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Query: UMLS:C0011849 (diabetes)
277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Survival of 312 patients with acute myocardial infarction was studied from data collected during the first 48 h in the coronary care unit. Only patients with recent onset of symptoms (48 h), with a 48-h survival, and with evidence of myocardial infarction, were selected. Mortality rate at 1 mth was 15.3% and 24.6% at 6. The following factors were significant for poor survival: increasing age, female sex, diabetes, previous angina, low blood pressure on admission and at the 48th h low average value and the lowest observed value of blood pressure, clinical and radiological left ventricular failure, high level of LDH, increased urea and leukocytosis. Among ECG data, the presence of signs related to extent of infarction, anterior as compared to inferior location, antero-lateral as compared to anterior, QRS frontal axis deviation, absence of sinus rhythm, sinus tachycardia, tachyarrhythmias with wide QRS complex, right bundle branch block, 3rd-degree AV block with wide QRS complex, was associated with significantly worse survival than the absence of these signs. A multivariate analysis of the 42 most significant data, assuming linear regression, was used to establish a discriminant prognostic index. Using this index, survival was predicted correctly in 90.2% of patients at 1 mth and 85.7% at 6 mth. Thus prognosis can be established in nonclear-cut groups of patients with myocardial infarction (severe and benign forms being excluded by criteria) from simple clinical data.
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PMID:Quantitative assessment of myocardial infarction prognosis to 1 and 6 mth--from clinical data. 72

Serial study of 72-lead precordial ST-maps, SGOT, and SLDH was done in 30 cases of acute myocardial infarction. Infarct size was estimated by sum of ST elevation in all leads (sigma ST), number of sites showing ST elevation (NST), peak SGOT, and peak SLDH levels, and correlated with each other and with clinical features and hospital course. sigma ST correlated well with NST (r=0.92), but the correlations of sigma ST with SGOT (r=0.99) and SLDH (r=3.84) were better than those of NST with SGOT (r=0.22) and SLDH (r=0.53). There were close agreements between sigma ST and peak SGOT and peak SLDH except in the cases of non-transmural infarction, in whom smaller sigma ST suggesting small infract occurred with higher enzyme peaks indicating moderate or large infarct. Longer duration of chest pain, larger number of associated conditions (e.g. angina, hypertension, diabetes), complications (e.g. congestive heart failure, shock, arrhythmias) and mortality were associated with larger infarcts.
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PMID:Precordial ST-segment changes and serum enzyme levels in acute myocardial infarction. 73 32

Four hundred sixty patients with ischemic heart disease (IHD) were examined: 226 of them--with myocardial infarction; 38--stenocardia, 196--myocardiosclerosis. With age advancing all forms of IHD increase. The incidence of the followed up risk factors progessively increases. Hypertension has the greatest share--56.30 per cent out of all the subjects examined. Second place as regards incidence is occupied by the emotional stress--46.52 per cent. Further they are as follows: heredity--38.91 per cent; tobacco smoking--34.57 per cent, sedentary life--32,83 per cent, obesity--31.52 per cent, overfeeding--30 per cent, hypercholesterinemia--30 per cent, diabetes--17.61 per cent. The significance of the indicated risk factors alarmingly grows, consideration given to their combined effect. An average of 3.18 risk factors fall on patient. In patients with myocardial infarction they are more frequent and appear at an earlier age. Such an accumulation of the noxae upon the contemporary man requires the complex effors of the whole society.
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PMID:[Risk factors in ischemic heart disease patients]. 73 28

The major independent role played by anxiety and severe psychosocial problems (especially family ones) is demonstrated by this multivariate analysis of a five year prospective study of the development of new angina pectoris among almost 10,000 adult men (average annual incidence = 5.7/1,000). The independent effect of these two variables is considerably augmented by the other significant risk factors of age, total serum cholesterol, systolic or diastolic blood pressure, certain electrocardiographic abnormalities and diabetes mellitus. The presence of all seven risk factors (at a high level) increases the probability of angina pectoris developing within five years to 289/1,000 from 14/1,000, when these factors are low or absent. The wife's love and support is an important balancing factor, which apparently reduces the risk of angina pectoris even in the presence of high risk factors. The implications of these findings to the pathophysiology and prevention of angina are stressed.
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PMID:Angina pectoris among 10,000 men. II. Psychosocial and other risk factors as evidenced by a multivariate analysis of a five year incidence study. 79 90

Angina pectoris is a subjective symptom recognized primarily by a careful history. It must be differentiated from nonatherosclerotic chest pain. Arteriography should be performed when the diagnosis is in doubt or when the stable from becomes unstable. Management must include: attention to risk factors; awareness of precipitating factors; treatment of other illnesses such as hypertension and diabetes, and the use of drugs: nitroglycerin and, for long-term therapy, propranolol. If this regimen fails, patients should be considered for surgery.
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PMID:The medical treatment of angina pectoris. 81 84

