Lipoprotein A also called “LP little a”, is a known marker for cardiovascular disease. Patients with high Lp(a) levels are at increased risk (up to 4x) from stroke or heart attack. Lp(a) levels are genetically determined and don’t significantly fluctuate with dietary/lifestyle changes. About 20% of the population has elevated levels of Lp(a). Compared to other forms of cholesterol such as LDL cholesterol, Lp(a) is linked to increased inflammation, atherosclerosis, and arterial thrombosis.
While LP(a) is clearly linked to increased to cardiovascular disease, it is still unclear if it is directly causal or just a marker for disease. It is not yet established whether reducing Lp(a) actually prevents future cardiovascular disease. Currently there is no FDA approved therapy for elevated Lp(a). PCSK9 inhibitors can reduce Lp(a) levels, but it is still unclear if this effect is strong enough to reduce disease apart from the cholesterol reduction (note: PCSK9 inhibitors are not FDA approved to lower Lp(a)).
In patients with elevated LP(a), it should be considered a risk enhancing factor for future atherosclerotic disease and may help shift patient-physician risk discussions toward favoring initiation of statin therapy. Current paradigms for treatment of elevated Lp(a) suggest aggressive risk factor modification. While it has been postulated the aspirin may be beneficial in a primary prevention setting, there is no clear consensus on routine use of aspirin in this setting. There is a genetic subtype of Lp(a) carries (rs-3798220-C) which may benefit from aspirin use.
There are several ongoing trials to determine if directly treating LP(a) levels will reduce cardiovascular disease. One trial sponsored by Novartis is called HORIZONS and another from Amgen is called OCEAN.
