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Patients with low LDL still demonstrated CAD progression

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Residual risk factors in patients with low LDL levels were associated with the likelihood of coronary artery disease, according to study findings.

A total of 3,437 patients with CAD underwent serial IVUS examination in seven clinical trials. Those who achieved an on-treatment LDL level ≤70 mg/dL (n=951) were categorized as progressors (≥5% increase in percent atheroma volume; n=200) or nonprogressors (n=751), and then they were compared.

CAD continued to progress in >20% of patients despite an LDL level ≤70 mg/dL. Progressors demonstrated higher baseline levels of glucose (117.1 ± 42.5 mg/dL vs. 112.1 ± 40 mg/dL; P=.02), triglycerides (157.5 mg/dL vs. 133 mg/dl, P=.004), and a smaller decrease of apolipoprotein B (–25.1 ± 3.4 mg/dL vs. 27.4 ± 3.35 mg/dL; P=.01) at follow-up. Multivariable analysis revealed that atheroma volume (P<.001), the presence of diabetes mellitus (P=.02), increase in systolic BP (P<.001), less increase in HDL (P=.01) and a smaller decrease in apolipoprotein B levels (P<.001), but not changes in C-reactive protein or LDL, were independently associated risk factors for progression.

“While achieving a very low LDL level is essential for CV prevention, the greatest impact is likely to be derived from the use of a combination of lifestyle and pharmacological therapies that reduce global risk by targeting multiple risk factors,” the researchers concluded. “These findings further highlight the multifactorial nature of atherosclerotic CVD and the ongoing need to improve current risk marker strategies.”

Basil S. Lewis, MD,and David A. Halon, MB, both of Lady Davis Carmel Medical Center in Haifa, Israel, wrote in an accompanying editorial that the findings suggest the fight to halt and reverse the pathology and progression of atherosclerotic vascular disease is on the right track.

“The findings redefine and confirm therapeutic targets beyond LDL lowering on which to focus if we are to halt progression of atheromatous disease,” they wrote.

Bayturan O. J Am Coll Cardiol. 2010;55:2736-2742.

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