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Elevated lipoprotein(a) and familial hypercholesterolemia in the coronary care unit: Between Scylla and Charybdis
Katrina L Ellis1,2, Jing Pang1, David Chieng3
1School of Medicine, University of Western Australia, Perth, Australia.
Insights
Elevated lipoprotein(a) (Lp[a]) and familial hypercholesterolemia (FH) are common in coronary care unit patients and increase premature coronary artery disease (CAD) risk, especially when combined.
Area of Science:
- Cardiology
- Genetics
- Lipidology
Background:
- Familial hypercholesterolemia (FH) and elevated lipoprotein(a) (Lp[a]) are inherited lipid disorders.
- Their prevalence, co-occurrence, and association with premature coronary artery disease (CAD) in coronary care unit (CCU) patients require definition.
Purpose of the Study:
- To determine the frequencies of elevated Lp(a) and FH in CCU patients.
- To investigate their independent and combined associations with premature CAD.
Main Methods:
- Measured plasma Lp(a) and LDL-C in consecutive CCU patients with acute coronary syndrome or prior CAD.
- Defined elevated Lp(a) as ≥0.5 g/L and FH phenotype as LDL-C ≥5 mmol/L.
- Used logistic regression to assess the relationship with premature CAD (age <60 years).
Main Results:
- Elevated Lp(a) and FH were found in 27.0% and 11.6% of 316 patients, respectively.
- Both conditions were more frequent in patients with premature CAD (32.0% and 15.5%) compared to others.
- Elevated Lp(a) alone, FH alone, and their combination increased premature CAD risk by 1.9, 3.2, and 5.3-fold, respectively.
Conclusions:
- Elevated Lp(a) and FH are common in CCU patients and associated with premature CAD.
- The combination of elevated Lp(a) and FH significantly elevates CAD risk.
- Routine screening for elevated Lp(a) and FH is recommended for CCU patients.
Background:
Elevated lipoprotein(a) (Lp[a]) and familial hypercholesterolemia (FH) are inherited lipid disorders. Their frequencies, coexistence, and associations with premature coronary artery disease (CAD) in patients admitted to the coronary care unit (CCU) remain to be defined.
Hypothesis:
Elevated Lp(a) and FH are commonly encountered among CCU patients and independently associated with increased premature CAD risk.
Methods:
Plasma Lp(a) concentrations were measured in consecutive patients admitted to the CCU with an acute coronary syndrome (ACS) or prior history of CAD for 6.5 months. Elevated Lp(a) was defined as concentrations ≥0.5 g/L. Patients with LDL-C ≥ 5 mmol/L exhibited phenotypic FH. Premature CAD was diagnosed in those age < 60 years, and the relationship between this and elevated Lp(a) and FH was determined by logistic regression.
Results:
316 patients were screened; 163 (51.6%) had premature CAD. Overall, elevated Lp(a) and FH were identified in 27.0% and 11.6% of patients, respectively. Both disorders were detected in 4.4% of individuals. Elevated Lp(a) (32.0% vs 22.2%; P = 0.019) and FH phenotype (15.5% vs 8.0%; P = 0.052) were more common with premature vs nonpremature CAD. Elevated Lp(a) alone conferred a 1.9-fold, FH alone a 3.2-fold, and the combination a 5.3-fold increased risk of premature CAD (P = 0.005).
Conclusions:
Elevated Lp(a) and phenotypic FH were commonly encountered and more frequent with premature CAD. The combination of both disorders is especially associated with increased CAD risk. Patients admitted to the CCU with ACS or previously documented CAD should be routinely screened for elevated Lp(a) and FH.
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