The report by Johnsen and colleagues details the changes in plaque composition and size as defined by duplex ultrasound at 2 time points 7 years apart
The report by Johnsen and colleagues details the changes in plaque composition and size as defined by duplex ultrasound at 2 time points 7 years apart. A multivariate analysis showed an independent relationship between high-density lipoprotein (HDL) cholesterol and plaque size and composition. The results suggest that high levels of HDL cholesterol inhibit the accumulation of lipids in common carotid plaques.
These results further support the beneficial role HDL cholesterol plays in retarding the growth of complex atheroma and raise the question of whether active therapy to increase HDL cholesterol is worthwhile in presymptomatic atherosclerosis. However, these data do not answer this question, nor do they support the hypothesis that HDL cholesterol leads to “plaque regression” (as opposed to retarding plaque growth). Furthermore, the study does not address the effect of HDL cholesterol levels on advanced or symptomatic atheromatous lesions.
The prospective population-based nature of the Tromsø study makes the findings of particular interest, but there are significant limitations to this study, including the limited follow-up, acknowledged by the authors. More important, however, is the fact that the study design rests on 2 isolated observations 7 years apart, with no data (particularly on HDL cholesterol levels) in between. Lack of interim information on cholesterol levels (either HDL or low-density lipoprotein cholesterol) severely limits any conclusions.
Medical treatment of atherosclerotic plaque remains a goal of all physicians treating patients with vascular disease. Most clinicians feel this will be most effective when plaque is at an early, presymptomatic state. This study suggests that higher levels of HDL cholesterol are associated with less plaque progression. It should be noted, however, that 70% of plaques in the study population showed progression over the 7-year period, not a surprising finding. This shows the limited influence of any single factor on plaque progression.
Strategies to increase HDL cholesterol remain elusive. Pharmacologic manipulation in large populations of presymptomatic patients, although attractive, would be expensive and might be associated with morbidity. In addition, the influence of therapy on symptoms of coronary or cerebral atherosclerosis, although intuitive, needs to be proven. The findings of Johnsen and colleagues clearly emphasize the need to focus on HDL cholesterol levels as a goal of risk factor reduction. How this can be applied clinically remains to be elucidated.