Lipoprotein(a) as a Predictor of Cardiovascular Disease in a Prospectively Followed Cohort of Patients With Type 1 Diabetes
- Barbara Kollerits, MPH1,
- Martin Auinger, MD2,
- Veronika Reisig, MD3,
- Thomas Kästenbauer, PHD, MSC2,
- Arno Lingenhel, PHD1,
- Karl Irsigler, MD2,
- Rudolf Prager, MD2 and
- Florian Kronenberg, MD1
- 1Division of Genetic Epidemiology, Innsbruck Medical University, Innsbruck, Austria
- 2Hospital Vienna-Lainz, Vienna, Austria
- 3Institute of Epidemiology, GSF, Neuherberg, Germany
- Address correspondence and reprint requests to Florian Kronenberg, MD, Division of Genetic Epidemiology, Schöpfstr. 41, A-6020, Innsbruck, Austria. E-mail: florian.kronenberg{at}i-med.ac.at
- CVD, cardiovascular disease
- eGFR, glomerular filtration rate
- ESRD, end-stage renal disease
- Lp(a), lipoprotein(a)
Lipoprotein(a) [Lp(a)] concentrations are genetically determined (1,2), and numerous epidemiological studies in the general population have identified elevated Lp(a) levels as a risk factor for atherosclerotic disorders (3,4). However, this association is not as clearly defined in patients with type 1 diabetes (5), since large prospective studies are missing. We therefore analyzed the role of Lp(a) for the incidence of cardiovascular disease (CVD) complications.
RESEARCH DESIGN AND METHODS
The 429 consecutive, unrelated type 1 diabetes patients included in this observational study were from the Hospital Lainz-Vienna. Inclusion criteria described recently (6) were regular attendance at the outpatient clinic in the last year and stable metabolic control. For patient characteristics, see Table 1. The recruitment period lasted from 1993 to 1999. Regular follow-ups were performed every 3–6 months. Yearly follow-ups included detailed history, laboratory parameters, measurement of peripheral and autonomic neuropathy, staging of retinopathy, and feet inspection.
Previous CVD complications were obtained by self reports verified from hospital records. Patients’ blood was drawn after an overnight fast. Lp(a) quantification was carried out, as described in detail (7). Apolipoprotein(a) phenotyping was performed by SDS agarose gel electrophoresis (8). Glomerular filtration rate (eGFR) was calculated from the Modification of Diet in Renal Disease equation (9).
A composite CVD end point during follow-up was defined as coronary artery disease, cerebrovascular disease, and …
