Factor VII levels in patients undergoing coronary angiography: factor VII and coronary artery disease.

BACKGROUND: Factor VII (F VII) has been widely investigated as a risk factor for coronary atherosclerosis, however there is still debate about its role in the progression of coronary artery disease (CAD). In this study F VII levels were measured in patients with angiographically proven CAD and its relation with disease severity, coronary events and with other risk factors of coronary atherosclerosis were examined. METHODS: Consecutive patients referred to coronary angiography were divided in three groups: 1. CAD group--those with a significant lesion in one or more coronary arteries (n = 155), 2. High-risk group--patients with normal coronary arteries and with two or more risk factors (n = 54), 3. Controls--patients with normal coronary arteries and with no or one risk factor (n = 90). CAD group was also studied according to the number of vessels involved and to the history of coronary events. RESULTS: Mean F VII levels were not different between the three groups of patients. In CAD group, F VII increased parallel to the number of vessels involved (one vessel disease: 85 +/- 20%, two vessel disease: 92 +/- 23%, three vessel disease: 105 +/- 23%). Patients with a history of coronary events had significantly higher F VII levels than those without such a history (96 +/- 25% versus 89 +/- 22% respectively, P = 0.02). However, logistic regression analysis revealed no significant relation between F VII and either the presence of CAD or coronary events. CONCLUSIONS: F VII levels increase in patients with previous coronary events, but it is not an independent risk factor for the progression or for the severity of CAD.

[Relation of HLA antigens and myocardial infarction]. / Akut miyokard infarktüsü ile HLA doku grubu iliskisi.

OBJECTIVE: Genetic predisposition and chronic inflammation play the leading role in the early stages and in the development of atherosclerosis. Previous studies have shown that substantial amounts of T-lymphocytes are present in both early fatty lesions and advanced fibrous lesions in humans. This observation suggests that HLA antigens may be used as genetic markers for the tendency to coronary artery disease. The aim of our study was to investigate the relation of atherosclerosis and HLA antigens in patients with acute myocardial infarction. METHODS: Thirty consecutive patients with acute myocardial infarction (15 male, 15 female, aged 54+/-8 years) and 30 subjects (15 male, 15 female, aged 52+/-7 years) without evidence of coronary artery disease--according to physical, fundoscopic, electrocardiographic and radiological examination--were enrolled to the study. Histocompatibility antigens (HLA-AB, -DR, -DQ) were studied with lymphocytotoxicity method. RESULTS: Age, gender, smoking, alcohol consumption, frequency of obesity and diabetes mellitus were similar between the two groups. In patients with myocardial infarction frequency of hypertension, family history and hyperlipidemia were significantly higher than the controls (p < 0.0003, p < 0.0001, p < 0.01 respectively). Frequency of HLA antigens in patients and in controls was 50% and 23% for HLA-A2, 63% and 20% for HLA-DQ4 and 90% and 50% for HA-DQ7. Logistic regression analysis revealed a significant relation with the disease and the presence of these antigens (p = 0.02, p = 0.02 and p = 0.03 respectively). CONCLUSIONS: It is concluded that in the Turkish population presence of HLA-A2, HLA-DQ4 ve HLA-DQ7 (3) may be used as genetic markers for the tendency to coronary artery disease.

Carbohydrate-deficient transferrin and sialidase levels in coronary heart disease.

Transferrin is a N-glycosylated glycoprotein and plays an important role in iron transport from sites of absorption and storage to sites of utilization. The main component of normal serum transferrin contains two biantennary glycans, each consisting of 2 mol of sialic acid (Tetrasialo transferrin). Normal serum also contains small amounts of tri- and disialotransferrin. We have undertaken this study to investigate the levels of serum carbohydrate-deficient transferrin (Desialotransferrin) and sialidase levels in patients with coronary heart disease. In patient group, serum desialotransferrin and sialidase levels were found to be significantly higher than control group (p < 0.01 and p < 0.001, respectively). We conclude that increased activity of sialidase may be responsible for increased desialotransferrin in patients with coronary heart disease. Serum desialotransferrin levels may be useful critaria to diagnosis and pathogenesis of coronary heart disease.

Discrete subaortic stenosis as part of a short stature syndrome.

Observations in a family point to the existence of autosomal dominant inheritance for discrete subaortic stenosis (DSS), which made up part of a multisystem disorder. Both parents, offspring of two full siblings, had short stature, obstructive lung disease (OLD), hoarseness and upturned nose. The father alone had aortic stenosis and inguinal hernia. The six offspring, aged from 13 to 28 years, were followed up for up to 8 years. While one of them was virtually normal, and one had only minor abnormalities, four siblings displayed clinical signs of progressive aortic stenosis. Of the two eldest siblings who eventually died, necropsy in one showed a discrete subaortic stenosis, which was hemodynamically proven in one and surgically corrected in another sibling. Upturned nose was present in each examined member of the family, short stature and hoarseness in five of the siblings, DSS in four, OLD, inguinal hernia and congested episcleral veins in three, kyphoscoliosis in two, while epicanthus, strabismus, microphthalmos and widely spaced teeth were noted in the deceased female. The prevalence of some of these traits in roughly three-quarters of the sibship was consistent with an underlying single gene abnormality in affected heterozygous parents. We proposed that this constitutes a new syndrome.

Anaesthesia in first degree atrioventricular block.

A patient with an intracardiac conduction defect characterised by first degree atrioventricular block due to slowed transmission through the atrioventricular node with increased refractoriness of the node, is described. Asymptomatic first degree block, rarely progressing to transient Wenckebach (type 1 second degree) block had been present for a period of 32 years until general anaesthesia was required, when profound bradycardia attributable to complete atrioventricular block developed abruptly. Subsequent investigations located delayed intracardiac conduction through the atrioventricular node, and indicated excess vagal activity rather than structural disease as the cause. The significance of first degree heart block is discussed in relation to other forms of atrioventricular conduction defect and the current recommendations for temporary pacing for elective general anaesthesia.

Heterogenous glycogen storage disease in one family.

Three brothers, aged 17, 14 and 4 ye presented. Deficiency of glucose-6-phosphatase was associated with deficiency of acid maltase in one and debranching enzyme in the other. Enzyme analyses could not be performed in the youngest sibling.