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Published on: October 12, 2017
Lipoprotein(a) Does Not Correlate with Hypertensive Mediated Organ Damage and Subsequent Cardiovascular Events in a
Chiara Tognola1, Davide Paolo Bernasconi2,3, Paola Rebora2,4
1Cardiology 4, ASST GOM Niguarda, Milan, Italy.
Insights
Elevated lipoprotein(a) [Lp(a)] did not correlate with organ damage or cardiovascular events in primary prevention patients. This study found no association between high Lp(a) levels and heart, vessel, or kidney damage, nor with mortality.
Area of Science:
- Cardiology
- Preventive Medicine
- Lipidology
Background:
- Elevated lipoprotein(a) [Lp(a)] is linked to cardiovascular risk.
- Association with Hypertension Mediated Organ Damage (HMOD) and CV events in primary prevention is unclear.
Purpose of the Study:
- Evaluate correlation between Lp(a) levels and HMOD (heart, vessels, kidney).
- Assess relationship between Lp(a) and CV events/all-cause mortality in primary prevention.
Main Methods:
- Recruited 747 low CV risk subjects.
- Assessed HMOD via Pulse Wave Velocity, carotid IMT, plaques, LVH, EF, GFR.
- Tracked CV events and mortality for a median of 10 years.
Main Results:
- No significant correlation found between Lp(a) levels and subclinical HMOD indices.
- No relationship identified between Lp(a) levels and CV events or all-cause mortality.
- Prevalence of hypertension (37.9%), dyslipidemia (67.2%), smoking (17.8%), and diabetes (8.7%) noted.
Conclusions:
- In primary prevention, elevated Lp(a) is not associated with significant HMOD.
- High Lp(a) levels did not correlate with increased CV events or all-cause mortality in this cohort.
Introduction:
Elevated lipoprotein(a) [Lp(a)] levels have been strongly related to cardiovascular (CV) risk. However, its association with Hypertension Mediated Organ Damage (HMOD) and CV events in the primary prevention setting remains unclear.
Aim:
To evaluate in these patients, the correlation between Lp(a) levels and: (i) heart, vessels and kidney HMOD and; (ii) CV events and all-cause mortality in a primary prevention setting.
Methods:
747 low CV risk subjects were recruited between 2009 and 2014. HMOD was assessed through Pulse Wave Velocity, carotid Intima-Media Thickness (IMT), presence of carotid plaques, Left Ventricular Hypertrophy (LVH) and Ejection Fraction and glomerular filtration rate. All-cause mortality and CV events up to 2021 were retrieved by electronic health records, for a median follow-up time of 10 years (I-III quartiles 9.6-11.1).
Results:
Mean age was 50.8 ± 13.0 years and 63.5% of the subjects were men. The prevalence of hypertension was 37.9%, dyslipidemia 67.2%, smoking 17.8%, and diabetes mellitus 8.7%. Median Lp(a) value was 17 mg/dL (5.9-56.0), and 26.5% of patients had values above 50 mg/dL. Regarding HMOD, 10.3% subjects had arterial stiffness, 7.2% increased IMT, 19.8% carotid plaques while only 0.7% had LVH. No significant correlation was found between Lp(a) levels and indices of subclinical HMOD. Furthermore, no relationship was found between CV events and all-cause mortality and Lp(a) levels.
Conclusions:
In this primary prevention cohort, elevated Lp(a) levels were not associated with significant structural damage to the heart, carotid arteries, or increased aortic stiffness and were not associated with CV events and all-cause mortality.
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