The early diagnosis of heart disease during or better before pregnancy is one of the most important problems, as cardiac diseases are the most common cause for maternal deaths throughout the world. The knowledge of hemodynamic alterations in circulatory and respiratory physiology during pregnancy complicated by heart disease is a prerequisite for their management. The following indications for therapeutic abortion of pregnancy complicated by heart disease can be concluded according to our own observations: 1. history of significant heart failure (more than grade IV according to the classification of the New York Heart Association), frequent attacks of angina pectoris and longstanding cyanosis: 2. in spite of the most careful heart treatment with digitalis, diuretics and salftree diet cardiac-thorax-rate of more than 55% in congenital heart disease, cardiac-thorax-rate of more than 60% in acquired heart disease, significant signs of heart failure, namely more severe than grade III, tachycardic atrial fibrillation, pulse deficit of more than 30/min, active inflammatory processes of the heart (rheumatic fever, subacute bacterial endocarditis, Takayasu's disease); 3. especially severe metabolic disorders, i.e. diabetes mellitus, malignant hypertension, kidney diseases; 4. primiparae of an age of more than 35 years with any heart disease. Commissurotomy can be accomplished during pregnancy if it is too late for therapeutic abortion. Pregnancy in case of artificial valves is not recommended in general because of impending hemorrhagic diathesis.
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PMID:[Indication for pregnancy interruption in patients with heart diseases]. 85 89

Left ventricular function was assessed by measuring sytolic time intervals in insulin-requiring diabetics with and without significant microangiopathy. The results were compared with those in normal controls. Significant microangiopathy was defined as proteinuria over 3 g/24 h or proliferative retinopathy. Left ventricular function was also assessed one and a half years later by echocardiography in four patients with microangiopathy. Patients with angina, previous myocardial infarction, hypertension, and alcoholism were excluded. All had normal electrocardiograms and chest radiographs. Diabetics with microangiopathy had impaired left ventricular function, whereas those with uncomplicated diabetes had normal function. This finding supports the existence of a specific diabetic cardiomyopathy due to microangiopathy rather than the metabolic defect. The association of microangiopathy and impaired left ventricular function may explain the high immediate mortality and the high incidence of cardiogenic shock and congestive heart failure after myocardial infarction in diabetics.
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PMID:Diabetic cardiomyopathy: the preclinical phase. 86 81

Fifty patients who suffered from an acute myocardial infarction at age 40 or below and underwent coronary arteriography, were studied from 8 to 184 months after the infarction (mean follow-up 56 months). Hyperlipidaemia (60%) and cigarette-smoking (82%) were the most common risk factors, while hypertension and diabetes mellitus were found in 10% of all patients. Thirty-seven patients had two or more risk factors. Preinfarction angina was present in 7 subjects. Death rate was 14% within five years and was related to the severity of symptoms. Out of the patients with normal coronary arteriogram (6 patients) or with a single vessel disease 21 were free of angina and 30 did not suffer a reinfarction. Out of 17 patients with two or more coronary vessel disease, angina was present in 14 and reinfarction was seen in 5.
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PMID:[Myocardial infarction in the young: evolution and clinico-coronarographic correlation (author's transl)]. 87 96

Ventricular ectopic beats (VEB) were studied in 100 consecutive patients prior to discharge after an acute myocardial infarction and again after 1 yr, on 6-h recordings. VEB were found in 71 patients prior to discharge. Reinfarction and sudden death taken together were significantly more common in the 35 patients who had severe VEB, i.e. multiform, paired, R-on-T or ventricular tachycardia (P less than 0.05). Reinvestigation after 1 yr of 73 survivors who had not reinfarcted revealed a nonsignificant overall increase in patients with VEB from 67 to 78% together with an increase in degree of severity. The intraindividual pattern, however, differed considerably. Several clinical findings including angina pectoris, heart fialure, hypertension, diabetes mellitus, hyperlipidemia, antiarrhythmic therapy, and smoking, failed to differentiate patients with increasing VEB severity from the remainder.
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PMID:Ventricular arrhythmias prior to discharge and one year after acute myocardial infarction. 89 82

Platelet hypersensitivity has been documented in diabetes and angina pectoris and can be partially reversed in hyperbetalipoproteinemia by clofibrate. We therefore examined the effects of incubating another lipid-lowering agent, halofenate, with both normal platelets and platelets made hypersensitive in vitro by incorporation of 55 per cent excess cholesterol into their membranes. At therapeutic concentrations, halofenate caused a time- and dose-dependent inhibition of the aggregation of normal platelets by epinephrine. After 30 minutes' incubation at 37 degrees C., halofenate significantly inhibited the extent of aggregation by 88 per cent (p less than 0.01), whereas clofibrate inhibited aggregation by 44 per cent (p less than 0.01). Halofenate was a more potent inhibitor of platelets than clofibrate (p less than 0.01). The mean threshold concentration of epinephrine necessary for aggregation of normal platelets (4.2 muM) was not significatnly increased with clofibrate (10 muM) but was markedly elevated with halofenate (245 muM; p less than 0.001). Significant but less dramatic increases in threshold concentration of ADP and collagen were found with halofenate but no clofibrate. Cholesterol-rich platelets were 114-fold more sensitive to epinephrine and twofold more sensitive to ADP than normal platelets but after incubation with halofenate became even less sensitive than normal. Clofibrate inhibited the extent of aggregation of hypersensitive platelets but did not alter the threshold concentration of epinephrine necessary for aggregation. Thus, halofenate is more potent than clofibrate in reducing the sensitivity of normal platelets to aggregating agents in vitro and can completely reverse experimentally produced platelet hypersensitivity. These data suggest that halofenate might be useful in reversing increased platelet sensitivity in cardiovascular diseases.
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PMID:Halofenate: a potent inhibitor of normal and hypersensitive platelets. 95 86


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