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)

After successful intracoronary and intravenous thrombolysis in acute myocardial infarction in about 90% of all cases highgrade organic stenoses of the diseased vessels can be found. These obstructions may impede coronary blood flow and be the reason for recurrent angina in the rehabilitation phase. In a prospective, controlled, randomized study with 127 patients (pts) with acute myocardial infarction 64 pts were treated with streptokinase (group I) and 63 pts were treated with streptokinase and additional PTCA procedures (group II). The patients of both groups did not differ with respect to age, distribution of sex and diseased vessels, time between onset of symptoms and start of lysis or time to maximum of CPK-curve. In group I 59 out of 64 pts had recanalized vessels (92%), in group II 56 out of 63 pts (89%). In 55/56 pts PTCA was attempted (success rate 65%) with an artificial reocclusion in two pts (4%). After four weeks in group I 47 pts were controlled angiographically. The stenosis rate did not differ between the acute phase and the control study (78.6 +/- 11.8% vs. 78.0 +/- 15.2%). Five reocclusions had occurred. In group II the resting stenosis after thrombolysis (81.7 +/- 6.6%) was diminished by PTCA to 33.0 +/- 18.2%. In the control study the remaining stenosis was 31.9 +/- 24.4%. The difference between groups I and II at the four week control was highly significant (p less than 0.001). In group I there were ten deaths during the hospital phase, nine of them of cardiac origin. In group II nine pts died, three from shock lung and five from cardiac causes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Percutaneous transluminal coronary angioplasty (PTCA) following thrombolysis. 293 24

The activities of cyclic 3',5'-nucleotide phosphodiesterases which hydrolyze cyclic 3',5'-nucleotides were measured in sera from patients with an acute myocardial infarction, angina pectoris and other heart diseases. Cyclic AMP and cyclic GMP phosphodiesterase activities were significantly elevated in acute myocardial infarction, but not in angina pectoris and other cardiovascular diseases. The peak activity appeared approximately within 24 hours following the acute attack of chest pain, and then gradually decreased as the patient recovered. The observed changes of cyclic 3',5'-nucleotide phosphodiesterase activity were similar to that of the other enzyme activities such as GOT, CPK and LDH in sera of acute myocardial infarction. These data reflect damage of myocardial cells during myocardial infarction.
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PMID:Serum cyclic 3',5'-nucleotide phosphodiesterase activity in myocardial infarction. 300 9

The clinical significance of long-standing (greater than or equal to 24 hours) coronary T waves without abnormal Q waves was evaluated in 24 patients with angina. They were categorized in two groups; 11 with ST elevation followed by coronary T waves (Group A), and 13 with coronary T waves alone (Group B). 1. The patients had long-standing or repetitive episodes of rest angina, with clinical features of unstable angina in all but one. Fifty-five % of patients in Group A and 85% in Group B had histories of effort angina. 2. Significant (greater than or equal to twice the upper normal) elevation of serum CPK value was observed in 36% of patients in Group A and in 46% in Group B. There was no correlation between the maximum CPK value and the number of leads with the coronary T wave. 3. Coronary angiography demonstrated significant (greater than 50%) coronary artery stenosis in 27% of patients in Group A and in 77% in Group B. The incidence of severe stenosis was greater in Group B than in Group A. Angioplasty was performed in 9% of patients in Group A and in 38% in Group B. 4. During the average follow-up period of 27 months, there was one cardiac event (unstable angina) in Group A, two events (one sudden death and one unstable angina) in Group B. Each cardiac event occurred after the patients themselves discontinued their medications. This was not related to the severity of coronary artery stenosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Angina with long-standing coronary T waves]. 324 80

