7 Elevated Lp(a): What Are the Risks? * Treatment strategy: Consider implementation of aggressive LDL-C lowering strategies in patients with elevated Lp(a). ** Treatment strategy: Maximally manage modifiable risk factors in patients with elevated Lp(a) by including more intensive control of lipids, blood pressure, and glycemic control. Of Note … Patients with elevated Lp(a) remain at increased ASCVD risk even when LDL-C is well controlled.7 The association of Lp(a) with ASCVD risk is independent of LDL-C and other cardiovascular risk factors, including among individuals with low LDL-C.7,22,23 People who have clinical CVD (including atherosclerosis-based cardiovascular diseases (ASCVD) such as acute coronary syndrome; stable angina or a history of MI or coronary or other arterial revascularization; stroke or transient ischemic attack; or PAD, including aortic aneurysm), are at higher risk for future events if Lp(a) is elevated. Elevated Lp(a) is also associated with onset16,17 and progression16 of CAVD, and progression to symptomatic heart failure.18 In the general population, Lp(a) levels ≥125 nmol/L (≥50 mg/dL) are associated with an approximately 20% increased risk of cardiovascular events: each 3.5-fold increase in Lp(a) is associated with a 16% increase of risk of events.14* People with borderline or slightly elevated LDL-C are three to four times more likely to have CVD events than those with low LDL-C.19 Lp(a) can pose increased risk for acute coronary syndrome when LDL-C is elevated.20** Lp(a): A Toolkit for Healthcare Professionals Elevated Lp(a) and LDL-C are independent and additive risk factors for ASCVD; a metaanalysis of statin trials showed risk in those with Lp(a) ≥125 nmol/L (≥50 mg/dL) was progressively attenuated at lower achieved levels of LDL-C.22 Elevated Lp(a) values represent an independent risk factor for ischemic stroke (more relevant in patients who have a stroke at a young age), PAD and aortic and mitral valve stenosis.21
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