Scandinavian Journal of Clinical and Laboratory Investigation
ISSN: 0036-5513 (Print) 1502-7686 (Online) Journal homepage: http://www.tandfonline.com/loi/iclb20
Lipoprotein(a) and acute-phase proteins in acute myocardial infarction L. Slunga, O. Johnson, G. H. Dahlén, S. Eriksson & Dr Lisbeth Slunga To cite this article: L. Slunga, O. Johnson, G. H. Dahlén, S. Eriksson & Dr Lisbeth Slunga (1992) Lipoprotein(a) and acute-phase proteins in acute myocardial infarction, Scandinavian Journal of Clinical and Laboratory Investigation, 52:2, 95-101 To link to this article: http://dx.doi.org/10.3109/00365519209088771
Published online: 08 Jul 2009.
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Citing articles: 4 View citing articles
Full Terms & Conditions of access and use can be found at http://www.tandfonline.com/action/journalInformation?journalCode=iclb20 Download by: [Australian National University]
Date: 07 November 2015, At: 11:15
Scand J Clin Lab Invest 1992; 52: 95-101
Lipoprotein(a) and acute-phase proteins in acute myocardial infarction L . S L U N G A , 0. J O H N S O N , G . H . D A H L E N " ; & S . E R I K S S O N t
Downloaded by [Australian National University] at 11:15 07 November 2015
Departments of Internal Medicine, *Clinical Chemistry and ?Geriatrics, University Hospital, Umei, Sweden
Slunga L, Johnson 0, Dahlen GH, Eriksson S. Lipoprotein(a) and acute-phase proteins in acute myocardial infarction. Scan J Clin Lab Invest 1992; 52: 95-101. Lipoprotein(a) (Lp(a)) and the acute-phase proteins, orosomucoid, haptoglobin and a,-antitrypsin, were studied in 32 patients with acute myocardial infarction. Samples were taken at admission and, after fasting overnight, on the following 6 days. In a subgroup of 21 patients total serum cholesterol, high-density lipoprotein (HDL) cholesterol and triglycerides were also estimated. In a linear regression model a significant relation between the relative values of Lp(a) and the time in days was obtained (p=0.001). Compared with the acute-phase proteins, however, Lp(a) showed a weak increase and the individual responses were very variable. There were no correlations between the individual changes in Lp(a) and the changes in the actue-phase proteins, but Lp(a) changes correlated significantly with the changes in total cholesterol and low-density lipoprotein (LDL) cholesterol. It is suggested that the Lp(a) reaction in myocardial infarction is linked to the reaction of the lipoproteins. There may also be several clinical conditions, including different medications, which influence the Lp(a) level. Key words: acute-phase proteins; lipoprotein(a); myocardial infarction Dr Lisbeth Slungu, Department of Medicine, University Hospitul, S-901 85 Umed, Sweden
Lipoprotein(a) (Lp(a)) was reported by Berg [l] to be an antigen in blood. Further studies have shown that Lp(a) consists of an LDL-like particle and the apolipoprotein(a) (apo(a)) linked to apo 9-100 by a disulphide linkage. Sequencing of apo(a) has revealed a striking homology to plasrninogen [2]. There is a great interindividual variation in the Lp(a) level, ranging from undetectable up to more than 1000 mg I-'. The distribution is highly skewed. Apo(a) has several isoforms of different molecular size, which are strongly genetically determined. There is an association
between phenotype and serum concentration of Lp(a) [3, 41. High levels of Lp(a) indicate an increased risk of developing atherosclerotic disease [5,6]. The metabolic control and physiological roles of Lp(a) have still not been determined. The intra-individual concentration of Lp(a) has been claimed to remain very stable throughout life and to be hardly changed by lifestyle factors. However, there are now several reports indicating that Lp(a) is influenced by disease states [7,&9, lo]. Lp(a) contains large amounts of sialic acid ill], and it has been proposed that 95
96
L . SIunga et al.
Lp(a) like the acute-phase reactants, might play a role in inflammation. This study was designed to evaluate if Lp(a) can be regarded as an acute-phase protein in patients with acute myocardial infarction.
PATIENTS A N D METHODS
Downloaded by [Australian National University] at 11:15 07 November 2015
Study population Patient characteristics are described in Table I. The study group comprised 32 patients with definite signs of myocardial infarction treated at the coronary care unit. The classical diagnostic criteria were observed: clinical symptoms, E C G findings and elevated serial total creatine kinase (CK) levels. CKMB activities were determined by immuno-inhibition, based on the presence of CKM-subunit antibodies. Patients with a symptom duration exceeding 24 h at admission were excluded from the study. Because of possible interactions between thrombolysis and Lp(a) levels, patients who received thrombolytic therapy were also excluded. During the study period 18% of all patients treated at the coronary care unit because of myocardial infarction received
TABLE I . Patient characteristics n Sex Age (years)
32 19 male 13 female
69.2f8.6 (45-80)
Previous myocardial infarction* Diabetes* Hypertension* Symptom duration at admission (h) Lp(a), basal value (mg I '1 CKMB, max. value (Fkat I I , normal value
ISSN: 0036-5513 (Print) 1502-7686 (Online) Journal homepage: http://www.tandfonline.com/loi/iclb20
Lipoprotein(a) and acute-phase proteins in acute myocardial infarction L. Slunga, O. Johnson, G. H. Dahlén, S. Eriksson & Dr Lisbeth Slunga To cite this article: L. Slunga, O. Johnson, G. H. Dahlén, S. Eriksson & Dr Lisbeth Slunga (1992) Lipoprotein(a) and acute-phase proteins in acute myocardial infarction, Scandinavian Journal of Clinical and Laboratory Investigation, 52:2, 95-101 To link to this article: http://dx.doi.org/10.3109/00365519209088771
Published online: 08 Jul 2009.