Ferritin (F) is an iron-protein (molecular weight 445.000) present in various organs including the heart. Using the immunoenzymatic method (Ferrizyme Abbott), ferritinemia (Fe) was determined daily in 28 patients with acute myocardial infarction (AMI). A significant rise was revealed, already evident in the first few days 8-9 after with Fe gradually returns to baseline levels. The results have shown that this pattern is not evident in patients with angina, heart failure, valve defects, pericarditis or cor pulmonale and may thus be considered a reliable, if not early, marker of myocardial cytolysis. In those cases studied no correlations were observed between CPK and Fe peak or between these and clinical intensity of AMI.
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PMID:[Behavior of blood ferritin in acute myocardial infarct]. 355 38

The evaluation of the CPK-peak time (CPK-p) during Acute Myocardial Infarction (AMI) is now considered as a reliable method to identify ischemic myocardial tissue reperfusion both spontaneous and pharmacologically-induced. The purpose of this study is to assess the clinical significance of this index over a non selected group of patients (pts) affected by a first episode of AMI looking for some variables possibly connected with it. This study includes 114 pts hospitalized in our Unit Coronary Care (UCC) and diagnosed as affected by AMI and not treated with anticoagulant and/or fibrinolytic drugs. They were divided according to CPK-p into 2 groups: group A (23 pts, 18M 5F, mean age 64.2 +/- 10.1y; CPK-p 11.9 +/- 3.3h, AMI Anterior 14/AMI Inferior 9) and group B (91 pts, 85M 6F, mean age 64 +/- 10.3y; CPK-p 25.7 +/- 4.5h, AMI Anterior 50/AMI Inferior 41). Moreover, a third group C has been studied including pts with similar clinical characteristics who underwent thrombolysis by intravenous infusion of Streptokinase (48 pts, 39M 9F, mean age 62.7 +/- 10.6y; CPK-p 15.2 +/- 7h, AMI Anterior 28/AMI Inferior 20). For each pt CKP-p has been evaluated as well as the pre-UCC time (T-pc), the maximum value of released CPK (CPK-max), the incidence of new coronary events such as angina, re-AMI, sudden death detected between the 1st (NEC-I) and the 6th month (NEC-II) after the acute event.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Early peak of CPK in acute myocardial infarct: a marker of clinical instability?]. 365 95

In order to discuss the mechanism of onset in myocardial infarction (MI), clinical cases were reviewed and various clinical findings were analyzed according to the premise that the onset of MI requires both a predisposition and a trigger. The majority of subjects did present conditions that constituted predispositions for MI, including a history of angina pectoris (especially unstable angina), poor therapeutic results for angina pectoris, organic stenosis of the coronary artery, life changes, and overwork. Patients with multiple factors tended to develop MI without a definite trigger, i.e., onset during sleep or rest whereas, in patients with fewer predisposing factors, it was obvious effort, excitation or stress that triggered MI. However, not a few of the patients presented with no organic stenosis of the coronary artery or no history of angina pectoris. There were patients without ST segment elevation at onset of MI, and patients in whom ST elevation was recorded after onset. These findings suggest the existence of mechanisms other than coronary occlusion in onset of MI. Occlusion of the coronary artery distributed to the infarct region occurred frequently among patients with delayed CPK efflux as well as prolonged chest pain and ST segment elevation. These lines of evidence suggest extension of infarction due to secondary coronary occlusion.
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PMID:Evaluation of clinical factors involved in onset of myocardial infarction. 372 78

Haemorrheological disturbances have already been described in ischaemic heart disease. However, it has not been established whether these changes are secondary to the ischaemia and/or myocardial infarction or whether they play a role in initiating or sustaining the haemodynamic abnormalities which cause infarction. We report our results observed in 14 patients aged 48 to 75 years admitted to the coronary care unit with a diagnosis of acute coronary insufficiency defined as typical persistent anginal pain resistant to glyceryl trinitrate associated with specific ECG changes (without pathological Q waves or increased serum CPK concentrations). Blood samples were obtained on admission for determination of: haematocrit, total blood viscosities at different levels of shear with the patients hematocrit and with corrected hematocrits, total blood filtrability, plasma viscosity and plasma albumin fraction. All patients received 800 mg lidocaine, 40 mg chlorezepate, adequate anticoagulant doses of heparin and a specific antianginal drug: amiodarone, nifedipine or diltiazem. Six patients had a favourable outcome and were discharged from the Coronary Care Unit without myocardial infarction (Group I); the remaining 8 patients (Group II) developed documented changes of myocardial infarction between the 12th and 4th day after admission (see the Table in the text). The haemorrheological parameters on admission of the two patients groups were compared. The abnormalities observed were significantly more severe in the group developing myocardial infarction. This suggests that these changes may play a major role in initiating conditions leading to myocardial necrosis. These observations confirm the results of other workers who have also shown a relationship between the severity of infarction and the incidence of haemodynamic complications and changes in blood viscosity and filtrability.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hemorheologic disorders in the threatened myocardial infarct syndrome]. 393 83

