Lipoprotein(a) and apolipoproteins B and A-I after acute myocardial infarction.

Lipoprotein(a) and apolipoproteins B and A-I after acute myocardial infarction. Research Abstract Details 

Research Abstract Table of Contents

Jump to the:

Lipoprotein(a) and apolipoproteins B and A-I after acute myocardial infarction. Abstract Text:

M Husain,P W Armstrong,P W Connelly,R A Hegele,

OBJECTIVE: To assess the temporal behaviour of plasma lipoprotein(a) [Lp(a)]--a low density lipoprotein-like particle whose plasma levels are associated with atherosclerosis risk--and apolipoproteins (apo) B and A-I (the major protein components of low and high density lipoproteins, respectively) in acute myocardial infarction (AMI), and to determined the effect of tissue plasminogen activator (tPA) on them. DESIGN AND PATIENTS: Serial Lp(a), apoB and apoA-I determinations were obtained over eight days in 19 AMI patients who were part of a randomized, placebo (n = 7) controlled trial of tPA (n = 12). MAIN RESULTS: At 48 h postinfarct, plasma Lp(a) and apoB concentrations were, respectively, 20% (24.9 +/- 3.0 to 19.9 +/- 2.9 mg/dL, P < 0.05) and 28% (1.37 +/- 0.10 to 0.99 +/- 0.11 mM/L, P < 0.05) below baseline values. ApoA-I concentrations were unchanged at 48 h postinfarct. At 192 h postinfarct, Lp(a) rebounded to 36% above baseline (24.9 +/- 3.0 to 33.9 +/- 3.9 mg/dL, P < 0.05), apoB returned to baseline (1.37 +/- 0.10 versus 1.33 +/- 0.11 g/L, P < 0.05) and apoA-I was 15% below baseline (1.43 +/- 0.06 to 1.21 +/- 0.06 g/L, not significant). Administration of tPA had no effect on any of these changes. CONCLUSIONS: Plasma Lp(a) and apolipoproteins undergo shifts from baseline values in the postinfarct period and tPA has no effect on these variations.

Lipoprotein(a) and apolipoproteins B and A-I after acute myocardial infarction. Publishing Authors By Initials

M Husain,PW Armstrong,PW Connelly,RA Hegele,

For similar enzymes and coenzymes: enzymes: hydrolases: peptide hydrolases: endopeptidases: serine endopeptidases: tissue plasminogen activator research abstracts see: enzymes and coenzymes: enzymes: hydrolases: peptide hydrolases: endopeptidases: serine endopeptidases: tissue plasminogen activator research

PUBMED ID PMID:

MEDLINE DATE:

Lipoprotein(a) and apolipoproteins B and A-I after acute myocardial infarction. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: The Canadian journal of cardiology

VOLUME: 11

Page Numbers: 206-10

Journal Abbreviation:

ISSN: 1916-7075

DAY: 3

MONTH: Mar

YEAR: 1995

Lipoprotein(a) and apolipoproteins B and A-I after acute myocardial infarction. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 8510280

Lipoprotein(a) and apolipoproteins B and A-I after acute myocardial infarction. Keywords Mesh Terms:

KEYWORDS: Tissue Plasminogen Activator

MESH TERMS: therapeutic use

Chemical & Substance for Abstract: Lipoprotein(a) and apolipoproteins B and A-I after acute myocardial infarction. Information

Substance Name: Tissue Plasminogen Activator

Registry Number: EC 3.4.21.68

Grant and Affiliation Information for Lipoprotein(a) and apolipoproteins B and A-I after acute myocardial infarction.

AFFILIATION: Department of Clinical Biochemistry, St Michael's Hospital, University of Toronto, Ontario.

Country: CANADA

AGENCY:

GRANT:

ACRONYM:

MEDLINETA: Can J Cardiol

REFSOURCE:

DATABASENAME:

ACCESSION NUMBER:

Number Hits: 0

Lipoproteina and apolipoproteins B and A-I after acute myocardial infarction Related Publications

• A Glimpse at HDL-based Therapy for Atherosclerosis.
• Abetalipoproteinemia: two case reports and literature review.
• Adaptation to visuomotor rotations in younger and older adults.
• Association between the -455T>C promoter polymorphism of the APOC3 gene and the metabolic syndrome in a multi-ethnic sample.
• Association between the FTO rs9939609 polymorphism and the metabolic syndrome in a non-Caucasian multi-ethnic sample.
• Clinical and genetic associations with hypertriglyceridemic waist in a Canadian aboriginal population.
• Common variants APOC3, APOA5, APOE and PON1 are associated with variation in plasma lipoprotein traits in Greenlanders.
• Effect of change in posture and exercise on repolarization in patients with long QT syndrome with HERG channel mutations.
• Efficacy and safety of pioglitazone in treatment of a patient with an atypical partial lipodystrophy syndrome.
• Emerging antidyslipidemic drugs.
• GCK and HNF1A mutations in Canadian families with maturity onset diabetes of the young (MODY).
• Gene-environment interactions in atherosclerosis.
• Gene-environment interactions in atherosclerosis: animal models.
• Genetic determinants of plasma lipoproteins.
• Genetics of metabolic syndrome.
• Genetics of metabolic syndrome: is there a role for phenomics?
• HIV-associated dyslipidaemia: pathogenesis and treatment.
• Heterozygous CAV1 frameshift mutations (MIM 601047) in patients with atypical partial lipodystrophy and hypertriglyceridemia.
• Human hepatocyte nuclear factor-1 beta (HNF1B) 1968A/G polymorphism.
• Is raising HDL a futile strategy for atheroprotection?
• Lipoprotein (a): an emerging risk factor for atherosclerosis.
• Lipoprotein(a) and apolipoproteins B and A-I after acute myocardial infarction.
• Lipoprotein(a) and fibrinolysis.
• Lipoprotein(a): biochemistry and genetics.
• Microsomal triglyceride transfer protein inhibition-friend or foe?
• Monogenic pediatric dyslipidemias: Classification, genetics and clinical spectrum.
• Phenomics, lamin A/C, and metabolic disease.
• Single nucleotide polymorphisms of the fukutin gene.
• Spectrum of HNF1A and GCK mutations in Canadian families with maturity-onset diabetes of the young (MODY).
• The failure of torcetrapib: what have we learned?