Can high levels of lipoprotein(a) (Lp(a)) cause hypertension (HTN)?

Elevated Lipoprotein(a) Does Not Cause Hypertension

High lipoprotein(a) levels do not cause hypertension, but the two conditions frequently coexist and may share common pathophysiological mechanisms involving endothelial dysfunction and oxidative stress. The available evidence demonstrates associations between elevated Lp(a) and hypertension rather than a causal relationship.

The Evidence on Lp(a) and Hypertension

The relationship between Lp(a) and blood pressure is correlative, not causal:

• A 2021 systematic review found limited data demonstrating an association between elevated Lp(a) and hypertension, with no mechanistic data establishing causality 1
• Approximately 30% of hypertensive patients have elevated Lp(a) levels, but this represents coexistence of two independent cardiovascular risk factors rather than one causing the other 1
• The NHLBI Working Group's comprehensive 2018 guidelines on Lp(a) do not identify hypertension as a consequence or mechanism of elevated Lp(a), focusing instead on atherosclerotic cardiovascular disease and aortic valve disease 2

Potential Shared Mechanisms (Not Causation)

While Lp(a) doesn't cause hypertension, both conditions may be linked through endothelial dysfunction:

• Elevated Lp(a) correlates with impaired endothelial function and oxidative stress in hypertensive patients, with significant correlations found between Lp(a) levels and nighttime blood pressure patterns (r=0.32 for systolic, r=0.30 for diastolic) 3
• Hypertensive patients show significantly higher Lp(a) concentrations (69-70 mg/dL) compared to normotensive controls (19 mg/dL), regardless of whether dyslipidemia is present 4
• The correlation between Lp(a) and blood pressure is further potentiated when oxidative stress is present (r=0.37 and r=0.40 for nighttime systolic and diastolic pressures, respectively) 3

Clinical Implications

The coexistence of elevated Lp(a) and hypertension creates compounded cardiovascular risk:

• The combination of elevated Lp(a) (>300 mg/L) with arterial hypertension was found to be the most important cardiovascular risk factor, exceeding the magnitude of gender, age, and the combination of hypertension with smoking 5
• Patients with both elevated Lp(a) and elevated LDL cholesterol face a 10-fold or higher risk of myocardial infarction 6
• Lp(a) contributes to cardiovascular disease through pro-inflammatory effects, pro-thrombotic mechanisms, and LDL-like atherogenic properties—not through blood pressure elevation 2

Important Clinical Pitfalls

• Do not attribute hypertension to elevated Lp(a)—treat hypertension according to standard guidelines based on blood pressure measurements and cardiovascular risk stratification
• Do not delay hypertension treatment while investigating Lp(a) levels—these are independent risk factors requiring separate management strategies
• Recognize that finding elevated Lp(a) in a hypertensive patient identifies a very high-risk individual who requires aggressive management of both conditions, with LDL-C targets <70 mg/dL 7, 6
• Consider measuring Lp(a) in hypertensive patients with premature cardiovascular disease, family history of premature CAD, or recurrent events despite optimal therapy 6, 8