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Familial hypercholesterolemia associated with high risk for aortic valve calcification
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A new study highlights a high prevalence and large extent of aortic valve calcification in patients with heterozygous familial hypercholesterolemia.
The study included 145 asymptomatic patients with heterozygous familial hypercholesterolemia (HeFH; 93 men; mean age, 52 years) and 131 participants with nonanginal chest pain and without HeFH. The data were collected from February 2008 to June 2011 for patients with HeFH and from November 2006 to January 2011 for the control group.
Aortic valve calcification was defined as calcium at the aortic valve leaflets. Calcium levels were measured by Agatston units. The researchers also measured coronary artery calcification and LDL receptor mutation status.
The overall prevalence of aortic valve calcification was 41% in the HeFH group compared with 21% in the control group (P < .001). The median aortic valve calcification score was also higher among patients with HeFH: 51 (interquartile range, 9-117) vs. 21 (IQR, 3-49; P for comparison = .007).
The relationship between CAC and aortic valve calcification varied, according to the researchers. Higher aortic valve calcification scores were linked to the presence of CAC in the HeFH and control groups, but CAC was present without aortic valve calcification in more than 39% of patients.
Forty-one percent of the 145 patients with HeFH had LDL mutations without residual function (LDLR-negative mutations). These patients had higher levels of total cholesterol, LDL and maximum untreated LDL compared with patients with LDLR-defective mutations. In addition, these patients tended to be younger, started statin therapy at an earlier age and had a longer duration of statin use.
The data also revealed an independent association between aortic valve calcification and age, CAC, diastolic BP and maximum untreated LDL. The strongest predictor of aortic valve calcification score was LDLR-negative mutational HeFH (OR = 4.81; 95% CI, 2.22-10.4; P < .001).
“The prevalence and extent of subclinical aortic valve calcification are clearly increased in patients with HeFH, especially in those carrying LDLR-negative mutations,” Gert-Jan R. ten Kate, MD, from the department of radiology at Erasmus Medical Center, Rotterdam, the Netherlands, and colleagues wrote.
The researchers called for more studies on the effectiveness of statin use in this population.
In an accompanying editorial, Nalini M. Rajamannan, MD, from the Most Sacred Heart of Jesus Cardiology and Valvular Institute in Sheboygan, Wisconsin, and the department of molecular biology and biochemistry at Mayo Clinic in Rochester, Minnesota, wrote, “the present study is the first to combine biochemical analysis with genetic LDL receptor function and the calcifying phenotype in the heart. The study further confirms the hypothesis regarding the possible modification and slowing of calcific aortic valve disease progression with the use of long-term lipid lowering if the therapy is initiated in the early stages of preclinical calcific aortic valve disease, the atherosclerotic phase.” – by Tracey Romero
Disclosure: The study was supported by a grant from the Dutch Heart Foundation and the Interuniversitair Cardiologisch Instituut Nederland. One researcher reports consulting for Bracco Diagnostics and another researcher reports receiving research support from Bayer Healthcare, GE Healthcare and Siemens Medical Solutions. Rajamannan is an inventor on a patent for methods to slow progression of aortic valve disease; the patent is owned by Mayo Clinic, with no royalty payments to the inventor.
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