Key result
Elderly subjects with heterozygous familial hypercholesterolemia on prolonged statin therapy had a higher prevalence of moderate/severe aortic stenosis than controls (7.1% vs 1.1%; OR 8.33, p=0.03).
Why the study?
Hypercholesterolemia and statins are risk factors for aortic stenosis and vascular calcification, but whether subjects with heterozygous familial hypercholesterolemia treated with statins are at risk of aortic stenosis was unknown.
Do elderly subjects with HeFH on prolonged statin therapy have a higher prevalence of aortic valvular disease compared to relatives without HeFH?
Case-Control (n=205)
Do elderly subjects with HeFH on prolonged statin therapy have a higher prevalence of aortic valvular disease compared to relatives without HeFH?
Odds Ratio: 8.33
Absolute Event Rate: 7.1% vs 1.1%
p-value: p=0.03
Elderly subjects with HeFH on prolonged statin therapy have a significantly higher prevalence of aortic stenosis and valvular disease compared to controls, which is driven by life-long elevated LDLc exposure rather than the duration of statin treatment.
May warrant aortic valve surveillance in elderly HeFH; leaves open causal role of lifelong LDL exposure versus statins.
Hypercholesterolemia and statins are risk factors for aortic stenosis (AS) and vascular calcification, respectively. Whether heterozygous subjects with familial hypercholesterolemia (HeFH) treated with statins are at risk of AS is unknown. We study the prevalence of AS, aortic valve calcification (AoVC), and aortic sclerosis (ASc) in elderly subjects with HeFH in a prolonged statin treatment. Case-control study, cases were adults ≥65 years of age with a genetic diagnosis of HeFH, LDLc >220 mg/dl, and statin treatment ≥5 years. Controls were relatives of HeFH patients, with LDLc <190 mg/dl. Participants underwent a cardiac ultrasound for aortic valve analysis. We studied 205 subjects, 112 HeFH and 93 controls, with mean age 71.8(6.5) years and 70.0(7.3) years, respectively. HeHF, with respect to controls, presented greater gradients of aortic transvalvular pressure, 7.4(7.3) mmHg versus 5.0(2.8) mmHg, and maximum aortic velocity, 1.7(0.7) m/s versus 1.5(0.4) m/s, and lower aortic valve opening area, 2.0(0.7) cm2 versus 2.4(0.6) cm2 (all p < 0.05). AoVC and ASc were also more prevalent in HeFH (p < 0.05 between groups). Moderate/severe AS prevalence was higher among HeFH: 7.1% versus 1.1% (age- and sex-adjusted odds ratio (OR) 8.33, p = 0.03). Independent risk factors for aortic valve disease in HeFH were age and LDLc before treatment. The number of years under statin treatment was not associated with any aortic valve measurement. Subjects ≥65 years with HeFH in prolonged statin treatment show more aortic valvular disease and higher frequency of AS than controls. Life-long elevated LDLc exposure, rather than time of exposure to statins, explains this higher risk.
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Marco-Benedí et al. (2019) conducted a case-control in Heterozygous Familial Hypercholesterolemia (n=205). Heterozygous familial hypercholesterolemia (HeFH) with prolonged statin treatment vs. Relatives of HeFH patients with LDLc <190 mg/dl was evaluated on Moderate/severe aortic stenosis (OR 8.33, p=0.03). Elderly subjects with heterozygous familial hypercholesterolemia on prolonged statin therapy had a higher prevalence of moderate/severe aortic stenosis than controls (7.1% vs 1.1%; OR 8.33, p=0.03).
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