Nick S R Lan1, Dick C Chan2, Jing Pang2, P Gerry Fegan3, Bu B Yeap4, James M Rankin5, Carl J Schultz6, Gerald F Watts6, Damon A Bell7. 1. Department of Endocrinology and Diabetes, Fiona Stanley Hospital, Perth, WA, Australia; Department of Cardiology, Fiona Stanley Hospital, Perth, WA, Australia. Electronic address: nick.lan@health.wa.gov.au. 2. Medical School, The University of Western Australia, Perth, WA, Australia. 3. Department of Endocrinology and Diabetes, Fiona Stanley Hospital, Perth, WA, Australia; Medical School, Curtin University, Perth, WA, Australia. 4. Department of Endocrinology and Diabetes, Fiona Stanley Hospital, Perth, WA, Australia; Medical School, The University of Western Australia, Perth, WA, Australia. 5. Department of Cardiology, Fiona Stanley Hospital, Perth, WA, Australia. 6. Medical School, The University of Western Australia, Perth, WA, Australia; Departments of Internal Medicine and Cardiology, Royal Perth Hospital, Perth, WA, Australia. 7. Medical School, The University of Western Australia, Perth, WA, Australia; Departments of Internal Medicine and Cardiology, Royal Perth Hospital, Perth, WA, Australia; Department of Clinical Biochemistry, PathWest Laboratory Medicine WA, Royal Perth and Fiona Stanley Hospitals, Perth, WA, Australia; Department of Biochemistry, Clinipath Pathology, Perth, WA, Australia.
Abstract
INTRODUCTION: Lipoprotein(a) [Lp(a)] and diabetes are independently associated with premature coronary artery disease (pCAD). However, there is an inverse relationship between Lp(a) concentration and type 2 diabetes (T2D) risk. We examine whether Lp(a) distribution in patients with pCAD differs between those with or without T2D, and whether elevated Lp(a) is associated with pCAD in patients with T2D. METHODS: Lp(a) concentration was measured in consecutive acute coronary syndrome (ACS) patients in two coronary care units (study one: ACS with or without diabetes, study two: ACS and diabetes). Elevated Lp(a) mass concentration was defined as ≥0.5 g/L and pCAD where CAD was diagnosed age <60 years. The association between elevated Lp(a) and pCAD was assessed using logistic regression. RESULTS: Of 449 patients, 233 (51.9%) had pCAD and 278 (61.9%) had T2D. In patients with pCAD, those with T2D had a significantly lower median Lp(a) concentration (0.13 g/L versus 0.27 g/L, p=0.004). In patients with T2D, elevated Lp(a) was significantly associated with pCAD (OR 2.419, 95% CI 1.513-3.867, p<0.001). After adjusting for gender, smoking, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol and triglycerides, elevated Lp(a) remained significantly associated with pCAD (OR 2.895, 95% CI 1.427-5.876, p=0.003) in patients with T2D. CONCLUSIONS: In coronary care patients with pCAD, patients with T2D had lower Lp(a) concentrations than those without T2D. Despite this, elevated Lp(a) remained predictive of pCAD in patients with T2D. Measurement of Lp(a) should be considered in younger adults with T2D to identify who may benefit from earlier preventative therapies to reduce pCAD burden.
INTRODUCTION:Lipoprotein(a) [Lp(a)] and diabetes are independently associated with premature coronary artery disease (pCAD). However, there is an inverse relationship between Lp(a) concentration and type 2 diabetes (T2D) risk. We examine whether Lp(a) distribution in patients with pCAD differs between those with or without T2D, and whether elevated Lp(a) is associated with pCAD in patients with T2D. METHODS:Lp(a) concentration was measured in consecutive acute coronary syndrome (ACS) patients in two coronary care units (study one: ACS with or without diabetes, study two: ACS and diabetes). Elevated Lp(a) mass concentration was defined as ≥0.5 g/L and pCAD where CAD was diagnosed age <60 years. The association between elevated Lp(a) and pCAD was assessed using logistic regression. RESULTS: Of 449 patients, 233 (51.9%) had pCAD and 278 (61.9%) had T2D. In patients with pCAD, those with T2D had a significantly lower median Lp(a) concentration (0.13 g/L versus 0.27 g/L, p=0.004). In patients with T2D, elevated Lp(a) was significantly associated with pCAD (OR 2.419, 95% CI 1.513-3.867, p<0.001). After adjusting for gender, smoking, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol and triglycerides, elevated Lp(a) remained significantly associated with pCAD (OR 2.895, 95% CI 1.427-5.876, p=0.003) in patients with T2D. CONCLUSIONS: In coronary care patients with pCAD, patients with T2D had lower Lp(a) concentrations than those without T2D. Despite this, elevated Lp(a) remained predictive of pCAD in patients with T2D. Measurement of Lp(a) should be considered in younger adults with T2D to identify who may benefit from earlier preventative therapies to reduce pCAD burden.