The above letter is very timely. It presents data demonstrating that subjects with nonalcoholic fatty liver disease have increased atheroma mass, as demonstrated by an increased carotid intima-medial thickness (IMT) when compared to controls. Carotid IMT is another marker of atheroma progression. While abnormalities of flow-mediated vasodilation identify early mechanical abnormalities in the arterial wall, IMT tends to demonstrate later atherosclerotic structural abnormalities. Interestingly, an IMT < 0.87 mm carries a low odds ratio of coronary heart disease, and an IMT ≥ 1.10 carries a high odds ratio of coronary heart disease: IMTs found by these authors in their controls and subjects with NAFLD.1 Although no specific structural characterization of the increased IMT (fatty infiltration, fibrofatty disease, or fibrocalcific) is made by the authors, it would seem that these patients most likely will have fatty and fibrofatty infiltrates. The fatty atheroma components are amenable to therapy.
Therefore, patients with nonalcoholic fatty liver disease having either altered flow-mediated vasodilation or increased carotid IMT could be candidates for aggressive treatment of the liver disease, cholesterol lowering, and treatment of any related metabolic syndromes. This would help to modify and potentially decrease atheroma mass and progression.
These findings emphasize the importance of evaluating cardiovascular risk and cardiovascular disease in patients diagnosed with nonalcoholic fatty liver disease.