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03-10-2011 | Stroke | Article

PRoFESS follow-up adds to ‘obesity paradox’ debate


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MedWire News: An analysis of patients in the PRoFESS trial appears to support the existence of the "obesity paradox" in patients with stroke who are at risk for vascular events, but the authors of an accompanying editorial dispute the claim.

"The idea that a known risk factor somehow transforms into a 'protective' agent after an occurrence of a vascular clinical event - the obesity paradox - is both surreal and troubling," say the editorialists - Michael Katsnelson and Tatjana Rundek (University of Miami, Florida, USA).

The research study, by Bruce Ovbiagele (University of California, San Diego, USA) and team looked at outcomes among 20,332 ischemic stroke patients in the PRoFESS (Prevention Regimen for Effectively Avoiding Second Strokes) trial, during 2.5 years of follow-up. In all, 24% of these patients were obese, defined as a body mass index (BMI) of at least 30 kg/m2 for non-Asian patients and 27.5 kg/m2 for Asian patients.

The cumulative rate of recurrent stroke was 8.89% in the obese patients and 9.06% in 600 lean patients (BMI ≤25 kg/m2 for non-Asians, 23 kg/m2 for Asians), the researchers report in the journal Stroke. This difference was not statistically significant after accounting for multiple confounders.

The researchers note that "perhaps the most plausible" explanation for the lack of effect of obesity on recurrent stroke risk is that the effect is mitigated by the introduction of secondary preventive medications.

Katsnelson and Rundek echo this viewpoint, saying: "More aggressive or frequent follow-up care may have been bestowed on corpulent stroke survivors simply due to them 'looking' like they were more at risk."

However, cumulative rates of a composite vascular endpoint of stroke, myocardial infarction, or vascular death were lower in the obese than lean patients, at 12.74% versus 14.47%, and this difference was significant on multivariate analysis. Overweight patients were also less likely than lean patients to meet the composite vascular endpoint.

Ovbiagele et al say that this supports the obesity paradox, but suggests that it has a cardiovascular, rather than cerebrovascular basis.

But Katsnelson and Rundek argue that by focusing the study design on obese patients with stroke, the researchers selected those in whom other stroke risk factors have a smaller impact relative to that in nonobese patients.

"Because we just implicitly selected our obese group to have a smaller nonadipose stroke risk burden by conditioning on the initial stroke, it seems reasonable that this lesser risk will lead to a smaller ensuing event rate," say the editorialists. "This leads to a surprising and paradoxical 'protective' effect of obesity and serves as a good example of an index event bias."

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By Eleanor McDermid