Submit your article to this journal
Article views: 3
View related articles
Citing articles: 4 View citing articles
Full Terms & Conditions of access and use can be found at http://www.tandfonline.com/action/journalInformation?journalCode=iclb20 Download by: [Australian National University]
Date: 07 November 2015, At: 11:15
Scand J Clin Lab Invest 1992; 52: 95-101
Lipoprotein(a) and acute-phase proteins in acute myocardial infarction L . S L U N G A , 0. J O H N S O N , G . H . D A H L E N " ; & S . E R I K S S O N t
Downloaded by [Australian National University] at 11:15 07 November 2015
Departments of Internal Medicine, *Clinical Chemistry and ?Geriatrics, University Hospital, Umei, Sweden
Slunga L, Johnson 0, Dahlen GH, Eriksson S. Lipoprotein(a) and acute-phase proteins in acute myocardial infarction. Scan J Clin Lab Invest 1992; 52: 95-101. Lipoprotein(a) (Lp(a)) and the acute-phase proteins, orosomucoid, haptoglobin and a,-antitrypsin, were studied in 32 patients with acute myocardial infarction. Samples were taken at admission and, after fasting overnight, on the following 6 days. In a subgroup of 21 patients total serum cholesterol, high-density lipoprotein (HDL) cholesterol and triglycerides were also estimated. In a linear regression model a significant relation between the relative values of Lp(a) and the time in days was obtained (p=0.001). Compared with the acute-phase proteins, however, Lp(a) showed a weak increase and the individual responses were very variable. There were no correlations between the individual changes in Lp(a) and the changes in the actue-phase proteins, but Lp(a) changes correlated significantly with the changes in total cholesterol and low-density lipoprotein (LDL) cholesterol. It is suggested that the Lp(a) reaction in myocardial infarction is linked to the reaction of the lipoproteins. There may also be several clinical conditions, including different medications, which influence the Lp(a) level. Key words: acute-phase proteins; lipoprotein(a); myocardial infarction Dr Lisbeth Slungu, Department of Medicine, University Hospitul, S-901 85 Umed, Sweden
Lipoprotein(a) (Lp(a)) was reported by Berg [l] to be an antigen in blood. Further studies have shown that Lp(a) consists of an LDL-like particle and the apolipoprotein(a) (apo(a)) linked to apo 9-100 by a disulphide linkage. Sequencing of apo(a) has revealed a striking homology to plasrninogen [2]. There is a great interindividual variation in the Lp(a) level, ranging from undetectable up to more than 1000 mg I-'. The distribution is highly skewed. Apo(a) has several isoforms of different molecular size, which are strongly genetically determined. There is an association
between phenotype and serum concentration of Lp(a) [3, 41. High levels of Lp(a) indicate an increased risk of developing atherosclerotic disease [5,6]. The metabolic control and physiological roles of Lp(a) have still not been determined. The intra-individual concentration of Lp(a) has been claimed to remain very stable throughout life and to be hardly changed by lifestyle factors. However, there are now several reports indicating that Lp(a) is influenced by disease states [7,&9, lo]. Lp(a) contains large amounts of sialic acid ill], and it has been proposed that 95
96
L . SIunga et al.
Lp(a) like the acute-phase reactants, might play a role in inflammation. This study was designed to evaluate if Lp(a) can be regarded as an acute-phase protein in patients with acute myocardial infarction.
PATIENTS A N D METHODS
Downloaded by [Australian National University] at 11:15 07 November 2015
Study population Patient characteristics are described in Table I. The study group comprised 32 patients with definite signs of myocardial infarction treated at the coronary care unit. The classical diagnostic criteria were observed: clinical symptoms, E C G findings and elevated serial total creatine kinase (CK) levels. CKMB activities were determined by immuno-inhibition, based on the presence of CKM-subunit antibodies. Patients with a symptom duration exceeding 24 h at admission were excluded from the study. Because of possible interactions between thrombolysis and Lp(a) levels, patients who received thrombolytic therapy were also excluded. During the study period 18% of all patients treated at the coronary care unit because of myocardial infarction received
TABLE I . Patient characteristics n Sex Age (years)
32 19 male 13 female
69.2f8.6 (45-80)
Previous myocardial infarction* Diabetes* Hypertension* Symptom duration at admission (h) Lp(a), basal value (mg I '1 CKMB, max. value (Fkat I I , normal value
