure sensation. Her chest X-ray showed migrating infiltration and marked cardiomegaly. Her ECG at the admission revealed abnormal Q wave and T wave inversion, though that of 3 years before had been almost normal. Hematology showed leukocytosis and eosinophilia of 8,000/mm3 without abnormal cells. All immunological tests were negative and the specific cause of the eosinophilia was unknown. 2 weeks after admission, she complained of severe chest pain suddenly and her ECG showed ST elevation on V1-4 and serum CPK level was elevated to 290 IU/l. By the thrombolytic agent and anticoagulant therapy, her symptom was lightened immediately. 2 months later, we made her cardiac catheterization and myocardial biopsy. Her LVG showed a small aneurysm of the apex, though her CAG was normal finding. The biopsy revealed moderate fibrosis and cellular infiltration including a few eosinophils. We thought that eosinophilic endocarditis had existed first, and secondary embolism continued led to the small infarction. The hypereosinophilia was spontaneously normalized 2 months after admission, but the patient complained of myalgia and sensory disturbance of extremities. The biopsy of quadriceps muscle could prove neither infiltration of eosinophils nor vasculitis. But we diagnosed mononeuritis multiplex due to hypereosinophilia. Judging from various symptoms and laboratory findings, this case was included to the hypereosinophilic syndrome. We also thought allergic granulomatosis and angitis as one of the differential diagnoses, but histologically vasculitis was not proved. In this case, eosinophilia was disappeared without using corticosteroids.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of hypereosinophilic syndrome associated with eosinophilic endocarditis]. 261 22


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