An examination of 400 coronary patients demonstrated a relationship between increased serum CPK, AST, LDH and LDH-1, and the spread and severity of myocardial infarction (MI). In transmural and large-focal MI, CPK activity peak observed on Day 1-2 of the disease was increased 4-12-fold, and that of AST, 5-fold, as compared to the upper limit of the normal range. In small-focal and subendocardial MIs, the increase was 1.5-8-fold and 3-fold, respectively. In angina pectoris, serum CPK activity also showed an increase, although a less manifest one. A CPK activity level of 175 IU is proposed as a discriminative level to be used in the diagnosis of large-focal myocardial infarctions.
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PMID:[Assessment of the results of serum enzyme studies in different forms of myocardial infarction]. 662 Aug 15

In a consecutive series of 297 patients prospectively evaluated at the time of admission for an acute myocardial infarction, the extension of necrosis was found to occur in 16,4% of the cases. The electrocardiographic site of extension was the same as during the initial episode in over 75% of cases suggesting the possibility of a similar pathogenetic mechanism and the involvement of the same coronary district. Patients in Killip class I were respectively 61% and 45% before and after the extension, in class II 33% and 14%, in class III 6% and 14%, in class IV 0 and 27% (p less than 0,001). In-hospital mortality was 16,1% without and 38,8% with extension (p less than 0,001). The peak level of CPK-MB was an average of 110 +/- 45 U/1 before and 96 +/- 34 after the extension (p = N.S.). It was not possible to recognize the patients at risk of extension according to the traditional clinical parameters (age, sex, site of necrosis, transmural involvement, residual angina, Norris index and Killip class before the extension). It is concluded that the protection of the myocardium at risk is of primary importance in the setting of acute myocardial infarction, regardless of the possibility of saving areas already compromised at the time of admission or the hypothetical "border zone".
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PMID:[Extension of necrosis in the acute phase of myocardial infarct. Clinical picture and prognosis]. 667 96

In order to evaluate differences between the initial manifestations of acute myocardial infarction (AMI) in diabetics (DM) and non-diabetics (N-DM), 94 consecutive AMIs (DM 40, N-DM 54) were studied over a four-year period. Cases with abrupt onset associated with chest pain and/or discomfort in the areas of the chest and back were classified as the typical group (I). All other cases were classified as the atypical group (II). In subjects over the age of 60, 12 out of 33 DM had atypical manifestations, but only 3 out of 29 N-DM (p less than 0.05). In subjects aged 59 or less, the incidence of atypical cases was similar in the DM and N-DM groups. The initial symptoms of AMI were not correlated with type or location of infarction, nor with the type of treatment or presence of the ankle jerk reflex. Pre-infarction symptoms were present in 69% of Group I and 74% of Group II DM subjects. In Group II, 5 out of 16 patients had a history of typical angina, but had no chest pain at the onset of infarction. The post-AMI mortality within one month was 15% in the DM and 18% in the N-DM group. It was 14% in Group I and 25% in Group II. Mean CPK did not differ statistically between Group I and Group II. However, the Peel prognostic index was 11.0 +/- 5.1 for Group I and 15.5 +/- 5.0 for Group II (p less than 0.05) in subjects over the age of 60.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Painless myocardial infarction in diabetics. 668 May 31


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